Podcasts about Neutropenia

Dr. Shaalan Beg and Dr.Mohamed Salem discuss key abstracts that will be presented at the 2024 ASCO Annual Meeting, including hypoxia-response CAR T- cell therapy for solid tumors, GPC3-specific CAR T- cell therapy in hepatocellular carcinoma, and the promising efficacy of targeted therapies in GI cancers.  TRANSCRIPT Dr. Shaalan Beg: Hello and welcome to the ASCO Daily News Podcast. I am Dr. Shaalan Beg, your guest host of the podcast today. I'm an adjunct associate professor at UT Southwestern's Simmons Comprehensive Cancer Center. In today's episode, we'll be discussing some key abstracts in GI cancers that will be presented at the 2024 ASCO Annual Meeting. I'm delighted to welcome Dr. Mohammed Salem, a GI medical oncologist at the Levine Cancer Institute at Atrium Health, for this discussion. Our full disclosures are available in the transcript of this episode. Mohammed, it's great to have you back on the podcast. Dr. Mohamed Salem: Thank you, Dr. Beg. It's always a pleasure to be here. Thanks for having me.  Dr. Shaalan Beg: So we're seeing more and more exciting data emerge on the role of ctDNA in GI cancers. And that's a topic that we've covered fairly extensively on the podcast. This year, in Abstract 3513, investigators used a novel, highly sensitive HPV ctDNA assay to evaluate the clinical outcomes of HPV ctDNA status in people with localized anal cancer treated with chemoradiation. And we know that prior HPV infection is associated with 90% of anal cancers. Can you give us a summary of the study and why it's so important to the clinical care we're giving our patients today?  Dr. Mohamed Salem: Sure. So, as you already alluded to, in the current era of precision oncology or precision medicine in general, there is an effort to try to maximize treatment efficacy and minimize the side effects. We're trying to understand how to do that by developing more biomarkers. I think this was a very interesting study that was led by Dr. Morris of MD Anderson. As you mentioned, he tried to determine the correlation between that circulating tumor DNA at different timelines and also associated that with the relapse. Obviously, as we all know, HPV infection is linked to about over 90% of anal cancers, and anal cancer is increasingly common in the U.S.  The study design includes patients from stage 1, 2, and 3 anal cancer treated with curative intent concurrent chemo radiation and the plot sample to collect circulating DNA was taken at five weeks of treatment and then at various intervals, including 3months, 6  months, 9 months and 12 months, to detect the HPV circulating DNA. And the analysis was done to correlate detection of circulating DNA with a relapse.  So what they observed is after collecting the samples at the end of the treatment, which is 5 weeks, followed by 3 months, 6 months, 9 months, and 12 months following treatment using the correlation between the detection of circulating tumor DNA as well as the recurrence rate, they were able to identify that about 22% was seen at 5 weeks, 13% was seen at three months, then 10% was seen at 6 months, and 0% actually was seen at 12 months. In the final analysis, they concluded that detection of circulating DNA at 3 months was significantly associated with a relapse rate of those patients. And also, they looked at the baseline stage, T stage, end stage, age and other perhaps prognostic factors. But the clinical implication of that trial is this finding supports the potential of integrating now the circulating DNA analysis and routine post-treatment surveillance, which hopefully will help us identify those patients with high risk of relapse and whether they can be treated with adjuvant therapy  in context-free drug trial or even like more close surveillance. Obviously, this is a very novel study, so it needs validation. Also, we need to understand more about the platform used because with the immersion technology and how fast this field is moving, I think it's important to look at this platform or other platforms. I think as a concept it's very interesting and hopefully will help us to identify patients with higher risk. So, I'm looking forward to hearing the full presentation. Dr. Shaalan Beg: Moving on to colorectal cancer, Abstract 3514 is a trial of hypoxia-responsive CEA CAR T-cell therapy for people with heavily pretreated solid tumors where this was administered intraperitoneally or intravenously. And you know, as a solid tumor oncologist or GI oncologist, we've been watching the hematologic space evolve so dramatically in the last five years with cellular therapies that it's exciting to see these CAR T-cell approaches being applied in solid tumors with some results. So can you talk about this study and whether you think it will influence clinical practice?  Dr. Mohamed Salem: Of course, I'm actually very excited to see this study because as you mentioned, CAR T-cell therapy has been utilized in hematological malignancies for the last several years and in fact it's becoming a center of care. As you know, it's very effective in certain tumors. Unfortunately, we did not see a similar result in solid tumors thus far. I know we are trying to make progress, but we are definitely not seeing the same efficacy in solid tumors. And also, of course, in CRC and many other tumors, we need more target options, so I was very excited to see this abstract. And I want to give a little bit of background why this abstract is important. Many solid tumors have a low oxygen level environment, hypoxia obviously, which can impact the effectiveness of CAR T therapy. So hypoxia can suppress the immune response, leading to poor performance of the immune cells like the T cell within the tumor. The investigators, to overcome that challenge, meaning hypoxia impacting the efficacy of the T cell, they were actually able to engineer a CAR T cell to be hypoxia responsive. And what does that mean? That the cells are designed to become more active in low oxygen conditions, which is more difficult in many of the solid tumors. The reason that's very interesting is because, one, it reduces exhaustion of the T cell, meaning like when you have the T cell active all the time, they get exhausted. So when you have the T cell in the resting state, until they reach the tumor environment and they get activated by the hypoxia status, now you reduce the expulsion of the T cell. But also that one overcomes the resistance. So once activated in the tumor hypoxic environment, this CAR T cell shows increased efficacy in targeting and killing the cancer cell.  Based on that concept, the investigators conducted a phase 1 dose escalation study in solid tumors. So this was a phase 1 open label group escalation study involving patients with tumor suppressed CEA and also had relapsed refractory second line treatment. The trial actually included 2 routes of administration, which I think was very interesting – IV versus intraperitoneal, IP, way of administration. And they enrolled about 40 patients between June of 2022 and January 2023. And 35 patients had colorectal cancer, 3 patients had gastric cancer, and 2 patients had non-small cell lung cancer. Overall, there was no surprising safety data. In terms of side effects, it was largely macrocystis, colitis. Unfortunately, they had 1 treatment that did not finish. But the interesting feature was the efficacy of that concept was demonstrated and in fact they were able to see more disease response and control at this rate with IP infusion, which I think is a very novel approach. I would look forward to trying and looking into this kind of delivery, especially in CRC and other tumors. Dr. Shaalan Beg: Because we've known that historically managing disease intraperitoneally has been challenging with cytotoxic chemotherapies and even surgical approaches that have been deployed can be fairly morbid as well. So looking at novel delivery mechanisms can help us understand, maybe be able to manage side effects of treatments in different ways and open doors for treatment in diseases that otherwise we couldn't manage. So definitely a very novel and exciting approach on this study.  Dr. Mohamed Salem: I agree. I think the idea of administering an IP route is a very interesting idea.   Well, Shaalan, there is another study in CRC, Abstract 3515. This is the first human study of ABBV-400, cMET–targeting antibody-drug conjugate in advanced solid tumors. Can you tell us about this promising data? Dr. Shaalan Beg: Yeah, so we've known that cMET is a very relevant biomarker across many cancers, particularly colorectal cancer, and it is overexpressed in a fairly large proportion of multiple diseases. But there hasn't been an effective regimen that has been found to be tolerable to target this specific biomarker. In this study, the investigators are evaluating an antibody drug conjugate, which takes the cMET targeting antibody telisotuzumab and conjugates it to a novel topoisomerase one inhibitor payload. And there's a phase one study that enrolled people across multiple different tumor types. This was presented at ASCO 2023. And this year, the investigators are coming in and giving the results of a colorectal cancer cohort within that study. Patients were enrolled in the dose escalation phase, and in the dose expansion phase, there were 122 colorectal cancer cases; so a fairly healthy size colorectal cancer population. And the median number of prior lines of therapy was 4, which is fairly consistent with what we would expect in our clinical population for people with colorectal cancer. So what they found in terms of efficacy is that the response rates, the confirmed overall response rates, were between 15 and 20%, depending on what dose of the medication the patients had received. They enrolled people regardless of cMET expression and then evaluated the response based on a higher or lower cMET expression. And those with higher cMET expression had an overall response rate of >30%, while those with lower cMET expression had a response rate of 10 to 15%. So they still had a response rate, which for fifth-line colorectal cancer is something to be aware of and it could be a marker of more significant clinical activity than other treatments that are out there.  And with the antibody drug conjugates, it's also important for us to keep an eye on the side effect profiles because a lot of these agents can have distinct side effect profiles that otherwise we wouldn't be familiar with. And in this study, 64% of participants had a grade 3 or above treatment emergent adverse events, and 41% had serious adverse events. So definitely something to think about. And most of these were hematologic toxicities, 30% had grade 3 or worse anemia. Neutropenia was seen, in grade three and above, was seen in 25%, leukopenia or grade three and above was seen in 12%, and thrombocytopenia again around 12%. And the non-hematologic toxicities were nausea, fatigue, vomiting and diarrhea. There was some interstitial lung disease, pneumonitis, which was seen in 7% of the total population, of which 2% had grade three or above. So definitely something to think about. From my perspective, I really am excited about this presentation because we're seeing evidence of clinical activity focused on cMET for refractory colorectal cancer compared to other agents that are out in the market. If this pans out in future studies, it could definitely change the way we deliver our treatments. Dr. Mohamed Salem: I totally agree that we actually need more therapy for those patients. And I'm not surprised that the myelosuppression, as you mentioned, was in fifth-line treatment. So this patient had large exposure to cytotoxic agents before.   So, looking at CAR T once more, there is a very interesting Abstract 4019, which is a study of C-CAR031, a GPC3-specific TGFβRIIDN armored autologous CAR T, in patients with advanced hepatocellular carcinoma (HCC). What are your key takeaways from this study, Shaalan? Dr. Shaalan Beg: This is a first-in-human study. It enrolled people with advanced HCC who failed on one or more lines of prior therapy and they were given one single infusion of C-CAR031 after standard lymphodepletion and they enrolled 24 patients across 4 dose levels. If we look at the overall response rate, 50% of the 22 people who were eligible for response assessments had a partial response. This response rate varies based on the dose level itself and the investigators claim a 90% disease control rate. So definitely when we think about standard treatments for hepatocellular cancer after first line therapy, this is something which will catch a lot of people's attention. Again, with CAR T-cell therapy, we need to be aware of the risk of potential toxicities. There were no dose limiting toxicities and CRS or cytokine release syndrome was observed in 91% of patients, while a very small proportion, about less than 5%, had grade three CRS. Most of the side effects here were, again, lymphocytopenia, neutropenia, thrombocytopenia, and some transaminitis in 16% of patients. They did see tumor reduction in 90%, not only in the intrahepatic disease, but also in the extrahepatic disease. And again, these are people who had BCLC stage C disease. So this included people with hepatic and extrahepatic metastases. And in terms of prior lines of therapy, 96% of patients had either received immune checkpoint inhibitors and TKIs.  If we think about how some other immune therapy regimens are being developed in the GI cancer space, there is some indication that liver lesions may respond differently compared to extra hepatic disease. So in this case, they saw responses in both scenarios, which makes it very exciting, because even though we've seen many approvals of TKIs and immunotherapy, anti-androgenic therapy in hepatocellular cancer, the treatment of these patients is still extremely difficult because of their underlying hepatic dysfunction. And it'll be very interesting to see how this treatment unfolds.  Dr. Mohamed Salem: You summarized it very well, Shaalan. I echo your thoughts. What is also interesting about that study, it's actually targeted at the GPC strain, which is prevalent in HCC but not normal tissue, which goes back to your comment about the toxicity, and hopefully we can also manage treatment in the context of underlying liver disease.  Dr. Shaalan Beg: I guess it's fair to say that we're both very excited to see what's ahead in GI cancers at the Annual Meeting.   Mohamed, thanks as always for sharing your great insights with us on the ASCO Daily News Podcast.  Dr. Mohamed Salem: Thank you all for having me, and I'm looking forward to meeting you and all our colleagues in Chicago in a couple of weeks. Dr. Shaalan Beg: And thank you to our listeners for your time today. You'll find links to the abstracts discussed today in the transcripts of this episode. I'll be back to cover late breaking abstracts and other key advances in GI oncology after the annual meeting, so please join me for more key insights from ASCO24 and on the ASCO Daily News Podcast. Finally, if you value the insights that you hear on the podcast, please take a moment to rate, review, and subscribe wherever you get your podcasts.   Disclaimer: The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement.   Find out more about today's speakers:  Dr. Shaalan Beg  @ShaalanBeg  Dr. Mohamed Salem  @SalemGIOncDoc    Follow ASCO on social media:  @ASCO on Twitter ASCO on Facebook ASCO on LinkedIn   Disclosures: Dr. Shaalan Beg:  Consulting or Advisory Role: Ispen, Cancer Commons, Foundation Medicine, Genmab/Seagen  Speakers' Bureau: Sirtex  Research Funding (An Immediate Family Member): ImmuneSensor Therapeutics  Research Funding (Institution): Bristol-Myers Squibb, Tolero Pharmaceuticals, Delfi Diagnostics, Merck, Merck Serono, AstraZeneca/MedImmune    Dr. Mohamed Salem: Consulting or Advisory Role: Taiho Pharmaceutical, Exelixis, Bristol-Myers Squibb, Exelixis, QED Therapeutics, Novartis, Pfizer, Daiichi Sankyo/Astra Zeneca  Speakers' Bureau: Genentech/Roche, Taiho Pharmaceutical, Daiichi Sankyo/Astra Zeneca, BMS, Merck 

This is Ep. 1 of SHEA's three-part series, Developments in Transmission-based Precautions. This episode focuses on preventing respiratory virus infections in patients with neutropenia or those undergoing hematopoietic stem cell transplantation. We'll explore characteristics of the patient population or local epidemiological trends that might warrant additional precautions and our speakers will provide a synopsis of the recommendations or data used to substantiate such measures. Speakers: Mini Kamboj, MD Lynne Strasfeld, MD Moderator: Chad Nix, MSc, CIC

Download for FREE today -  special Mnemonics Cheatsheet - so you can be SURE that you have that Must Know information down:  bit.ly/nursing-memory   Outline ANT A-Anemia N-Neutropenia T-Thrombocytopenia Description Leukemia can lead to anemia as it will disrupt the production of blood within the bone marrow. Neutropenia is a natural result of leukemia as the body's supply of white blood cells is decreased. Thrombocytopenia is a reduced platelet count which can also result from leukemia, especially in infants.

Episode 146: RA vs OA    Future Dr. Magurany explains how to differentiate rheumatoid arthritis from osteoarthritis.  Written by Thomas Magurany, MSIV, Ross University School of Medicine. Comments by Hector Arreaza, MD. You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.1. Etiology: Rheumatoid Arthritis (RA): RA is an autoimmune disease wherein the immune system mistakenly attacks healthy tissues, particularly the synovial joints, usually between the ages of 30-50. Genetic predisposition, environmental factors such as smoking or infections, hormonal imbalances, and lower socioeconomic status have been associated with an increased risk of developing RA(1).Osteoarthritis (OA): OA primarily arises due to mechanical stress on the joints over time. Factors contributing to OA include age, obesity, joint injury or trauma, repetitive joint use or overuse, genetic abnormalities in collagen structure, and metabolic disorders affecting cartilage metabolism (2).The greatest risk factor for the development of OA is age with most patients presenting after 45 years of age. The greatest modifiable risk factor for OA is weight. People with a BMI >30 were found to have a 6.8 times greater risk of developing OA. (3) Primary OA is the most common and is diagnosed in the presence of associated risk factors such as: older age, female gender, obesity, anatomical factors, muscle weakness, and joint injury (occupation/sports activities) in the absence of trauma or disease. Secondary OA occurs alongside a pre-existing joint deformity including trauma or injury, congenital joint disorders, inflammatory arthritis, avascular necrosis, infectious arthritis, Paget disease, osteopetrosis, osteochondritis dissecans, metabolic disorders (hemochromatosis, Wilson's disease), Ehlers-Danlos syndrome, or Marfan syndrome.2. Pathogenesis:Rheumatoid Arthritis (RA):In some patients, RA is triggered by some sort of environmental factor in a genetically predisposed person. The best example is tobacco use in a patient with HLA-DRB1. The immune response in RA starts at sites distant from the synovial joints, such as the lung, gums, and GI tract. In these tissues, modified proteins are produced by biochemical reactions such as citrullination. (4)In RA, an abnormal immune response leads to chronic inflammation within the synovium lining the joints. The inflammatory cytokines released cause synovitis and lead to the destruction of articular cartilage and bone erosion through pannus formation. Immune cells infiltrate the synovium causing further damage. (4) In summary: formation of antibodies to citrullinated proteins, these antibodies begin attacking wrong tissues.Osteoarthritis (OA):The primary pathological feature of OA is the degeneration of articular cartilage that cushions the joints causing surface irregularity, and focal erosions. These changes progress down the bone and eventually involve the entire joint surface. Mechanical stress triggers chondrocyte dysfunction, leading to an imbalance between cartilage synthesis and degradation that cause cartilage outgrowths that ossify and form osteophytes. This results in the release of enzymes that degrade the extracellular matrix, leading to progressive cartilage loss. As more of the collagen matrix is damaged, chondrocytes undergo apoptosis. Improperly mineralized collagen causes subchondral bone thickening; in advanced disease, bone cysts infrequently occur (5). In summary: Osteophytes formation and cartilage loss.3. Clinical Presentation:Rheumatoid Arthritis (RA):The most common and predominant symptoms include joint pain and swelling, usually starting insidiously over a period of weeks to months. RA typically affects multiple joints symmetrically, commonly involving small joints of the hands, wrists, feet and progresses to involve proximal joints if left untreated. Morning stiffness lasting more than an hour is a characteristic feature. The affected joint will be painful if pressure is applied to the joint or on movement with or without joint swelling. Synovial thickening with a "boggy" feel on palpation will be noted. The classical physical findings of ulnar deviation, metacarpophalangeal joint subluxation, swan neck deformity, Boutonniere deformity, and the "bowstring" sign (prominent and tight tendons on the dorsum of the hand) are seen in advanced chronic disease. (4) Around ¼ of patients with RA may present with rheumatoid noduleswhich are well demarcated, flesh-colored subcutaneous lumps. They are usually described as being doughy or firm and are not typically tender unless they are inflamed. They are usually found on areas susceptible to repeated trauma or pressure and include the elbows, fingers and forearms. Osteoarthritis (OA):OA primarily affects weight-bearing joints such as knees, hips, spine, and hands. Symptoms include joint pain aggravated by activity and relieved with rest, morning stiffness lasting less than 30 minutes, joint swelling due to secondary inflammation, and occasionally the formation of bony outgrowths called osteophytes (6). Tenderness may be present at joint lines, and there may be pain upon passive motion. Classic physical exam findings in hand OA include Heberden's nodes (posterolateral swellings of DIP joints), Bouchard's nodes (posterolateral swellings of PIP joints), and “squaring” at the base of the thumb (first Carpal-Metarcapal or CMC joints), bony enlargement, crepitus, effusions (non-inflammatory), and a limited range of motion. Patients may also experience bony swelling, joint deformity, and instability (patients complain that the joint is “giving way” or “buckling,” a sign of muscle weakness). (5)4. Lab findings:Rheumatoid Arthritis: Laboratory testing often reveals anemia of chronic disease (increased ferritin, decreased iron and TIBC) and thrombocytosis. Neutropenia may be present if Felty syndrome is present. RF is present in 80-90% of patients with a sensitivity of 69%. In patients who are asymptomatic or those that have arthralgias, a positive RF and especially CCP predicts the onset of clinical RA. Patients with RA with RF, ACPA, or both are designated as having seropositive RA. About 10% of RA patients are seronegative. ESR and levels of CRP are usually elevated in patients with active disease and can be used to assess disease activity. The synovial fluid in RA will also reveal low C3 and C4 levels despite elevated serum levels.(4) Some non-specific inflammatory markers such as ESR, CRP can help you guide your diagnosis of RA.Osteoarthritis:Lab findings are not significant. Clinical diagnosis if the following are present: 1) pain worse with activity and better with rest, 2) age more than 45 years, 3) morning stiffness lasting less than 30 minutes, 4) bony joint enlargement, and 5) limitation in range of motion. Blood tests such as CBC, ESR, rheumatoid factor, ANA are usually normal but usually ordered to rule out an inflammatory process. Synovial fluid should show a white blood cell count less than 2,000/microL, predominantly mononuclear cells (non-inflammatory). X-rays of the affected joint can show findings consistent with OA, such as marginal osteophytes, joint space narrowing, subchondral sclerosis, and cysts; however, radiographic findings do not correlate to the severity of the disease and may not be present early in the disease. (5)5. Treatment Approaches:Rheumatoid Arthritis (RA):There is no cure for RA.The goal of treatment in RA is inducing remission and optimizing quality of life. This is initially done by beginning DMARDs, include methotrexate, hydroxychloroquine, sulfasalazine, and leflunomide. Methotrexate is the initial DMARD of choice. Anti-TNF-alpha inhibitors include etanercept, infliximab, adalimumab, golimumab, and certolizumab may be used if DMARDs fail. NSAIDs are used to control joint pain and inflammation. Corticosteroids may be used as a bridge therapy to DMARDs in a newly diagnosed patient with a very active disease. (7) Coronary artery disease has a strong association with RA. RA is an independent risk factor for the development of coronary artery disease (CAD) and accelerates the development of CAD in these patients. Accelerated atherosclerosis is the primary cause of morbidity and mortality. There is increased insulin resistance and diabetes mellitus associated with RA and is thought to be due to chronic inflammation. When treated with specific DMARDs such as hydroxychloroquine, methotrexate, and TNF antagonists, there was a marked improvement in glucose control in these patients. (8) RA is not just a disease of the joints, it is able to affect multiple organ systems.Osteoarthritis (OA):OA treatment aims at reducing pain and improving joint function through a combination of non-pharmacological interventions like exercise programs tailored to strengthen muscles around affected joints, weight management strategies, and assistive devices like braces or walking aids if required (9). Medications including analgesics or nonsteroidal anti-inflammatory drugs may be prescribed for pain relief when necessary. Duloxetine has modest activity in relieving pain associated with OA. Intraarticular glucocorticoid joint injections have a variable response but are an option for those wanting to postpone surgical intervention. In severe cases where conservative measures fail, surgical options like joint replacement may be considered (9). Weight loss is a critical intervention in those who have overweight and obesity; each pound of weight loss can decrease the load across the knee 3 to 6-fold. (5) Summary: Medications (NSAIDs, topical, duloxetine), weight loss, PT, intraarticular injections of corticosteroids, and joint replacement.________________________________Conclusion: Now we conclude episode number 146, “RA vs. OA.” Future Dr. Magurany explained that rheumatoid arthritis is an autoimmune disease that presents with joint pain and inflammation, mostly on hands and small joints, accompanied by morning stiffness longer than 1 hour. The rheumatoid factor and ACPA may be positive in a percentage of patients but not always. The base of treatment is early treatment with disease-modifying antirheumatic drugs to induce remission of the disease. OA affects weight-bearing joints with little to no inflammation, treatment is mainly lifestyle modifications, analgesics, intraarticular injections, and joint replacement.This week we thank Hector Arreaza and Thomas Magurany. Audio editing by Adrianne Silva.Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! _____________________References:Myasoedova E, Crowson CS & Gabriel SE et al. (2010). Is the incidence of rheumatoid arthritis rising?: Results from Olmsted County, Minnesota, 1955-2007. Arthritis and Rheumatism, 62(6), 1576-1582.Goldring MB & Goldring SR. (2007). Osteoarthritis. Journal of Cellular Physiology, 213(3), 626-634.King LK, March L, Anandacoomarasamy A. Obesity & osteoarthritis. Indian J Med Res. 2013;138(2):185-93. PMID: 24056594; PMCID: PMC3788203.Chauhan K, Jandu JS, Brent LH, et al. Rheumatoid Arthritis. [Updated 2023 May 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-.Sen R, Hurley JA. Osteoarthritis. [Updated 2023 Feb 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-.Hunter DJ, Bierma-Zeinstra S. & Eckstein F. (2014). OARSI Clinical Trials Recommendations: Design and conduct of clinical trials for primary hip and knee osteoarthritis: An expert consensus initiative of the European Society for Clinical and Economic Aspects of Osteoporosis and Osteoarthritis (ESCEO) Task Force in collaboration with the Osteoarthritis Research Society International (OARSI). Osteoarthritis Cartilage, 22(7), 363-381.van Everdingen AA, Jacobs JW, Siewertsz Van Reesema DR, Bijlsma JW. Low-dose prednisone therapy for patients with early active rheumatoid arthritis: clinical efficacy, disease-modifying properties, and side effects: a randomized, double-blind, placebo-controlled clinical trial. Ann Intern Med. 2002 Jan 1;136(1):1-12. doi: 10.7326/0003-4819-136-1-200201010-00006. PMID: 11777359.Nicolau J, Lequerré T, Bacquet H, Vittecoq O. Rheumatoid arthritis, insulin resistance, and diabetes. Joint Bone Spine. 2017 Jul;84(4):411-416.Fernandes L, Hagen KB, Bijlsma JWJ et al. (2019). EULAR recommendations for non-pharmacological core management of hip and knee osteoarthritis. Annals of Rheumatic Diseases, 79(6), 715-722.Royalty-free music used for this episode: "Driving the Point." Downloaded on July 29, 2023, from https://www.videvo.net/ 

Este pódcast está destinado exclusivamente a profesionales de la salud. La neutropenia se define como un recuento absoluto de neutrófilos (RAN) de menos de 500/µL, o menos de 1000/µL con una disminución anticipada a menos de 500/µL en el siguiente periodo de 48 horas. La fiebre neutropénica es una temperatura oral única de 38,3 ºC o una temperatura superior a 38,0 ºC sostenida durante más de 1 hora en un paciente con neutropenia. Nuestra invitada: Dra. Armelle Pérez-Cortés Villalobos (Twitter: @ArmelleID)  

On episode #31 of the Infectious Disease Puscast, Daniel and Sara review the infectious disease literature for the weeks of 6/8 – 6/20/23. Hosts: Daniel Griffin and Sara Dong Subscribe (free): Apple Podcasts, Google Podcasts, RSS, email Become a patron of Puscast! Links for this episode Relative effectiveness of the cell-based quadrivalent influenza vaccine in preventing cardiorespiratory hospitalizations (OFID) Evaluation of Oseltamivir used to prevent hospitalization in outpatients with influenza (JAMA) Pan-ebolavirus monoclonal antibody cocktail provides protection against Ebola and Sudan viruses (JID) Inappropriate antibiotic prescribing and its determinants among outpatient children in low-and middle-income countries (PLOS) IDSA 2023 Guidance on the treatment of antimicrobial resistant gram-negative infections (IDSA) Evaluating antimicrobial duration for gram-negative bacteremia in patients with neutropenia (TID) Antibiotic myths for the ID clinician (CID) Dalbavancin for the treatment of acute bacterial skin and skin structure infection in patients with obesity or Diabetes (OFID) Global differences in the management of S. aureus bacteremia (CID) Clinical risk Scores to Predict Trimethoprim-Sulfamethoxazole, Fluoroquinolone, Nitrofurantoin, and Cephalosporin non-susceptibility among outpatient episodes of complicated UTI among adults (OFID) Continuous vs intermittent meropenem administration in critically ill patients with sepsis (JAMA) Current pyuria cutoffs promote inappropriate UTI diagnosis in older women (CID) Paenibacillus infection as a novel cause of sepsis in term neonates with high risk of sequelae in Uganda (CID) Antimicrobial for 7 or 14 Days for febrile urinary tract infection in men (CID) Candida auris‒associated hospitalizations (EID) Fatal invasive mold infections after transplantation of organs recovered from drowned donors (EID) Music is by Ronald Jenkees

Drs. Allison Zibelli and Arielle Heeke discuss the NATALEE trial's novel approach to high-risk HR+ breast cancer, the potential of delaying CDK4/6 inhibitors in HR+, HER2-negative mBC to decrease toxicities and costs in the SONIA trial, and de-escalation strategies in HER2+ early-stage breast cancer. TRANSCRIPT Dr. Allison Zibelli: Hello. I'm Dr. Allison Zibelli, your guest host for the ASCO Daily News Podcast today. I'm an associate professor of medicine and a breast medical oncologist at the Sidney Kimmel Cancer Center at Jefferson Health in Philadelphia. My guest today is Dr. Arielle Heeke, a breast medical oncologist at the Levine Cancer Institute at Atrium Health in North Carolina.  Today, we'll be discussing practice-changing studies and other key advances in breast cancer that were featured at the 2023 ASCO Annual Meeting.   Our full disclosures are available in the show notes and disclosures of all guests on the podcast can be found on our transcripts at asco.org/DNpod.   Arielle, it's great to speak with you today.   Dr. Arielle Heeke: Thank you so much for having me.  Dr. Allison Zibelli: Let's start with LBA500. This was the NATALEE trial of ribociclib and endocrine therapy as adjuvant treatment in patients with hormone receptor-positive HER2-negative early breast cancer. What are your key takeaways from the study, and how do you think this changes our approach to high-risk ER-positive breast cancer?  Dr. Arielle Heeke: Yeah, this was definitely the study for which many of us were waiting to see the results. It was exciting to see the results come through so quickly. As you mentioned, the NATALEE trial was a phase 3 study that evaluated three years of adjuvant ribociclib at a dose of 400 milligrams, which is a little different than what we're used to in the metastatic space at 600 milligrams. But essentially, it randomized patients to receive this 400-milligram dose with their adjuvant aromatase inhibitor therapy versus just the standard of care adjuvant endocrine therapy in patients that are high risk with early-stage breast cancer.   What made NATALEE somewhat unique is they defined high risk a little bit more broadly than we've seen in previous studies, such as monarchE. So, what I mean by that is NATALEE enrolled patients with stage 2 and 3 early-stage breast cancer. And notably, they allowed for patients that were lymph node-negative but had some other high-risk features, such as a grade 3 tumor or a grade 2 tumor with high-risk genomics, such as oncotype or a high Ki-67. So, by broadening who was eligible, NATALEE captured more patients at risk for recurrence. Of course, we know that recurrence is not specific for patients with lymph node-positive disease. We can see recurrence even with stage 1, but certainly, we start to see more recurrence risk as patients drift into stage 2 and stage 3.   In the NATALEE study, the majority of these patients did receive prior chemotherapy, which I also think is interesting. We've kind of seen in the metastatic space that sometimes chemotherapy can augment patients' responsiveness to CDK4/6 inhibitors. But specifically in NATALEE, 88% of patients had received prior chemotherapy, and ultimately, about a third of the patients were lymph node-negative.   So, diving into some of the results with this first analysis that we saw at ASCO, with the median follow-up for invasive disease-free survival of just 27.7 months, they were able to show that the risk for invasive disease was reduced by 25.2% with the addition of ribociclib plus endocrine therapy compared to endocrine therapy alone. And this three-year invasive disease-free survival rate was 90.4% for the combination therapy compared to 87.1% for endocrine therapy alone, which is an absolute difference of 3.3%. Additionally, patients treated with ribociclib and endocrine therapy had a 26.1% reduced risk for distant disease-free survival compared with endocrine therapy alone, and this was a rate of 90.8% for ribociclib with endocrine therapy compared to 88.6% with endocrine therapy alone, which correlates to an absolute benefit of 2.2%.    They did show results for overall survival as well, but again, follow-up was just a median of 27.7 months. So, data was essentially immature to show any true overall survival benefit from this approach. And in fact, only 20% of patients had completed three years of ribociclib at this data cutoff. And as a reminder, again, NATALEE involved ribociclib for three years compared to two years, which we've seen with other studies in this space.   Also, what was encouraging from NATALEE were the readouts for toxicities. Neutropenia is definitely a concern with this class of medication, and they were able to show that rates of neutropenia were overall lower than what we've seen in the pooled data in the metastatic space. And also that problematic QTc prolongation for which we have to get EKGs baseline two weeks and four weeks. They also showed that the likelihood of having QTc prolongation on this therapy was significantly less at that 400-milligram dose compared to 600.   I think the key takeaway is yes, this drug is effective as adjuvant therapy, which is perhaps not surprising since we've seen such promising results in the metastatic space, but numerically not as striking as what we have at this point with adjuvant abemaciclib, but of course, this is a newer study. We hope to see that continued separation of the curves as we were fortunate enough to see with the abemaciclib data, but obviously we'll be looking for additional analyses from NATALEE.    And then how this will change practice, of course, we'll have to wait to see if the therapy is approved for use in the adjuvant setting for early-stage hormone receptor-positive breast cancer, but it certainly will be a nice option for patients that struggle with GI toxicity kind of at baseline. But also, if they were previously on abemaciclib and were not able to tolerate due to the GI toxicity, this would be an option for them. Also, as mentioned, it's a broader patient population, so we can consider this perhaps for a patient with lymph node-negative disease.   Although we will have to ask ourselves that just because someone meets eligibility for the NATALEE  study, and if the therapy is ultimately approved, is it appropriate to give it to all those patients? Or do we need to still kind of think of this in the setting of the highest-risk patient, not just any patient with stage 2 plus disease? There was a lot of talk at the meeting, certainly about biomarkers and potentially using ctDNA to try to find these predictors of benefit from CDK4/6 inhibitor therapy, but obviously, still a long way to go before we can use that type of technology in this space.  Dr. Allison Zibelli: Thank you. Staying on the topic of CDK4/6 inhibitors, everybody was excited about the SONIA trial, which was LBA1000, and this trial was asking if we can delay using CDK4/6 inhibitors for newly diagnosed ER-positive HER2-negative metastatic breast cancer as a way to decrease both toxicity and cost. Tell us about this study.  Dr. Arielle Heeke: The SONIA trial was such a cool study to see, and the presenter reported findings in such a thought-provoking way. Really great to see this sort of work being done because I think we all wonder deep down in our gut, if more is more, or if we do need to kind of be a little bit more thoughtful about how we introduce these therapies certainly from a patient perspective. Patients that participate at ASCO [meetings] have been saying for years how important it is to consider the toxicities in terms of side effects, but also, of course, financial toxicities. So, it was great to see the SONIA trial at center stage.   Essentially, as you mentioned, it was a study that randomized patients in the first-line setting with metastatic hormone receptor-positive breast cancer to receive either first-line CDK4/6 inhibitor therapy or second-line CDK4/6 inhibitor therapy. So basically, there was a mandated crossover, so patients that received the CDK4/6 inhibitor first-line did not receive a second line and vice versa. Patients that were randomized to receive their endocrine therapy as monotherapy first line went on to receive CDK4/6 inhibitor at second-line. And the second-line endocrine therapy was fulvestrant in both of those situations.    We kind of run into this problem with patients now where we have so many therapies available to us that we don't typically run out of treatment options, but rather we run up against treatment toxicity or ultimate failure of the human body to keep up with the demands of ongoing therapy. So, again, while it's maybe somewhat attractive to start treatments earlier using things first-line rather than second-line or longer, just kind of post-CDK4/6 inhibitor progression, you know using this CDK4/6 inhibitor again with a different endocrine therapy backbone is probably not offering a meaningful benefit to that many patients. So this type of study is so necessary to really try to help us frame who needs those therapies sooner and longer or perhaps is there a substantial portion of patients that we don't need to put them through that sort of toxicity.   So that's the SONIA trial. Some things to note about the patient population, these patients were a bit older than what we've seen in some of our metastatic CDK4/6 inhibitor trials. There was a median age of 64 and 87% were postmenopausal. Additionally, just 40% had received prior chemotherapy. And as is true for most of our studies, 91% have received palbociclib on study with just 8% receiving ribociclib. And the choice of the CDK4/6 inhibitor was per the treating provider, and at the time of the of study globally, palbociclib was the more commonly prescribed CDK4/6 inhibitor. But over the last year or so, data has certainly emerged favoring ribociclib in the metastatic setting.   On the SONIA trial, patients were monitored for a median of 37.3 months. And looking at the primary endpoint of the second progression-free survival, which is defined as the time for random assignment to the second objective disease progression or death, for those patients who received first-line CDK4/6 inhibition, had a PFS2 of 31 months compared to 26.8 months with second-line CDK4/6 inhibitor use. And this slight difference was non-statistically significant. So the conclusion was that time to second progression was not impacted by whether or not a patient received first-line CDK4/6  inhibition or second-line CDK4/6 inhibition. Additionally, there were no differences in overall survival between the 2 arms with a median overall survival of 45.9 months with first-line CDK4/6 inhibitor use versus 53.7 months in second-line CDK4/6 inhibitor use.  And that actually equates to significant differences in time on drug. The median duration of CDK4/6 inhibitor use with first-line therapy was 24.6 months compared to 8.1 months with second-line use. And by being on therapy for an additional 16.5 months if you use CDK4/6 inhibitor first-line, this, of course, leads to increased toxicity and certainly increased financial burden. And it was estimated that for each patient that receives this therapy first-line, there is an additional $200,000 spent on getting them the CDK4/6 inhibitor first-line, whereas the results from SONIA suggested that whether you use it first-line or second-line, the outcomes are essentially exactly the same.   And then specific for the SONIA trial, by conducting the study, they saved approximately €25 million on drug expenditure during the conduct of the trial. It's just amazing when you take it to that scale. And then lastly just to mention, they looked at quality of life assessments as well and there were no differences in the two arms whether they got first-line or second-line CDK4/6 inhibition.  Dr. Allison Zibelli: I thought this study was remarkable, and it got a long ovation when it was presented at the meeting. I'm certainly going to use this strategy and prioritize who needs upfront CDK4/6 inhibitor therapy.  I think that we have to think of not just drug toxicity for our patients, but financial toxicity. A lot of these drugs have very high copays and the number one cause of bankruptcy in the United States is medical costs. So that's something we really have to keep in mind. I also thought it was very interesting that the study was designed in cooperation with the patient advocacy group and patients themselves were very enthusiastic about this study and helped design it and helped recruit to it. So all in all, I thought this was a remarkable study.    So moving on, LBA1013 was the TORCHLIGHT study of toripalimab versus placebo in combination with nab-paclitaxel for patients with metastatic or recurrent triple-negative breast cancer. Many of us are not familiar with toripalimab. Can you tell us about the drug and how it was used in this study?  Dr. Arielle Heeke: Yes, toripalimab is essentially an immunotherapy agent. It's an IgG4K monoclonal antibody that targets PD-1. In this study, TORCHLIGHT, patients were randomized to receive toripalimab versus placebo in combination with nab-paclitaxel in newly metastatic triple-negative breast cancer. The patients on study were randomized two to one to receive drug or placebo. The drug is given on day 1 of a 3-week cycle at 240 milligrams and then patients of course also receive nab-paclitaxel on a day 1 and day 8 schedule of a 21-day cycle. They did look at outcomes on the study based on PD-L1 positivity status and they assessed for PD-L1 with an IHC assay JS311 antibody that ultimately generated a combined positive score. And PD-L1 positivity was defined as a CPS of greater than or equal to one based off of this assay. In the study population, about a third of patients were- patients' tumors were CPS negative, a third had a CPS of 1 to 10 and about a quarter had a CPS of greater than or equal to 10. And then approximately 7% of the tumors had an unknown status.   And then getting right into the results, we were provided results in the PD-L1 positive subgroup as well as the whole patient population. Looking at the primary endpoint of PFS, there were significant improvements seen in median PFS with the addition of toripalimab to nab-paclitaxel, again in the first line setting with a median PFS of 8.4 months with the addition of the immunotherapy agent versus 5.6 months with placebo. And this was statistically significant.  And then in the intent to treat population, there were some numeric improvements, in median, progression-free survival at 8.4 months with the addition of toripalimab versus 6.9 months with placebo.   We also got some results with overall survival that were quite intriguing, although this initial analysis was not designed to necessarily prove statistically significant differences in overall survival. But again, there were some promising trends. Looking first at the PD-L1 positive subgroup, the median overall survival was 32.8 months with the addition of toripalimab versus 19.5 months with placebo. Breaking it down a little bit further based on CPS values, for a CPS of 1 to 10, median overall survival was 32.8 months versus 19.5 months. And then for those very high CPS or greater than or equal to ten, median overall survival was not reached in this group versus 18.3 months with placebo. Also, looking in the intent-to-treat population, there were also improvements in overall survival with the addition of toripalimab with a median overall survival of 33.1 months with the addition of immunotherapy versus 23.5 months with nab-paclitaxel alone. So potentially, depending on next steps of this study, we would potentially have an option to add immunotherapy that is not biomarker specific, meaning we can potentially provide toripalimab to all patients regardless of their PD-L1 status.  Dr. Allison Zibelli: Very interesting new drug to look forward to. So, one of the major themes of this year's meeting was de-escalation strategies. For example, LBA506 reported the three-year invasive disease-free survival of the PHERGain trial, which looked at eliminating chemotherapy for HER2-positive patients getting neoadjuvant therapy. Tell us about the design of this study and how will it impact the care of these patients?   Dr. Arielle Heeke: The design was very complicated. I had to look at it a few times to really make sure I got my head around it. But I think once you do figure it out, you can see how there might be a path forward in clinical practice. Although I think for all of this work, it's maybe not ready yet for primetime, but certainly thought-provoking. But the PHERGain clinical trial, I feel like we've heard about this study for a little while and this concept of de-escalation really kind of started in the HER2-positive space. But this study was a randomized study of chemotherapy de-escalation and early HER2-positive breast cancer using PET/CT as a marker of response to therapies that don't involve chemotherapy.   Patients were eligible for the study if they had stage 1 to 3a HER2-positive breast cancer with no prior therapy for breast cancer, and ultimately 356 patients were enrolled in a 1 to 4 randomization scheme with the majority of patients ultimately enrolled into the experimental group, which is called Group B. So, to break down Group A and Group B, Group A essentially were patients that receive typical standard of care, which at this point is TCHP for six cycles, neoadjuvantly or prior to surgery. Once they complete those cycles they move into surgery and then Herceptin-PERJETA adjuvantly for additional twelve cycles.  I should also note that this study was conducted prior to results of the KATHERINE trial that showed benefit of switching to adjuvant T-DM1 if there's residual disease. So, patients in Group A as well as Group B did not receive T-DM1 at any point. So, again, Group A is kind of your standard of care. Group B was the “experimental arm.” And so, what they did in this arm to assess potential de-escalation strategies, patients first received Herceptin-PERJETA alone for two cycles with or without endocrine therapy, if they were also hormone receptor-positive. But after those two cycles, they underwent a PET/CT, and then if a response was garnered, they would continue with Herceptin-PERJETA and again plus or minus endocrine therapy to complete six cycles total before proceeding on with surgery. Then if they were fortunate enough to achieve complete response at the time of surgery, then they just continued with Herceptin-PERJETA maintenance, whereas if they did not achieve a complete response at the time of surgery, then they actually received TCHP 6 times adjuvantly. So, the chemotherapy was introduced after surgery.   And then going back to that PET/CT time point, if patients did not achieve a response at that check-in point, after 2 cycles of Herceptin-PERJETA, at that point they were transitioned to chemotherapy with TCHP, again, for six cycles. So, either they could kind of ride all the way through if they got that complete response at the time of surgery with Herceptin-PERJETA only, or if at surgery there was residual disease, they went on to receive TCHP after surgery, or if they did not have a response on that interim PET/CT after 2 cycles of HP then they would go on to receive TCHP neoadjuvantly.    So, looking at the results, they actually had 2 primary endpoints. The first primary endpoint was rates of a complete response at the time of surgery in patients that had a PET response. So, PET responses were actually seen in nearly 80% of all the patients treated with Herceptin-PERJETA without chemotherapy. And in those PET responders, a complete response rate at the time of surgery was seen in approximately 38% of patients. So, 37.9% of PET responders actually achieved a complete response when they went to surgery after receiving Herceptin-PERJETA alone, which is pretty amazing. I mean, we're used to seeing higher complete response rates with neoadjuvant therapy for HER2-positive disease, but again, this is a chemo-free regimen so that is encouraging for that 38% of patients that really didn't need chemotherapy.   And then the second primary endpoint, and this was what we saw basically for the first time with the 2023 ASCO Meeting, was results for the 3-year invasive disease-free survival in Group B or this experimental de-escalation group. And ultimately it was shown that the three-year invasive disease-free survival and the intent to treat group B population was 95.4%, which met its statistical endpoint, or, basically the null hypothesis was rejected. They just needed some sort of outcome that was not worse in terms of the 3-year invasive disease-free survival of 89%.   And then looking actually at the patients that kind of did the best. So, the patients that were PET responders and achieved a complete response at the time of surgery and therefore really only ever received Herceptin-PERJETA, their three-year invasive disease-free survival was 98.8%. So, really very good. Additional endpoints they looked at in Group A and Group B were favorable in terms of three-year invasive disease-free survival in Group A, and then three-year distant disease-free survival and three-year overall survival in both groups, all approximately 98%. So, very favorable.   So, ultimately, these findings reflect a potential role for a chemotherapy-free treatment approach for some patients with early-stage HER2-positive breast cancer. And this particular study, they used PET/CT to influence chemotherapy decision-making, which potentially identified 1 in 3 patients who can omit chemotherapy. With that, 80% of patients receiving the response with a PET/CT, and then of that, 80%, again, 38% actually having that complete response. And ongoing work is also being done to look at other mechanisms to assess for an opportunity to de-escalate with MRI imaging or HER2DX testing to again try to identify patients who can potentially defer chemotherapy in this setting. I did not see from the results what proportion of patients were hormone receptor-positive, which I think is also interesting when thinking about chemotherapy de-escalation, can you lean a little bit more heavily on endocrine therapy? Perhaps we'll get that data in the future.   Dr. Allison Zibelli: That's a very important point.  I would like to thank you, Dr. Heeke, for coming on the podcast today and sharing your valuable insights with us. We really appreciate it.  Dr. Arielle Heeke: Absolutely. It was a great meeting to dive into. It's always exciting to see what comes out of ASCO in the breast space. We're usually well represented there, and I hope that these studies will lead to further exploration.   Dr. Allison Zibelli: And thank you to our listeners for joining us today. You'll find links to all abstracts discussed today in the transcript of this episode. Finally, if you value the insights that you hear on the ASCO Daily News Podcast, please take a moment to rate, review, and subscribe wherever you get your podcasts.  Disclaimer:   The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement.  Follow today's speakers:   Dr. Allison Zibelli   Dr. Arielle Heeke  @HeekeMD     Follow ASCO on social media:    @ASCO on Twitter   ASCO on Facebook   ASCO on LinkedIn      Disclosures:    Dr. Allison Zibelli:    None Disclosed   Dr. Arielle Heeke:   Honoraria: Merck  Consulting or Advisory Role: Jazz Pharmaceuticals, Caris Life Sciences, Amgen, Daiichi Sankyo/Astra Zeneca, Pfizer, AstraZeneca, Menarini, Genome Insight  Speakers' Bureau: Daiichi Sankyo/Astra Zeneca      

No episódio da vez, Jordan, João Prats e Klinger irão discutir sobre a Neutropenia Febril: qual a definição, fatores de risco e principalmente como manejar esse paciente! Vem com a gente!

Neutropenia is a condition characterized by an abnormally low level of neutrophils, a type of white blood cell that helps to fight infection. Neutropenia is a common side effect of cancer treatment, particularly chemotherapy, which can damage the bone marrow where neutrophils are produced. When a cancer patient develops neutropenia, they are at increased risk for developing infections, which can be severe and life-threatening. Patients with neutropenia may experience symptoms such as fever, chills, sore throat, and mouth sores, which can be signs of infection. We have discuss more in this episode. Do listen and share with someone you think might get benefited. See you soon. Jai Hind

The First Principles of Febrile Neutropenia that can get you through an oncological emergency: First Principles summary version. === Other Links === Check out our new website ⁠⁠⁠1pm.wiki⁠⁠⁠ for the ⁠⁠⁠Notion document⁠⁠⁠, free Anki flashcards, and podcast episodes. Check out our Instagram: ⁠⁠⁠https://www.instagram.com/firstprinciplesofmedicine/⁠⁠⁠ Recorded 22 March 2023 Co-hosts: ⁠⁠⁠⁠⁠⁠⁠JT Yeung⁠⁠⁠⁠ & Adian Izwan feat. Michael Offerman & Lucy Variakojis. Produced by Adian Izwan. If you have any ideas or feedback, comment on this Notion document, or shoot us an email at ⁠⁠⁠hello@1pm.wiki⁠⁠ *** We're really excited to be collaborating with Becky from Becky's notes, a UK based resource, to produce infographics for our visual learners out there. Becky's notes brings together all the key topics medical students need to know in a readily available place, reviewed by specialists in the field. These visually striking notes are a refreshing change from all the boring textbooks. You can check her out on instagram at @beckysnotes01 and get her books at ⁠⁠⁠https://linktr.ee/Beckysnotes⁠

The First Principles of Febrile Neutropenia that can get you through an oncological emergency: What are neutrophils, what do they do, and how many do we need? === Other Links === Check out our new website ⁠⁠1pm.wiki⁠⁠ for the ⁠⁠Notion document⁠⁠, free Anki flashcards, and podcast episodes. Check out our Instagram: ⁠⁠https://www.instagram.com/firstprinciplesofmedicine/⁠⁠ Recorded 22 March 2023 Co-hosts: ⁠⁠⁠⁠JT Yeung⁠⁠⁠ & Adian Izwan feat. Michael Offerman & Lucy Variakojis. Produced by Adian Izwan. If you have any ideas or feedback, comment on this Notion document, or shoot us an email at ⁠⁠hello@1pm.wiki⁠⁠ *** We're really excited to be collaborating with Becky from Becky's notes, a UK based resource, to produce an infographic for our visual learners out there. Becky's notes brings together all the key topics medical students need to know in a readily available place, reviewed by specialists in the field. These visually striking notes are a refreshing change from all the boring textbooks. You can check her out on instagram at @beckysnotes01 and get her books at ⁠⁠https://linktr.ee/Beckysnotes⁠⁠ === Timestamps === (01:31) Normal body temperature (02:02) Neutrophils & bone marrow  (06:06) Normal neutrophil ranges (08:35) Decreased making vs increased breaking (11:29) What is febrile neutropenia (13:31) MASC risk index (14:47) Clinical features (16:21) Investigations (20:14) Michael's oncological emergency (22:41) Management (29:55) 3 key takeaways 

In 2022, Dr. Maura Abbott, Associate Professor of Nursing at the Columbia University School of Nursing, served as faculty for i3 Health's CME/NCPD approved activity, New Insights Into Preventing and Managing Chemotherapy-Induced Neutropenia. Now, in this follow-up interview with Oncology Data Advisor, Dr. Abbott reinforces the importance of educating patients who are at risk for chemotherapy-induced neutropenia and shares some of the therapeutic developments in both prevention and management that are coming down the pipeline in the near future. Listen to the free CME/NCPD activity, New Insights Into Preventing and Managing Chemotherapy-Induced Neutropenia, after the interview and click here to claim credit: i3health.com/44-policies/503-i3health-com-cin

Discover recent developments in the prevention, treatment, and management of chemotherapy-induced neutropenia, including a comprehensive understanding of the risk factors and current clinical practice guidelines. This activity is presented by Gary H. Lyman, MD, MPH, FASCO, FACP, FRCP, Professor, University of Washington, and Maura Abbott, PhD, AOCNP®, CPNP, Columbia University School of Nursing. Listen now to earn free CME/NCPD! Click here to claim credit: http://bit.ly/3nT8TQJ

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:    Ryan: Hi Dr Cabral, I love your podcast , and your equilife products too! My question is for father . He has ESRD because of untreated hypertension. His BP was 284/165 his last trip to ER. He gets dialysis. He eat relatively good for a 65 year old. He eats lots of fruit and veggies. He likes beef , chicken an pork. He's not overweight, small belly. Sorry just wanted you to have as much info to make possible suggestions. Every since he started dialysis and years before , his uncontrolled BP in return gave him ckd, an now ESRD . He feels so wiped-out afterwards and gets cramps in back legs and feet. Maybe something revitalizing a little and replenishing him? And maybe electrolyte products or shakes of your line. Love the podcast . So incredibly grateful to have stumbled upon your podcast !   Kenzie: My boyfriend is getting his deviated septum fixed. They want him on antibiotics because it's a surgery. Any tips for supporting the gut during? Any thoughts on this surgery?   Shannon: Hi Dr. Cabral, my 12-year-old son has been suffering from post-concussive syndrome since May 2022. He has had daily pounding headaches, accompanied sometimes by nausea, dizziness, difficulty concentrating etc. I had to withdraw him from school and his mood is very low and he cries a lot which is not normal for him. My heart is breaking as I don't know how to help him. We've seen the chiropractor, Osteopath, function Medicine practitioner, naturopath had acupuncture, cranial sacral therapy, massage and tried so many different things such as essential oils, food eliminations, high dose Omega 3, magnesium, homeopathic remedies. His sleep is poor and he is not himself in so many ways. I feel like this nightmare will never end. What am I missing? Please give me hope that this will get better.   Leora: My 22 month old son has been diagnosed with Severe Congenital Neutropenia with a mutation of the ELANE gene. We are currently investigating whether it is cyclic or not. Is there anything natural I can do to boost his neutrophils level? Moreover, he has chronic ear infections. Every time he has a virus he gets an ear infection. Of course the doctors always want him on antibiotics but I have found that onion juice works well to clear up the ear infection. However, is there anything I can do to prevent the ear infection occuring in the first place? His doctor believes it is caused by a fluid buildup that doesn't release due to the architecture of his ear.   Kenzie: Hello! Any tips for cutting down emf when living in apartment? I can't shut off my wifi. And obviously I live next to above and under other apartments.   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 and Resources: StephenCabral.com/2598 - - - Get a FREE Copy of Dr. Cabral's Book: The Rain Barrel Effect - - - Join the Community & Get Your Questions Answered: 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 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) - - - Get Your Question Answered On An Upcoming HouseCall: StephenCabral.com/askcabral - - - Would You Take 30 Seconds To Rate & Review The Cabral Concept? The best way to help me spread our mission of true natural health is to pass on the good word, and I read and appreciate every review!  

Guest host Dr. Neeraj Agarwal and Dr. Christian Kollmannsberger discuss practice-changing abstracts that were presented at the 2023 ASCO Genitourinary Cancers Symposium, including results from the TALAPRO-2, PROpel, TRITON3, ARASENS, KEYNOTE-057, CheckMate 274, and CheckMate 9ER studies. TRANSCRIPT Dr. Neeraj Agarwal: Hello and welcome to the ASCO Daily News Podcast. I'm Dr. Neeraj Agarwal, the director of the Genitourinary Oncology Program, and professor of Medicine at the Huntsman Cancer Institute at the University of Utah, and editor-in-chief of the ASCO Daily News.  Today, we will be discussing practice-changing abstracts and other key advances in GU Oncology featured at the 2023 ASCO Genitourinary Cancers Symposium. Joining me for this discussion is Dr. Christian Kollmannsberger, the chair of this year's ASCO GU. Dr. Kollmannsberger is a GU medical oncologist at the BC Cancer Vancouver Cancer Center and a clinical professor at the University of British Columbia.  Our full disclosures are available in the transcript of this episode, and the disclosures of all guests on the podcast can be found on our transcripts at asco.org/DNpod.  Christian, thank you for joining us on the podcast today.  Dr. Christian Kollmannsberger: Thank you very much, Neeraj. It's a real pleasure to be here and have this discussion. Dr. Neeraj Agarwal: Thank you. So, Christian, the GU meeting featured remarkable progress in various GU malignancies. Could you please share some of the prominent topics that made the headlines this year and give us an overall feel of ASCO GU this year? Dr. Christian Kollmannsberger: Absolutely. I think it was a great meeting with over 5,800 attendees from more than 70 countries. And most of the attendees were in person, so it was a great event. ASCO GU is truly the premier global event to feature the very best of GU cancer research and treatment. The theme of this year's meeting was "Today's Science, Tomorrow's Treatment," and that was reflected in the novel scientific and clinical findings that were presented and will potentially lead to changes in our daily clinical practice. It also reminds us how quickly the development today is and how quickly novel scientific progress is immediately translated into clinical practice, particularly oncology.   I was very impressed by the meeting's emphasis on diversity, interactivity, networking, multidisciplinary collaboration, and evidence-based care. We introduced several new features such as a “Meet the Professor session, a women's networking event, etc. And the first day really kicked off with a very rich focus on prostate cancer and much attention given to PARP inhibitors in our first session. As an example, LBA 17 was the first late-breaking abstract presented. And congratulations to you, Neeraj, on delivering this exciting data on the TALAPRO-2 trial, which were eagerly awaited. Let's start with that. Can you tell us about this trial? Dr. Neeraj Agarwal: Yes, of course. So the TALAPRO-2 trial was a phase 3 randomized trial where patients in newly diagnosed metastatic CRPC settings were randomized to standard of care enzalutamide plus placebo versus enzalutamide plus talazoparib PARP inhibitor. And as we know, Christian, the rationale has been that dual inhibition of PARP and AR may enhance the efficacy of each. And there's a laboratory preclinical rationale and based on which other studies have been done in the past. So, without getting into too much detail into the rationale for the trial, I'll come right to the results of the trial. So, this was the first-line mCRPC setting where rPFS was the primary endpoint as assessed by the independent radiology assessment. And in this trial, patients were recruited regardless of the homologous recombination repair gene alterations. So, patients were recruited and they were prospectively tested for whether they had these HRR gene alterations or not, but all comer population was included in this trial. And after a median follow-up of approximately 23 months, the trial read out, and we found that trial made the primary endpoint was improved radiographic progression-free survival with the rPFS being about 22 months in the enzalutamide arm and not reached in the combination arm with a 37% reduction in risk of progression or death.  If you look at the subgroup analysis of patients who were HRR+, there was a 54% reduction risk of progression or death. If you look at patients who were stratified in HRR- or unknown group, there was a 30% reduction risk of progression or death. If you specifically look at an exploratory analysis we did to look for patients who were HRR- by prospective tumor tissue testing; there was a 34% reduction in risk of death with a hazard ratio of 0.66 favoring the combination arm. So overall, the rPFS primary endpoint was met in all groups. We also see significant delay in PSA progression in the combination arm by more than nine months. We also see delays in the time to cytotoxic chemotherapy. We saw delay in progression or death on subsequent neoplastic therapy after the protocol treatment. We saw delays in deterioration of quality of life and global health status. All these were significant and happened on the talazoparib plus enzalutamide arm.  So overall, if you look at the totality of the data, these all favored the combination of talazoparib plus enzalutamide compared to enzalutamide alone. I want to highlight that overall survival is immature at 31% maturity with a hazard issue of 0.89, currently favoring enzalutamide plus talazoparib. But we'll have to look at more mature data as time passes.  Dr. Christian Kollmannsberger: Wow. Thank you, Neeraj. So, it sounds like that was a very positive trial, and it's potentially practice-changing. One of the concerns is always safety and toxicity. So can you tell us whether there were any new safety signals, and can you tell us more about the common adverse events that were noticed in TALAPRO-2? Dr. Neeraj Agarwal: No discussion is complete without talking about safety results, so I'm glad you asked me, Christian. The most common dose-affecting toxicity, if you will - so toxicities which led to dose modification and dose discontinuation of talazoparib were cytopenias, as we expect from this class of agents. So anemia, neutropenia, thrombocytopenia, these were the common toxicities. In fact, rate with anemia was 46.5%. Neutropenia and cytopenia were much less common.  I would like to highlight one fact which also came up during the discussion section after our oral presentation. The qualifying criteria for entry in this trial was a hemoglobin of 9-gram percent. And 49% of patients had grade 1 to 2 anemia at baseline, that is before starting treatment with talazoparib. So, we knew that if you mandate dose reduction, a lot of patients will not get adequate dosing of talazoparib. So, we waited for grade 3 anemia and then instituted dose reduction. And that I thought personally was a good strategy because the grade 3 anemia happened after a median duration of three months, 3.3 months to be more precise. And then, these patients underwent protocol-mandated dose reduction, following which the dose discontinuations were quite low actually. Only 8.3% patients discontinued talazoparib because of anemia, and the median dose intensity or median relative dose intensity of talazoparib in the talazoparib arm remained quite high at more than 80%, which translates to a talazoparib dose of 0.4 milligram daily when the starting dose was 0.5 milligram. So those were the hallmark of toxicities.   I do like to mention that those grade 3, 4 toxicities which are more known to affect the quality of life of our patients, such as grade 3, 4 anorexia, fatigue, nausea and vomiting, they were quite rare, happening in 1 to 4% patients who were on talazoparib. So overall, regarding the side effects, they were manageable, there were no new safety signals, and we could maintain adequate talazoparib dosing with dose reduction, which happened quite early during the protocol treatment.  Dr. Christian Kollmannsberger: Thank you, Neeraj. Very impressive results indeed. The patient population included in TALAPRO-2 was very similar to those included in the PROpel phase 3 trial, which tested the combination of abiraterone and olaparib in the first-line mCRPC setting. So, I'd like to just mention that we also saw LBA16 on the PROpel study, which was the final overall survival in PROpel, which was presented by Noel Clarke. So PROpel, as you know, was a randomized phase 3 trial evaluating efficacy and safety of olaparib plus abiraterone versus placebo plus abiraterone as first-line therapy for mCRPC in the first-line metastatic castration resistance setting. The enrollment in that study was independent of known defects in the homologous recombination repair gene pathway in contrast to other studies, such as MAGNITUDE, which tested the biomarker upfront. A total of 796 patients were randomly assigned to either olaparib plus abiraterone or placebo plus abiraterone. And we saw similar results, significant radiographic progression-free survival with olaparib plus abiraterone in PROpel, which was the primary endpoint similar to TALAPRO-2, and that was published last year in the New England Journal of Medicine Evidence.  Now, this abstract presented here at ASCO GU reported on overall survival with an overall survival majority of 47.9% and showed that with the addition of the PARP inhibitor olaparib to abiraterone, a statistically non-significant but clinically meaningful improvement in overall survival of about seven months were achieved compared to standard of care in abiraterone alone. The numbers were 42.1 versus 34.7 months in the all-comers population of patients in the first-line mCRPC setting. Importantly, I think the median overall survival of more than 42 months really represents the longest reported median overall survival thus far in a phase III trial for first-line metastatic castration-resistant prostate cancer. Although the median overall survival for the non-HRR group remains not statistically significant, with a hazard ratio of 0.89. Dr. Neeraj Agarwal: Such a great synopsis of the PROpel result data. Thank you, Christian, for highlighting these results. As we know, the combination is already approved by the EMA, the European Medical Agency, for patients in the first-line mCRPC setting who are not candidates for docetaxel chemotherapy. If this combination is approved by the FDA, we may have one more therapeutic option for our patients in first-line mCRPC.  So, just continuing on the PARP inhibitors, there was one more oral presentation with PARP inhibitor rucaparib by Dr. Alan Bryce from the Mayo Clinic, Arizona. This was Abstract 18 on the primary result of the TRITON3 trial. So to complete our PARP inhibitor section, I would like to summarize the result of the TRITON3 trial, which was a randomized phase III trial evaluating rucaparib versus physician choice, which notably included docetaxel in addition to abiraterone or enzalutamide in patients with chemotherapy-naive mCRPC with BRCA1, BRCA2 or ATM alterations. These patients had disease progression after having one novel hormonal therapy, or we call them second-generation androgen pathway inhibitors in any setting. So these patients had to have disease progression on a novel hormonal therapy.   In the BRCA subgroup and the subsequent intention to treat the population, the primary endpoint tested first was radiographic progression-free survival, and overall survival was the key secondary endpoint. The subgroup of patients with BRCA-altered disease had a median rPFS of 11.2 months with rucaparib compared to 6.4 months with physician choice of treatment - looks like almost doubling of the rPFS with the rucaparib. In the overall ITT population, median rPFS was 10.2 months with rucaparib and 6.4 months with the physician's choice of treatment. Although the overall survival data are immature, we still see a trend for improved overall survival with rucaparib. Regardless, the study clearly demonstrates the value of rucaparib for treating BRCA1 and BRCA2-altered mCRPC after disease progression on an androgen receptor pathway inhibitor. So these were the impressive results from the TRITON3 trial.  But before we switch to non-prostate abstract, I would like to complete the prostate cancer discussion by talking about the Abstract 15, which was based on the results of the ARASENS trial presented by Dr. Maha Hussain. As we know, ARASENS is a randomized phase 3 trial evaluating the efficacy and safety of darolutamide plus androgen deprivation therapy plus docetaxel versus androgen deprivation therapy or ADT plus docetaxel. So the triplet of ADT plus darolutamide plus docetaxel being compared to ADT plus docetaxel chemotherapy in patients with newly diagnosed metastatic castration-sensitive prostate cancer. A total of 1,300 patients were randomly assigned to the doublet versus triplet. As presented in the last ASCO GU meeting exactly one year ago, the primary endpoint of the study was met with a significant improvement in overall survival and a 32% reduction in risk of death for patients on the triplet therapy with ADT plus docetaxel plus darolutamide versus ADT plus docetaxel chemotherapy. So triplet therapy was already approved based on these data.  The abstract presented by Dr. Hussain this year is a post-talk analysis where Dr. Hussain and colleagues investigated the impact of triplet therapy across patients with high volume versus low volume per chartered criteria and higher risk versus low risk using latitude trial criteria. And investigators knew that these results would be highly attractive to practicing oncologists who are now choosing treatment based on volume of disease or risk of disease, more commonly, volume of disease.  So, let's come to what was presented this ASCO GU. So, after 1,305 patients in ARASENS, the majority had high-volume disease and high-risk disease. Among patients with high-volume disease, the addition of darolutamide reduced the risk of death by 30% compared with ADT and docetaxel, with a hazard ratio of 0.69. In the risk groups, the addition of darolutamide seems to favor both high-risk and low-risk groups. Among patients with low-volume disease, there was a trend towards improvement in overall survival with the addition of darolutamide, but it did not reach statistical significance. The great news was that there was no new safety signal. So, to summarize these data, the triplet of darolutamide plus ADT plus docetaxel showed superior overall survival compared to doublet of ADT plus docetaxel, with an important caveat that triplet was not compared with any of the modern doublets of ADT plus a second generation androgen receptor pathways inhibitor such as abiraterone, apalutamide, or enzalutamide, or even darolutamide. So, I wish there was a third arm of ADT plus darolutamide.  Having said that, triplet can be considered a standard of care now based on these data for patients with metastatic hormone sensory prostate cancer, where we would be using ADT plus docetaxel chemotherapy. And from this meeting data, this efficacy of triplet can be applied to high-volume disease and all risk disease. And we just need more time to see how the data pans out in low-volume patients with metastatic hormone-sensitive prostate cancer.  Dr. Christian Kollmannsberger: Yes, I completely agree, Neeraj. I think all the data presented in these abstracts are really impressive and will impact our daily clinical practice and our patients more or less immediately. I think the use of PARP inhibitors, whether as a monotherapy or in combination with androgen receptor pathway inhibitors, as well as now the option of triplet therapy in the metastatic castration sensitive setting really offer patients with metastatic prostate cancer new treatment strategies and most importantly, improved survival outcomes. And it is impressive to see how we have pushed the prognosis and the outcomes for our patients with prostate cancer, I would say, in the last five to ten years. And similar to last year, I think the entire Prostate Cancer Day at ASCO GU 2023 was full with impressive data and featured dynamic content throughout the day. Dr. Neeraj Agarwal: Indeed. So, let's move on to bladder cancer. Christian, what are your key takeaways from the bladder cancer studies presented at the meeting? Dr. Christian Kollmannsberger: I think there were interesting abstracts in both the non-muscle-invasive and the muscle-invasive setting and the metastatic setting. So, for example, Abstract 442 was presented by Dr. Andrea Necchi on the cohort B of the phase 2 KEYNOTE-057 trial. As a background here, the standard treatment for high-risk non-muscle-invasive bladder cancer involves transurethral resection of the bladder tumor, a TURBT, followed by intravesical BCG therapy to eradicate any residual disease. And patients who fail to adequately respond to BCG are usually recommended to undergo radical cystectomy. So in the cohort B of the phase 2  KEYNOTE-057 trial that investigated the safety and efficacy of pembrolizumab as a single agent for patients with BCG-unresponsive, high-risk non-muscle-invasive bladder cancer who were ineligible or declined to undergo radical cystectomy, enrolled patients received standard-dose pembrolizumab of 200 milligrams every three weeks for up to 35 cycles. So very common as we do it with other disease sites. And at a median follow-up of 45.4 months, the primary endpoints of disease-free survival at twelve months was 43.5%. The median disease-free survival duration was 7.7 months. These are encouraging results, and we should keep in mind that a radical cystectomy has immense impact on our patients' quality of life. So I think it is important that we do these trials.  Now in order to address potential biases in this phase II trial, such as the underlying heterogeneity of transurethral resection of bladder tumor quality, and to obtain a more comprehensive understanding of pembrolizumab's efficacy relative to a particular control group, we need further evaluation of pembrolizumab in a randomized trial before we can really go for regulatory approval. But overall, I think for the first time in a long time that we seem to be able to move the needle in non-muscle-invasive bladder cancer. Dr. Neeraj Agarwal: Thank you, Christian, for this great overview. Could you please also share the findings presented by Dr. Matt Galsky on Abstract 443? Dr. Christian Kollmannsberger: Of course, Neeraj. Abstract 443, presented by Matt Galsky, reported the extended follow-up results from the CheckMate 274 trial, which looked at another very important field where we haven't made that much progress, which is the adjuvant setting. And CheckMate 274 examined adjuvant nivolumab compared to placebo for patients with high-risk resected muscle-invasive urothelial carcinoma. In this trial, nivolumab was given at 240 milligrams every two weeks or placebo every two weeks for up to one year of treatment. After following up with patients for a median of 36.1 months, the study found that those who received nivolumab had a median DFS of 22 months compared to only 10.9 months for those who received placebo among the ITT patients. So basically, a doubling of the DFS with the addition of adjuvant nivolumab.  The results were particularly notable for patients with high PD-L1 expressions or PD-L1 expression of 1% or more, as those who are treated with nivolumab had a median DFS of 52.6 months, which was six times higher than the DFS in the control group where patients received placebo, which was only 8.4 months. And I think that is truly impressive. One year of adjuvant therapy with nivolumab continues to show a sustained disease-free survival benefit over a period of three years in both the ITT and the PD-L1-high patient population. In my view, these results reinforce the utility of nivolumab in the adjuvant urothelial carcinoma setting after surgery. And it will be interesting to see how the overall survival pans out in this study.  So, Neeraj, moving on to kidney cancer, what were your key takeaways from these studies on kidney cancer presented in this meeting?  Dr. Neeraj Agarwal: So, there were exciting results presented from multiple studies in this area as well. For example, Abstract 603 presented by Dr. Mauricio Burotto, senior author was, Dr. Toni Choueiri on the three-year follow-up from the phase 2 CheckMate-9ER trial. So, in this trial, patients were randomized one-to-one to nivolumab 240 milligrams every two weeks, plus cabozantinib 40 milligrams daily versus sunitinib 50 milligrams daily for four weeks, and it was a six-week cycle for sunitinib until disease progression or unacceptable toxicity. So this was the design of the phase 3 CheckMate-9ER trial. And after a median follow-up of three years, the benefit of nivolumab plus cabozantinib remained consistent with previous follow-ups. So, as we know, these data have been presented in the past, also published in the New England Journal of Medicine. But this meeting was a clear follow-up of these data.  Notably, the median overall survival of patients treated with cabozantinib plus nivolumab in the ITT population, which included all favorable intermediate and poor IMDC score patients, was significantly improved at 49.5 months compared to 35.5 months in the sunitinib arm. It is so heartening to see that median overall survival breaching the four-year mark in our patients with metastatic RCC in a consistent fashion. We saw similar data with the combination of ipilimumab plus nivolumab recently. And as these trials are maturing, we are probably going to see more combinations breaching this four-year mark. So importantly, no new safety signals emerged with the additional follow-up in either arm. And I think these results provide further support for the use of cabozantinib plus nivolumab as a first-line treatment option for patients with metastatic or advanced renal cell carcinoma. Dr. Christian Kollmannsberger: Indeed, I think it is extremely impressive what we've seen over the last 15 years in metastatic kidney cancer, going from a median overall survival of about a year to now more than four years. I think that is a great achievement, and we can see it on a daily basis in our clinical practice.  Now, before we wrap up, I would like to highlight another potentially practice-changing trial, LBA602, which titled, “Results from Phase 3 Study of 89Zr-DFO-Girentuximab for PET/CT Imaging of Clear Cell Renal Cell Carcinoma: The ZIRCON Trial” presented by Dr. Brian Shuch. The background of this is that the detection of renal masses poses a challenge due to the limitations of diagnostic options such as imaging and biopsy. And we often, in clinical practice, are confronted with "What exactly is this?" And what's even more importantly, “What's the histology of this?” And a non-invasive, accurate method is needed for pre-treatment risk stratification. Girentuximab, a monoclonal antibody that targets carbonic anhydrase IX expressed on clear cell renal cell carcinoma, can obviously now aid in the differentiation between clear cell renal cell carcinomas and other renal lesions when radiolabeled with this new agent.  The ZIRCON trial was open-label and designed to include patients with renal masses up to 7 cm in size or clear tumor stage cT1 who were scheduled for partial nephrectomy within 90 days of planned TLX250-CDx administration. The enrolled patients received a single intravenous dose of girentuximab on day 0 and underwent FDG PET/CT imaging on day 5 before their scheduled surgery. And the co-primary endpoints were to assess the sensitivity and specificity of girentuximab PET/CT imaging for detecting clear cell renal cell carcinoma in patients with indeterminate renal masses, with histology as the reference standard, which I think is a great way to test these agents because you get 100% validation.  In the primary analysis of 284 patients, the average sensitivity and specificity across all three central readers were 86% and 87%, respectively, exceeding the prespecified thresholds. The positive and negative predictive values were 93.4% and 78%, respectively. And with very few related adverse events reported, the study affirms that girentuximab PET/CT is safe and effective in identifying clear cell renal cell carcinoma in patients with indeterminate renal masses. And the findings hold potential for developing optimal management strategies for patients with indeterminate renal masses. I think this is important that we add a non-invasive method to this because we are confronted on a regular basis with patients who either cannot tolerate a biopsy or where the biopsy is indeterminate. And this could potentially be a great tool to help us with our pre-treatment planning of our treatment strategy. Dr. Neeraj Agarwal: Wow. So, it looks like a new PET scan using a unique tracer and antibody to detect the clear cell renal cell carcinoma with high specificity and sensitivity. It reminds me of drawing a crude analogy from the PSMA PET scan in prostate cancer. And hopefully, we will be able to use these newer scans that we call TLX250-CDx PET/CT scan. I hope they have a simpler name for this very soon. Or maybe follow up for patients who had kidney cancer, localized kidney cancer taken out by radical surgery, and then we are following them. And sometimes, we don't know if a small lung nodule is metastatic or not. And these kinds of imaging studies may help us down the line in monitoring those patients as well. So indeed, very exciting progress not only in the therapeutic area now but also in diagnostic fields at this GU ASCO.   So with that, we have seen multiple abstracts on prostate, bladder, and kidney cancer with real impact on how we practice medicine. Thank you, Christian, for sharing your insight with us today. It is an exciting time in GU Oncology, and we appreciate you taking the time to contribute to the discussion. Thank you so much.   Dr. Christian Kollmannsberger: Thank you, Neeraj, thank you for having me. And I completely agree it remains an exciting time in GU oncology.   Dr. Neeraj Agarwal: And thank you to our listeners for joining us today. You will find links to the abstracts discussed today on the transcripts of this episode.  Finally, if you value the insights that you hear on the ASCO Daily News Podcast, please take a moment to rate, review, and subscribe wherever you get your podcasts.   Disclaimer: The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement.   Find out more about today's speakers:   Dr. Neeraj Agarwal  @neerajaiims Dr. Christian Kollmannsberger Follow ASCO on social media:    @ASCO on Twitter    ASCO on Facebook    ASCO on LinkedIn    Disclosures:   Dr. Neeraj Agarwal:    Consulting or Advisory Role: Pfizer, Bristol-Myers Squibb, AstraZeneca, Nektar, Lilly, Bayer, Pharmacyclics, Foundation Medicine, Astellas Pharma, Lilly, Exelixis, AstraZeneca, Pfizer, Merck, Novartis, Eisai, Seattle Genetics, EMD Serono, Janssen Oncology, AVEO, Calithera Biosciences, MEI Pharma, Genentech, Astellas Pharma, Foundation Medicine, and Gilead Sciences   Research Funding (Institution): Bayer, Bristol-Myers Squibb, Takeda, Pfizer, Exelixis, Amgen, AstraZeneca, Calithera Biosciences, Celldex, Eisai, Genentech, Immunomedics, Janssen, Merck, Lilly, Nektar, ORIC Pharmaceuticals, crispr therapeutics, Arvinas   Dr. Christian Kollmannsberger: None disclosed  

In 2022, Dr. Maura Abbott, Associate Professor of Nursing at the Columbia University School of Nursing, served as faculty for i3 Health's CME/NCPD approved activity, New Insights Into Preventing and Managing Chemotherapy-Induced Neutropenia. Now, in this follow-up interview with Oncology Data Advisor, Dr. Abbott reinforces the importance of educating patients who are at risk for chemotherapy-induced neutropenia and shares some of the therapeutic developments in both prevention and management that are coming down the pipeline in the near future. Click here to view and claim credit for New Insights Into Preventing and Managing Chemotherapy-Induced Neutropenia, an accredited CME/NCPD activity provided by i3 Health: https://i3health.com/new-cme/44-policies/503-i3health-com-cin

CME credits: 0.25 Valid until: 29-12-2023 Claim your CME credit at https://reachmd.com/programs/cme/alloimmune-neutropenia-of-the-fetus-and-newborn/13910/ Program Chairman:Roberto Romero, MD, DMedSciChief, Perinatology Research BranchDivision of Maternal-Fetal Medicine and ObstetricsDivision of Intramural ResearchNICHD/NIH/DHHSEditor-in-Chief for ObstetricsThe American Journal of Obstetrics and Gynecology Neonatal alloimmune neutropenia (NAIN or NIN) is a neutrophil blood group antagonism similar to HDFN and FNAIT. Its presentation varies clinically and ranges from asymptomatic to severe manifestations such as sepsis and meningitis. Listen in as Drs. Masja de Haas and Lee Shulman discuss clinical clues that should catch your eye. Discover novel yet simple ways to be vigilant and make the right clinical calls.

Host: Lee P. Shulman, MD, FACMG, FACOG Guest: Masja de Haas, MD, PhD Program Chairman:Roberto Romero, MD, DMedSciChief, Perinatology Research BranchDivision of Maternal-Fetal Medicine and ObstetricsDivision of Intramural ResearchNICHD/NIH/DHHSEditor-in-Chief for ObstetricsThe American Journal of Obstetrics and Gynecology Neonatal alloimmune neutropenia (NAIN or NIN) is a neutrophil blood group antagonism similar to HDFN and FNAIT. Its presentation varies clinically and ranges from asymptomatic to severe manifestations such as sepsis and meningitis. Listen in as Drs. Masja de Haas and Lee Shulman discuss clinical clues that should catch your eye. Discover novel yet simple ways to be vigilant and make the right clinical calls.

Guest: Ilene Galinsky BSN,MSN,ANP-C Patients with acute myeloid leukemia (AML) are at high risk for febrile neutropenia or profound, protracted neutropenia. So how can we monitor for the risk of neutropenia in AML patients starting venetoclax therapy? That's what Ilene Galinsky, Senior Program Research Nurse Practitioner for the Leukemia Program at Dana Farber Cancer Institute, is here to explain.

Guest: Ilene Galinsky BSN,MSN,ANP-C Patients with acute myeloid leukemia (AML) are at high risk for febrile neutropenia or profound, protracted neutropenia. So how can we monitor for the risk of neutropenia in AML patients starting venetoclax therapy? That's what Ilene Galinsky, Senior Program Research Nurse Practitioner for the Leukemia Program at Dana Farber Cancer Institute, is here to explain.

Guest: Lisa Nodzon PhD, ARNP, AOCNP Both the disease itself and the treatments for chronic lymphocytic leukemia (CLL) can cause neutropenia, which is why Dr. Lisa Nodzon from the Moffitt Cancer Center is here to discuss neutropenia in relation to CLL treatment with venetoclax.

Guest: Ilene Galinsky BSN,MSN,ANP-C Patients with acute myeloid leukemia (AML) are at high risk for febrile neutropenia or profound, protracted neutropenia. So how can we monitor for the risk of neutropenia in AML patients starting venetoclax therapy? That's what Ilene Galinsky, Senior Program Research Nurse Practitioner for the Leukemia Program at Dana Farber Cancer Institute, is here to explain.

Guest: Lisa Nodzon PhD, ARNP, AOCNP Both the disease itself and the treatments for chronic lymphocytic leukemia (CLL) can cause neutropenia, which is why Dr. Lisa Nodzon from the Moffitt Cancer Center is here to discuss neutropenia in relation to CLL treatment with venetoclax.

Dr Mary Riedy discuss an infant with infantile-onset Pompe disease and the challenges of an unusual neutropenia phenotype. Infantile-onset Pompe disease with neutropenia: Treatment decisions in the face of a unique phenotype Mary Riedy, et al https://doi.org/10.1002/jmd2.12337

Dr. Centor discusses benign neutropenia with Drs. Cecelia Chung and Jonathan Mosley.

Divya A. Khandekar, PharmD, MS (Twitter: @pharmdiv) describes the etiology of febrile neutropenia in patients with hematological malignancies, summarizes guideline-based recommendations for antibiotic discontinuation in patients with febrile neutropenia and discusses primary literature supporting early antibiotic discontinuation in patients with febrile neutropenia. For more pharmacy content, follow Mayo Clinic Pharmacy Residency Programs @MayoPharmRes or the host, Garrett E. Schramm, Pharm.D., @garrett_schramm on Twitter! You can also connect with the Mayo Clinic's School of Continuous Professional Development online at https://ce.mayo.edu/ or on Twitter @MayoMedEd. 

Approvals in psoriasis, hepatorenal syndrome, and neutropenia; novel therapy gains Priority Review for Rett Syndrome; and the effects of multivitamin supplementation assessed on cognitive function.  

Show notes at pharmacyjoe.com/episode741. In this episode, I'll discuss the safety of early antibiotic discontinuation in hematology patients with fever of unknown origin during chemotherapy-induced neutropenia. The post 741: Is it safe to use early antibiotic discontinuation in hematology patients with fever of unknown origin during chemotherapy-induced neutropenia? appeared first on Pharmacy Joe.

Show notes at pharmacyjoe.com/episode741. In this episode, I ll discuss the safety of early antibiotic discontinuation in hematology patients with fever of unknown origin during chemotherapy-induced neutropenia. The post 741: Is it safe to use early antibiotic discontinuation in hematology patients with fever of unknown origin during chemotherapy-induced neutropenia? appeared first on Pharmacy Joe.

In this interview, Maura Abbott describes the current landscape of chemotherapy-induced neutropenia and the activity she co-led earlier this year.

“It's actually the nurse who most often first identifies the subtle signs of sepsis in patients. Trust your clinical judgement,” ONS member Laura Zitella, MS, RN, ACNP-BC, AOCN®, nurse practitioner at the University of California, San Francisco, told listeners during a conversation with Stephanie Jardine, BSN, RN, oncology clinical specialist at ONS. Zitella explained the nursing and management considerations for febrile neutropenia and what to do if it transitions into sepsis. This episode is part of a series about oncologic emergencies; the previous episodes are also linked below. You can also earn free NCPD contact hours after listening to this episode by completing the evaluation linked below. Music Credit: "Fireflies and Stardust" by Kevin MacLeod Licensed under Creative Commons by Attribution 3.0 Earn 0.5 contact hours of nursing continuing professional development (NCPD) by listening to the full recording and completing an evaluation at myoutcomes.ons.org by August 12, 2024. The planners and faculty for this episode have no relevant financial relationships with ineligible companies to disclose. ONS is accredited as a provider of NCPD by the American Nurses Credentialing Center's Commission on Accreditation. Episode Notes Complete this evaluation for free NCPD. Previous Oncology Nursing Podcast episodes on oncologic emergencies Clinical Journal of Oncology Nursing articles: Sepsis: Symptoms, Assessment, Diagnosis, and the Hour-1 Bundle in Patients With Cancer NEWS Scoring System: Use in Hematologic Malignancies and Cellular Therapeutics Patient Populations Febrile Neutropenia: Decreasing Time to Antibiotic Administration in a Community Hospital Emergency Department ONS book: Understanding and Managing Oncologic Emergencies: A Resource for Nurses (third edition) ONS courses: Oncologic Emergencies Treatment and Symptom Management—Oncology RN Essentials in Oncologic Emergencies for the Advanced Practice Provider ONS Huddle Cards™ International Guidelines for Management of Sepsis and Septic Shock National Comprehensive Cancer Network guidelines on prevention and treatment of cancer-related infections Sepsis Alliance Surviving Sepsis Campaign To discuss the information in this episode with other oncology nurses, visit the ONS Communities. To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org. Highlights From Today's Episode “We know that fever and neutropenia in combination needs to be treated immediately. This is a high-risk oncologic emergency. Our patients who have febrile neutropenia are at very high risk of having a severe infection or sepsis.” Timestamp (TS) 03:44 “Patients with cancer are at an increased risk for infection because of the inherent immunosuppression of the cancer itself and also the treatment.” TS 08:28 “There are some very, very basic things that patients can do [to decrease risk for infection]. The most important is good handwashing. I explain to patients that your skin is the best barrier against getting an infection. If there's no break in the skin, then infection cannot get in. So, if your hands get contaminated and you wash them before you touch your eyes or your mouth or your nose, then that is a good way to prevent infection.” TS 11:42 “Even if a patient does everything perfect, most of the time when you're neutropenic, the infections that develop come from endogenous organisms. So, our body is colonized with probably 10 times as many microbes as human cells, and when the immune system is suppressed, it allows these organisms sometimes to cause infection. So, it's very important for patients to know that if they have signs of infection that they should let us know so that we can start immediate treatment to treat the infection.” TS 14:01 “If patients are higher risk or they have any organ dysfunctions, or other symptoms—like they're unwell, nausea, vomiting, diarrhea, any symptoms like that—they should be admitted to the hospital, and we would initiate IV antibiotics.” TS 17:37 “It's actually the nurse who's most often the person that first identifies sepsis in patients, so I think it's really important to trust your clinical judgement. When you look at a patient, it's really easy to tell when something is wrong. When they're starting to breathe too heavy or they're a little bit off and they're starting to get some altered mental status, or suddenly their heart rate is elevated for no reason even though they're just lying in bed. So, nurses are really positioned and are most often the ones who first pick up on these subtle signs.” TS 27:17

  Clozapine is often prescribed for patients with treatment-resistant schizophrenia, but its use is sometimes discontinued if it is suspected of inducing neutropenia. In this podcast, author Laurent Béchard discusses a consecutive case series published in the July-August 2022 issue of the Journal of Clinical Psychopharmacology assessing the continuation or reintroduction of this drug despite a neutropenia episode. In addition to suggesting further research to better define severe vs. moderate cases, Dr. Béchard proposes the use of pharmacovigilance tools to assess possible causes of neutropenia so clinicians can better determine if this highly effective antipsychotic should remain part of a patient's treatment plan.

In this episode, Julia LaBarbera, MSN, RN, AGACNP-BC, discusses the latest evidence and guidance on how advanced practice providers can optimize patient outcomes with CDK4/6 inhibitors for HR+/HER2- breast cancer. Topics include:An overview of the monarchE study leading to FDA approval of adjuvant abemaciclibKey trial data on abemaciclib, palbociclib, and ribociclib for metastatic HR+/HER2- breast cancerManaging adverse events associated with CDK4/6 inhibitorsPromoting adherence to oral therapyPresenter:Julia LaBarbera, MSN, RN, AGACNP-BCNurse PractitionerDivision of Hematology/OncologyDepartment of MedicineUniversity of California, Los AngelesSanta Monica, CaliforniaLink to full program:PCE.is/Onc22

Neste episódio, o especialista em hematologista e colunista do Portal PEBMED, Felipe Mesquita, comenta sobre a abordagem e tratamento da neutropenia febril. Para abordar o assunto, o especialista analisa o artigo “How I Treat Febrile Neutropenia”, publicado em março/2021 no Mediterranean Journal of Hematology and Infectious Disease. O estudo é do médico brasileiro Márcio Nucci, referência no tratamento de infecções do paciente imunossuprimido, em especial do paciente oncohematológico submetido ou não ao transplante de células tronco hematopoéticas. Aperte o play e confira o podcast!

Discover recent developments in the prevention, treatment, and management of chemotherapy-induced neutropenia, including a comprehensive understanding of the risk factors and current clinical practice guidelines. This activity is presented by Gary H. Lyman, MD, MPH, FASCO, FACP, FRCP, Professor, University of Washington, and Maura Abbott, PhD, AOCNP®, CPNP, Columbia University School of Nursing. Listen now to earn free CME/NCPD!

In our final stop in our Cytopenias series, we discuss the ins and outs of neutropenia. This is another very commonly seen issue in the clinic and in the hospital so most definitely high yield!Why is neutropenia dangerous?Prone to infections, especially gut translocation of bacteriaDefinition of neutropenia:NORMAL: WBC 4400-11000 cells/microL; neutrophils make up 40-70% of thatNeutropenia defined by ANC: WBC (cells/microL) x percent (PMNs + bands) ÷ 100 Breakdown:Neutropenia: ANC

How should a primary care physician evaluate neutropenia, and decide when it's time to worry? Kandace Gollomp, MD, pediatric hematologist, Children's Hospital of Philadelphia, discusses: tips for evaluating a CBC with differential; absolute neutrophil count (ANC) parameters for mild/moderate/severe neutropenia; when to worry about increased risk of infection, both in previously well children and in those with risk factors; a review of risk factors; lymphopenia, granulocytopenia and agranulocytosis and how they are different; benign ethnic neutropenia; post-infectious neutropenia and when you should re-check the CBC; when an infectious history should raise a red flag; when to order a peripheral smear or refer a patient to hematology for bone marrow biopsy or other evaluation; and more.  Published February 2022. This podcast is for general informational and educational purposes only and is not to be considered as medical advice for any particular patient. Clinicians must rely on their own informed clinical judgment in making recommendations to their patients. ©2022 by Children's Hospital of Philadelphia, all rights reserved.

In this episode, Eileen M. O'Reilly, MD, and Naureen Starling, MD, FRCP,  discuss emerging therapeutic strategies involving PARP inhibitor therapy in the treatment of pancreatic cancer. Topics include:Current treatment landscape and testing in the United States vs the United Kingdom  Testing for molecular subgroups beyond BRCAmUsing PARP inhibitors in earlier stages of the diseaseLearning from other cancers, such as prostate, breast, and ovarian  Presenters:Eileen M. O'Reilly, MDWinthrop Rockefeller Chair in Medical OncologySection Head, Hepatopancreaticobiliary/Neuroendocrine CancersGastrointestinal Oncology ServiceAssociate DirectorDavid M. Rubenstein Center for Pancreatic CancerAttending Physician, MemberMemorial Sloan Kettering Cancer CenterProfessor of MedicineWeill Medical CollegeNew York, New York, USANaureen Starling, MD, FRCPAssociate Director of Clinical ResearchDepartment of GI CancersConsultant Medical Oncologist, GI CancersThe Royal Marsden HospitalLondon, United KingdomContent based on an online CME program supported by an educational grant from AstraZeneca.Link to full program:https://bit.ly/3s6AnSz

In this podcast episode, Ashley Leak Bryant, PhD, RN, OCN, FAAN, discusses therapeutic options for younger, fit patients with AML and no targetable mutations. Topics include:Induction chemotherapy and consolidation therapyUse of gemtuzumab ozogamicinManagement of sinusoidal obstruction syndrome  Nursing considerations for younger, fit patients with AMLPresenter:Ashley Leak Bryant, PhD, RN, OCN, FAANAssociate ProfessorSchool of NursingUNC Lineberger Comprehensive Cancer Center  University of North Carolina at Chapel HillChapel Hill, North Carolina 

CME credits: 0.50 Valid until: 06-01-2023 Claim your CME credit at https://reachmd.com/programs/cme/expert-answers-to-common-questions-for-whos-at-risk-preventing-and-managing-tumor-lysis-syndrome-and-neutropenia-in-cll/13144/ Many CLL treatments cause a high risk for tumor lysis syndrome (TLS), an oncologic emergency due to the release of intracellular contents of tumor cells characterized by hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia. These electrolyte imbalances may be severe enough to cause acute renal failure, cardiac arrhythmias, seizures, loss of muscle control, and even death. In addition, neutropenia is a common side effect associated with CLL therapies, which increases the risk for infection and can disrupt or delay treatment, ultimately affecting patient outcomes. A greater understanding of assessment and management of TLS and neutropenia is critical for reducing the likelihood of life-threatening complications in patients with CLL, which allows patients to continue to receive treatment. AXIS routinely collects and analyzes data gathered from participants in our live activities. These questions provide incredible insight regarding the persistent challenges that clinicians face when trying to optimize treatment and management of patients with cancer to verify where clinical practice gaps exist. This activity will provide expert answers to questions asked during a recent educational series on preventing and managing tumor lysis syndrome and neutropenia in CLL.

CME credits: 0.50 Valid until: 06-01-2023 Claim your CME credit at https://reachmd.com/programs/cme/expert-answers-to-common-questions-for-whos-at-risk-preventing-and-managing-tumor-lysis-syndrome-and-neutropenia-in-cll/13144/ Many CLL treatments cause a high risk for tumor lysis syndrome (TLS), an oncologic emergency due to the release of intracellular contents of tumor cells characterized by hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia. These electrolyte imbalances may be severe enough to cause acute renal failure, cardiac arrhythmias, seizures, loss of muscle control, and even death. In addition, neutropenia is a common side effect associated with CLL therapies, which increases the risk for infection and can disrupt or delay treatment, ultimately affecting patient outcomes. A greater understanding of assessment and management of TLS and neutropenia is critical for reducing the likelihood of life-threatening complications in patients with CLL, which allows patients to continue to receive treatment. AXIS routinely collects and analyzes data gathered from participants in our live activities. These questions provide incredible insight regarding the persistent challenges that clinicians face when trying to optimize treatment and management of patients with cancer to verify where clinical practice gaps exist. This activity will provide expert answers to questions asked during a recent educational series on preventing and managing tumor lysis syndrome and neutropenia in CLL.

On this week's episode of Fast Facts - Perio Edition, Katrina Sanders, we are continuing the conversation that we started last week in discussing periodontitis as a manifestation of systemic disease highlighting familial and cyclic neutropenia!   Quotes:    “These are individuals who experienced episodes of abnormally low white blood cells.”   “It's important for us to understand that when patients present to our chairs, there is a possibility that these individuals may not know that they have this disease process.” Resources:   DentistRX: https://www.dentistrx.com  More Fast Facts: https://www.ataleoftwohygienists.com/fast-facts/    Katrina Sanders Website: https://www.katrinasanders.com  Katrina Sanders Instagram: https://www.instagram.com/thedentalwinegenist/    Sources: Papapanou, P. N., Sanz, M., Buduneli, N., Dietrich, T., Feres, M., Fine, D. H., ... & Tonetti, M. S. (2018). Jepsen S, Caton JG, Albandar JM, Bissada NF, Bouchard P, Cortellini P, Demirel K, de Sanctis M, Ercoli C, Fan J, Geurs NC, Hughes FJ, Jin L, Kantarci A, Lalla E, Madianos PN, Matthews D, McGuire MK, Mills MP, Preshaw PM, Reynolds MA, Sculean A, Susin C, West NX, Yamazaki K. Periodontal manifestations of systemic diseases and developmental and acquired conditions: Consensus report of workgroup 3 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018 Jun;89 Suppl 1:S237-S248. doi: 10.1002/JPER.17-0733. PMID: 29926943.

Learn about one of the medical emergencies in oncology: febrile neutropenia! Written and recorded by our fabulous Leanne Kim, McMaster University Medical Student, Graduating class of 2021. What is the definition of febrile neutropenia and why is it important to know? Who is at risk for developing febrile neutropenia? Why does febrile neutropenia develop? How should you approach history-taking and physical examination of a patient with febrile neutropenia? What investigations should be ordered for work-up of a patient with febrile neutropenia? Are there any risk-stratifying tools for febrile neutropenia? How do you treat febrile neutropenia?

The post QOD 099: Peds Neutropenia (Safety and Infection Control) appeared first on NURSING.com.

In this episode, we cover the definition of febrile neutropenia, management, and risk stratification for inpatient vs outpatient treatment. Written by: Dr. Anna Whalen-Browne (Internal Medicine Resident) Reviewed by: Dr. Paul Barnfield (Medical Oncology) & Dr. Sara Piran (General Internal Medicine)

In this episode I cover myelodysplastic syndrome.If you want to follow along with written notes on myelodysplastic syndrome go to zerotofinals.com/medicine/haematology/myelodysplasticsyndrome/ or the haematology section in the Zero to Finals medicine book.This episode covers the definitions, types, tests, causes and treatments of myelodysplastic syndrome. The audio in the episode was expertly edited by Harry Watchman.