Podcasts about allopurinol

Shocked to find that Gout reared its ugly head yet again despite taking Allopurinol daily for the past few years, the reason is Aspartame. Aspartame cancels out the effectiveness of Allopurinol.

On this episode of the Top 200 Drugs pharmacology podcast, I cover fluticasone nasal spray, allopurinol, alendronate, famotidine, and cefdinir. Fluticasone is a corticosteroid that can be used nasally for the treatment of allergic rhinitis. Allopurinol is a xanthine oxidase inhibitor used to reduce uric acid and prevent gout flares. Alendronate is a bisphosphonate that inhibits the action of osteoclasts. This action helps treat osteoporosis. Famotidine is a histamine-2 receptor antagonist that helps reduce gastric acid secretion and alleviate heartburn symptoms. Cefdinir is a third-generation cephalosporin that is often used as an alternative for those who cannot take penicillin antibiotics. There is a small risk for cross-reactivity that a clinician has to consider.

Gibt es Belege für die Entität "verschleppter Infekt"? Was soll das sein? Und: Sport beim Infekt - macht das eine Myocarditis? Heavy Metal und Erkältung: Wozu Zink? Workload in der Primärversorgung: Geteiltes Leid ist doppelte Freude. Eine Simulation zum Workload von Einzelkämpfern vs Team-Praxen. Ein Modell für Deutschland?

Découvrez en 10 minutes avec Dr Didier POIVRET, rhumatologue, l'essentiel à savoir concernant la goutte en MG. ✅ Comment traiter une crise de goute en 2024 ? ✅ Quand et comment introduire un traitement de fond hypouricémiant par Allopurinol ? ✅ Chez qui demander le typage HLA B 508 ? ✅ Quand adresser le malade au rhumatologue ou néphrologue ? ✅ Que sait-on de nouveau sur la goutte en 2024 que vous devriez connaître en MG ? Les RÉPONSES du CAS CLINIQUE (COMMENTÉES EN VIDEO par Dr POIVRET ), cliquez-ici

Dr Dave updates Dr Jo about superficial venous thrombosis, ACE inhibitors and angioedema, scabies treatment with Ivermectin, complications with use of Allopurinol, pain relief in leg ulcers, ethical issues around breast screening, and the complementary use of light piano music and topical hop cream.

Allopurinol hypersensitivity syndrome (AHS) affects approximately 1 in 1,000 patients prescribed allopurinol, with reported mortality rates between 20% and 25%. The risk of AHS is nearly 100 times higher in carriers of the HLA-B*58:01 allele than in noncarriers. Populations with a high allele frequency include Han Chinese (6%-8%), Korean (12%), and Thai (6%-8%) people.In this episode, Drs. Wid Yaseen and Jonathan Zipursky discuss their paper published in CMAJ, titled "Five things to know about…allopurinol hypersensitivity syndrome". Dr. Jonathan Zipursky is a general internist, clinical pharmacologist, and clinician scientist at Sunnybrook Health Sciences Centre. Dr. Yaseen is a second-year internal medicine resident physician at the University of Toronto. They argue that the syndrome's frequency is often underestimated and emphasize the importance of genetic testing in susceptible populations.Next, Dr. David Juurlink broadens the discussion beyond allopurinol to describe other common medications whose effectiveness and safety are significantly influenced by genetic predispositions. Dr. Juurlnk is a staff internist and head of division of clinical pharmacology and toxicology at Sunnybrook Health Sciences Centre in Toronto. He is also a medical toxicologist at the Ontario Poison Centre.  He explores the need for expanded genetic testing to protect patients and ensure proper dosing.Join us as we explore medical solutions that address the urgent need to change healthcare. Reach out to us about this or any episode you hear. Or tell us about something you'd like to hear on the leading Canadian medical podcast.You can find Blair and Mojola on Twitter @BlairBigham and @DrmojolaomoleCMAJTwitter (in English): @CMAJ Twitter (en français): @JAMC FacebookInstagram: @CMAJ.ca The CMAJ Podcast is produced by PodCraft Productions

Welcome to The Hormone Prescription Podcast, where we empower midlife women to live their best lives through balancing their hormones, understanding their bodies, and unlocking the potential for optimal health!   In today's episode, we're thrilled to have Dr. Richard Johnson as our special guest. Dr. Johnson is a practicing physician and a Professor of Medicine at the University of Colorado. With over 25 years of research experience, he is an international expert on sugar as well as uric acid and its role in obesity and diabetes. Dr. Johnson has recently authored the book "Nature Wants Us to be Fat", which dives into the intriguing story of why we are becoming obese and what we can do about it.   Episode Highlights: Introducing Dr. Richard Johnson: Discover the extensive background and expertise of today's guest, Dr. Richard Johnson. The Role of Sugar and Uric Acid: Learn how these two factors play a significant role in obesity, and how modern diets have contributed to the current obesity epidemic. How Hormones Affect Weight Gain: Understand the connection between hormonal imbalances and weight gain, and what midlife women can do to regain control. Impact of Stress on Weight: Dr. Johnson explains how stress impacts our bodies and can lead to weight struggles. Preventing & Reversing Weight Gain: Learn simple yet powerful dietary and lifestyle changes that can help prevent and even reverse obesity and diabetes. A Brief Look at Dr. Johnson's Book: Dr. Johnson shares some insights from his latest book "Nature Wants Us to be Fat" and discusses how it can help midlife women in their journey to better health. We hope you enjoy this insightful conversation with Dr. Richard Johnson, which provides not only a deeper understanding of the surprising science behind weight gain but also practical advice on how to prevent and reverse it.    Don't forget to subscribe, rate, and review our podcast on your preferred platform to stay updated with new episodes.   (00:00): The only good thing about a donut is the whole Jack Le Lane. Today we're gonna talk about the science behind how sugar is not food, but poison. Thank you, Robert Lustig. (00:14): So the big question is, how do women over 40 like us keep weight off, have great energy, balance our hormones and our moods, feel sexy and confident, and master midlife? If you're like most of us, you are not getting the answers you need and remain confused and pretty hopeless to ever feel like yourself Again. As an ob gyn, I had to discover for myself the truth about what creates a rock solid metabolism, lasting weight loss, and supercharged energy after 40, in order to lose a hundred pounds and fix my fatigue, now I'm on a mission. This podcast is designed to share the natural tools you need for impactful results and to give you clarity on the answers to your midlife metabolism challenges. Join me for tangible, natural strategies to crush the hormone imbalances you are facing and help you get unstuck from the sidelines of life. My name is Dr. Kyrin Dunston. Welcome to the Hormone Prescription Podcast. (01:08): Hi everybody. Welcome back to another episode of the Hormone Prescription with Dr. Kyrin.. Thank you so much for joining me today. My guest today is Dr. Richard Johnson, and he loves fat. I know you don't, but he does, and it's a good thing because he is been studying it for years and he's got some epic information to share with you about why nature wants us to be fat, the surprising science behind why we gain weight and how to prevent and reverse it. And he's done the research. He loves research. He went into medicine because he wanted to figure out what was causing diseases and treat the reason why we had diseases, not just medicate them with drugs and surgery. So he's a doctor after my own heart. He is an internal medicine doctor. He is also trained in nephrology and infectious disease, and he's an avid researcher. (02:02): So he has a book. Nature Wants Us to Be Fat. We're gonna talk about it today. We're gonna dive into some of the details about sugar and really how bad it is, and you can't hear about this enough. And the ways in which, which types of sugar contribute to overweight and obesity, how you can mitigate these types of sugar in your diet, how your water and hydration status, your salt status, your uric acid status, all affect these, how menopause is associated with insulin resistance. And these link into these other factors. So before I get too technical, I'm gonna bring in Dr. Richard Johnson, who is the researcher. And he, I love the way he describes these things. He tells it almost like a story with a plot and a murder mystery. And I love a good murder mystery. So you're gonna love hearing him talk because he really has a passion for the science behind what makes us overweight and why nature is conspiring to make us overweight. (03:02): And he's really going to spell it out for you and give you some practical, actionable tips. I know you want those. He's got 'em. And I've already told you a little bit about him. Let me just check out his bio and see if there's anything else important that you need to know. He is a professor of medicine at University of Colorado. He does practice medicine, but he really loves research and he is done it for more than 25 years. He is an international expert on sugar and uric acid and its role in obesity, their role in obesity and diabetes. He is book is Nature, wants us to Be Fat. It tells the story of why we are becoming obese and what to do about it becoming, I mean, we're kind of in the the era of epidemic obesity. So we're in it, folks, and if you wanna get out, then you wanna listen to Doctor Rick as he likes to be called. (03:55): Thank you Kyrin. It's wonderful. We'll be on your show. (03:58): I'm so excited to have you here talking about one of my favorite topics, fat, right? What woman doesn't love talking about fat and how to get rid of it. And we're gonna dive into why nature is conspiring against us to make us fat. And the surprising science, why we gain weight and how to prevent and reverse it. But first, I always like to get some type of background for everybody listening. Why are you so passionate about this? How did that happen? You come from an internal medicine background, also nephrology, infectious disease. So how did you become fascinated with that? (04:34): Well, it began when I was becoming a doctor, I just really have been interested in the causes of disease even more so than the treatment of disease. And my, I come from a family where there've been a lot of scientists. And so I, you know, from the very beginning, I always was wondering, why do they have diabetes? Why do they have this condition or that, as opposed to just giving them insulin and having them come back to see you in clinic, you know? And so very early on I started my research career and I was very, I initially, I studied high blood pressure and high blood pressure, as you know, is linked with obesity. And it's linked with insulin resistance. And one thing led to another. And over the last 20 some years, over 30 years, actually, I've been doing research and probably about half of my time is doing research from the basic laboratory to animals in the wild to studies of people. And I've been a very active researcher, but I also have a clinical practice. I see people treat people. And so I have kind of a, I try to do both, both ends of the spectrum. Yeah. (05:44): You know, it reminds me of that Hippocrates quote. Oh gosh. Somebody shared it in one of the podcast episodes recently about the goal of good medicine is to make you not need it. And so you came into this field thinking that you were more interested in why people got disease. Wh if we can figure out why they get it and fix the why, then they won't get it Right (06:09): Ex. Exactly. It's much more effective, it's a much more effective way of helping people. And you know absolutely. That's been the main driver I've been studying, particularly got interested in this thing called the metabolic syndrome, where people develop obesity and pre-diabetes and high blood pressure. And it seems to be the precursor for just about, you know, many of the diseases that are affecting us today. So, you know, when I would go on, when I go on the ward, you know, the residents would come up to me and say, you know, well we have a patient with diabetes and hypertension and heart disease and gout and fatty liver. And, and it's just kind of like a litany of these common diseases. And I believe they're all linked. And so my research took me into diet and into nutrition and into what was it in the diet that triggers these changes that we're seeing? (07:08): And I was particularly puzzled by the fact that in 1900, only one in 30 people were obese. Only one in 50,000 had diabetes. It was like diabetes was almost unheard of. High blood pressure was seen in less than 5% of the population. Heart disease really hadn't even been described. The coronary artery disease wasn't described till 1910. And so, you know, there were only 500 cardiologists in the entire United States in 1940. I mean, it was just not a very common problem. But today, you know, it's just gone crazy. So the question is, you know, why, why did this increase? And obviously the biggest thought has been its relates to diet. And, and then that, that led me to, to my research. (07:59): Right? And those are some very sobering statistics. Nowadays, hypertension, diabetes, coronary artery disease are so commonplace that we consider it normal. It's part of our normal vocabulary. But you're right, what a hundred, just over a hundred years ago, these were kind of anomalies, but now we consider them common. And I'll go ahead and plug in my hormones because it's the same when it comes to menopause. You know, over a hundred years ago, women didn't live any significant amount of time in menopause. So it really wasn't an issue. Now that our lifespan has increased due to medical advances and improved healthcare, we will live some, sometimes a third to a half of our life in menopause in a state of what I call hormonal poverty. And it seems like all the symptoms of what I call midlife metabolic mayhem and disease and premature death from menopause are quote unquote normal. (08:58): And because most women suffer from them. But I think that we have to kind of take a page out of the book of these other metabolic diseases that you described, where they're now commonplace. And so we have physicians that are dedicated to treating these disorders and medications and whole fields of study. And really it should be the same with menopause. But if you compare , the amount of funding and doctors who do research on menopause and treatment, it's really not equivalent to that of diabetes, hypertension, and coronary artery disease. So I just wanted to get that in. Cause I think it's, (09:36): You're right, absolutely right after menopause happens, there's such a dramatic increase in the risk of high blood pressure and obesity and diabetes and all of these metabolic complications go way up in women after menopause. And it is related for sure to these hormonal changes. And actually it's very much linked to our research. And I agree with you. I like that phrase, hormonal poverty. That really does describe the situation. Well. Yes. (10:09): So let's dive into your research on sugar, uric acid, all kinds of wonderful things. Where would you like to start? (10:19): Well, I can begin by kind of how we approached this problem. So the question we, we were asking ourselves is, I'm not afraid to ask big questions, . Yeah. So the, the question that we asked ourselves is, you know, what's driving obesity? And so many people study it and usually they study it from this standpoint of obesity is a disease, it's associated with metabolic syndrome and diabetes. And they kind of come at it like it's a, you know, it is a very bad thing to have. But we decided to kind of take a twist on it and kind of look at it from the standpoint of nature. And in nature, obesity can be lifesaving. And you probably know this well, you know, if you're a big brown bear yeah, and you wanna make it through the winter, you better have enough fat. And so what happens is they, in the spring, they're, they're kind of lean and during the summer they, they actually stay lean and mean as they say. (11:22): But then about eight weeks before they hibernate, they purposefully get fat. And so I realized that it was kind of like a switch. They're eating normally every day and if they eat too much one day, they eat less the other. And actually there's data in animals that regulate their weight. Normally if you fast it an animal for a month and make it lose 20% of its weight, which is sort of mean, but if you do that and you stop that, they'll go right back to the weight they're supposed to be at. If you feed an animal force, feed it so that it has to gain weight and then you stop that, they'll go back to their normal weight. So normally animals regulate their weight, but, you know, all I had to do is look acro, you know, walk to the supermarket and you would recognize that people are not regulating their weight today. (12:13): But interestingly, if you look at a bear, it regulates its weight perfectly. And then eight weeks before it hibernates, it suddenly starts eating voraciously. It looks for food, it starts foraging dramatically, it increases its weight, eight to 10 pounds a day. It becomes insulin resistant. It gets fat in its blood, it gets fat in its silver, it develops the metabolic syndrome. But it is purposeful because it wants to get that fat so that when it goes into its den and it sleeps through the winter, it lives off the fat and the guts not from just the energy from the fat, you know, it breaks down the fat to produce energy. So you don't have to eat when you ha fat enough. You don't have to eat when you're breaking down the fat cuz you can get your energy from the fat, but they even get their water from the fat. (13:09): So when a bear hibernates it doesn't drink water for four months, doesn't eat food for four months and it lives off its fat. Mm-Hmm. . So when we think about animals like this or animals that do long distance migration or nesting, we see that nature wants them to be fat, at least for that period of time. And the question is what triggers them to go from kind of a normal weight to one where they're really gaining weight fast. And then we thought to ourselves, if we can figure this out, then maybe if we can see if people have accidentally turned on this switch all the time. That was sort of the question. And I had also, I have to admit, I'd been studying this for quite a while. At the time we started studying, we did study hibernating bears and we studied hibernating squirrels. And so we did do studies, but I already had an idea, I have to admit. (14:07): And the idea I had related to sugar and particularly to fructose, and I was thinking about, I don't know if you know it, but the little hummingbird Yeah. Has a metta metabolic rate. That's unbelievable. I mean they, they're bidding their wings so fast and their heartbeat so high. I mean, it's like they are metabolically fantastic. They can do anything. They can actually, they can fly long distances even. I mean they, they are just an amazing species. They are. Yeah. And beautiful. But, but they, and beautiful and they eat sugar, they're eating sugar and they, they nectar, you know, with, they put their little bills and those flowers and they pull out, they suck out the the nectar. Nectar is like sugar water. And you know what happens during the day, that's all they eat and they become internally fat like you can't believe it. (15:03): Their liver turns white. Mm-Hmm. , it becomes white with fat. They call it the pearly white liver of the hummingbird. It's supposed to be like the fattest of all livers of birds. And their glucose levels go up to like 700 in their blood. So they actually become diabetic. They're diabetic fat, visceral fat, liver fat all in one day. And then at the end of the day they quit eating, they actually will start resting and when they rest they burn. They continue with that high metabolic rate and they burn off the fat and they drop their blood glucose levels by hundreds of, you know, milligrams mm-hmm. . And basically they go back to normal by the morning and then they start over. And so I was well aware that fructose can really make an animal fat one day if you eat enough, you know, if you're a hummingbird, even with your metabolic rate, it can overcome you and mm-hmm. (16:06): , it just told me that there's something about sugar that's particularly strong. And, actually that's one of my quotes, sugar turns to fat because when you feed animals sugar, they increase their fat content and they decrease their muscle mass actually a little bit. And so it's really powerful, it's a powerful food for increase in fat. And when we started looking at this, we realized it was the fructose that was really the key, you know, sugar or table sugar is sucrose, but it's actually two sugars. It's fructose and glucose bound together and high fructose corn syrups, another added sugar that's in foods and by the name you can tell it's got fructose in it. It's got fructose, high amounts (16:55): . (16:56): Yeah. High amounts, high fructose corn syrup. But let's remember that it's high and it is higher than fat sugar. So yeah, bear (17:05): A fruit hummingbird. It started there with sugar. Sugar turns to fat. A lot of people still think that it's fat that makes you fat. It's not, it's sugar. Right. And can you talk a little bit about high fructose corn syrup because it used to hear a lot more about it and then I don't think it's so much in the media, but it's still being served daily (17:26): . It's unbelievable. So, here was the problem, I don't know, you know, I'm old enough that I remember when ice cream was made with regular sugar and if the ice cream got in the freezer a long time, it would form crystals and it wasn't as good. And so then they found that they could make a syrup of sugar. High fructose corn syrup is basically a syrup and you know, it has a little bit more fructose cuz fructose is the sweeter of the two sugars. So there's fructose and glucose and it has a little more of the fructose, which is sweeter and people like that. And because it's liquid, they can mix it into food really well, it doesn't crystallize. It's got a good shelf life. And so when it was introduced, they found that they could put it in all kinds of food. And when they put it in the food, they can blend it. They, so they can make it strong. So it's really sweet or they can make it just subtle. And actually if it's just subtle, it just makes, makes it taste better. You know, like crackers, if you add just a tiny bit of sugar, you know, I don't know if when you eat a wheat then it, it's got a little sweetness that's so subtle that you can't tell (18:40): It hits that, that bliss point, you know, that everybody has biologic. Right. (18:46): And we did it (18:46): For the fat, salt and sugar. So Yes, go ahead. I'm sorry to interrupt. (18:50): Yeah, no, no, no. I'm sorry to my enthusiasm getting ahead of me here. So sorry. But, but anyway, so it turns out that, you know, when they added the high fructose corn syrup, they found that they could just really, that people would buy the food more. And so a lot of processed foods where you, where, you know, they add things into it, they'll add this high fructose corn syrup or sugar and salts, another one. And so these processed foods have about 70, 70%, 75% of them contain either sugar or high fructose corn syrup and a lot of salt too. And so this, this turns out to be a great way to trigger this switch because, in animals in the wild, a lot of them will eat fructose as their means to trigger the switch. And bears is they eat fruit. And although I like fruit and you like fruit and normally small amounts of fruit, like what humans eat is healthy cuz it contains so many good things. (19:49): A bear won't eat, you know, two apples or one apple at a time. It'll eat as many as it can stuff in its mouth. And so they can get a hundred fruits and then when you eat that much, the sugar adds up. So that's how they do it. They eat a lot of fructose and they can trigger this, this thing. And we did studies in animals then, and we could show that fructose triggers this switch. And when you feed an animal fructose, not only do they get hungry, they get hungry, they get thirsty, they want to eat more food, and they do, they don't control their appetite anymore. So they eat more than they should. They drop their energy metabolism when they're resting, they start becoming insulin resistant and they raise their blood pressure and they put Liv fat in their liver. Anyway, they do all these things, they even get behavioral changes where they start foraging. (20:56): It's an incredible program. So it's like a whole orchestra is initiated, it isn't just about eating more. And this is all triggered by fructose and it turns out to be unique. It's unique to fructose. And we actually figured out how it worked. And it's really cool because when you eat food, you're getting energy, right? We get our energy from the food we eat. And so when we eat food, we make energy in our bodies that we use to do what we do. That's why we eat. But there's two types of energy, there's really two major types of energy. There's the act of energy that we use everyday and we call that a t p, that's the energy we make. We make it in our mitochondria and other places in our body. And then the other energy is the stored energy and the stored energy is fat because it can be turned into energy when you break it down. (21:58): That's how the bear gets through the winter. So, so it turns out that when you eat, most people were thinking that when you eat, you get this energy and if we fill up our atp and once the gas tank is full, then the extra goes into fat. And it turns out that's not the way it works. Once the ATTP is full, you count your weight is regulated, you, you're not going to eat anymore. It's like a system that controls your weight. Mm-Hmm. . But what fructose does is it, it lowers the a t p, it's the only nutrient that lowers the a t P in the cell. And when that happens, it makes you hungry because you wanna have a full, you wanna have a full tank. And so what you do is you eat more, but be the way fructose works is it doesn't allow you to really build up that attp. It makes the energy that comes in go over to the fat. So energy the same. You're you're eating energy and you're, you're storing energy. But instead of, or using it, but instead of using it for, at tp, it's going preferentially to the fat mm-hmm. . And, and because the a t P levels are low, you keep eating. And so it's a fantastic system for making an animal want to gain weight. You (23:18): Know, as you're saying that I've experienced this, maybe people listening have, so I don't consume a lot of fruit because the more fruit I eat, the more fruit I want, the more food I want. I've always noticed that. And you know, all these diet wars going on and people say, well why do you hate fruit? And Dr. Kiran, I say, I don't hate fruit. It just is not necessarily the best option when there are other options. So you're saying that the switch that triggers it for the hummingbird and for the hibernating bears is sugar and that's what's switching us Yes. The survival switch that's causing us to gain weight as well. (24:00): Yes. So originally, okay, originally our work said it was from, just from the sugars that we were eating. And you know, like a hummingbird gets it from nectar, the bear gets it by eating a lot of fruit. To address your question, you know, we've done a fair number of studies and if, and for most people, if they eat a few fruits, it's actually good because you got fiber and potassium and all this. But if you eat a lot of fruit or if you eat certain fruits that are sweeter than others, you can activate the switch from fruit. I have had people who couldn't lose weight and they were eating, drinking smoothies of fruits and I had them stop that and they were able to lose weight very quickly. So it is true, but in general, fruits in our work, we actually did a clinical trial where we gave people on a low fructose diet with or without some fruit supplements. (24:56): And for most people, natural fruit supplements are good. Now, if you're eating bananas, if you're eating, you know, apples, bananas, plums, pears, those in particular can either raise your glucose a lot or or raise, provide a big fructose load mm-hmm. . So anyway, so I I I think we're in agreement actually. Totally. But anyway, so then how about we did have, we had a big bad discovery though. It's really important for me to bring this up for your Okay. People listened and that was that, you know, so in the beginning I said, that's all high fructose corn syrup, it's all added sugars. It's these, these are the foods that have the fructose, this is the food that activates the switch. It's gotta be that. And so I was targeting them and, and high fr you know, and then I found out too that you're like, if you knocked out the taste of an animal so that it can't taste sweet, it's still like sugar. (25:51): And so I realized that even when people were putting sugar in the foods, even if you can't taste it, it's like a mechanism to make you like it because the animals that can't taste sweet still seek sweet foods. So I thought it was all that. And then of course I started thinking and I realized that not all animals that hibernate are eating fruit. And also, you know, the penguin can really get fat very easily and there's not much fruit done in Antarctica. So, you know, I realized that there had to be other foods that could trigger the switch. And the big discovery was when we figured out that the body can make fructose from carbs. You know, so french fries for example, probably not our favorite food, right? , right. But yeah. But anyway, french fries do not contain fructose. They contain starch, they don't contain sugar, really, they contain starch. (26:48): Now when the starch is broken down, it makes glucose and glucose, I is a sugar, but it's not fructose. Right. So, but when the glucose goes up in the blood, it stimulates insulin, which helps drive fat of course. But it also is producing fructose. And so glucose can be converted to fructose. And especially when you eat a high glycemic carbs like rice, potatoes, all those foods that we love, bread, hot bread, you know, there's very few people who, you know, didn't, don't enjoy, you know, hot bread or you know, french fries or things like that. But we know that they're not good for us. And, and what we, why we know that it's not good for us is because when you give animals a lot of carbs, they also can gain weight. And we did studies where we gave glucose and the animals actually became fat just like giving fructose did. But when we studied and we figured out that what was happening was they were converting the glucose to fructose in their body mm-hmm. . And then we went and proved it, you know, by using, you know, special animals that can only metabolize fructose and stuff like that, or can't. And so what we did, so basically it turns out that we realized that it wasn't just sugar and high fructose corn syrup. They are the, they're definitely bad guys. Right. They're bad guys. (28:21): , I love how you're telling this like, it's like a murder mystery. I can't wait to hear. Okay, so go ahead. (28:26): Yeah, they, they're so then what they, they're definitely villains at the scene, right? But there are other villains too. And those villains include bread, rice, potatoes, and all these foods that I love. So it's really disappointing. But I do wanna say that it isn't that you should never eat sugar or cake or ice cream. And I think probably many of the people listening to me, maybe you're having some ice cream in front of you right now. But, the truth is, I'm telling you that it is not that you can eat this stuff or shouldn't, but that it's clearly that we're eating too much of it. Yeah. And there's something, and I, and I would say like, don't ever drink a soft drink. I mean that it's just pure sugar. It's gonna activate this switch, you know, so try really to, if you wanna get healthy, try to cut back on these things, (29:20): Right? I would say I'm in Argentina right now and there's lots of bread and there's lots of potatoes and there's really no obesity here. You rarely see an obese person on the street or even overweight. And so I've been kind of looking around and figuring out why that is. And I guess it's cuz they don't eat it all day every day with every meal. And they're also extremely active so they burn it off. And, and the same was true when I was in . You know, rice is a staple in many countries. Bread is a staple in many countries, but they don't consume the sheer volume of these sp fructose containing items that we do. Right. So go off and, and, and (30:06): There is a, there is a secret there, there's a secret weapon too for you to consider when you're wandering around there. And I, there's two secret weapons. So let me tell you, and you probably already know about the one, but the one is salt. You know, for years people were saying, ah, you know, salt's, you know, have been linked with hypertension, but if anything, a lot of us should eat a lot of salt. But it turns out that when you eat a lot of salt, salt can be really good for sure. But if you eat a lot of salt so that the salt concentration goes up into your blood, goes up in your blood and the way you'll know that is you'll feel thirsty if you start feeling thirsty from eating salt, it turns out that your salt concentration in the blood is high. And when that happens, it is like it stimulates the chemical reaction that converts glucose to fructose. So glucose, you have to have glucose around to make fructose, but if you have the chemical reaction turned on, you can make a lot more. And so it turns out that if I eat a baked potato that has no salt on it and it's just a, you know, plain potato, I'm not gonna make as much fructose as if I salt it. So salted french fries are much worse than regular potatoes just because of that. But (31:37): Now Rick, are we talking about sodium chloride or potassium chloride? Cause (31:44): Sodium chloride, (31:46): You're talking about sodium. So that's, we're not talking about sea salt. Because sea salt should not, not have that. Okay. Just wanna make sea salt clarify for everyone. (31:54): Right. Sea salt does not do it. Potassium chloride does not do it. Mm-Hmm. , it's specifically sodium chloride. And actually animals love salt licks and they do it, they actually want the sodium chloride if they've been studied where they take deer and they make these licks with different kinds of salts. Mm-Hmm. , it's only the sodium, sodium chloride that they'll like. (32:17): Okay. (32:18): And it's because we think that that raises the serum sodium, which is a trigger to make fructose. So if you're eating a lot of salt, you can make more fructose. Now there's another twist, and this twist is sort of interesting because it's a little, it will sound challenging initially, but it turns out that fats and seed oils and fats can play a role in obesity as well. And you know, there are the, the, the low carb people will say, well, I'm on a low carb diet and I'm on a, which is a high fat diet and I'm losing weight on it. And I'll explain how that works because the reason that is, is because you need the carbs to trigger the switch. So if you trigger the switch and lower the a t p, then you're going to eat more. Okay. So the carbs, the fructose is really there to make you hungry and to disrupt your ability to control your weight. (33:22): So if you don't have a lot of fructose in your system, the fructose makes you hungry and can't control your appetite. But to actually gain weight, it is calories at that point. And the thing about fat is it's like nine calories per gram. So if you go to countries where there's not a lot of fat, a lot of fat in the diet, they'll, people will, can trigger the switch. They can become diabetic, they can become hypertensive, all those things of the switch. But to get really massively overweight, it's a little bit harder to do if there's not a lot of fat around because the fat just has so many calories per gram. So the, in our country where we have all this processed food and fried this and fried that, the, it's not that the fried food will make you fat by itself, but if you have that fructose, that sugar that or, or you're making fructose that triggers you to the switch, then the high fat food will, will, will be like putting wood on the fire. (34:28): So think of fructose as the actual fire and food is the firewood, but of the firewood, the one that burns the biggest and the strongest are the ones that have a lot of fat in it. So seed oils have become really popular and fat has in general, but we're, because we're eating so much fat in our processed food as well, you know, it's the triple whammy because you've got sugar and you and i or high fructose corn syrup, you've got salt and you got fat. So the, the, the sugar tri triggers the switch, the salt helps really convert things into fructose. And then you got the fat that that really is giving you the calories to gain weight. So this is why on a low carb diet, you can eat all the, a very high fat diet and you're not gonna gain fat gain weight because you're regulating your weight. So well, you, fill up people in a low carb diet don't have to actually go on a diet re caloric restriction cuz they naturally won't eat as much because they fill up or easier mm-hmm. . And that's because they're, they haven't activated the switch. They're, so they, you know, they can eat that high fat food, but they're not going to mm-hmm. to really gain a lot of weight from. (35:47):So there's so many things I wanna ask you. And we're, we are getting some time, so I'm gonna kind of try and let's see if we can get really targeted here. So you just mentioned something that made me think of intermittent fasting, which is all the rage right now with the research on how it helps diseases like certain autoimmune diseases, weight loss, the list is long cognitive decline, et cetera, et cetera. Can you comment on the utility of intermittent fasting from the research that you've done and your perspective? (36:20): I love intermittent fasting. I think it's a fantastic way to lose weight. Mm-Hmm. , it's easy. I think it's a fantastic system. I also think low carb diets in general are very good. And if you do intermittent fasting, so long as you're not getting hypoglycemic from it, I would try to cut back as well on those bad foods that we talked about. And I would focus on drinking, staying really well hydrated. And actually that's one of my, my second quote for you is, is, you know, keep hydrated or stay hydrated because it turns out it really makes a difference. And if you keep your serum electrolytes or sodium normal, it helps keep the fructose from being produced and it's really good. And we actually did studies where we gave animals water and we could slow the development of obesity even with sugar. So I try to stay hydrated. (37:17): What I recommend is drinking a glass of water before each meal. It's so easy. Mm-Hmm. , just make it, make it a requirement and, you know, drink a glass of water as soon as you wake up in the morning. And if you're gonna have a snack, drink a glass of water before the snack, you know mm-hmm. , it will make a huge difference. I have people emailing me saying, this is unbelievable how powerful this is. You know, I've lost that weight that I couldn't lose. And so when you see it's so true. Yeah. So when you see somebody running around, you know, these young athletic types that are lean and mean and you know, they have their huge water bottle next to them. That is an association that is real and they need the water to stay hydrated, but the water is keeping them healthy. So That's right. It's just really important. (38:11): I gotta ask you Dr. Rick, about uric acid. Is there anything you wanna add about that when it comes to gaining weight? (38:18): Yes. Especially related to you, your point about hormones and postmenopausal effects. So estrogen has many, many beneficial effects, and we've studied estrogen in our research and, you know, it keeps blood vessels healthy in many respects. But one of the most powerful benefits of estrogens is that they lower uric acid. So young women have uric acid levels that tend to be lower than men. And uric acid turns out to be important in how fructose works. And so when, when you make or eat fructose it, it's broken down. Remember I talked about how it lowers the energy in the cell, it uses uric acid to lower the energy in the cell. And when it does that, that's how it triggers the switch. So uric acid is considered biologically active. It isn't just a waste product that we get rid of and we get uric acid. (39:23): When we eat fructose, we make uric acid when we drink alcohol, especially beer. And so uric acid is a bad guy. So it's another villain at the dinner table when you look around at what you want to eat, what you don't want to eat. You know, sugar can make uric acid alcohol canned. You don't want to drink a lot of alcohol, especially beer and certain shellfish in which we love like shrimp, they can make uric acid, but the uric acid can play a role in driving these diseases. And people with high uric acid are at risk for diabetes and obesity. And when you are postmenopausal and you lose your estrogen uric acid levels go up and it's associated with women getting increased risk for obesity and diabetes and all this. And, and it's even worse for women because at the same level of uric acid, women seem to be more sensitive to it. So when the uric acid goes up postmenopausally, it becomes the same levels as it does for men, but it's worse because it's doing more for, for at the same level in women than it does in men. So a very strong argument for hormones for hormones and hormonal therapy, and I believe it's a major player in why following menopause people are at risk for, you know, everything going to hell, going to, you know, into pieces. Right. (40:55): And so just as a fellow physician, is that at all controversial anymore? Because, you know, even acog, American College of Obstetricians and Gynecologists, the only indications they have for estrogen therapy are vasomotor symptoms like hot flashes, urogenital atrophy, osteoporosis, that's it. But all these diseases are increased in women who are hormonally deficient or in the hormonal poverty of menopause. And yet just what you said, how estrogen improves blood vessels and it affects weight and 75% of us at 60 are overweight or obese. Yeah. So I'm just wondering from your perspective, is that all a controversial statement? (41:37): Well, it is. It is. But you know, no one has really like the Women's health Initiative in some of these trials. What they really need to do is they need to consider uric acid as a potential mechanism to explain the effects post-menopause. Mm-Hmm. and to, when they do these studies, like with estrogens, they should include, you know, measuring what happens to the uric acid to see if this really re can predict the better a, you know, can predict the results. So in other words, if the uric acid levels don't go down, it suggests to me it would suggest that that person is less likely to show a benefit. I've been studying uric acid for 30 years, and I can tell you that biologically it's really powerful. And, we even did some studies in humans that we published in the JAMA showing that uric acid can raise blood pressure in people especially in younger people, there's links with insulin resistance and a variety of things. (42:37): It is controversial, we need to do more clinical studies, but experimentally and in the animal and in the cell culture, it is very clear that uric acid is biologically active and is doing things that we tend not to want to have done to us. So right. I would say yes, we need to do more studies, but like I've published studies showing that lowering uric acid improves insulin resistance. I've shown it improves blood pressure. There's studies showing that it improves vascular function. There's hundreds of studies that show that if you have a high uric acid associated with poorer outcomes, including cancers and all these things. So I believe that there's enough evidence there that everyone should measure their uric acid and know what it is. Now whether or not you should go on a medication to lower the uric acid, I think that, you know, that may be a little more controversial because medications can carry side effects. (43:38): But there are some things you can do to lower the uric acid. We just talked about 'em, you know, reduce your sugar and drink more water. Another one is vitamin C. Vitamin C is a vitamin. It's healthy. And if you take 500 milligrams twice a day, it's been shown in placebo controlled trials to lower uric acid. So it's a good move. It helps the energy factories. You certainly, there's enough evidence that high uric acid levels are associated with bad outcomes and there's good evidence that low uric acids are associated with good outcomes. And there's pilot studies that show that lowering uric acid improves things. So in my mind, estrogen's, lower uric acid, vitamin C lowers uric acid hydration, lowers uric acid, exercising daily can lower uric acid, reducing sugar. These are all good things. They're all associated with good outcomes. We should use diet, exercise vitamins, maybe hormones as you recommend. And I think that a lot can be gained and you don't necessarily have to go on Allopurinol or a drug like that, but if your uric acid is really high and you have gout, I would recommend it. (44:54): Well, you are a font of information about fat and sugar and uric acid and all these things. That is for sure. I'm gonna direct everyone to your book and we're gonna have Dr. Richard share all his links and we'll have 'em in the show notes too. But he has chapters on the optimal diet for blocking the fat switch. In his book. He has one for restoring your original weight and improving your health span. So he's got all the how-tos in his book. But Dr. Richard, please tell everyone where they can find your book and where they can connect with you online and find out more about the work that you're doing. (45:33): Thank you, Kyrin. So my book called Nature Wants us to be Fat . Mm-Hmm. , and you know exactly right, there's a section on, you know, the science and why and, but there's also, at least half of the book is devoted to how to block the switch and how to turn it off. And there's food that turns it off. And so I do think that you'll find it useful and how to restore your energy. So that book can be, you can get it through almost all sites. Amazon Books A million Barnes and Noble. You can find it. And my, I have a nice website. Well at least I think it's nice . Anyway, I didn't make it so it's great. (46:16): It's (46:16): Really good. Yeah. But it's called Dr. Richard johnson.com and that's a really good place to find me. I have a thing called Link Bio, which you can use Dr. Richard Johnson and it connects to all kinds of podcasts as well. But my website's the, my main site mm-hmm. and I'm findable on Instagram and Twitter. And so I think you should be able to find me. (46:41): Okay. I love this quote you have on your website from Robert Lusting, the Science Behind How Sugar is Not Food but Poison. And it reminds me of, there's a TED Talk that is entitled I believe It's Sugar is Not a Treat. And I really think this, this gets to the truth that we really need to stop idolizing Sugar . (47:07): Yes, absolutely. Yeah. Rob Lustig's, one of my heroes. And anyway, thank you so much for having me on your show, and thank you for those who've been listening. Yes. (47:17): Thank you for joining us, Dr. Johnson. Super happy to have you here. Important topic, great research you're doing, direct everybody to the book. You can find it wherever books are sold. Nature wants us to be fat, definitely check out Dr. Johnson's website. It is Dr. Richard johnson.com. He has lots of wonderful resources on there and you can find out about all the wonderful research he is participating with. So thank you for the work that you are doing. Dr. Johnson, thank you for really being a true healer and being more interested in why people get disease than just treating it with drugs and surgery. Thank you so much for that. Thank you. And thank you all for joining us for another episode of The Hormone Prescription with Dr. Kyrin. Hopefully you've learned something that you can put into effect in your life to impact your health and move it in the right direction. A journey of a thousand miles starts with a single step. So what's one thing you could do today? Just drink water when you wake up. Right? That's so super simple. If you take simple actions, put them in effect in your life, before you know it, you will have improved health. (48:34): So thanks so much (48:35): For joining me. I look forward to seeing you again next week. Until then, peace, love, and hormones, y'all. (48:41): Thank you so much for listening. I know that incredible vitality occurs for women over 40 when we learn to speak hormones and balance these vital regulators to create the health and the life that we deserve. If you're enjoying this podcast, I'd love it if you'd give me a review and subscribe. It really does help this podcast out so much. You can visit the hormone prescription.com where we have some free gifts for you, and you can sign up to have a hormone evaluation with me on the podcast to gain clarity into your personal situation. Until next time, remember, take small steps each day to balance your hormones and watch the wonderful changes in your health that begin to unfold for you. Talk to you soon.   ► Learn more about Dr. Richard Johnson's works, research and books - CLICK HERE.   ► Feeling tired? Can't seem to lose weight, no matter how hard you try? It might be time to check your hormones. Most people don't even know that their hormones could be the culprit behind their problems. But at Her Hormone Club, we specialize in hormone testing and treatment. We can help you figure out what's going on with your hormones and get you back on track. We offer advanced hormone testing and treatment from Board Certified Practitioners, so you can feel confident that you're getting the best possible care. Plus, our convenient online consultation process makes it easy to get started. Try Her Hormone Club for 30 days and see how it can help you feel better than before. CLICK HERE.  

Un nouvel épisode du Pharmascope est maintenant disponible! La saison des congrès en cardiologie vient de se terminer et a laissé derrière elle plein de nouveautés. Dans de ce 108ème épisode, Sébastien, Nicolas et Isabelle discutent notamment de diurétiques thiazidiques, d'allopurinol et d'inhibiteurs du SGLT2. Les objectifs pour cet épisode sont les suivants: Discuter des bénéfices et des risques des inhibiteurs du SGLT2 en néphropathie chronique et en insuffisance cardiaque avec fraction d'éjection préservée ou faiblement diminuée Comparer l'efficacité et l'innocuité de la chlorthalidone et de l'hydrochlorothiazide en hypertension Discuter de l'efficacité et de l'innocuité de l'allopurinol en maladie cardiovasculaire athérosclérotique Étude EMPA-KIDNEYEMPA-KIDNEY Collaborative Group, Herrington WG et coll. Empagliflozin in Patients with Chronic Kidney Disease. N Engl J Med. 2022. Epub ahead of print. doi: 10.1056/NEJMoa2204233. Étude Diuretic Comparison ProjectIshani A et coll; Diuretic Comparison Project Writing Group. Chlorthalidone vs. Hydrochlorothiazide for Hypertension-Cardiovascular Events. N Engl J Med. 2022. doi: 10.1056/NEJMoa2212270. Epub ahead of print. Étude DELIVERSolomon SD et coll; DELIVER Trial Committees and Investigators. Dapagliflozin in Heart Failure with Mildly Reduced or Preserved Ejection Fraction. N Engl J Med. 2022;387:1089-98. Étude ALL-HEARTMackenzie IS et coll; ALL-HEART Study Group. Allopurinol versus usual care in UK patients with ischaemic heart disease (ALL-HEART): a multicentre, prospective, randomised, open-label, blinded-endpoint trial. Lancet. 2022;400:1195-205.

If you are too busy to read the EMEUNET What Is New contributions (https://emeunet.eular.org/what_is_new.cfm), this podcast is exactly for you. Now you can get updated while on the go, with highlights of the most recent publications in the field of Rheumatology, selected for you by EMEUNET members.

GET TRANSCRIPT AND FULL SHOWNOTES: melanieavalon.com/uricacid 2:15 - IF Biohackers: Intermittent Fasting + Real Foods + Life: Join Melanie's Facebook Group At Facebook.com/groups/paleoOMAD For A Weekly Episode GIVEAWAY, And To Discuss And Learn About All Things Biohacking! All Conversations Welcome! 2:15 - Follow Melanie On Instagram To See The Latest Moments, Products, And #AllTheThings! @MelanieAvalon 2:30 - AVALONX SERRAPEPTASE: Get Melanie's Serrapeptase Supplement: A Proteolytic Enzyme Which May Help Clear Sinuses And Brain Fog, Reduce Allergies, Support A Healthy Inflammatory State, Enhance Wound Healing, Break Down Fatty Deposits And Amyloid Plaque, Supercharge Your Fast, And More!  AvalonX Supplements Are Free Of Toxic Fillers And Common Allergens (Including Wheat, Rice, Gluten, Dairy, Shellfish, Nuts, Soy, Eggs, And Yeast), Tested To Be Free Of Heavy Metals And Mold, And Triple Tested For Purity And Potency. Order At AvalonX.us, And Get On The Email List To Stay Up To Date With All The Special Offers And News About Melanie's New Supplements At melanieavalon.com/avalonx 5:55 - FOOD SENSE GUIDE: Get Melanie's App At Melanieavalon.com/foodsenseguide To Tackle Your Food Sensitivities! Food Sense Includes A Searchable Catalogue Of 300+ Foods, Revealing Their Gluten, FODMAP, Lectin, Histamine, Amine, Glutamate, Oxalate, Salicylate, Sulfite, And Thiol Status. Food Sense Also Includes Compound Overviews, Reactions To Look For, Lists Of Foods High And Low In Them, The Ability To Create Your Own Personal Lists, And More! 6:30 - BEAUTYCOUNTER: Non-Toxic Beauty Products Tested For Heavy Metals, Which Support Skin Health And Look Amazing! Shop At beautycounter.com/melanieavalon For Something Magical! For Exclusive Offers And Discounts, And More On The Science Of Skincare, Get On Melanie's Private Beautycounter Email List At melanieavalon.com/cleanbeauty! Find Your Perfect Beautycounter Products With Melanie's Quiz: melanieavalon.com/beautycounterquiz 11:45 - Why Does Fructose Threaten Our Health? 13:50 - Can We Evolve Out Of The Obesity Signaling Pathway From Fructose? 20:20 - Triggering The Pathway 21:20 - Orange Juice 22:05 - BEAUTY AND THE BROTH: Support Your Health With Delicious USDA Organic Beauty & The Broth Bone Broth! It's Shelf Stable With No Preservatives, And No Salt Added. Choose Grass-Fed, Grass-Finished Beef, Free Range, Antibiotic And Hormone-Free Chicken, Or Their NEW Organic Vegan Mushroom Broth Concentrate Shipped Straight To Your Door! The Concentrated Packets Are 8x Stronger Than Any Cup Of Broth: Simply Reconstitute With 8 Ounces Of Hot Water. They're Convenient To Take Anywhere On The Go, Especially Travel! Go To melanieavalon.com/broth To Get 15% Off Any Order With The Code MelanieAvalon! 23:55 - The Historical Consumption Of Fructose 25:45 - Depletion Of Energy In The Cell By Fructose Metabolism 30:15 - AMPD 34:05 - Neurological Effects Of High Uric Acid 36:00 - Uric Acid's Role As An Independent Risk Factor In Mortality 40:50 - Does Metabolic Syndrome Come With High Uric Acid Exclusively 41:40 - Purines 46:00 - Checking Uric Acid 47:20 - "Normal Levels" 48:30 - Recommended Sugar Consumption Per Day 52:00 - Allopurinol  54:45 - Does Ketosis Create Uric Acid? 56:50 - NUTRISENSE: Get Your Own Personal Continuous Glucose Monitor (CGM) To See How Your Blood Sugar Responds 24/7 To Your Food, Fasting, And Exercise! The Nutrisense CGM Program Helps You Interpret The Data And Take Charge Of Your Metabolic Health! Learn More About Nutrisense In Melanie's Interview With Founder Kara Collier At melanieavalon.com/nutrisense. Get $40 Off A CGM At nutrisense.io/melanie With The Code MelanieAvalon! 1:00:10 - Cycling Keto 1:03:30 - Healthy Mitochondria 1:06:00 - Gender And Uric Acid 1:09:20 - Endogenous Fructose Production 1:11:15 - Why Is The Body Making Fat If It Feels Its Dehydrated? 1:13:30 - The Evolution Of Storing Fat For Metabolic Water 1:15:00 - Sodium In The Diet 1:16:15 - Drugs That Elevate Uric Acid 1:17:40 - Quercetin Daily

In 2017, Frank Bruni suffered a stroke while sleeping in the middle of the night, an event that led to blindness in his right eye. His new memoir, “The Beauty of Dusk,” examines not only his physical condition but the emotional and spiritual counsel he sought from others in order to deal with it. On this week's podcast, he discusses the experience, including his initial reaction to it.“I woke up one October morning and I felt like I had some sort of smear — some gunk or something — in my eye, because the right side of my field of vision had this dappled fog over it,” Bruni says. “I think like a lot of boomers, I had this sense of invincibility. When I was diagnosed, at one point, with mild gout, I took Allopurinol every day and that was solved. When my cholesterol was un-ideal, I took a statin, and that was solved. I kind of thought modern medicine solves everything and we boomers, with our gym workouts, et cetera, are indestructible. So for hours I thought, ‘This is just an oddity.' I took a shower and washed my eye, but the fog didn't go away. I thought, ‘Maybe I haven't had enough coffee.' I thought, ‘Maybe I had too much wine last night.' It was a good 12 to 24 hours later before I accepted, something is really wrong here.”Meghan O'Rourke visits the podcast to talk about her latest book, “The Invisible Kingdom: Reimagining Chronic Illness,” which is also about personal pain and the larger context around it. O'Rourke spent many years experiencing symptoms that were misdiagnosed or dismissed.“I just kept getting sicker and sicker, but it took so long to realize, OK, something is quite wrong.” She attributes some of this delayed realization to the “problem of subjectivity,” especially when younger. “None of us know what others are experiencing, so I thought, ‘OK, maybe pain is normal. Maybe brain fog is normal. Maybe I just should never eat dessert. It really did take maturing into my 30s and getting really sick to cross that line where it became unignorable.”Also on this week's episode, Elizabeth Harris has news from the publishing world, and Dwight Garner and Alexandra Jacobs talk about books they've recently reviewed. Pamela Paul is the host.Here are the books discussed by The Times's critics this week:“Black Cloud Rising” by David Wright Faladé“The Founders” by Jimmy SoniWe would love to hear your thoughts about this episode, and about the Book Review's podcast in general. You can send them to books@nytimes.com.

Allopurinol is often considered to be one of the top 100 most-prescribed medications in the U.S., so it will definitely be on your exams or something you'll see in the clinical setting. In this episode, we're going through all the things you need to know about allopurinol using the Straight A Nursing DRRUGS framework. See references for this lesson and get it in written format here. For more pharmacology articles and podcast episodes, click here. Follow me on instagram Study Sesh features PodQuizzes and other forms of dynamic audio learning to free you from your desk. It truly does change the way you study! RATE, REVIEW AND FOLLOW! If this episode helped you, please take a moment to rate and review the show! This helps others find the podcast, which helps me help even more people :-) Click here, scroll to the bottom, then simply tap to rate with 5 stars and select, "write a review." I'd love to hear how the podcast has helped you! If you're not following yet, what are you waiting for? It takes just a quick moment and the episodes show up like magic every Thursday. And, when I release a bonus episode, those show up, too! You'll never miss a thing! In Apple Podcasts, just click on the three little dots in the upper right corner here. Know someone who would also love to study with me? Share the show or share specific episodes with your classmates...when we all work together, we all succeed! On Apple Podcasts, the SHARE link is in the same drop-down as the follow link. Spread the love! Thanks for studying with me! Nurse Mo

Marcela, Pedro e Fred discutem 7 armadilhas sobre a crise de gota. Pode usar alopurinol na crise? Precisa puncionar toda monoartrite? Colchicina, AINEs ou corticoide, qual é o melhor? Essas armadilhas e mais algumas são discutidas nesse episódio. Referências: Richette P, Doherty M, Pascual E, et al. 2016 updated EULAR evidence-based recommendations for the management of gout. Ann Rheum Dis 2016. Hill EM, et al. Does Starting Allopurinol Prolong Acute Treated Gout? A Randomized Clinical Trial. JCR - Journal of Clinical Rheumatology Apr 2015. Vol21 Issue 3. Taylor TH. Initiation of Allopurinol at First Medical Contact for Acute Attacks of Gout: A Randomized Clinical Trial. The American Journal of Medicine. Vol 125, Issue 11. Nov 2012.  Xin Feng, Yao Li, Wei Gao. Significance of the initiation time of urate-lowering therapy in gout patients: A retrospective research. Joint Bone Spine Volume 82, Issue 6, December 2015.  Park Y, Park Y, Lee S, et al. Clinical analysis of gouty patients with normouricaemia at diagnosisAnnals of the Rheumatic Diseases 2003;62:90-92.  LOGAN JA, MORRISON E, McGILL PE. Serum uric acid in acute goutAnnals of the Rheumatic Diseases 1997;56:696-697.  FitzGerald, J. D., Dalbeth, N., Mikuls, T., Brignardello‐Petersen, R., Guyatt, G., Abeles, A. M., ... & Neogi, T. (2020). 2020 American College of Rheumatology guideline for the management of gout. Arthritis care & research, 72(6), 744-760. Ragab, Gaafar, Mohsen Elshahaly, and Thomas Bardin. "Gout: An old disease in new perspective–A review." Journal of advanced research 8.5 (2017): 495-511. Janssens, H. J., Janssen, M., Van de Lisdonk, E. H., van Riel, P. L., & van Weel, C. (2008). Use of oral prednisolone or naproxen for the treatment of gout arthritis: a double-blind, randomised equivalence trial. The Lancet, 371(9627), 1854-1860. Parperis, K. (2021). Open-label randomised pragmatic trial (CONTACT) comparing naproxen and low-dose colchicine for the treatment of gout flares in primary care. Annals of the Rheumatic Diseases, 80(12), e202-e202. Barthélémy, I., Karanas, Y., Sannajust, J. P., Emering, C., & Mondié, J. M. (2001). Gout of the temporomandibular joint: pitfalls in diagnosis. Journal of Cranio-Maxillofacial Surgery, 29(5), 307-310. Terkeltaub, R. A., Furst, D. E., Bennett, K., Kook, K. A., Crockett, R. S., & Davis, M. W. (2010). High versus low dosing of oral colchicine for early acute gout flare: twenty‐four–hour outcome of the first multicenter, randomized, double‐blind, placebo‐controlled, parallel‐group, dose‐comparison colchicine study. Arthritis & Rheumatism, 62(4), 1060-1068. Lumezanu, E., Konatalapalli, R., & Weinstein, A. (2012). Axial (spinal) gout. Current rheumatology reports, 14(2), 161-164. Kienhorst, Laura BE, et al. "The validation of a diagnostic rule for gout without joint fluid analysis: a prospective study." Rheumatology 54.4 (2015): 609-614. Clebak, Karl T., Ashley Morrison, and Jason R. Croad. "Gout: Rapid evidence review." American family physician 102.9 (2020): 533-538. Robin, F., et al. "External validation of Gout-calculator performance on a cohort of acute arthritis (SYNOLACTATE) sparing distal joints such as hallux and midfoot. A cross-sectional study of 170 patients." Clinical Rheumatology 40.5 (2021): 1983-1988. Ma, Lingling, Ann Cranney, and Jayna M. Holroyd-Leduc. "Acute monoarthritis: what is the cause of my patient's painful swollen joint?." Cmaj 180.1 (2009): 59-65. Yu, K. H., et al. "Concomitant septic and gouty arthritis—an analysis of 30 cases." Rheumatology 42.9 (2003): 1062-1066. NBR 6023Janssens, Hein JEM, et al. "A diagnostic rule for acute gouty arthritis in primary care without joint fluid analysis.Archives of Internal Medicine170.13 (2010): 1120-1126

Welcome back to our weekend Cabral HouseCall shows! This is where we answer our community's wellness, weight loss, and anti-aging questions to help people get back on track! Check out today's questions:  Anonymous: Hi Dr. Cabral- First I would like to thank you for everything you do. You have educated me so much and changed my life for the better. I have a three year old daughter who was diagnosed with febrile seizures at the age of two. If she catches a virus or infection at school (very common) and gets a fever to spike quickly she can have a febrile seizure. Fevers as low as 101 can cause these. While terrifying when they are happening we have been told around 5% of children have this condition and they typically go away around age 5 or 6 and is nothing to be worried about. The pediatrician and neurologist have told us this. When these fevers occur we spend one to two days constantly giving her Tylenol and motrin to bring the fever down. We are constantly testing the temperature and if it gets above 99, it causes us great anxiety that a seizure is coming. I am looking for what the root causes could be here to try and prevent them from occurring and how to possibly bring the fever down without constantly pumping her with drugs. Basically if this was your daughter what would you do? Based on what I have learned from you there has to be a root cause here and some type of action we can take.   Victoria: Hi Dr Cabral. I tend to eats lots of raw nuts like Almonds and seeds I'm very active and it doesn't makes me fats I eat very healthy No sugar takes al the vitamins from your practice But I'm wondering if Therese is something I'm missing Thank you   Anonymous: Hi Dr. Cabral, I wanted to get your thoughts on how to effectively identify the root cause and reduce high uric acid. I had a Uric acid level of over 10 and made some lifestyle changes including losing 50lbs, reducing alcohol intake and taking tart cherry extract to reduce it. I was only able to reduce it to 9.6 so my doctor put me on Allopurinol as he said since I have had a gout attack (one time) it should test below 6 to avoid future attacks. He told me that sometimes the medication is the only thing that can keep this to below 6 due to genetic disposition. I wanted to get your thoughts on how to reduce this naturally and/or ID what is causing this. What would you do if you were faced with this situation? I don't want to be on this medication for the rest of my life and I figured there had to be something naturally I could do or at least try. Thanks!   Trevor: Dr Cabral sir, My name is Trevor and I am one of your IHP students currently healing my body. I was just told I need to put in a lift in my shoe due to hip displacement and believed to be the length of my legs. I did fracture my growth plate in my ankle when I was 17, and I am now 32. Is there anyway for my body to heal back to normal and not need the lift? Thank you very much   Sage: Hi doctor Cabral, I am very health conscious and try to eat clean and organic food most of the time. To my horror, I discovered that the supplement that I've been using for a few months contained Titanium Dioxide, which is apparently unsafe and can cause cancer. Do you know if this is correct? It's said to be accumulating in the body tissues and I really want to get it out of my body ASAP. What would be the best way to do this? Thanks so much for your help! Love your podcast, keep up the amazing work! Sage   Molly: Hi doctor Cabral, I have an important question for you: I have been a vegan for about 10 years now, and I'll be honest - I'm doing it more for health benefits, rather than the ethical/environmental ones. Lately, I've been thinking about maybe adding fish and or eggs tp my diet, in order to boost the omega 3', choline, B12 protein and other nutrients naturally, rather than using the supplements. It's really difficult to make this decision though, as being vegan has become a bit of an identity for me and I've built a business and some great relationships because of it. I'm afraid of losing that if I'm no longer considered “vegan”. In your professional opinion, what would you advise? Staying fully vegan or adding eggs/fish once a week. I know it's a difficult question, but my health is very important to me and there are few people I trust more than you when it comes to the health advice. I can't wait to hear your thoughts and I'm grateful for you and all you do! Molly   Thank you for tuning into today's Cabral HouseCall and be sure to check back tomorrow where we answer more of our community's questions!  - - - Show Notes & Resources: http://StephenCabral.com/2206 - - - Get Your Question Answered: http://StephenCabral.com/askcabral   - - - Dr. Cabral's New Book, The Rain Barrel Effect https://amzn.to/2H0W7Ge - - - Join the Community & Get Your Questions Answered: http://CabralSupportGroup.com - - -  Dr. Cabral's Most Popular At-Home Lab Tests: > Complete Minerals & Metals Test (Test for mineral imbalances & heavy metal toxicity) - - - > Complete Candida, Metabolic & Vitamins Test (Test for 75 biomarkers including yeast & bacterial gut overgrowth, as well as vitamin levels) - - - > Complete Stress, Mood & Metabolism Test (Discover your complete thyroid, adrenal, hormone, vitamin D & insulin levels) - - - > Complete Stress, Sleep & Hormones Test (Run your adrenal & hormone levels) - - - > Complete Food Sensitivity Test (Find out your hidden food sensitivities) - - - > Complete Omega-3 & Inflammation Test (Discover your levels of inflammation related to your omega-6 to omega-3 levels) - - - > View all Functional Medicine lab tests (View all Functional Medicine lab tests you can do right at home for you and your family)

Watch the full video interview on YouTube here: https://bit.ly/drdavidperlmutter457 Dr. David Perlmutter (IG: @davidperlmutter) is a Board-Certified Neurologist and five-time New York Times bestselling author. He serves on the Board of Directors and is a Fellow of the American College of Nutrition. Today we're discussing David's new book, Drop Acid. It focuses on the pivotal role of uric acid in metabolic diseases. Reducing high uric acid levels through dietary and lifestyle tweaks will help you lose weight, prevent (and reverse) disease, and live a long and healthy life. In this episode, we discuss: The role of uric acid Fructose is directly metabolized into uric acid Fruit in moderation does not elevate uric acid Sources of fructose to avoid What is the optimal range for uric acid levels Estrogen helps with uric acid excretion after menopause Alternative sweetener recommendations + what to avoid Purines increase uric acid Beer stimulates uric acid Foods high in purines The correlation between salt consuption and obesity Lack of restorative sleep is associated with an elevation of uric acid Walking after dinner improves sleep Time-restricted eating is a powerful tool to improve metabolic health Uric acid levels rise during longer fasts + how long it takes to lower Luteolin is as effective as Allopurinol for lowering uric acid The powerful benefits of quercetin Counteracting roles of AMP kinase vs AMP deaminase Exercise activates AMP kinase When did the uricase mutation take place? The problem with sports drinks + healthy alternatives Check your blood sugar levels with a continuous glucose monitor Consuming coffee is associated with lower uric acid levels The dietary approach to lowering uric acid Show sponsors: Paleovalley

"Dagáll læknanemans" er hlaðvarp fyrir læknanema og annað áhugasamt fólk um hvaðeina sem viðkemur klínik og læknisfræði. Stjórnendur eru Sólveig Bjarnadóttir og Teitur Ari Theodórsson. Í þessum ræða þeir Ragnar Freyr Ingvarsson gigtarlæknir og Ólafur Orri Sturluson sérnámslæknir í almennum lyflækningum um þvagsýrugigt. Af hverju fáum við þvagsýrugigt? Hvernig er hún greind? Hvaða meðferðarmöguleikar eru í boði? Ennfremur er rætt um þvagsýrugigt í sögulegu samhengi, gildi smásjáskoðunar og hvernig hægt er að beita ómun við mismunagreiningu bólgins liðar. Að lokum uppljóstra viðmælendur þáttarins hver jólagjöfin í ár er (var)!Dagáll læknanemans er sjálfstæð þáttasyrpa innan Hlaðvarps Landspítala. Þættirnir eru aðgengilegir á helstu samfélagsmiðlum Landspítala og einnig í streymisveitunum Spotify og Apple iTunes, ásamt hlaðvarpsveitum á borð við Simplecast, Pocket Casts og Podcast Addict.(Tónlist: "Garden Party" með Mezzoforte. Notað með leyfi frá hljómsveitinni.)SIMPLECAST:https://landspitalihladvarp.simplecast.com/episodes/dagall-23

Diving deeper into relevant illnesses during the festivities, Fadhli and Esther sat down to discuss gout or hyperuricemia. The condition once dubbed as the "rich man's disease" turned out to have quite a bit of genetic implication, both on the pathophysiology and even on the pharmacogenomics of it. We focused on the important mainstay drug for gout, Allopurinol, and the presence of certain genetic variation that increases the likelihood of Stevens-Johnson Syndrome. The episode also spoke about how this condition is markedly higher in certain populations, including Asians. Learn more about us: www.nalagenetics.com

Not another one! Music: Time Travellin' Nancy by Shane Ivers - www.silvermansound.com

1:08 - Take-home thoughts for R/R MM 3:47 - Summary of BCMA-targeted CAR T-cell therapy; Use of novel agents for R/R MM6:47 - Information on melphalan flufenamide; Combination approaches with selinexor in clinical practice9:59 - Cost considerations for treatment options in R/R MM12:25 - Administration considerations for subcutaneous daratumumab and venetoclax in R/R MMFacultyKathryn Maples, PharmD, BCOPClinical Pharmacy Specialist, Multiple MyelomaWinship Cancer Institute, Emory HealthcareAtlanta, GeorgiaTim Peterson, PharmD, BCOPClinical Pharmacy Specialist – Multiple MyelomaMemorial Sloan Kettering Cancer CenterNew York, New York Content based on a CE activity supported by educational grants from Karyopharm Therapeutics, Inc. and Oncopeptides, Inc.Link to full activity: https://www.proce.com/RRMM

Altbewährte Gicht Medikamente wie Allopurinol oder Kolchizin der Herbstzeitlosen sind wichtige Bestandteile der Behandlung von chronischer Gicht bzw. dem akuten Gichtanfall. Doch was hilft schnell, wenn z.B. die Harnsäure effektiv gesenkt werden muss doch Niere oder Leber eine Behandlung mit diesen etablierten Mitteln nicht zulassen? Meine Website: https://medizinmensch.de Kaffee spenden: https://buymeacoffee.com/Medizinmensch Glossar: Interleukin-1 (IL-1): Ein wichtiger Botenstoff bei Gicht Canakinumab: Ein monoklonaler Antikörper gegen Interleukin-1 Allopurinol: Medikament dass die Harnsäure senkt Kolchizin (Gift der Herbstzeitlosen): Mittel gegen Gicht dass die Beweglichkeit von neutrophilen Granulozyten hemmt Uratoxidase: Ein Enzym zum Abbau von Harnsäure, beim Menschen im Verlauf der Evolution verloren gegangen. Weitere Videos zu Gicht & Pseudogicht: https://bit.ly/MM-Gicht Links / Sources: Volker Brinkmann et al. Neutrophil Extracellular Traps Kill Bacteria https://science.sciencemag.org/content/303/5663/1532.abstract Lizenzen: CC0: https://creativecommons.org/publicdomain/zero/1.0 CC BY 3.0: https://creativecommons.org/licenses/by/3.0 CC BY 4.0: https://creativecommons.org/licenses/by/4.0 Wichtiger Hinweis: Die Videos dienen ausschließlich der Allgemeinbildung. Die Informationen ersetzen keine persönliche Beratung, Untersuchung oder Diagnose. Die zur Verfügung gestellten Inhalte ermöglichen nicht die Erstellung eigenständiger Diagnosen. Medizinisches Wissen unterliegt fortwährendem Wandel und es kann nicht garantiert werden dass die Informationen zu jedem Zeitpunkt noch korrekt sind, oder selbst korrekt waren. Haftung ausgeschlossen. Merk-würdiges Medizinwissen für Alle. Abonniere jetzt und erhalte neue Folgen, jeden Medizin-Sonntag. Folge direkt herunterladen

Leo's channel: https://www.youtube.com/c/LeoandLongevity  Steve's channel: https://www.youtube.com/user/VigorousSteve

Today's episode is dedicated to Tumor Lysis Syndrome management in the PICU. Join us as we discuss the patient case, symptoms, and treatment. We are delighted to be joined by Dr. Himalee Sabnis, Assistant Professor of Pediatrics at Emory University School of Medicine. She is also a pediatric hematologist/oncologist and the Co-Director of the High-Risk Leukemia Team at the AFLAC Cancer & Blood Disorders Center at Children's Healthcare of Atlanta.  Show Highlights: Our case, symptoms, and diagnosis: A three-year-old female with pre-B ALL presents on Day 2 of chemotherapy to the PICU. She is admitted with telemetry findings of arrhythmia, decreased urine output, and an EKG notable for peaked T waves. Her labs are notable for elevated WBC, hyperkalemia, hyperphosphatemia, and low ionized calcium. Tumor Lysis Syndrome is a life-threatening medical emergency stemming from rapid tumor cell destruction that overwhelms the usual metabolic and excretory pathways.  Why TLS is the most common pediatric oncologic emergency for pediatric cancer patients When the tumor cells die or lyse, what's inside those cells comes out into the blood Key metabolic abnormalities that affect organ function are too much potassium and phosphorus, low calcium, and uric acid buildup. Those metabolic abnormalities can result in cardiac arrhythmia and kidney failure. Certain patient populations have an increased risk for TLS: Hematological cancers have a higher risk than solid tumors Patients with fast-growing tumors, like lymphoma and leukemia, are at high risk Key pathophysiologic principles that drive TLS: The imbalance of electrolytes can impact heart function TLS is characterized by hyperkalemia, hyperphosphatemia, hypocalcemia, and uric acid, which is a by-product of DNA breakdown If untreated, the uric acid can lead to acute kidney injury and renal failure Electrolyte and metabolic disturbances can progress to renal insufficiency, cardiac arrhythmias, seizures, and death TLS releases cytokines that can cause a systemic inflammatory response and multi-organ failure Other lab markers in patients with TLS include uric acid, LDH, CBC, DIC panel, and daily blood gas (these are typically trended every 4-6 hours). Key factors in TLS management are to understand the risk and know your resources. Steps taken would be continuous cardiac monitoring, uric acid control, administering Allopurinol to combat uric acid formation, and managing electrolyte disturbances in conjunction with an intensivist. Chemotherapy would not be delayed due to TLS because the patient's condition won't improve until the cancer is treated. How the complications of TLS are treated: Hyperphosphatemia should be treated by using oral phosphate binders such as aluminum hydroxide. Hypocalcemia does not require therapy unless cardiac function is affected. How renal replacement therapy might be required and indications are similar to other forms of acute kidney injury. Besides Allopurinol being given at the initiation of chemotherapy, patients at high risk for TLS may receive low-intensity initial therapy to prevent rapid cell lysis. Takeaway clinical pearls regarding TLS: Know what you're dealing with because every cancer is different. Fluid management is important and will vary from patient to patient. Be proactive in monitoring. Intervene early and quickly.  

Video auf YouTube: Medizinmensch Starker Gelenk-Schmerz durch extreme Entzündung ist typisch, sowohl beim Gichtanfall also auch bei der Pseudogicht. Anders als die durch Harnsäure ausgelöste Gicht, tritt Pseudogicht typischerweise im Knie oder Sprunggelenk und anderen größeren Gelenken auf, während bei der Gicht der Zeh typisch ist. Auslösender Reiz des Pseudogicht-Anfalls sind im Gegensatz zur Gicht sog. Kalziumpyrophosphat-Kristalle. Ein möglicher Hinweis auf Pseudogicht sind ein normaler Harnsäurespiegel, eine Ablagerung von Kalziumkristallen, die im Röntgenbild sichtbar ist (sog. Chondrokalzinose). Harnsäuresenkende Mittel wie z.B. Allopurinol, sind für die Vermeidung hier somit unwirksam und sollten vermieden werden! Meine Website: https://medizinmensch.de Kaffee spenden: https://buymeacoffee.com/Medizinmensch Glossar: Allopurinol: Ein wichtiges Mittel zur Senkung der Harnsäure, jedoch unwirksam bei Pseudogicht Arthrose: "Verschleißliche" Gelenkerkrankung, die die entwicklung von Pseudogicht, vorallem im Knie, begünstigt Chondrokalzinose: Die Ablagerung von Kalzium-Kristallen, typisch für Pseudogicht Colchizin: Das "Gift der Herbstzeitlosen" das zur Behandlung und Vorbeugung von Gicht angewendet wird und vermutlich auch zur Vorbeugung von Pseudogicht wirksam ist Hämochromatose (Eisenspeicherkrankheit): Eine Ursache für Pseudogicht Hyperurikämie: Eine Ursache für Gicht Magnesiummangel: Eine weitere Ursache für Pseudogicht Weitere Videos von mir (Playlists): Autoimmunerkrankungen: https://bit.ly/MM-Autoimmunerkrankungen Blutwerte erklärt: https://bit.ly/MM-Blutwerte Coronavirus & Covid-19: https://bit.ly/MM-Corona Gicht & Pseudogicht: https://bit.ly/MM-Gicht Medizin leicht erklärt: https://bit.ly/MM-Medizin-erklaert Merk-würdiges Medizinwissen für Alle. Abonniere jetzt und erhalte neue Folgen, jeden Medizin-Mittwoch. Folge direkt herunterladen

Neste episódio, contamos com a participação da Dra. Rosa Telles, professora da faculdade de medicina da UFMG, pesquisadora do ELSA Brasil Musculoesquelético e integrante da comissão de artrites microcristalinas da Sociedade Brasileira de Reumatologia e da Dra. Ana Beatriz Vargas, staff do ambulatório de gota da UERJ e coordenadora da comissão de artrites microcristalinas da Sociedade Brasileira de Reumatologia, para nos atualizar sobre o novo guideline para tratamento de Gota do American College of Reumatology (ACR) de 2020. Minutagem: 00:48 Definição de hiperuricemia assintomática 02:53 Hiperuricemia assintomatica tem indicação de tratamento medicamentoso? 05:28 Medicações que aumentam ou diminuem acido úrico 07:41 Mudança de estilo de vida: quais são as evidências e o impacto no tratamento? 12:04 Mudança de estilo de vida: como fazer na prática? 15:08 Agradecimentos 16:07 Convite para Jornada Mineira de Reumatologia 18 a 20 de março: Inscrições gratuitas no reumatominas.com.br/jornada2021 Se aproxime de nós também pelo Instagram: @sociedademineiradereumatologia Referências: 1) FitzGerald JD, Dalbeth N, Mikuls T, et al. 2020 American College of Rheumatology guideline for the management of gout. Arthritis Care Res. 2020; doi: 10.1002/acr.24180. 2) Badve SV, et al. Effects of Allopurinol on the Progression of Chronic Kidney Disease. N Engl J Med 2020; 382:2504-2513 DOI: 10.1056/NEJMoa1915833

This podcast presents, Dr. Michael Edwards, a rheumatologist with Ridgeview Specialty Clinics, who provides a discussion some unique arthritis cases. Enjoy the podcast! Objectives:     Upon completion of this podcast, participants should be able to: Identify various causes of monoarthritis. Review the evaluation and management of monoarthritis. Recognize that lower back pain may be inflammatory in nature, and how to further evaluate and manage the inflammation/pain. CME credit is only offered to Ridgeview Providers & Allied Health Staff for this podcast activity. Complete and submit the online evaluation form, after viewing the activity.  Upon successful completion of the evaluation, you will be e-mailed a certificate of completion within approximately 2 weeks.  You may contact the accredited provider with questions regarding this program at  rmccredentialing@ridgeviewmedical.org. Click on the following link for your CME credit: CME Evaluation: "Bone to Pick: Rheumatology Cases with Dr. Edwards" (**If you are listening to the podcasts through iTunes on your laptop or desktop, it is not possible to link directly with the CME Evaluation for unclear reasons. We are trying to remedy this. You can, however, link to the survey through the Podcasts app on your Apple and other smart devices, as well as through Spotify, Stitcher and other podcast directory apps and on your computer browser at these websites. We apologize for the inconvenience.)  DISCLOSURE ANNOUNCEMENT  The information provided through this and all Ridgeview podcasts as well as any and all accompanying files, images, videos and documents is/are for CME/CE and other institutional learning and communication purposes only and is/are not meant to substitute for the independent medical judgment of a physician, healthcare provider or other healthcare personnel relative to diagnostic and treatment options of a specific patient's medical condition; and are property/rights of Ridgeview Medical Center & Clinics.  Any re-reproduction of any of the materials presented would be infringement of copyright laws.  It is Ridgeview's intent that any potential conflict should be identified openly so that the listeners may form their own judgments about the presentation with the full disclosure of the facts. It is not assumed any potential conflicts will have an adverse impact on these presentations. It remains for the audience to determine whether the speaker’s outside interest may reflect a possible bias, either the exposition or the conclusions presented. Ridgeview's CME planning committee members and presenter(s) have disclosed they have no significant financial relationship with a pharmaceutical company and have disclosed that no conflict of interest exists with the presentation/educational event. SHOW NOTES: CASE 1 - Psoriatic Arthritis: For our first case, our 77 year old male ended up with psoriatic arthritis. Key points of the work up include ruling out a septic joint, looking for articulation problems or soft tissue concerns like chronic infections, skin lesions, or breakdown and assessing for polyarthritis. Further work up includes sedimentation rate, C-reactive protein, and imaging, starting with x-rays. Key points of the work up include ruling out a septic joint, looking for articulation problems or soft tissue concerrns like chronic infections, skin lesions or breakdown and assessing for polyarthritis. Further work up includes sedimentation rate, C-reactive protein, and imaging - starting with x-rays. To tap or not to tap? That is the question for joint complaints. Arthrocentesis through an area of cellulitis or inflamed soft tissue is generally contraindicated. However, if a tap is feasible, the three C's:  culture, WBC count, and crystals should be send. A cell count greater than 10,000 would be indicative of an inflammatory effusion. In the acute setting, the pros and cons should be weighted as to whether or not to inject steroids. If you suspect infection, though, do NOT inject corticosteroids. Long-term treatment of psoriatic arthritis is individualized to the patient. Some patients manage with methotrexate, while others might need a biologic. Cost is a barrier in prescribing biologics, requiring referrals, and prior insurance authorization. Biologics target a specific part of the immune system. Contraindications would be patients who are already immunosuppressed, have TB, hepatitis or multiple sclerosis, or are in late stages of CHF. Other contraindications include breast, lung or melanoma cancer with a high risk of recurrence. When running a fever or prior to surgery, biologic doses should be delayed or paused. CASE 2 - Ankylosing Spondylitis:  In case number 2, a young man with a long history of back pain ended up with ankylosing spondylitis. Again, the history becomes important in the diagnosis, keying us to be suspicious of this patient's chronic pain. For this case, though lab work was normal, an AP x-ray of the pelvis showed narrow and sclerotic sacroiliac joints with erosion. Like psoriatic arthritis, this diagnosis falls under the category of seronegative spondylarthropathy. When tested, the patient will not have antibodies or positive rheumatoid factor. It is a reactive condition: sacroiliitis causes inflammatory changes and therefore pain. Inflammatory bowel conditions like Crohns and Ulcerative colitis fall into this same family of reactive conditions. First line treatment for ankylosing spondylitis is NSAIDS taken on a scheduled basis to protect the joints. Long term management includes physical therapy and back education. Biologics can be used for pain refractory to NSAIDS. This pain can go undiagnosed for years, and cause irreparable fusion of the spine, otherwise known as a bamboo sign as seen on x-ray. Again, a thorough history is key to catching and diagnosing these patients early, and preventing long-term complications. CASE 3 - Gout:  Out last patient is a woman with a swollen knee, normal wbc, and elevated sed rate. Due to her history, and RA flare up would be considered in the differential, but unlikely due to a monoarthritic presentation. Following a similar work up as the first two cases, labs and imaging are obtained and the knee is tapped. The three C's mentioned earlier:  culture, WBC count  and  crystals are sent and the results are positive for needle-like crystals which are negative birefringent when examined with polarizing microscopy. The patient has gout. Treatment includes NSAIDS like Naprosyn or indomethacin. In an acute setting, oral steroids can be prescribed. Dosing for gouty monoarthritis is 20-30mg for 3-5 days. For patients already on baseline steroids, include a steroid taper back to baseline. Additional work up could include uric acid levels. While not diagnostic, a uric acid greater than 9 may help identify patients at risk for future episodes. If the patient has 2 or more gout attacks a year. Allopurinol can be prescribed. CONCLUSION:  To sum up all our cases today; a thorough history and exam are critical, keep the differential broad, and management is weighing the pros and cons of NSAIDS, steroids and whether or not to tap that joint. Septic arthritis can not be overlooked. Early recognition and diagnosis is key. Thanks for listening.

日本 批准2个新的口服HIF羟化酶抑制剂用于治疗CKD贫血NEJM 尚无证据证明降尿酸药物可以延缓慢性肾脏病的进展Kidney International 一种新型的泛磷酸转运蛋白抑制剂治疗慢性肾脏病-矿物质骨病伐度司他（vadadustat） 伐度司他 （Vadadustat）是一种口服缺氧诱导因子羟化酶抑制剂（HIF-PHI），药理机制是模拟高海拔情况下身体对缺氧的生理反应，提高缺氧诱导因子（HIF）的生成。HIF会调控铁元素的动员、和红细胞生成素（EPO）的产生来刺激红细胞的生成，从而改善氧气运输，用于治疗慢性肾病（CKD）引起的贫血。与目前临床上使用的罗沙司他（Roxadustat）是一类的药物。2020年6月，伐度司他 （vadadustat）被日本厚生劳动省批准用于治疗CKD贫血。《随机双盲研究：治疗慢性肾病贫血的两项2期临床研究》Nephrology Dialysis Transplant，2020年7月 (1)这2项、2期、多中心、双盲、安慰剂对照研究，选取非透析依赖的、慢性肾脏病患者51人，或透析依赖的、慢性肾脏病患者60人，随机分入伐度司他150mg组、伐度司他300mg组、伐度司他600 mg组或安慰剂组。6周后，所有伐度司他组与安慰剂组相比，平均血红蛋白会睡均出现了显著的、剂量依赖性的升高。安慰剂组和伐度司他 150、300和600 mg组中，非透析依赖的患者血红蛋白变化分别为-0.47g/dL、0.43g/dL、1.13g/dL和1.62g/dL，透析依赖的患者血红蛋白变化分别-1.48g/dL、-0.28g/dL、0.08g/dL和0.41g/dL。第16周，91%的非透析依赖的患者和71%的透析依赖的患者，经过伐度司他治疗后，达到了目标血红蛋白水平（10.0-12.0 g/dL），并观察到铁利用和动员的生物标志物的、显著的、剂量依赖性变化。最常见的不良事件是恶心、高血压、腹泻、鼻咽炎和分流管狭窄。结论：这项研究的支持了伐度司他用于治疗慢性肾脏病相关的贫血的安全性和有效性。达普司他（daprodustat） 达普司他（daprodustat）也是一种缺氧诱导因子羟化酶抑制剂。2020年6月达普司他被日本厚生劳动省批准用于治疗CKD贫血。《随机双盲研究：达普司他治疗血液透析患者的贫血问题的3期临床研究》Clinical Journal of American Society of Nephrology，2020年8月 (2)这项随机的、第三期、双盲、主动对照研究，研究对象是接受规律血液透析的、慢性肾脏病患者共271人，患者从促红素改为达普司他4mg qd、或继续使用促红素。第40-52周后，两组的患者的平均血红蛋白均维持在目标范围内（10.0-12.0 g/dl），达普司他的疗效不劣于促红素。其中88%的达普司他组患者和90%的促红素组患者血红蛋白在目标范围内。在第52周时，达普司他组观察到铁调素下降、总铁结合力增加。两组的不良事件发生频率大致相似。结论：血液透析的日本患者中，口服达普司他治疗40-52周后，平均血红蛋白水平不亚于促红素。慢性肾脏病和高尿酸血症之间的关系慢性肾脏病患者可因尿液中排出的尿酸减少而发生高尿酸血症。观察性研究中，高尿酸血症可能促进慢性肾脏病的进展，可能因为高尿酸血症刺激入球小动脉血管平滑肌细胞增殖而使肾脏灌注减少。但也有研究认为尿酸与肾脏疾病或心血管疾病没有因果关系，属于风险标志物。反方观点：降尿酸治疗不能延缓肾功能恶化的进展《CKD-FIX研究：别嘌呤醇对慢性肾病进展的影响》New England Journal of Medicine，2020年6月 (3)这项随机、对照研究中，纳入CKD3期或4期的、无痛风、尿白蛋白/肌酐≥265mg/g，或前一年eGFR下降至少3.0ml/min/1.73m2的患者共369人，随机分配到别嘌呤醇100mg qd组、别嘌呤醇300mg qd组或安慰剂组，共104周。eGFR的年平均变化，在别嘌呤醇组和安慰剂组中，分别为−3.33ml/min/1.73m2和−3.23ml/min/1.73m2（P = 0.85）。在别嘌呤醇组和安慰剂组发表有46%和44%的患者报告了严重不良事件。结论：与安慰剂相比，在慢性肾病和进展高风险患者中，别嘌呤醇降低尿酸治疗并没有减缓eGFR的下降。�《随机对照研究：别嘌醇降低1型糖尿病患者血清尿酸水平不能延缓肾脏功能进展》New England Journal of Medicine，2020年6月 (4)尿酸升高与糖尿病肾病的风险增加有关，研究旨在评估1型糖尿病合并早中期糖尿病肾病患者中，使用别嘌醇降尿酸是否可以减缓肾小球滤过率的下降。在这个双盲研究中，纳入GFR在40～99.9ml/min/1.73m2的1型糖尿病合并糖尿病肾病的患者，随访3年。3年后，服用别嘌醇的患者尿酸从362umol/L降至220umol/L，安慰剂组不变；两组患者GFR平均每年下降3.0和2.5ml/min/1.73m2。结论：在1型糖尿病合并糖尿病肾病患者中，没有证据证明采用别嘌醇降尿酸可以延缓肾脏功能进展。《回顾性观察研究：非布司他与别嘌呤醇对慢性肾病患者尿酸降低及肾预后的比较》Science Report，2020年7月 (5)本研究旨在比较黄嘌呤氧化酶抑制剂非布司他和别嘌呤醇在CKD患者中降低尿酸和保护肾脏的作用。来自台湾高雄的研究人员对一家大型医疗服务系统2010 - 2015年的电子健康记录进行分析，纳入刚开始接受降尿酸治疗的成年、CKD患者，总共1050例，观察时间为2.5年。与别嘌呤醇相比，非布司他治疗后，80%的情况下患者的尿酸水平可以维持在

日本 批准2个新的口服HIF羟化酶抑制剂用于治疗CKD贫血NEJM 尚无证据证明降尿酸药物可以延缓慢性肾脏病的进展Kidney International 一种新型的泛磷酸转运蛋白抑制剂治疗慢性肾脏病-矿物质骨病伐度司他（vadadustat） 伐度司他 （Vadadustat）是一种口服缺氧诱导因子羟化酶抑制剂（HIF-PHI），药理机制是模拟高海拔情况下身体对缺氧的生理反应，提高缺氧诱导因子（HIF）的生成。HIF会调控铁元素的动员、和红细胞生成素（EPO）的产生来刺激红细胞的生成，从而改善氧气运输，用于治疗慢性肾病（CKD）引起的贫血。与目前临床上使用的罗沙司他（Roxadustat）是一类的药物。2020年6月，伐度司他 （vadadustat）被日本厚生劳动省批准用于治疗CKD贫血。《随机双盲研究：治疗慢性肾病贫血的两项2期临床研究》Nephrology Dialysis Transplant，2020年7月 (1)这2项、2期、多中心、双盲、安慰剂对照研究，选取非透析依赖的、慢性肾脏病患者51人，或透析依赖的、慢性肾脏病患者60人，随机分入伐度司他150mg组、伐度司他300mg组、伐度司他600 mg组或安慰剂组。6周后，所有伐度司他组与安慰剂组相比，平均血红蛋白会睡均出现了显著的、剂量依赖性的升高。安慰剂组和伐度司他 150、300和600 mg组中，非透析依赖的患者血红蛋白变化分别为-0.47g/dL、0.43g/dL、1.13g/dL和1.62g/dL，透析依赖的患者血红蛋白变化分别-1.48g/dL、-0.28g/dL、0.08g/dL和0.41g/dL。第16周，91%的非透析依赖的患者和71%的透析依赖的患者，经过伐度司他治疗后，达到了目标血红蛋白水平（10.0-12.0 g/dL），并观察到铁利用和动员的生物标志物的、显著的、剂量依赖性变化。最常见的不良事件是恶心、高血压、腹泻、鼻咽炎和分流管狭窄。结论：这项研究的支持了伐度司他用于治疗慢性肾脏病相关的贫血的安全性和有效性。达普司他（daprodustat） 达普司他（daprodustat）也是一种缺氧诱导因子羟化酶抑制剂。2020年6月达普司他被日本厚生劳动省批准用于治疗CKD贫血。《随机双盲研究：达普司他治疗血液透析患者的贫血问题的3期临床研究》Clinical Journal of American Society of Nephrology，2020年8月 (2)这项随机的、第三期、双盲、主动对照研究，研究对象是接受规律血液透析的、慢性肾脏病患者共271人，患者从促红素改为达普司他4mg qd、或继续使用促红素。第40-52周后，两组的患者的平均血红蛋白均维持在目标范围内（10.0-12.0 g/dl），达普司他的疗效不劣于促红素。其中88%的达普司他组患者和90%的促红素组患者血红蛋白在目标范围内。在第52周时，达普司他组观察到铁调素下降、总铁结合力增加。两组的不良事件发生频率大致相似。结论：血液透析的日本患者中，口服达普司他治疗40-52周后，平均血红蛋白水平不亚于促红素。慢性肾脏病和高尿酸血症之间的关系慢性肾脏病患者可因尿液中排出的尿酸减少而发生高尿酸血症。观察性研究中，高尿酸血症可能促进慢性肾脏病的进展，可能因为高尿酸血症刺激入球小动脉血管平滑肌细胞增殖而使肾脏灌注减少。但也有研究认为尿酸与肾脏疾病或心血管疾病没有因果关系，属于风险标志物。反方观点：降尿酸治疗不能延缓肾功能恶化的进展《CKD-FIX研究：别嘌呤醇对慢性肾病进展的影响》New England Journal of Medicine，2020年6月 (3)这项随机、对照研究中，纳入CKD3期或4期的、无痛风、尿白蛋白/肌酐≥265mg/g，或前一年eGFR下降至少3.0ml/min/1.73m2的患者共369人，随机分配到别嘌呤醇100mg qd组、别嘌呤醇300mg qd组或安慰剂组，共104周。eGFR的年平均变化，在别嘌呤醇组和安慰剂组中，分别为−3.33ml/min/1.73m2和−3.23ml/min/1.73m2（P = 0.85）。在别嘌呤醇组和安慰剂组发表有46%和44%的患者报告了严重不良事件。结论：与安慰剂相比，在慢性肾病和进展高风险患者中，别嘌呤醇降低尿酸治疗并没有减缓eGFR的下降。�《随机对照研究：别嘌醇降低1型糖尿病患者血清尿酸水平不能延缓肾脏功能进展》New England Journal of Medicine，2020年6月 (4)尿酸升高与糖尿病肾病的风险增加有关，研究旨在评估1型糖尿病合并早中期糖尿病肾病患者中，使用别嘌醇降尿酸是否可以减缓肾小球滤过率的下降。在这个双盲研究中，纳入GFR在40～99.9ml/min/1.73m2的1型糖尿病合并糖尿病肾病的患者，随访3年。3年后，服用别嘌醇的患者尿酸从362umol/L降至220umol/L，安慰剂组不变；两组患者GFR平均每年下降3.0和2.5ml/min/1.73m2。结论：在1型糖尿病合并糖尿病肾病患者中，没有证据证明采用别嘌醇降尿酸可以延缓肾脏功能进展。《回顾性观察研究：非布司他与别嘌呤醇对慢性肾病患者尿酸降低及肾预后的比较》Science Report，2020年7月 (5)本研究旨在比较黄嘌呤氧化酶抑制剂非布司他和别嘌呤醇在CKD患者中降低尿酸和保护肾脏的作用。来自台湾高雄的研究人员对一家大型医疗服务系统2010 - 2015年的电子健康记录进行分析，纳入刚开始接受降尿酸治疗的成年、CKD患者，总共1050例，观察时间为2.5年。与别嘌呤醇相比，非布司他治疗后，80%的情况下患者的尿酸水平可以维持在

On continue notre série goutteuse! Dans ce 61ème épisode du Pharmascope, Nicolas, Sébastien et Isabelle discutent des mesures non pharmacologiques et du traitement prophylactique de la goutte. Les objectifs pour cet épisode sont les suivants: Expliquer les mesures non pharmacologiques utilisées dans le traitement chronique de la goutteIdentifier les indications pour débuter un traitement prophylactique en goutteExpliquer les bénéfices et les risques associés aux traitements prophylactiques en goutte Ressources pertinentes en lien avec l’épisode Lignes directrices portant sur la prise en charge de la goutteFitzGerald JD et coll. 2020 American College of Rheumatology Guideline for the Management of Gout. Arthritis Rheumatol. 2020;72:879-95. Richette P et coll. 2018 updated European League Against Rheumatism evidence-based recommendations for the diagnosis of gout. Ann Rheum Dis. 2020;79:31-8. Qaseem A et coll. Management of Acute and Recurrent Gout: A Clinical Practice Guideline From the American College of Physicians. Ann Intern Med. 2017;166:58-68. Articles de revue portant sur la prise en charge de la goutteDrug and Therapeutics Bulletin. Latest guidance on the management of gout. BMJ. 2018;362:k2893. Sidari A, Hill E. Diagnosis and Treatment of Gout and Pseudogout for Everyday Practice. Prim Care. 2018;45:213-36. Dugré N. L’hyperuricémie et la goutte. Québec Pharmacie. Juin/juillet 2015. 25p. Études portant sur les traitements chroniques de la goutteBadve SV et coll. Effects of Allopurinol on the Progression of Chronic Kidney Disease. N Engl J Med. 2020;382:2504-13. Doria A et coll. Serum Urate Lowering with Allopurinol and Kidney Function in Type 1 Diabetes. N Engl J Med. 2020;382:2493-2503. Kimura K et coll. Febuxostat Therapy for Patients With Stage 3 CKD and Asymptomatic Hyperuricemia: A Randomized Trial. Am J Kidney Dis. 2018;72:798-810. Schumacher Jr HR et coll. Effects of febuxostat versus allopurinol and placebo in reducing serum urate in subjects with hyperuricemia and gout: a 28-week, phase III, randomized, double-blind, parallel-group trial. Arthritis Rheum. 2008;59:1540-8. Seth R et coll. Allopurinol for chronic gout. Cochrane Database Syst Rev. 2014;10:CD006077. Ramasamy SN et coll. Allopurinol Hypersensitivity: A Systematic Review of All Published Cases, 1950–2012. Drug Saf. 2013;36:953-80. White WB et coll. Cardiovascular safety of febuxostat or allopurinol in patients with gout. N Engl J Med 2018;378:1200-10.

The Filtrate:Joel TopfSwapnil HiremathSamira FaroukAnd special guests:Katalin Susztak, Professor of Medicine Perlman School of Medicine, University of Pennsylvania. @KSusztakShow Notes:CKD-FIX: Effects of Allopurinol on the Progression of Chronic Kidney DiseasePERL: Serum Urate Lowering with Allopurinol and Kidney Function in Type 1 DiabetesCoverage at NephJC: Effects of Allopurinol on the Progression of Chronic Kidney DiseaseRichard Johnson’s theory in pay-walled Nature Reviews Nephrology: Hypothesis: fructose-induced hyperuricemia as a causal mechanism for the epidemic of the metabolic syndromeRichard Johnson’s theory in open access Nehrology Dialysis and Transplantation: Uric acid and chronic kidney disease: which is chasing which?PERL: Preventing early renal lossIohexol, good for measuring GFR as well as causing contrast associated nephropathy?Uric acid versus urate: The Crystallization of Monosodium UrateAssociation of HLA-B*5801 allele and allopurinol-induced Stevens Johnson syndrome and toxic epidermal necrolysis: a systematic review and meta-analysisWHO list of essential medicationsFixing the numbers, specifically phosphorousGFR Decline as an End Point for Clinical Trials in CKD: A Scientific Workshop Sponsored by the National Kidney Foundation and the US Food and Drug AdministrationCost of allopurinol: $7/month but it is only $9 for 3 monthsFebuxostat Therapy for Patients With Stage 3 CKD and Asymptomatic Hyperuricemia: A Randomized TrialTipping point analysis - multiple imputation for stress test under missing not at random (MNAR) or a YouTube video if that’s your speed (sorry, I couldn’t find a TikTok on imputation stress tests).Mendelian randomization study of urate and CKD by Ron Do and teamDad jokesFake systematic review by Johnson’s group showing Urate lowering prevented CKDHyperuricemia As a trigger of Immune Response in Hypertension and Chronic Kidney Disease by Claudio Ponticelli published the week after these two RCTs were published.NEJM Editorial: Urate-Lowering Therapy and Chronic Kidney Disease Progression by Daniel FeigCOVID and PPI manuscriptHashtag the cowboy‘WhatsApp®’ening in nephrology trainingArkana LIVE Pathology SessionsNephJC Summer Book Club. Read Rana Awdish’s In Shock

(Actualidad Médica 015) La gota es la artropatía inflamatoria más frecuente afectando alrededor de 10 millones de adultos en los Estados Unidos de América. Aunque su etiología está bien comprendida y existen medicamentos de bajo costo que permiten su tratamiento, existe aún una brecha terapéutica en el tratamiento de esta enfermedad. A pesar de múltiples recomendaciones que han sido publicadas desde el 2012 por diferentes organismos, no ha habido un aumento importante del uso de medicamentos para la reducción del ácido úrico, la adherencia a estos es baja y ha habido un aumento considerable de la evidencia disponible para el manejo de esta enfermedad en los últimos años. ENLACE: https://onlinelibrary.wiley.com/doi/full/10.1002/acr.24180

The Journal of Rheumatology's Editor-in-Chief Earl Silverman talks about this month's selection of articles that are most relevant to the clinical rheumatologist. This month's selections include: Cardiovascular Event Risk in Rheumatoid Arthritis Compared with Type 2 Diabetes: A 15-year Longitudinal Study by Rabia Agca, Luuk H.G.A. Hopman, Koen J.C. Laan, Vokko P. van Halm, Mike J.L. Peters, Yvo M. Smulders, Jacqueline M. Dekker, Giel Nijpels, Coen D.A. Stehouwer, Alexandre E. Voskuyl, Maarten Boers, Willem F. Lems and Michael T. Nurmohamed DOI: https://doi.org/10.3899/jrheum.180726 Treating Psoriatic Arthritis to Target: Defining the Psoriatic Arthritis Disease Activity Score That Reflects a State of Minimal Disease Activity by Anthony V. Perruccio, Matthew Got, Suzanne Li, Yang Ye, Dafna D. Gladman and Vinod Chandran DOI: https://doi.org/10.3899/jrheum.181472 Neutrophil Extracellular Traps Profiles in Patients with Incident Systemic Lupus Erythematosus and Lupus Nephritis by Maurizio Bruschi, Alice Bonanni, Andrea Petretto, Augusto Vaglio, Federico Pratesi, Laura Santucci, Paola Migliorini, Roberta Bertelli, Maricla Galetti, Silvana Belletti, Lorenzo Cavagna, Gabriella Moroni, Franco Franceschini, Micaela Fredi, Giulia Pazzola, Landino Allegri, Renato Alberto Sinico, Giampaola Pesce, Marcello Bagnasco, Angelo Manfredi, Giuseppe A. Ramirez, Paola Ramoino, Paolo Bianchini, Francesco Puppo, Francesca Pupo, Simone Negrini, Federico Mattana, Giacomo Emmi, Giacomo Garibotto, Domenico Santoro, Francesco Scolari, Angelo Ravelli, Angela Tincani, Paolo Cravedi, Stefano Volpi, Giovanni Candiano and Gian Marco Ghiggeri DOI: https://doi.org/10.3899/jrheum.181232 Effect of Timing and Duration of Statin Exposure on Risk of Hip or Knee Revision Arthroplasty: A Population-based Cohort Study by Michael J. Cook, Antony K. Sorial, Mark Lunt, Tim N. Board and Terence W. O'Neill DOI: https://doi.org/10.3899/jrheum.180574 Factors Influencing the Effectiveness of Allopurinol in Achieving and Sustaining Target Serum Urate in a US Veterans Affairs Gout Cohort by Jasvinder A. Singh, Shuo Yang and Kenneth G. Saag DOI: https://doi.org/10.3899/jrheum.190522 To read the full articles visit www.jrheum.org Music by David Hilowitz

Should we target uric acid levels when working to reduce cardiovascular risk? Cardiovascular (CV) disease remains the leading cause of death with many contributing risk factors, including hyperuricemia. Evidence suggests an elevation in uric acid levels is associated with and can lead to worse outcomes for individuals with CV disease and heart failure.  The Cardiovascular Safety of Febuxostat and Allopurinol in Patients with Gout and Cardiovascular Morbidities (CARES) trial was conducted to evaluate whether febuxostat was noninferior to allopurinol with regard to CV events in patients with gout and CV disease. Guest Authors:  Sophia Dietrich, PharmD and Michael W. Nagy, PharmD, BCACP Music by Good Talk

Dr. Jan Dutz speaks with JCMS Editor-in-chief Dr Kirk Barber about the article Dutz co-authored in the Nov/Dec 2019 edition of the Journal of Cutaneous Medicine and Surgery. The article focuses on how East Asians exposed to the urate-lowering drug allopurinol have a predilection for severe cutaneous drug reactions such as drug-induced hypersensitivity syndrome or drug reaction with eosinophilia and systemic symptoms and Stevens-Johnson syndrome/toxic epidermal necrolysis. Dr Barber and Dr Dutz discuss why screening of patients of East Asian descent for the presence of HLA-B*58:01 prior to allopurinol initiation has been a Canadian missed opportunity. And what more can be done to encourage wider use of this inexpensive screening test.Dr. Jan Dutz is Professor and Head of the Department of Dermatology and Skin Science at UBC. He is also a Senior Scientist with the British Columbia Children's Hospital Research Institute.Theme music by Lee RosevereProduced by David McGuffin - Explore Podcast Productions 

Dr. Jan Dutz speaks with JCMS Editor-in-chief Dr Kirk Barber about the article Dutz co-authored in the Nov/Dec 2019 edition of the Journal of Cutaneous Medicine and Surgery. The article focuses on how East Asians exposed to the urate-lowering drug allopurinol have a predilection for severe cutaneous drug reactions such as drug-induced hypersensitivity syndrome or drug reaction with eosinophilia and systemic symptoms and Stevens-Johnson syndrome/toxic epidermal necrolysis. Dr Barber and Dr Dutz discuss why screening of patients of East Asian descent for the presence of HLA-B*58:01 prior to allopurinol initiation has been a Canadian missed opportunity. And what more can be done to encourage wider use of this inexpensive screening test. Dr. Jan Dutz is Professor and Head of the Department of Dermatology and Skin Science at UBC. He is also a Senior Scientist with the British Columbia Children’s Hospital Research Institute. Theme music by Lee Rosevere Produced by David McGuffin - Explore Podcast Productions  

We want to live longer… and healthier too! Dr Peter Attia, a physician focusing on the applied science of longevity, walks us through lifespan and healthspan, exploring tactics aimed at extending both. Listeners will challenge the conventional approach to primary care and explore tactics to optimize exercise, nutrition, and health, including counseling on different dietary patterns, fasting, exercise, emotional well-being and how to prepare for the Centenarian Olympics! Show Notes | Subscribe | Spotify | Schwag! | Top Picks | Mailing List | thecurbsiders@gmail.com Credits Written and Produced by: Matthew Watto MD, FACP and Elena Gibson MD  Cover Art and Infographic: Elena Gibson MD Hosts: Elena Gibson MD, Stuart Brigham MD; Matthew Watto MD, FACP; Paul Williams MD, FACP    Editor: Emi Okamoto MD Audio Editor: Clair Morgan of Nodderly Guest: Peter Attia MD    Time Stamps 00:00 Intro, disclaimer, guest bio 04:22 Guest one-liner, Career Advice, Picks of the Week* 14:30 Case: A couple seeking maximize longevity; Defining longevity, healthspan, lifespan and the 4 types of death 19:30 Lifespan, the longevity curve and the long tail 23:50 Peter’s approach to shepherding patients toward longevity; Exploring motivations 32:06 Back to our couple: What exercises should they perform 42:09 Peter’s advice on nutrition; the standard American diet; Intermittent fasting; Dietary Restriction 51:20 Periodic fasting and water only fasting 54:33 Genetics and longevity 56:40 Metformin; SGLT2 inhibitors; Allopurinol and uric acid lowering 61:47 Peter’s take home points and a plug for David Foster Wallace’s commencement speech from Kenyon College 66:40 Outro *The Curbsiders participates in the Amazon Services LLC Associates Program, an affiliate advertising program designed to provide a means for sites to earn advertising commissions by linking to Amazon. Simply put, if you click on my Amazon.com links and buy something we earn a (very) small commission, yet you don’t pay any extra. Goal Listeners will learn a framework for thinking about longevity and practical tips for improving lifespan and healthspan. Learning objectives After listening to this episode listeners will…   Define longevity, healthspan,and lifespan  Recall the four types of death. Explain the objectives of improved aging (longer lifespan, delayed rate of decline, and compressed period of morbidity). Learn basic dietary principles to improve lifespan/healthspan and compare various dietary patterns Describe some tactics to promote lifespan/healthspan (in nutrition, exercise physiology, sleep, distress management, medications and supplements, etc.) Explore the possible longevity benefits of fasting Disclosures Dr Peter Attia reports the following relevant financial disclosures: Peter receives speaking honorariums from organizations including hospitals and health-related businesses when he is asked to speak on longevity, metabolic-related topics, athletic performance, and his personal experience. Peter is the co-founder and Chief Medical Officer of the fasting app Zero. Peter is an advisor to, and/or investor in, the companies Virta Health, Hu Kitchen, Oura Health Oy, Magic Spoon Cereal, Inevitable Ventures, Salutoceuticals, and Supercast. Further information can be found at his website https://peterattiamd.com/about/.  The Curbsiders report no relevant financial disclosures.  Citation Attia P, Gibson E, Williams PN, Brigham SK, Watto MF. “#183 Longevity, Healthspan and Lifespan with Peter Attia MD”. The Curbsiders Internal Medicine Podcast. https://thecurbsiders.com/episode-list November 18, 2019.

I am joined by Spiro Koulouris, a sufferer from gout. Spiro has dramatically improved his condition through lifestyle and dietary changes. He tells us how. Spiro's website: Gout & You:www.goutandyou.comSpiro's Facebook page:https://www.facebook.com/GoutandYou/

A look at this deadly mucocutaneous reaction and how to best manage these patients in the ED https://media.blubrry.com/coreem/content.blubrry.com/coreem/SJS.mp3 Download Leave a Comment Tags: Critical Care, Dermatology Show Notes Episode Produced by Audrey Bree Tse, MD Rash with dysuria should raise concern for SJS with associated urethritis Dysuria present in a majority of cases SJS is a mucocutaneous reaction caused by Type IV hypersensitivity Cytotoxic t-lymphocytes apoptose keratinocytes → blistering, bullae formation, and sloughing of the detached skin Disease spectrum SJS = 30% TBSA SJS/ TEN Overlap = 10-30% TBSA Incidence is estimated at around 9 per 1 million people in the US Mortality is 10% for SJS and 30-50% for TEN Mainly 2/2 sepsis and end organ dysfunction. SJS can occur even without a precipitating medication Infection can set it off especially in patients with risk factors including HIV, lupus, underlying malignancy, and genetic factors SATAN for the most common drugs Sulfa, Allopurinol, Tetracyclines, Anticonvulsants, and NSAIDS Anti-epileptics include carbamazepine, lamictal, phenobarb, and phenytoin Can have a curious course Hypersensitivity reaction can develop while taking medication, or even one to four weeks after exposure In pediatric population, mycoplasma pneumonia and herpes simplex have been identified as precipitating infections Patients often have a prodrome 1-3 days prior to the skin lesions appearing May complain of fever,

A look at this deadly mucocutaneous reaction and how to best manage these patients in the ED https://media.blubrry.com/coreem/content.blubrry.com/coreem/SJS.mp3 Download Leave a Comment Tags: Critical Care, Dermatology Show Notes Episode Produced by Audrey Bree Tse, MD Rash with dysuria should raise concern for SJS with associated urethritis Dysuria present in a majority of cases SJS is a mucocutaneous reaction caused by Type IV hypersensitivity Cytotoxic t-lymphocytes apoptose keratinocytes → blistering, bullae formation, and sloughing of the detached skin Disease spectrum SJS = 30% TBSA SJS/ TEN Overlap = 10-30% TBSA Incidence is estimated at around 9 per 1 million people in the US Mortality is 10% for SJS and 30-50% for TEN Mainly 2/2 sepsis and end organ dysfunction. SJS can occur even without a precipitating medication Infection can set it off especially in patients with risk factors including HIV, lupus, underlying malignancy, and genetic factors SATAN for the most common drugs Sulfa, Allopurinol, Tetracyclines, Anticonvulsants, and NSAIDS Anti-epileptics include carbamazepine, lamictal, phenobarb, and phenytoin Can have a curious course Hypersensitivity reaction can develop while taking medication, or even one to four weeks after exposure In pediatric population, mycoplasma pneumonia and herpes simplex have been identified as precipitating infections Patients often have a prodrome 1-3 days prior to the skin lesions appearing May complain of fever, myalgias,

I break down the mechanism of action, side effects, and important drug interactions you need to know. I give you a sense of what things you might actually encounter in practice when working with patients who take allopurinol. Allopurinol is a top 200 drug. Remember to subscribe to the website reallifepharmacology.com for the Free 31 page PDF where I give you three highly testable pearls on the top 200 drugs. In addition to the 31 page PDF for subscribing, you will get a free 100 question pharmacology test designed for healthcare professionals. I hope you enjoy this episode the pharmacology of allopurinol!

Master the management of gout with tips from expert, Tuhina Neogi MD, PhD, Professor of Medicine at Boston University School of Medicine. Topics include: how to initiate and titrate urate lowering therapy, guidelines controversy over uric acid targets, colchicine & NSAIDS for anti-inflammatory prophylaxis, uricosuric agents, febuxostat, HLA B5801, use of uric acid levels in the acute setting and more random gout facts. Full show notes available at http://thecurbsiders.com/podcast. Join our mailing list and receive a PDF copy of our show notes every Monday. Rate us on iTunes, recommend a guest or topic and give feedback at thecurbsiders@gmail.com. Credits: Written and produced by: Matthew Watto MD Hosts: Paul Williams MD, Stuart Brigham MD, Matthew Watto MD Guest: Tuhina Neogi MD, PhD Time Stamps 00:00 Intro and guest bio 01:30 Allopurinol initiation and titration 07:10 Uricosuric therapy 09:10 Controversy over uric acid targets for gout 17:40 Parachutes and randomized controlled trials 19:15 Colchicine or NSAIDS for prophylaxis 23:20 Who needs febuxostat? 26:20 When to refer for gout, HLA B5801, and checking uric acid levels in the acute setting   33:29 Take home points 36:15 Outro Tags: allopurinol, uric, urate, acid, level, therapy, management, gout, flare, crystal, arthritis, titration, probenecid, febuxostat, target, acr, acp, guidelines, nsaids, colchicine, hla b5801, septic, rheumatology, assistant, care, doctor, education, family, FOAM, FOAMim, FOAMed, health, hospitalist, hospital, internal, internist, meded, medical, medicine, nurse, practitioner, professional, primary, physician, resident, student

Commentary by Dr. Valentin Fuster

This week we'll be discussing a trial addressing a controversial topic - starting allopurinol during an acute attack of gout.  It's a short podcast on a short paper, but one that could have a big impact on your practice. Be sure to follow us on Twitter @EBRheum! Access the paper itself here.

Se noter og links på sivp.dk/9 Leishmania hos hunde Eva fortæller at Leishmania præsenterer sig næsten altid med hudproblemer om symmestrisk alopeci og noduli. Der kan også ses vægttab, nedstemt humør, tegn på begyndende nyresvigt og nogle gange øget blødningstendens. Promastigoter udvikles i sandfluen. Disse injiceres i værten når sandfluen bider. Her optages promastigoterne af makrofager og spredes i kroppen. Inkubationstiden er 1 måned op til 7 år. Intracellulære amastogoter (non-flagellat-form) giver kutane læsion hvorfra sandfluer re-inficeres. Den intracellulære form kan desuden inducere et kraftigt immunrespons der resulterer i glomerulonefritis og polyartritis på grund af udviklingen af immunkomplekser. Anamnesen Indeholder næsten altid information om udlandsrejse inden for 7 år eller om oprindelse af Syd- og mellemeuropa. Cases er set i Mellemeuropa (bl.a. Tyskland) hos hunde, der ikke har været ude og rejse. Klinisk undersøgelse Eva forklarer at vi klassisk vil se hudproblemer og tegn på systemiske lidelse. For en stor del af patienterne vil det være lymadenopati og forstørret milt og evt. forstørret lever Paraklinisk undersøgelse Antistof kan måles i serum med høj specificitet og sensitivitet. Amastigote kan ses ved direkte mikroskopi af lymfeknude- og knoglemarvsaspirat og ved direkte hudaftryk. Dette giver en definitiv diagnose. Eva beskriver at paraklinisk ses ofte: Azotæmi (øget crea og urea) og polyclonal hyperglobulinæmi (altså fra forskellelige celleliner) Proteinuri kan forekomme i en ren urinprøve uden aktivt sediment og Urin/Protein-Creatin-ratio vil ofte være større end 0,5. Differentialdiagnoser Immunmedierede sygdomme som Pemphigus foliaceus og SLE er differentialdiagnoser. Det er neoplasi som Lymfoma Multipelt myelom. Behandling I følgelige Eva kan Leishmania behandles med Allopurinol, der er det mest effektive pt. Forebyggelse af infektion ved at forhindre sandfluers bid er eneste medicinske mulighed for forebyggelse. Til dette bruges rappellerende medicin som Permethrin (Bayvantic Vet eller Effitix) Desuden bør hunde holdes inde og under flue-/myggenet om natten. Hunde med nyresvigt bør monitoreres herfor.

Professor Michael Doherty from the University of Nottingham, Nottingham, UK, speaks to Prof Jaap van Laar, Editor of Rheumatology about their study published in the Journal. The questions they discussed were around when allopurinol is given to pat

Professor Michael Doherty from the University of Nottingham, Nottingham, UK, speaks to Prof Jaap van Laar, Editor of Rheumatology about their study published in the Journal. The questions they discussed were around when allopurinol is given to pat

Professor Michael Doherty from the University of Nottingham, Nottingham, UK, speaks to Prof Jaap van Laar, Editor of Rheumatology about their study published in the Journal. The questions they discussed were around when allopurinol is given to pat

How the gout drug allopurinol could be a new anti-anginal therapy.

Thyroid parameters in tortoises and turtles frequently presented at the veterinary practise The present study is concerned with the examination of thyroid parameters in those tortoisespecies frequently presented at the veterinary practise. 338 tortoises and turtles were examined over a period of one year. The examinations included case history, clinical examinations, diagnosis and determination of fT3, fT4, T3, and T4 levels by way of electrochemiluminescence immunoassay and sonographic examinations of the thyroid gland with determination of the thyroid size by measuring. One of the first steps was to determine the thyroid hormone concentrations of fT3, fT4, T3, T4 in 103 healthy tortoises and turtles. Subsequently the levels were examined for dependencies regarding species, age, sex, and season. This revealed significantly higher fT4- and T4-concentrations in turtles compared to tortoises. A diagnostical dependence regarding age, sex, and season could not be detected. Accordingly a reference range, defined as 95% percentile interval, was established for those tortoises frequently presented at the veterinary practise (Testudo hermanni, Testudo graeca, Testudo marginata, Agrionemys horsfieldii). In a second step the fT3, fT4, T3, and T4 concentrations of 235 ill tortoises were determined. The animals were divided according to manner and severity of their illness into three groups (slightly ill animals, profoundly ill animals, and animals under medication by Allopurinol). Significant differences were revealed in the thyroid hormone concentrations of healthy compared to profoundly ill animals. The main parameter for diagnostic use, it became, is apparently fT3. There is evidence suggesting an increase of this parameter in excess of the reference range indicates that the animals suffer from a severe illness with possibly fatal consequences. This test has a high specificity and a comparatively low sensitivity. At the same time the thyroid glands of 338 tortoises were examined sonographically. Position, shape, echogenicity and echotexture were described. The maximum diameter of the thyroid gland was established and put in relation to the body weight. Dependencies between the size of the thyroid and the state of health or illness on the one hand and the concentration of thyroid hormones on the other hand were checked. This showed that animals under medication by Allopurinol frequently feature bigger thyroid glands than healthy animals. A correlation between thyroid hormone concentration and thyroid-size could not be proven. The results of this study are compared to evidence from to literary references and the diagnostical applicability is discussed.