Podcasts about hla b27

Too busy to read the Lens? Listen to our weekly summary here! In this week's episode we discuss… Recurrent acute anterior uveitis is associated with Māori ethnicity and HLA-B27 disease, and moderate vision loss is associated with shorter time to first recurrence JAK1 inhibitors may reduce the rate of treatment failure in inflammatory uveitis when compared to patients receiving placebo Asymptomatic vitreoretinal lymphoma (VRL) associated with primary CNS lymphoma exhibits lower rates of anterior segment involvement, vitritis, and subretinal infiltrates when compared to primary vitreoretinal lymphoma and symptomatic vitreoretinal lymphoma associated with primary CNS disease A study identifies patient factors that influence the presence of non-retinal hemorrhage ocular abnormalities in infants

Vissa genvarianter är kopplade till specifika smärttillstånd, förklarar professor Johan Frostegård som svar på en fråga från en lyssnare som genomgått en smärtutredning som visade att hen hade genotyp HLA B27. Vad innebär det och hur hänger det ihop med smärta?

If you would like to get a hold of him and or to check out his website. I know he would love to hear from you. Don't be shy. https://www.nottherestofyourlife.com If you would like to get a hold of me for coaching or a free conversation. I am happy to pass as much as I can and support you on your path. Asguidedintent@gmail.com or asguided.ca Craig is 37 years old and grew up on a farm in South Dakota. He always had big dreams and high anxiety. He was brought up in a stable family, his parents are still together and his mother and father both had anxiety and he now realizes how much that imprinted on him. He dropped out of law school to be a comedian at age 23 and did some shows, but by then he was 5 years into a pretty heavy alcohol addiction to cope with panic attacks. He worked odd jobs, until he was 28 years old, at which point he had a mental breakdown and quit alcohol. He always had aches and pains, injuries that lasted all summer, foot issues, etc. He never took care of the mental aspect after getting sober, and then the stress of 2020 spring at age 34, the pandemic kicked things into overdrive, suddenly his leg and S.I. joint were constantly inflamed to the point of not sleeping, not being able to walk. Went to dozens of doctors, orthopaedics, brain and spine doctors, and finally, he was the one who suggested an HLA-B27 test. Then finally after waiting..in Feb 2022 his rheumatologist told him biologics are the answer since he had tried NSAIDs for so long, and that he would have this for life. He didn't accept this, and that's when he started searching (meat-only diet, CBD oil, and seed gut protocols, stretching, special hip apparatuses for relieving muscle tension, and massages. For his career, he does freelance drone photography, auctioneering, and cattle farming with his dad.

Notre 1er invité est Kepa pour la sortie de son 2ème album Divine Morphine (Éditions Miliani). C'est toujours la même chanson, celle qui tient en un mot. Cinq lettres, trois consonnes et deux voyelles. Un B, un L, un U, un E et la marque du pluriel au bout. Un mot international, qui désigne à la fois une musique, un état émotionnel et vaguement une couleur. Vous l'avez, là ? Chut… Il ne faut plus l'écrire, ni le nommer, pour ne pas tomber dans ses clichés, ni y emmener les auditeurs du deuxième album de Kepa. Kepa ne veut plus en entendre parler, pourtant il l'a. Dans sa guitare en métal qui, entre de bonnes mains, ressemble à une lampe d'Aladin, à une épée mythologique. Dans son harmonica, cet instrument qui fait trembler le cerveau quand on en joue avec le cœur. Dans sa vie de tous les jours et même de tous les hiers. Au fond de ses tripes, comme un frisson qui remonte jusqu'à ses cordes vocales, un super pouvoir dont il faut aussi avoir peur. Dans ses gênes, son corps endolori, son sang altéré. Dans le titre de ce nouvel album, Divine Morphine. Le premier, sorti il y a trois ans, s'appelait Doctor, Do Something. Un début de concept, toujours la même chanson, comme une affection longue durée. Kepa l'a attrapé comme une maladie. En 2013, Kepa s'appelait Bastien Duverdier et il vivait la vie de skater professionnel, humain augmenté capable de voyager loin et de s'envoler sur une planche à roulettes. Quant tout à coup, il s'est senti devenir vieux. Rongé par une maladie auto-immune qui a bouleversé sa vie, les chiens de l'enfer à ses trousses, qui ne le lâcheront jamais. Il a trouvé une planche de salut, sans roulettes mais avec des cordes, dans la musique, pratiquée sur sa guitare en métal et de préférence sur un ou deux accords qui tournent, à la recherche d'une transe intérieure, d'une vibration musico-thérapeutique, d'un rite auto-chamanique. Bastien est devenu musicien, sortant donc en 2018 Doctor, Do Something, premier album réalisé avec Taylor Kirk du groupe canadien Timber Timbre. L'album a été très bien accueilli, et des centaines de concerts ont fait connaître Kepa, son humour, sa musique et ses jolies chemises.   Mais, malgré tout le bien qu'on a pensé de Doctor, Do Something, on peut l'affirmer sans forfanterie : Divine Morphine est mille fois mieux. Doctor, Do Something était une carte de visite. Divine Morphine est le récit d'une expédition au fond de soi, d'un voyage au bout de l'enfermement. Personne ne t'entendra crier. Il a fait ce disque pour chercher à comprendre, dompter et raconter cette maladie qui l'a chamboulé jusqu'à l'implosion, à l'orée de la folie. «Du plomb dans l'Eldorado», chante-t-il en duo avec Sarah McCoy sur l'incroyable dark-pop song Eldorado, un vrai tube du nouveau monde. Du plomb dans l'Eldorado, c'est un peu ce que tout le monde ressent depuis l'année 2020, non ? Le calvaire des uns est la Covid-19, le sien s'appelle HLA-B27, pour human leucocyte antigen. Personne ne peut le vivre à sa place, mais tout le monde peut ressentir et apprécier comment il s'est soigné avec Divine Morphine. Le premier morceau est un peu son All Aboard (Muddy Waters) à lui. Un solo d'harmonica basse façon train song, qui aurait eu sa place sur Doctor, Do Something, mais qui d'un coup tourbillonne, se dérègle et annonce la suite. Le train vient de dérailler et d'entrer dans une autre dimension, celle du vertige opiacé, de la perte de contrôle, de la musique qui rêve et dérive… Une chanson va sonner comme la bande-son d'un western où Kepa fait un duel avec lui-même (Dog Days). Une autre emmène les vieux Bukka White et Alan Vega danser dans un club de Détroit pendant un tremblement de terre (Wet Dream). Le temps de deux reprises, Kepa s'agenouille sans se prosterner devant des totems intimes : Hard Time Killin Floor Blues de Skip James (avec Rodolphe Burger), et Sodade de Cesaria Evora dans une version hallucinée, où l'on voit l'océan geler autour des îles du Cap-Vert.   Six pieds sous terre reste sous les tropiques le temps d'une murder ballad. La chanson Divine Morphine est presque badine, indolente, ritournelle dans un état second. L'instrumental Messe HLA-B27 montre les progrès guitaristiques fulgurants de Kepa, affranchi des exercices de styles, devenu son propre maître. Sa voix aussi a changé, il la pousse vers la plainte dans des aigus hululants. Il joue différents instruments, des claviers comme des stalactites, la trompette et d'autres choses avec sa bouche, des bruitages d'origine non identifiée. Il est l'homme-orchestre du Titanic, au final seul survivant du naufrage, puis échoué sur une île déserte – le dernier morceau, Merle, ressemble à la prière païenne d'un Robinson en lévitation. L'album est maintenant terminé. Personne n'en sortira indemne. Et tout le monde n'aura qu'une envie : y retourner. Stéphane Deschamps. Titres interprétés - Divine Morphine, Live RFI - Sodade, extrait de l'album Divine Morphine - Eldorado, Live RFI - Hard Time Killing Floor, extrait de l'album Divine Morphine. Puis nous recevons Jawhar pour la sortie de l'album Tasweerah (62TV/PIAS).   Tasweerah est le quatrième album du singer / songwriter tunisien Jawhar. Tasweerah veut dire en tunisien à la fois : portrait, image, mais aussi : projection de l'esprit… L'album est une série d'arrêts sur image, de portraits plus ou moins personnels. Les chansons sont, chacune à leur manière, des tentatives vers un portrait universel de l'artiste. Elles questionnent sa place et celle de l'imaginaire dans la société, posent «la création et la quête de la beauté» au centre de l'album. Volontairement brut et sans artifice, Tasweerah nous replonge dans la folk / pop claire-obscure de Jawhar, proclamé dans la catégorie Arabic Dream Pop. Né d'une mère professeure de Littérature arabe, éprise de musique et de poésie, et d'un père qui se consacre au théâtre puis à la politique culturelle, Jawhar grandit dans la banlieue au sud de Tunis, à Radès. Très tôt, il est fasciné par une certaine culture populaire, par la force de ses images et de ses expressions verbales, musicales et gestuelles. Quand il part à l'âge de vingt ans étudier l'anglais à Lille, c'est plutôt la poésie abstraite qui l'attire, celle de William Blake et d'Emily Dickinson… En plus d'un amour grandissant pour un certain Nick Drake qui le liera de manière irrévocable à sa folk impressionniste. Titres interprétés - Malguit Live RFI - Schizo Hyout, extrait de l'album Tasweerah voir le clip  - Sayyed Ezzin, extrait de l'album Tasweerah - Foug Layyem Live RFI voir le clip. Son : Fabien Mugneret, Mathias Taylor, Benoît Letirant. (Rediffusion du 27 mars 2022)

In this episode I discuss an article from Myspondyloarthritisteam.com on HLA-B27. Here is a link to the https://www.myspondylitisteam.com/resources/hla-b27-and-the-genetics-of-spondylitis?utm_source=iterable&utm_medium=email&utm_campaign=spondylitis_roc (article). Make sure to check out The Faces of Ankylosing Spondylitis. Here is a link to https://thefacesofankylosingspondylitis.com/?blogsub=confirming#subscribe-blog (website). I'm number 158 if you are curious. If you are not part of this wonder page, submit your story. Cookie wants to get to 2700 people on the site, but I bet we can get her way past this. All the below links are affiliate links. If you purchase any of the items, I may earn a small commission. It does not change the price of items. Get paid to take tests. Here is a link to Rare Patient Voice. If you take participate in a study, you can get paid (amount varies). https://rarepatientvoice.com/TheAxialSpondyloarthritisPodcast/ (https://rarepatientvoice.com/TheAxialSpondyloarthritisPodcast/) Here are some links to Amazon showing some of the items I discussed. Uberlube - https://amzn.to/3i604N2 (https://amzn.to/3i604N2) Here is the Bean Bag neck warmer https://amzn.to/3uN6mcg (https://amzn.to/3uN6mcg) Biofreeze - https://amzn.to/33gygBS (https://amzn.to/33gygBS) Cane - https://amzn.to/3uN9fts (https://amzn.to/3uN9fts) Heating Pad - https://amzn.to/3Bjd5vz (https://amzn.to/3Bjd5vz) Weighted Blanket - https://amzn.to/36RCdi7 (https://amzn.to/36RCdi7) Steff Di Pardo's new book - I Am Not Invisible - https://amzn.to/3JpDScA (https://amzn.to/3JpDScA) All My Ankylosing Spondylitis Shit: Pain and Symptom Tracker by Kinsella Love https://amzn.to/34CHhpx (https://amzn.to/34CHhpx)

Notre 1er invité est Kepa pour la sortie de son 2ème album Divine Morphine (Éditions Miliani). C'est toujours la même chanson, celle qui tient en un mot. Cinq lettres, trois consonnes et deux voyelles. Un B, un L, un U, un E et la marque du pluriel au bout. Un mot international, qui désigne à la fois une musique, un état émotionnel et vaguement une couleur. Vous l'avez, là ? Chut… Il ne faut plus l'écrire, ni le nommer, pour ne pas tomber dans ses clichés, ni y emmener les auditeurs du deuxième album de Kepa. Kepa ne veut plus en entendre parler, pourtant il l'a. Dans sa guitare en métal qui, entre de bonnes mains, ressemble à une lampe d'Aladin, à une épée mythologique. Dans son harmonica, cet instrument qui fait trembler le cerveau quand on en joue avec le cœur. Dans sa vie de tous les jours et même de tous les hiers. Au fond de ses tripes, comme un frisson qui remonte jusqu'à ses cordes vocales, un super pouvoir dont il faut aussi avoir peur. Dans ses gênes, son corps endolori, son sang altéré. Dans le titre de ce nouvel album, Divine Morphine. Le premier, sorti il y a trois ans, s'appelait Doctor, Do Something. Un début de concept, toujours la même chanson, comme une affection longue durée. Kepa l'a attrapé comme une maladie. En 2013, Kepa s'appelait Bastien Duverdier et il vivait la vie de skater professionnel, humain augmenté capable de voyager loin et de s'envoler sur une planche à roulettes. Quant tout à coup, il s'est senti devenir vieux. Rongé par une maladie auto-immune qui a bouleversé sa vie, les chiens de l'enfer à ses trousses, qui ne le lâcheront jamais. Il a trouvé une planche de salut, sans roulettes mais avec des cordes, dans la musique, pratiquée sur sa guitare en métal et de préférence sur un ou deux accords qui tournent, à la recherche d'une transe intérieure, d'une vibration musico-thérapeutique, d'un rite auto-chamanique. Bastien est devenu musicien, sortant donc en 2018 Doctor, Do Something, premier album réalisé avec Taylor Kirk du groupe canadien Timber Timbre. L'album a été très bien accueilli, et des centaines de concerts ont fait connaître Kepa, son humour, sa musique et ses jolies chemises.     Mais, malgré tout le bien qu'on a pensé de Doctor, Do Something, on peut l'affirmer sans forfanterie : Divine Morphine est mille fois mieux. Doctor, Do Something était une carte de visite. Divine Morphine est le récit d'une expédition au fond de soi, d'un voyage au bout de l'enfermement. Personne ne t'entendra crier. Il a fait ce disque pour chercher à comprendre, dompter et raconter cette maladie qui l'a chamboulé jusqu'à l'implosion, à l'orée de la folie. "Du plomb dans l'Eldorado", chante-t-il en duo avec Sarah McCoy sur l'incroyable dark-pop song Eldorado, un vrai tube du nouveau monde. Du plomb dans l'Eldorado, c'est un peu ce que tout le monde ressent depuis l'année 2020, non ? Le calvaire des uns est la Covid-19, le sien s'appelle HLA-B27, pour human leucocyte antigen. Personne ne peut le vivre à sa place, mais tout le monde peut ressentir et apprécier comment il s'est soigné avec Divine Morphine. Le premier morceau est un peu son All Aboard (Muddy Waters) à lui. Un solo d'harmonica basse façon train song, qui aurait eu sa place sur Doctor, Do Something, mais qui d'un coup tourbillonne, se dérègle et annonce la suite. Le train vient de dérailler et d'entrer dans une autre dimension, celle du vertige opiacé, de la perte de contrôle, de la musique qui rêve et dérive… Une chanson va sonner comme la bande-son d'un western où Kepa fait un duel avec lui-même (Dog Days). Une autre emmène les vieux Bukka White et Alan Vega danser dans un club de Détroit pendant un tremblement de terre (Wet Dream). Le temps de deux reprises, Kepa s'agenouille sans se prosterner devant des totems intimes : Hard Time Killin Floor Blues de Skip James (avec Rodolphe Burger), et Sodade de Cesaria Evora dans une version hallucinée, où l'on voit l'océan geler autour des îles du Cap-Vert.     Six pieds sous terre reste sous les tropiques le temps d'une murder ballad. La chanson Divine Morphine est presque badine, indolente, ritournelle dans un état second. L'instrumental Messe HLA-B27 montre les progrès guitaristiques fulgurants de Kepa, affranchi des exercices de styles, devenu son propre maître. Sa voix aussi a changé, il la pousse vers la plainte dans des aigus hululants. Il joue différents instruments, des claviers comme des stalactites, la trompette et d'autres choses avec sa bouche, des bruitages d'origine non identifiée. Il est l'homme-orchestre du Titanic, au final seul survivant du naufrage, puis échoué sur une île déserte – le dernier morceau, Merle, ressemble à la prière païenne d'un Robinson en lévitation. L'album est maintenant terminé. Personne n'en sortira indemne. Et tout le monde n'aura qu'une envie : y retourner. Stéphane Deschamps.   Titres interprétés - Divine Morphine, Live RFI - Sodade, extrait de l'album Divine Morphine - Eldorado, Live RFI - Hard Time Killing Floor, extrait de l'album Divine Morphine.   Puis nous recevons Jawhar pour la sortie de l'album Tasweerah (62TV/PIAS).   Tasweerah est le quatrième album du singer / songwriter tunisien Jawhar. Tasweerah veut dire en tunisien à la fois : portrait, image, mais aussi : projection de l'esprit… L'album est une série d'arrêts sur image, de portraits plus ou moins personnels. Les chansons sont, chacune à leur manière, des tentatives vers un portrait universel de l'artiste. Elles questionnent sa place et celle de l'imaginaire dans la société, posent "la création et la quête de la beauté" au centre de l'album. Volontairement brut et sans artifice, Tasweerah nous replonge dans la folk / pop claire-obscure de Jawhar, proclamé dans la catégorie Arabic Dream Pop. Né d'une mère professeure de Littérature arabe, éprise de musique et de poésie, et d'un père qui se consacre au théâtre puis à la politique culturelle, Jawhar grandit dans la banlieue au sud de Tunis, à Radès. Très tôt, il est fasciné par une certaine culture populaire, par la force de ses images et de ses expressions verbales, musicales et gestuelles. Quand il part à l'âge de vingt ans étudier l'anglais à Lille, c'est plutôt la poésie abstraite qui l'attire, celle de William Blake et d'Emily Dickinson… En plus d'un amour grandissant pour un certain Nick Drake qui le liera de manière irrévocable à sa folk impressionniste.     Titres interprétés - Malguit Live RFI - Schizo Hyout, extrait de l'album Tasweerah voir le clip  - Sayyed Ezzin, extrait de l'album Tasweerah - Foug Layyem Live RFI voir le clip.   Son : Fabien Mugneret, Mathias Taylor, Benoît Letirant.

Inflammation can occur in any part of the body and the eye is no exception. In this episode, we discuss uveitis and scleritis, two specific inflammatory conditions of the eye. Uveitis, one of the major causes of vision loss, is an intraocular inflammatory condition that can be broken up into three categories: infectious, non-infectious, and traumatic. It can further be classified by where the inflammation occurs in the eye: anterior (front part - iris), intermediate (middle part – ciliary body), posterior (back part – choroid), and panuveitis (entire eye).Infectious uveitis can be caused by bacteria, viruses, fungi, and parasites in the eye or by a systemic infection like herpes, tuberculosis, syphilis, toxoplasmosis, or Lyme disease. Noninfectious uveitis, the most common type, can be caused by autoimmune conditions like rheumatoid arthritis, lupus, sarcoidosis, Reiter syndrome, ankylosing spondylitis, Behcet's disease, psoriatic arthritis, and inflammatory bowel disease. The most common reason for uveitis is called idiopathic – no reason can be found. Symptoms of uveitis will vary according to its location in the eye. Anterior uveitis, also called iritis, can cause ocular pain, photophobia (light sensitivity), red eye, and decreased vision. Uveitis in the back of the eye mainly causes vision loss but usually does not cause pain.After a thorough eye examination, a lab work-up should be performed especially after the second recurrent episode or if the first episode affects both eyes. Ruling out an infectious cause can be done in the office. Bloodwork to rule out some of the autoimmune diseases is the next step. Sometimes a chest x-ray may be necessary to help rule out TB or sarcoidosis.Treatment of infectious uveitis is directed at the pathogen causing the infection. This may involve a combination of topical antibiotics or anti-virals and systemic medications. Steroids are the mainstay of treatment of non-infectious uveitis. Most anterior uveitis is treatable with topical steroid eye drops. Intermediate and posterior uveitis is mainly treated with oral steroids and steroid injections around or in the eye. For patients with chronic or recurrent uveitis, immunomodulatory therapies may be necessary. Some of these medications may include methotrexate, Cellsept, Humira, and Remicade.Scleritis is an inflammatory condition of the outer coating of the eye (sclera). Symptoms include severe eye pain, red eye, and sometimes a decrease in vision. If the back part of the eyewall is inflamed, the eye may not appear red. An ultrasound of the eye may be necessary to properly diagnose this condition. Some of the causes of scleritis include rheumatoid arthritis, HLA-B27-related diseases, and gout. Oral and injectable steroids are the primary treatments for this condition. Sometimes immunomodulatory therapies are also needed to control the inflammation. Here are some more links to learn more about inflammation in the eye.Uveitis.orgPreventblindness.org/uveitis/Scleritis To find out more about Dr. Lou Chorich and his practice, go to Midwest Retina's website.This is intended for informational and educational purposes only, and nothing in this podcast/blog is to be considered as recommending or rendering medical advice or treatment to a specific patient. Please consult your eye care specialist for proper diagnosis and treatment of any eye conditions that you may have.

YouTube-Kanal: bit.ly/Medizinmensch-YT Entzündung im Gelenk ist ein wichtiger Grund für Rheuma Diagnostik. Die Diagnose von Rheuma erfolgt unter anderem mithilfe von Bluttests und dieses Video erklärt die schrittweise Vorgehensweise vom Verdacht bis hin zur Bestätigung der rheumatischen Diagnose: Rheumatoide Arthritis, Systemischer Lupus Erythematodes (SLE), und Morbus Bechterew und Psoriasis-Arthritis (Krankheiten der sog. seronegativen Spondylarthritiden) sind typische Ergebnisse bei der Diagnostik. 0:00 Intro 0:35 Körper attackiert sich selbst 0:44 Entzündlicher Schmerz und körperliche Anzeichen als Ausgangspunkt der Rheuma-Diagnose 2:19 Blutsenkungsgeschwindigkeit (BSG) 2:54 C-reaktives Protein CRP 4:00 Blutbild und Ferritin 5:27 Blutchemie (Leberwerte und Nierenfunktion) 6:03 Drei Bausteine zur Rheuma-Diagnostik 6:47 Tests bei Verdacht auf Rheumatoide Arthritis, Rheumafaktor und CCP 10:50 Tests bei Verdacht auf Lupus, ANA 12:18 Tests bei Verdacht auf Morbus Bechterew, Psoriasis-Arthritis (seronegative Spondyloarthritis) Meine Website: https://medizinmensch.de Kaffee spenden: https://buymeacoffee.com/Medizinmensch Weitere Videos von mir (Playlists): Autoimmunerkrankungen: https://bit.ly/MM-Autoimmunerkrankungen Blutwerte erklärt: https://bit.ly/MM-Blutwerte Coronavirus & Covid-19: https://bit.ly/MM-Corona Gicht & Pseudogicht: https://bit.ly/MM-Gicht Medizin leicht erklaert: https://bit.ly/MM-Medizin-erklaert Lizenzen: CC0: https://creativecommons.org/publicdomain/zero/1.0 CC BY 3.0: https://creativecommons.org/licenses/by/3.0 CC BY 4.0: https://creativecommons.org/licenses/by/4.0 Wichtiger Hinweis: Die Videos dienen ausschließlich der Allgemeinbildung. Die Informationen ersetzen keine persönliche Beratung, Untersuchung oder Diagnose. Die zur Verfügung gestellten Inhalte ermoeglichen nicht die Erstellung eigenständiger Diagnosen. Medizinisches Wissen unterliegt fortwaehrendem Wandel und es kann nicht garantiert werden dass die Informationen zu jedem Zeitpunkt noch korrekt sind, oder selbst korrekt waren. Haftung ausgeschlossen. Merk-würdiges Medizinwissen für Alle. Abonniere jetzt und erhalte neue Folgen, jeden Medizin-Mittwoch. Folge direkt herunterladen

In this week's episode of the Spine & Nerve podcast Dr. Nicolas Karvelas and Dr. Brian Joves review a common cause of low back pain, sacroiliac joint (SI) pain. The SI joint is a large complex joint that involves the iliac bone and sacrum. The SI joint is a critical component of the connection between the spine and lower limbs, and one of the primary functions of the SI joint is stability. Chronic SI joint pain is a relatively common cause of low back pain with epidemiologic studies demonstrating that SI joint pain significantly contributes to 10-38% of cases of chronic low back pain. Risk factors for SI joint pain include: leg length discrepancy, gait abnormality, scoliosis, spinal fusion, hip pathology, pregnancy, high force/velocity injury, seronegative HLA-B27 spondyloarthropathies, repetitive shear stress injuries in athletes. The common clinical presentation for SI joint pain includes aching pain below the belt line, with radiating/referred pain to gluteal/buttock region, groin, posterior leg, and less commonly thigh. This pain is often worsened with prolonged sitting, sleeping positions, movement. Physical exam results supportive of a diagnosis of SI joint pain include at least 3 positive tests, with at least one of these tests being thigh thrust or compression test. The 5 recommended provocative maneuvers include: 1) Distraction test 2) thigh thrust test 3) FABERE 4) Compression test 5) Gaenslen's maneuver. A recent expert opinion article titled A Review and Algorithm in the Diagnosis and Treatment of Sacroiliac Joint Pain, works to clarify the approach to diagnosis and treatment of SI joint pain. This review article highlights the importance of optimizing the diagnosis as soon as possible to guide treatment, and image guided injection remains the gold standard for the diagnosis of SI joint pain. Listen as the doctors review SI joint pain, and discuss the algorithm presented in the recent expert opinion review article. This podcast is for information and educational purposes only, it is not meant to be medical or career advice. If anything discussed may pertain to you, please seek council with your healthcare provider. The views expressed are those of the individuals expressing them, the may not represent the views of Spine & Nerve. References: 1. Falowski S, Sayed D, Pope J, Patterson D, Fishman M, Gupta M, Mehta P. A Review and Algorithm in the Diagnosis and Treatment of Sacroiliac Joint Pain. J Pain Res. 2020;13:3337-3348. 2. Wallace P, Bezjian Wallace L, Tamura S, et al. Effectiveness of Ultrasound-Guided Platelet-Rich Plasma Injections in Relieving Sacroiliac Joint Dysfunction. American Journal of Physical Medicine & Rehabilitation. 2020 Aug;99(8):689-693.

FDA 连续批准2个IL-17A单抗治疗中轴型脊柱关节炎Annals of Rheumatic Diseases 发表2篇真实世界的研究讨论TNF抑制剂在中轴型脊柱关节炎治疗中的疗效Science Advance 纳米颗粒包裹环孢素靶向治疗狼疮肾炎依奇珠单抗中轴型脊柱关节炎（axial spondyloarthritis，SpA）是慢性炎症性疾病，主要表现为背痛和进展性脊柱僵直。分成两种类型：影像学可见骶髂关节炎改变的称为强直性脊柱炎（ankylosing spondylitis，AS）；没有骶髂关节炎改变的称为影像学阴性的中轴型脊柱关节炎（nonradiographic axial spondyloarthritis，nr-axSpA）。常用的治疗药物包括非甾体类抗炎药和TNF-α抑制剂。依奇珠单抗（ixekizumab）是抗IL-17A的单克隆抗体，2016年被批准用于治疗银屑病和银屑病性关节炎；2020年6月适应症被扩展放射学阴性的中轴型脊椎关节炎、和强直性脊柱炎。《COAST-X研究：依奇珠单抗用于放射学阴性的中轴型脊椎关节炎的3期临床研究》Lancet，2020年1月 (1)COAST-X是一项52周、随机、双盲、安慰剂对照、平行组研究。共303名、活动性的、放射学阴性的中轴型脊椎关节炎的、对非甾体抗炎药效果不好的患者，被随机分配依奇珠单抗80mg q4w组，依奇珠单抗80mg q2w组或安慰剂组。第16周后，可根据情况开放标签。研究的主要终点设定为中轴型脊椎关节炎评估国际标准改善≥40%（ASAS40）。16周时，q4w组中35%的患者和q2w组中40%的患者病情缓解，安慰剂组仅19%。52周时，q4w组中30%的患者和q2w组中31%的患者病情缓解，安慰剂组仅13%。依奇珠单抗最常见的不良事件是鼻咽炎和注射部位反应，而且有1例出现严重感染。总的来说，三组的严重不良事件发生率都很低，没有肿瘤或死亡。结论：在治疗放射学阴性的中轴型脊椎关节炎方面，依奇珠单抗疗效优于安慰剂。《COAST-V和COAST-W研究：依奇珠单抗在治疗活动性强制性脊柱炎的有效性和安全性的3期临床研究》Annals of Rheumatology，2020年2月 (2)在2项3期临床研究中，旨在研究连续52周使用依奇珠单抗治疗活动性强制性脊柱炎的疗效和安全性，纳入研究的患者有的从未使用过生物抗风湿药（COAST-V），有的正在使用TNF抑制剂（COAST-W）。研究将患者随机分入依奇珠单抗q4w组，依奇珠单抗q2w组、安慰剂组或阿达木单抗组。在第16周时，安慰剂组和阿达木单抗组随机加用依奇珠单抗q2w或依奇珠单抗q4w，直至第52周。研究的主要终点设定为中轴型脊椎关节炎评估国际标准改善≥40%（ASAS40）。COAST-V研究中，在第16周和第52周达到ASAS40的比例分别为48%和53% （依奇珠单抗q4w），52%和51%（依奇珠单抗q2w），36%和51%（依奇珠单抗+阿达木单抗），19%和47%（依奇珠单抗+安慰剂）。COAST-W研究中，16周和52周达到ASAS40的比例分别为25%和34%（依奇珠单抗q4w），31%和31%（依奇珠单抗q2w），14%和39%（依奇珠单抗+安慰剂）。依奇珠单抗两种给药方案持续改善疾病活动度、患者身体功能、炎症的客观指标、生活质量、健康状况和整体功能达52周。依奇珠单抗52周安全性与16周的安全性一致。结论：对于未使用过生物制剂和曾经使用过TNF抑制剂的患者，依奇珠单抗的疗效从16周持续至52周。最初接受阿达木单抗治疗的患者换到依奇珠单抗后，有进一步改善。苏金单抗苏金单抗（secukinumab）是人源抗IL-17A的单克隆抗体。2015年被批准用于治疗银屑病和银屑病性关节炎；2020年6月适应症被扩展放射学阴性的中轴型脊椎关节炎。《苏金单抗治疗影像学阴性的中轴型脊椎关节炎的3期研究》Arthritis and Rheumatology，2020年8月 (3)研究旨在评估苏金单抗在治疗活动性、影像学阴性的中轴型脊椎关节炎的患者中的疗效。共555例患者，分别苏金单抗150mg负荷组，苏金单抗150mg无负荷组或安慰剂，前4周q1w负荷剂量给药，4周后q4w给药。20周后，允许切换到开放标签。研究的主要终点设定为国际中轴型脊椎关节炎评估国际标准改善≥40%（ASAS40）。16周时苏金单抗负荷组41.5%的患者，52周时非负荷组39.8%的患者出现病情缓解，安慰剂组仅为29.2%（P < 0.05)。没有新的安全发现报告。结论：苏金单抗治疗影像学阴性的中轴型脊椎关节炎优于安慰剂，疗效持续52周。中轴型脊柱关节炎中轴型脊柱关节炎的背痛的特点有：40岁以前出现背部不适、起病隐匿、随运动而改善、休息时无缓解、夜间痛。患者还可以伴有以下症状：交替性臀区疼痛、附着点炎导致的足跟痛、指炎、下肢非对称性关节炎、前葡萄膜炎（虹膜炎）、克罗恩病或溃疡性结肠炎、银屑病、疼痛对NSAID类药物反应良好、脊柱关节炎家族史。实验室检查包括HLA-B27阳性，和影像学骶髂关节炎。对于慢性背痛发病时3个月、后因无效而停用、并开始另一项抗风湿药物的患者，进行了一项回顾性队列研究。137例患者中，抗阿达木单抗抗体的存在并不能预测换用其他TNFi的药物反应性（敏感性/特异性 18%/75%），也不能预测非TNFi药物的反应性（敏感性/特异性 33%/70%）。阿达木单抗的血药浓度不能预测换用TNFi的药物反应性（敏感性/特异性 50%/52%），也不能预测非TNFi药物反应性（敏感性/特异性 32%/69%）。结论：对于抗阿达木单抗抗体或阿达木单抗血药浓度，作者无法找到二次使用TNFi或非TNFi药物反应的预测价值。《BSRBR-RA研究：抗TNF的早期反应预测长期获益》Rheumatology，2020年7月 (9)研究的目的是评估，类风湿关节炎患者在启动第一个抗TNF（TNF）的药物后，长期的疾病活动情况的轨迹。研究选取2001年至2013年首次使用抗TNF药物的类风湿关节炎患者，共14436例。类风湿关节炎活动评分的最低点出现在用药250天内。第180天时，已经出现了4种不同的、稳定的响应轨迹。55.3%的患者属于“适度”反应型；32.4%的患者属于“显著”反应型。其余的8.7%和3.6%分别符合“最大”和“最小”反应型。在2001-2008年和2010-2013年之间，达到“最大”反应的比例显著增加(P < 0.01)。结论：抗TNF药物使用6个月时，疾病活动的长期轨迹轮廓已经可以确定。大多数患者有持续的“适度”反应，维持中度的疾病活动；大约1/3的患者达到最大程度的缓解。《注册研究：一线TNF抑制剂与非TNF抑制剂生物制剂和靶向合成制剂在类风湿性关节炎患者中的疗效比较》Annals of Rheumatic Diseases，2020年7月 (10)本研究评估了TNF（TNF）抑制剂与非TNF抑制剂（生物疾病修饰抗风湿药物，bDMARDs）和靶向合成抗风湿药物（tsDMARDs）的疗效比较。TNF抑制剂治疗组和非TNF抑制剂治疗组在疗效评估方面无统计学差异。贫血的发生率上，TNF抑制剂组略优于非TNF抑制剂组（24.01 / 100人年，p=0.03)。结论：一线TNF抑制剂和一线非TNF抑制剂的疗效没有显著差异，支持指南中建议的“基于临床判断和考虑患者偏好的个体化治疗”。狼疮性肾炎《高效淋巴系统靶向纳米颗粒包裹的环孢霉素预防狼疮小鼠模型肾小球肾炎》Science Advance，2020年6月 (11)环孢素A是一种强大的免疫抑制剂，但由于其生物利用度低需要增加剂量，但大剂量又存在肾毒性，故它无法单独用于治疗系统性红斑狼疮。贝勒医学院的研究人员设计了一个以CD71为靶点的、生物可降解的聚酯纳米颗粒，直接向淋巴系统递送环孢素A。其中藤黄酸偶联纳米颗粒显著增加了纳米颗粒与CD3+或CD20+淋巴细胞以及肠道淋巴组织的结合率。在口服给药的小鼠模型中，经纳米颗粒包裹的环孢素A增加了4-18倍的淋巴给药量。环孢素A淋巴生物利用度的提高，与抗双链DNA抗体IgG滴度、血浆细胞因子和肾小球肾炎的缓解一致。结论：本研究证明了纳米颗粒增强淋巴组织靶向性的潜力。参考文献1.Deodhar A, van der Heijde D, Gensler LS, Kim TH, Maksymowych WP, Østergaard M, et al. Ixekizumab for patients with non-radiographic axial spondyloarthritis (COAST-X): a randomised, placebo-controlled trial. Lancet. 2020;395(10217):53-64.2.Dougados M, Wei JC, Landewé R, Sieper J, Baraliakos X, Van den Bosch F, et al. Efficacy and safety of ixekizumab through 52 weeks in two phase 3, randomised, controlled clinical trials in patients with active radiographic axial spondyloarthritis (COAST-V and COAST-W). Ann Rheum Dis. 2020;79(2):176-85.3.Deodhar A, Blanco R, Dokoupilová E, Hall S, Kameda H, Kivitz AJ, et al. Secukinumab improves signs and symptoms of non-radiographic axial spondyloarthritis: primary results of a randomized controlled phase III study. Arthritis Rheumatol. 2020.4.Renson T, Depicker A, De Craemer AS, Deroo L, Varkas G, de Hooge M, et al. High prevalence of spondyloarthritis-like MRI lesions in postpartum women: a prospective analysis in relation to maternal, child and birth characteristics. Ann Rheum Dis. 2020;79(7):929-34.5.Abdelaziz MM, Gamal RM, Ismail NM, Lafy RA, Hetta HF. Diagnostic value of anti-CD74 antibodies in early and late axial spondyloarthritis and its relationship to disease activity. Rheumatology (Oxford). 2020.6.Jones GT, Dean LE, Pathan E, Hollick RJ, Macfarlane GJ. Real-world evidence of TNF inhibition in axial spondyloarthritis: can we generalise the results from clinical trials? Ann Rheum Dis. 2020;79(7):914-9.7.Koo BS, Oh JS, Park SY, Shin JH, Ahn GY, Lee S, et al. Tumour necrosis factor inhibitors slow radiographic progression in patients with ankylosing spondylitis: 18-year real-world evidence. Ann Rheum Dis. 2020;79(10):1327-32.8.Ulijn E, den Broeder N, Wientjes M, van Herwaarden N, Meek I, Tweehuysen L, et al. Therapeutic drug monitoring of adalimumab in RA: no predictive value of adalimumab serum levels and anti-adalimumab antibodies for prediction of response to the next bDMARD. Ann Rheum Dis. 2020;79(7):867-73.9.Hamann PDH, Pauling JD, McHugh N, Hyrich K, Shaddick G. Early response to anti-TNF predicts long-term outcomes including sustained remission: an analysis of the BSRBR-RA. Rheumatology (Oxford). 2020;59(7):1709-14.10.Pappas DA, St John G, Etzel CJ, Fiore S, Blachley T, Kimura T, et al. Comparative effectiveness of first-line tumour necrosis factor inhibitor versus non-tumour necrosis factor inhibitor biologics and targeted synthetic agents in patients with rheumatoid arthritis: results from a large US registry study. Ann Rheum Dis. 2020.11.Ganugula R, Arora M, Zou D, Agarwal SK, Mohan C, Kumar MNVR. A highly potent lymphatic system–targeting nanoparticle cyclosporine prevents glomerulonephritis in mouse model of lupus. Science Advances. 2020;6(24):eabb3900.

The Effect of HLA-B27 on Susceptibility and Severity of Covid-19 James T. Rosenbaum, Hedley Hamilton, Michael H. Weisman, John D. Reveille, Kevin L. Winthrop and Dongseok Choi The Journal of Rheumatology October 2020, jrheum.200939; DOI: https://doi.org/10.3899/jrheum.200939

This week, Tiffany and Patrice discuss the importance of biomarkers. Do biomarkers hold the key to understanding disease severity and predicting disease onset? In this episode, we talk about biomarkers, or a measurable indicator present in the blood or tissues, and how their presence in our bodies can predict disease severity and guide treatment development. Furthermore, evidence that identifying biomarkers early - BEFORE DISEASE ONSET - could actually prevent a person from developing the disease.  Now, there is still the environmental plus genetic factors to consider, but the findings are promising.  While the research focuses on Rheumatoid Arthritis (RA), showing how those who are sero-positive - in addition to having other genetic biomarkers - have a higher likelihood of developing severe disease and bone erosion,  Tiffany points out this is similar to Axial Spondyloarthritis, where many of those with non-radiographic disease do not have the biologic HLA-B27 gene that is present in most with radiographic evidence.   The bottom line is that learning about biomarkers can help patients navigate their own healthcare journey, but also could possibly prevent their loved ones from developing these diseases in the future.  Now, if you are a patient or parent of a juvenile patient - are you ready to join the conversation? It's your turn to pull up a seat! Join Tiffany and Patrice to continue this conversation inside our new, coordinating AiArthritis Voices ONLINE COMMUNITY - where patients unite with others around the world to talk, learn, and connect.  JOIN TODAY! Other stakeholders - are you a doctor, nurse, researcher, industry representative, or other health services person who wants to join us "at the table", too?  Then message your comments or questions about this show to podcast@aiarthritis.org OR message us on any of our social media accounts at @IFAiArthritis.    AiArthritis Voices 360 is the official talk show for the International Foundation for Autoimmune & Autoinflammatory Arthritis (AiArthritis). You can find us on the web at www.aiarthritis.org. 

Hello, and welcome to today's episode of The Ankylosing Spondylitis Podcast. I'm really glad that you could join me today because we're going to have fun today, we're going to be combining some of my favorite subjects history, modern medicine, and a little bit of speculation mixed in. So stay tuned. This one should be a lot of fun.  I've partnered up with a couple of really good companies. One is Joy Organics and you can find the link in the show notes. If you use that link. It doesn't change the price of anything for you. It just reverts a little commission back to the show to help keep the show going and hopefully growing and Joy Organics make some of the best organic based CBD products that you'll find whether it be tinctures pills that I take the soft gel tablets, I really like those and also a drink mix that I just put it into a jar water, shake up the water and drink it and it adds a bit of CBD through the day as I drink that water. So it's a great way to help level it out through the day as you're drinking that. So they have all sorts of products, lotions. So check out the link to go to Joy Organics. They're 100% organic hemp grown in the United States is where they derive all their CBD oil from so you can't go wrong going to Joy Organics link in the shownotes. The other one is new. Now, if you have kids cover their ears Foria is an intimacy lotion that is really fantastic and it works. I don't even know how to describe it beyond just that it works. It has a CBD base to it, and you apply it and it helps. So again, go to the show notes where you can access the link for Foria and then go and read about it and see if that fits something that might be of interest to you. Again, no price increases but it does pay a commission back to the show which helps to keep the show going and growing. Thank you.  So in today's episode by the title, you saw the word Neanderthal and you go, “What does that have to do with ankylosing spondylitis at all?” Well, I wondered the same thing. And then I was directed towards a few interesting articles and I started reading them and it really was a very interesting hypothesis. So about 30,000 years ago, give or take a few thousand years. What we would know as the modern homosapien came wandering out of the continent of Africa as they were migrating north. And as they got into the colder climates, they walked right into and head on confrontations with an ancestor of theirs that was already living there. But that hadn't changed in the hundreds of thousands of years. The Neanderthal was they got there, what you would expect took place, conflict, fighting, death as one type of species tried to basically conquer the other. Which one was going to win? Well, it ended up obviously being humans, you know,Homo sapiens. But did we walk away with a gift or maybe a curse From Neanderthals? Well, let's look at that. It's an interesting hypothesis or interesting series of debates that had gone on around this. So I was directed to a website called Everyday Battle, where there was an article entitled How a weird fetish among our ancestors led to Ankylosing Spondylitis. And so I started to delve into this article and found it to be really interesting, and I'll have a link down below what the studies are showing where now this is from some information that came out in the 2013, 2012 somewhere back in that area. But it was based upon looking at the DNA of Neanderthals and (modern day)humans and what they found in that and what may have carried over to us as modern humans. Studies suggest that Neanderthal genetics may be responsible for autoimmune diseases in modern humans. The author discusses a documentary called Decoding Neanderthals and in that documentary, they talked about discovering in the ancient DNA of these Neanderthals, the HLA alleles, and one particular HLA, HLA-B27 is the main genetic marker that's used to diagnose Ankylosing Spondylitis. It's found in 95% of the people with AS. Now, Support this podcast

Hello and welcome to this episode of The Ankylosing Spondylitis Podcast. How is everyone doing? I hope everyone is having just a fantastic week. So if you're on my website spondypodcast.com, you'll notice a link on the main page called https://www.buymeacoffee.com/ASpodcast (Buy Me A Coffee). And that's a link that I used for anybody that wants to provide, you know, a donation to help keep the show going. And I have a fantastic message that I got last night through that link. Lisa, who is from Ireland sent a donation, which is fantastic and much appreciated and on it she wrote,  I've had AS for 22 years, everything you describe is true. And I cry when I listen. I cry because I'm so sad for myself and because I'm not alone. Thank you from the bottom of my heart. Love Lisa, the cat lady from Dublin, Ireland. Well Lisa, I'm glad you like the show. I'm glad you find some benefit to it. Also Lisa and many others have done on spondee podcast comm you can sign up for the newsletter that I occasionally when I feel like it when I get around to it create. So I'd encourage you to go there to spondypodcast.com sign up for the newsletter and join Lisa and all the others receiving information when I get around to sending it out. This last one I sent out had pictures of Bandit in it, my service dog and training so you never know what I'm going to include in there.  Now on to today's show, I see a lot of questions asked online every day about Ankylosing Spondylitis and these questions ranged from real basic, I've just been diagnosed, what do I expect? What should I expect? Should I take medication? Can I cure it? To very detailed questions specifically in relation to is this part of Ankylosing Spondylitis or not? So I put together these nine questions and some answers to them that hopefully this will help you as you start off your journey with Ankylosing Spondylitis.  Number one is Ankylosing Spondylitis an autoimmune disease? Ankylosing Spondylitis is both an autoimmune type of arthritis and a chronic inflammatory disease. An autoimmune disease develops when your body attacks its own healthy tissues. Ankylosing Spondylitis is also an inflammatory condition that involves inflamed or swollen joints. It often affects joints and bones in the spine, lower back spinal bones confused together over time, and this is what is known as bamboo spine and, and how the name developed.  Number two, what exactly is Ankylosing Spondylitis? Ankylosing Spondylitis is a type of inflammatory arthritis that affects the spine and the sacroiliac joints in the pelvis. Like many types of arthritis, Ankylosing Spondylitis can cause pain and swelling in the joints. This condition affects the bones of the spine, the vertebrae, and joints in the lower back. It also causes swelling were the tendons and ligaments attached to the bones in your spine. Your doctor might call this and Enthisitis pain and discomfort from Ankylosing Spondylitis can lead to symptoms in other joints such as shoulders, hips, you know, basically, if there's bones that come together, or there's muscles or ligaments AS can affect those areas.  Number three, how is Ankylosing Spondylitis diagnosed? The doctor will likely start by asking about your symptoms and family history of AS. An exam can reveal symptoms like pain, tenderness and stiffness of your spine. The doctor then might send you for an X ray or MRI, or maybe even both, though generally not on the same day. Both tests can show damage to bones and soft tissues in your spine. An MRI creates more detailed images, and it can show damage earlier in the disease than an X ray can. Another way to diagnose this condition is with a blood test for the HLA-B27 gene. Now, some people don't have this gene, but have Ankylosing Spondylitis and not everybody that's positive with the HLA-B27 gene will have Ankylosing Spondylitis. So it's just one of the things they look at. You know, the... Support this podcast

Jayson: Michael, welcome to this episode of the Ankylosing Spondylitis podcast. And based upon the introduction and what we're going to cover today, I may have to change that name at some point down the road. Welcome to the show. Michael Thank you, Jayson. And thank you for having me. And yes, there's certainly time to change terminology around our disease. Jayson: Well, I was diagnosed 35 years ago, things tend to change slowly. So hopefully, I'll get around to figuring that out and what I want to do and how we structure it, but you know, you and I met through a forum on Facebook that deals with ankylosing spondylitis and the whole disease structure itself. You've made multiple posts that have been met differently with people's reactions on why the correct terminology might not be calling the disease itself ankylosing spondylitis, but maybe better off calling it Axial Spondyloarthritis. Tell me a little bit about that. Michael: Well, I can I understand why people are married to the next Ankylosing Spondylitis because like you that's what I was diagnosed with. And after my disease onset 40 years ago, but times change the technology changes, and also the name Ankylosing Spondylitis was never a universally used name, still isn't. In many parts of Europe, especially German speaking countries, the disease is referred to as Mobis Bechterew. In Russia, for example, it's named after Vladimir Bekhterev who was a Russian doctor who documented some of the symptoms of Ankylosing Spondylitis, but it's also been called Marie-Strumpell disease as well after two researchers who described the disease but what's more important, from our point of view is that Axial Spondyloarthritis is very difficult to diagnose. Originally, it was diagnosed by X ray radio graphically. So back in 1973, people recognized that there was a very common association with the gene HLA-B27 and spondyloarthritis. And looking into that further, they started seeing that people with Axial Spondyloarthritis or then called Ankylosing Spondylitis had this radiographic stage. And that was used as a diagnostic tool. There are no diagnostic criteria for this disease, but there are lots of different classifications. So, if you had radiographic sacral sacral le itis, and you displayed some other spondyloarthritis symptoms like family history or morning stiffness, etc. You were diagnosed with Ankylosing Spondylitis, then MRI came into being in the 1970s By the 1980s it was out there in the general hospital population and in general use and people who could read MRIs started noticing that if they were taking an MRI of the sacroiliac joint, they could see sacroillitis. But was this the same as the sacroillitis evident by X ray in Ankylosing Spondylitis? And there was a long debate about that. And that debate really wasn't resolved until the last year or two. So it's now understood that what we call Axial Spondyloarthritis is a continuum of disease from what had been called non-radiographic axial spondyloarthritis through to radiographic axial spondyloarthritis. So it's all recognized as one disease. And the important thing about that is that to exclude people, from patient organizations from help and support from the treatments available for Ankylosing Spondylitis, because they have non-radiographic axial spondylitis writers is extremely unfair. The disease burden is the same. Somebody with non-radiographic axial spa has exactly the same symptoms, the same pain, the same stiffness, the same mental issues as somebody who they ankylosing spondylitis. There's a further important part and that is that we know from a lot of evidence that the earlier the treatment, the better the outcome for the patient. So if you're waiting 6,7,8,9,10 years for diagnosis, and you don't get onto a treatment plan, until you're sort of seven or eight years into your disease progress. That's pretty serious, because by then you could have disfigurement, you could have kyphosis, you could have fusion, Support this podcast

Hello, and welcome to this week's episode of The Ankylosing Spondylitis Podcast. I hope this show finds everybody doing well. In today's show, I want to look at the relationship between your microbiome and Ankylosing Spondylitis. The reason for this came about from looking at a few items online and in some of the forums on Facebook. I was seeing one particular thread I believe an example that there was a number of people giving definitive, this is how I got Ankylosing Spondylitis. This caused my Ankylosing Spondylitis and that might have triggered a flare that brought the Ankylosing Spondylitis to your attention, or made you notice some of the symptoms that made you look further into what was causing them. But at this time, there really is nothing that I've ever found that says the doctors can pinpoint to this one exact reason as to why you got Ankylosing Spondylitis. No, there are some different contributing factors and there are some items that again, may have happened that triggered the domino to happen and and Ankylosing Spondylitis to finally come to life. There's nothing that at this time, they know, this is what exactly triggered anybody's Ankylosing Spondylitis. And that's what's really frustrating for a lot of us with the disease, is that we all present differently. We all get different symptoms, different reactions to medications. And if you listen to my episode a few back with Dr. Fox (Episode 42), he said there are some tests coming down the road that could help to better pinpoint which biologics you'll respond to better versus others. And that way, it's not such a guessing game like there is now with biologics where it's like, well take Enbrel if it doesn't work take Humira, if it doesn't work, take this one. It might take you four, five, or six until you find one that works. And if they have a way to narrow that down to one or two, that in of itself would be a great start to treating Ankylosing Spondylitis. The real big breakthrough is going to come when they can figure out what underlying symptoms make you susceptible to having it at some point in the future. One of those things is the gene, HLA-B27. Many people have that gene and it doesn't mean that if you have it, you will develop Ankylosing Spondylitis. Because there's people that don't have it, that develop Ankylosing Spondylitis. So it's just one of those factors to look at. So I happened to be looking around on ankylosingspondylitis.net, which is a fantastic resource, that if you're not using it you should be. People with Ankylosing Spondylitis write many of the articles and the editorial team writes many. I encourage you to head over, it's just a fantastic resource. And it got me thinking, I found this article, which is where I tell the show about the relationship between the microbiome and Ankylosing Spondylitis. And I thought it was really interesting. I've also saw a lot of people coming onto the forum saying, I'm brand new. I need to learn. Where do I start? What do I do? So this is something that might be a good spot to start to think about as you try to develop your game plan for dealing with Ankylosing Spondylitis. What we know is that about 40 years ago, researchers found out that people with HLA-B27 are much more likely to get Ankylosing Spondylitis.  HLA-B27 is a genetic trait associated with the immune system and the inflammatory conditions like Ankylosing Spondylitis. Well, scientists still don't know why. There is connection between Ankylosing Spondylitis and HLA-B27. They continue to study that relationship, and the potential link to help find further treatments for the condition of, of ALS and, and potentially other items. So, one of the areas that is being researched and I want to look at some more, and this is the microbiome. What is the microbiome? Well, all of us have trillions of bacteria living, you know, in us and on us on our bodies, you know, in our bodies, and this collection of bacteria is called your microbiome. Most Support this podcast

Welcome to AiArthritis Voices 360. This week, join your host, Tiffany, as she and co-host Charis Hill discuss the evolution of the term Ankylosing Spondylitis into the new umbrella term:  Axial Spondyloarthritis. What does this new term mean? How will it impact treatment options or the patient experience? Does it even matter what your diagnosis is if the treatments for AiArthritis are all basically the same? Listen in as they talk about these and other issues surrounding finding the right diagnosis. Then visit us on social media or online to make your voice heard in the ongoing discussion. AiArthritis Voices 360 is produced by the International Foundation for Autoimmune and Autoinflammatory Arthritis. Find us on the web at www.aiarthritis.org/podcast. Join our online private forum to have your seat at the table.  Show Notes: Episode 10 – “The Right Diagnosis” 00:57 – Tiffany welcomes listeners and fellow patient co-host, Charis Hill03:14 - The diagnosis of ankylosing spondylitis has been replaced with the umbrella term “axial spondyloarthritis”03:46 - Non-radiographic axial spondyloarthritis was also added as a diagnosis that would cover early or atypical disease presentation that isn’t visible on radiographic imaging06:10 - Some physicians within the rheumatology community do not believe there is a meaningful reason to differentiate between radiographic and non-radiographic diagnoses 06:25 - There is still a lack of clarity with regard to diagnostic coding which can impact patient access to treatments and the ability of researchers to track diseases08:08 - Charis’ diagnosis story15:08 - Early research suggests that non-radiographic axial spondylitis may be equally common in men and women, is often found in people who are HLA-B27 negative, and may have lower inflammation markers on blood work than the radiographic variety16:35 - Biologically female patients are more likely to have neck involvement than biologically male patients, who present with the traditional lower spine involvement18:16 - Axial spondyloarthritis is a more clinically accurate term because ankylosing spondylitis references only fusion of the spine, whereas axial spondyloarthritis encompasses inflammation or arthritis involvement anywhere in the center of the body21:30 - Within the medical community, there is still significant conversation about what terminology to use22:40 - Tiffany wonders whether radiographic patients would object to sharing a diagnosis with non-radiographic patients23:47 - The Spondylitis Association of America has detailed information on their website about the differences in the changing terminology24:37 - Spondyloarthrtis is the umbrella term that encompasses radiographic, non-radiographic, and peripheral disease presentations24:57 - Patients want to be informed about their diagnosis terminology and understand what it means26:05 - There has been considerable effort to raise awareness about Ankylosing Spondylitis, and now some people fear that changing the term will make it even more difficult to educate the public about this disease family27:43 - Possibly grouping several diagnoses together will help raise awareness by increasing the numbers of people united toward the same goal29:05 - Patients are still reporting that doctors don’t believe them without radiographic evidence29:15 - Hopefully using the umbrella terminology with the subset diagnoses will help all rheumatologists to understand that not all patients will present with radiographic evidence30:28 - The CDC does not have an accurate count of the number of patients with axial spondyloarthritis because many people with non-radiographic AxSpa were given a different diagnosis code so they could have access to treatments32:05 - Even if the treatment isn’t going to change, patients want validation that their doctor knows exactly what is going on with them32:15 - Patients want an accurate diagnosis so that they will have access to the right treatments in the future as new medications may be approved for their specific diagnosis33:08 - Rheumatoid arthritis research has been applied to AxSpa patients, even though those diseases are very different34:46 - Accurate diagnosis in medical records may also be important to future generations for reporting their medical history accurately39:45 - Rheumatologists treat 200+ different diseases, so it is important for the patient to be knowledgable about their own disease because you may be 1 of only 10 patients your doctor sees with your specific disease41:30 - Tiffany thanks Charis for co-hosting the episode41:55 - Tiffany invites everyone to visit www.aiarthritis.org/podcast to access resources and provide your thoughts on this topic42:53 - Visit aiarthritis.org/podcast to nominate yourself or someone else to co-host an episode of AiArthritis Voices 360

Welcome to AiArthritis Voices 360. This episode join your host, Tiffany, as she and co-host Suz Schrandt discuss the importance of early detection and diagnosis. They address barriers to receiving an accurate diagnosis, as well as what patients can do to increase their chances of receiving an accurate diagnosis in a timely fashion. Research consistently shows that early intervention improves patient outcomes. Whether you are a patient looking to confirm the accuracy of your diagnosis or avoid diagnostic delays in the event of new disease onset or a member of the public wondering if you or someone you love could be experiencing the onset of a rheumatological disease, this episode is a must-listen!   AiArthritis Voices 360 is produced by the International Foundation for Autoimmune and Autoinflammatory Arthritis. Find us on the web at www.aiarthritis.org/podcast. Join our online private forum to have your seat at the table.  Show Notes: Episode 6 – “Early Diagnosis” 00:56 – Tiffany welcome listeners and Co-Host Suz Schrandt01:35 – Suz explains Expect, a patient engagement initiative she founded02:44 – The topic for today’s episode is early diagnosis because so many people        experience delays in diagnosis that last months or years04:15 – People frequently receive the wrong rheumatological diagnosis and treatment before discovering the correct one07:15 - Delays lead to regret and distress as people wonder if they could be in remission if they had been diagnosed and received treatment sooner07:48 - Suz’s diagnostic story16:20 - Suz explains Polyarticular, Oligoarticular, and Systemic JIA (3 of the most   common types of Juvenile Idiopathic Arthritis)16:57 - Systemic JIA can be difficult to differentiate from juvenile lupus 19:25 - Clinicians have a tendency to focus on specific symptoms or parts of the body instead of seeing the whole picture, which adds to diagnostic delays 19:40 - Institutional barriers like short appointment times, overcrowded physician schedules, and cost concerns also cause delays in diagnosis20:50 - Some of the hallmark symptoms of arthritis (like pain and fatigue) are invisible 21:17 - People will delay seeking medical help until they exhaust all options to manage symptoms themselves because amongst other things we assume it’s something we can manage or because we’re afraid of navigating the healthcare system23:16 - Early age onset can also contribute to diagnostic delays because the patient appears very healthy 23:29 - Diagnostic delays also occur when medical professionals do not believe patients’ stories24:50 - There are between 40,000 and 80,000 deaths per year in the United States due to delayed and missed diagnoses 25:12 - Age, gender, race, and ethnicity can all cause diagnostic delays25:56 - Patients need to receive all of their test results in a timely fashion and may need to advocate to receive access to them27:27 - Patients do not need positive bloodwork to receive an RA diagnosis, but it is very common for doctors to dismiss patients without supporting bloodwork results29:35 - ACR diagnostic criteria only requires 1 or more swollen joints for more than 6 weeks without another explanation, but many clinicians - especially primary care - do not know that30:26 - If your erythrocyte sedimentation rate (SED rate) is elevated or your RA factor is positive, that can be helpful for a diagnosis, but it is not required31:35 - Testing positive for the HLA-B27 antigen increases the chances that you have ankylosing spondylitis (but some with radiographic changes may not have the gene).32:38 - Suz explains work she has done to teach medical students how to diagnose aiarthritis 35:34 - The work Suz has done to teach practicing clinicians to identify aiarthritis diseases has increased referrals to a rheumatologist by 11% among doctors who completed the training she provides36:30 - Treatment in the first two years is critical to preventing longterm damage and destruction38:22 - You can review the diagnostic criteria for any rheumatological illness on the ACR or EULAR websites and use the information to discuss your concerns with your clinician39:19 - Tracking your symptoms can really help avoid diagnostic delays and maximize the value of your appointment time with your doctor41:13 - SIDM (Society to Improve Diagnosis in Medicine) collects stories from patients of delayed or missed diagnoses 42:23 - Tiffany invites listeners to visit aiarthritis.org/podcast and view the page for this episode to share your diagnosis story with SIDM or view diagnostic criteria on the ACR site43:08 - Tiffany invites listeners to visit aiarthrits.org/voices to register and participate in discussions about this and other important issues surrounding aiarthritis diseases 43:46 - Tiffany thanks Suz for stopping by to discuss early detection and diagnosis of aiarthritis diseases 

Hello, and welcome to The Ankylosing Spondylitis Podcast. Can you believe that this is almost the end of 2019? Man this year has just flown by. It's been a really, really interesting year for me from the great highs with this show, the great numbers that have come in and the positive feedback I've got from everybody about liking the show, to going from highs like that to dealing with the passing of my father in August and the whole dynamic that created for me. I know I'm grateful for the almost 75 years that he was around and he was here for me. So that was fantastic, but I'm not going to lie. It still stinks to you know, I want to call him. Even though he didn't have Ankylosing Spondylitis, he and my stepmother listen to all these episodes, and were two of my biggest cheerleaders for these episodes. It's fantastic to know the years that I had with him.  So with that, on to the show. Now for the Question of the Week, this is going to be a little bit different because I happened to be online and I saw a posting from a fellow AS person in Australia named Tieran Brownlee. He posted an article, now I'm going to butcher this so up front, I apologize, but it is from the xinhua.net, and I'll have a link to it. So don't try to write any this down. It was dated December 7, 2019 and it says Scientists uncover potential nuclear of “bamboo spine”, otherwise known as Ankylosing Spondylitis. So here in Taipei, team of scientists from Taiwan uncovered how the human gene HLA-B27, triggered Ankylosing Spondylitis, which might lead to symptoms of bamboo spine, leading them to find a promising new cure for the disease. Can you believe that? The words Ankylosing Spondylitis and potential promising cure don't even seem like they should be in the same paragraph. So a collaborated research team led by a Dr. Lin Kuo-i with Genomics Research Center of the Academia Sinica in Taiwan, and they found the gene HLA-B27, triggers a miscoded protein response, and then a series of abnormal signal transduction, which eventually causes an isozyme called “tissue-nonspecific alkaline phosphatase” (TNAP) to be highly activated. The elevated tip was demonstrated to be the cause of bone like cell formation around a person's spine, the research team sent a press release. So that's the extent of the article I'm going to read. There will be a link in the show notes to it and I would encourage everybody to read it. It really caught my eye because farther down you'll see that researchers have found that two existing medicines that are already out there to treat items may be possible cure for Ankylosing Spondylitis. So they may have stumbled across something. As they look at this, we don't know. It's from China. It's not anything that's apparently maybe cleared through the FDA. So it could be years and years and decades away. We don't know. But it's definitely an interesting article to read. So I hope you all go out and read that article, and I'll have a link to it.  Now, on to the main topic of today, this week, as I was looking through some ideas about what to do for the show, I happened to be going through one of the Ankylosing Spondylitis forums online and I saw some people talking about you know, I hate it when somebody says this, right I hate it when somebody says that in relation to Oh, my back is bad or Yeah, I had AS but I cured it. You know, people say the craziest things to you. I generally like to think the best of people in that they aren't trying to be mean or be off putting their generally trying to be helpful. They just realize they're not being helpful. They're actually being a pain in the rear sometimes.  So I have to come across this article by Ricky white. That name sounds familiar. I did an interview with Ricky few months back for the show. He has Ankylosing Spondylitis. And the last episode, we talked about his book called Taking Charge - Making your Healthcare Appointments Work for You. So the article that I... Support this podcast

Hello, and welcome to The Ankylosing Spondylitis Podcast. Well, this is the month of November and I hope everybody's doing well. First I want to take a minute to talk about the show itself. I cannot thank everybody enough for making October just an amazing month for the show. The download numbers were through the roof and the feedback I got on the episodes was fantastic. So I really appreciate that and we added in a number of new countries that have access to show Let's get right into the show for the Question of the Week, I saw several people asking the same question online and it is can Ankylosing Spondylitis be inherited? Is it an inheritable disease you know, from one family member to the next generation to generation, in essence, it can run in families. In one of those markers, they used to look at it as the HLA- B27 gene. Now having this gene doesn't mean that you will get Ankylosing Spondylitis, but it is one of those markers that they look for. I found this kind of interesting in that research has shown that more than nine out of 10 people with AS carry the HLA-B27 gene, that's pretty amazing. It's almost 100% of everybody has it having this gene does not necessarily mean you'll develop as, as I said, it's estimated eight in every 100 people in the general population have the HLA-B27 gene, but most do not have AS so if you have it, you may end up getting AS but it doesn't mean you will. It also shows that's one of things you can look at it and family members and this particular person in the Question of the Week, they were wondering if they should have some family members tested for it because they and the other sibling had it. So I kind of replied back that it's not going to hurt anything. It never hurts to know if that gene is present because it could go along to explaining some future medical conditions if they run into AS it's also something to know that as we said as can run in families that gene can be inherited from familymembers to family member and if you have AS and test show you carry the HLA-B27 gene and their is a one in two chance that you could pass on the gene to any children you have is estimated that between five to 20% of children with this gene will then go out and develop AS that's still quite a wide variants of it. I have three kids they were all tested for the gene and if I remember right to came back with it, one didn't maybe all three had it. I don't remember exactly what it was, but they were tested and I believe my two older ones did have the gene one is showing some effects. I don't know if she'll come to grips with it. And hope you know, personally, I hope nothing ever develops of it. The other one is not nor is the youngest one. With that said, let's move on to today's topic of discussion. The Question of the Week done, let's look at this week's topic. You know, when I was diagnosed with Ankylosing Spondylitis, I was told a couple of things. Now,granted, you know, this was 35 years ago, so a lots changed. But when I was diagnosed, I was told this is primarily a man's disease, you'll rarely if ever see it in women. And it's primarily disease people of Mediterranean descent. What we found out is that is obviously not the case. So we know that today all these advances have been done in the research for Ankylosing Spondylitis that in fact, women get it probably just as much as men. I found this really cool article and it talked about different things dealing with a woman's diagnosis with Ankylosing Spondylitis. Again, as we've all heard, and been told women don't get it, but we know that that is incorrect. And I've had to do is look through the boards on Facebook, you'll see that there's just a ton of women dealing with this condition. So as we know, Ankylosing Spondylitis is an inflammatory form of arthritis that we get that starts in our SI joints or spine moves up the spine and then or can affect your ribs, your shoulders, your neck, move down affect your knees. It's going to... Support this podcast

¡Gracias por escuchar! En este episodio repaso algunos conceptos relevantes sobre la dactilítis, una manifestación común en espondiloartritis. Les pido amablemente que califiquen este episodio en iTunes, o dejen sus comentarios en esta página. El podcast se encuentra disponible también en Spotify y a través de la aplicación gestora de podcasts de su elección.Abajo enlisto referencias útiles, algunas mencionadas en el episodio: Olivieri, I., Scarano, E., Padula, A., Giasi, V. & Priolo, F. Dactylitis, a term for different digit diseases. Scand. J. Rheumatol. 35, 333–340 (2006). Gladman, D. D., Ziouzina, O., Thavaneswaran, A. & Chandran, V. Dactylitis in psoriatic arthritis: prevalence and response to therapy in the biologic era. J. Rheumatol. 40, 1357–1359 (2013). Ritchlin, C. T., Colbert, R. A. & Gladman, D. D. Psoriatic arthritis. N. Engl. J. Med. 376, 957–970 (2017). Rothschild, B. M., Pingitore, C. & Eaton, M. Dactylitis: implications for clinical practice. Semin. Arthritis Rheum. 28, 41–47 (1998). Taylor, W. J. et al. Classification criteria for psoriatic arthritis: development of new criteria from a large international study. Arthritis Rheum. 54, 2665–2673 (2006). Rudwaleit, M. et al. The Assessment of Spondyloarthritis International Society classification criteria for peripheral spondyloarthritis and for spondyloarthritis in general. Ann. Rheum. Dis. 70, 25–31 (2011). Brockbank, J. E., Stein, M., Schentag, C. T. & Gladman, D. D. Dactylitis in psoriatic arthritis: a marker for disease severity? Ann. Rheum. Dis. 64, 188–190 (2005). Kavanaugh, A., Helliwell, P. & Ritchlin, C. T. Psoriatic arthritis and burden of disease: patient perspectives from the population-based multinational assessment of psoriasis and psoriatic arthritis (MAPP) survey. Rheumatol. Ther. 3, 91–102 (2016). Kaeley, G. S., Eder, L., Aydin, S. Z., Gutierrez, M. & Bakewell, C. Dactylitis: a hallmark of psoriatic arthritis. Semin. Arthritis Rheum. 48, 263–273 (2018). McGonagle, D., Conaghan Philip, G. & Emery, P. Psoriatic arthritis: a unified concept twenty years on. Arthritis Rheum. 42, 1080–1086 (2001). Tinazzi, I. et al. ‘Deep Koebner’ phenomenon of the flexor tendon-associated accessory pulleys as a novel factor in tenosynovitis and dactylitis in psoriatic arthritis. Ann. Rheum. Dis. 77, 922 (2018). Pattison, E., Harrison, B. J., Griffiths, C. E., Silman, A. J. & Bruce, I. N. Environmental risk factors for the development of psoriatic arthritis: results from a case-control study. Ann. Rheum. Dis. 67, 672–676 (2008). Ng, J., Tan, A. L. & McGonagle, D. Unifocal psoriatic arthritis development in identical twins following site specific injury: evidence supporting biomechanical triggering events in genetically susceptible hosts. Ann. Rheum. Dis. 74, 948–949 (2015). Jacques, P. et al. Proof of concept: enthesitis and new bone formation in spondyloarthritis are driven by mechanical strain and stromal cells. Ann. Rheum. Dis. 73, 437–445 (2014). Jacques, P. & McGonagle, D. The role of mechanical stress in the pathogenesis of spondyloarthritis and how to combat it. Best Pract. Res. Clin. Rheumatol. 28, 703–710 (2014). Thorarensen, S. M. et al. Physical trauma recorded in primary care is associated with the onset of psoriatic arthritis among patients with psoriasis. Ann. Rheum. Dis. 76, 521–525 (2017). Wilkins, R. A., Siddle, H. J., Redmond, A. C. & Helliwell, P. S. Plantar forefoot pressures in psoriatic arthritis-related dactylitis: an exploratory study. Clin. Rheumatol. 35, 2333–2338 (2016). Tan, A. L. & McGonagle, D. The need for biological outcomes for biological drugs in psoriatic arthritis. J. Rheumatol. 43, 3–6 (2016). Mumtaz, A. et al. Development of a preliminary composite disease activity index in psoriatic arthritis. Ann. Rheum. Dis. 70, 272–277 (2011). Helliwell, P. S. et al. The development of candidate composite disease activity and responder indices for psoriatic arthritis (GRACE project). Ann. Rheum. Dis. 72, 986–991 (2013). Ramiro, S., Smolen, J. S., Landewe, R., van der Heijde, D. & Gossec, L. How are enthesitis, dactylitis and nail involvement measured and reported in recent clinical trials of psoriatic arthritis? A systematic literature review. Ann. Rheum. Dis. 77, 782–783 (2017). Salvarani, C. et al. A comparison of cyclosporine, sulfasalazine, and symptomatic therapy in the treatment of psoriatic arthritis. J. Rheumatol. 28, 2274–2282 (2001). Antoni, C. E. et al. Sustained benefits of infliximab therapy for dermatologic and articular manifestations of psoriatic arthritis: results from the infliximab multinational psoriatic arthritis controlled trial (IMPACT). Arthritis Rheum. 52, 1227–1236 (2005). Clegg, D. O. et al. Comparison of sulfasalazine and placebo in the treatment of psoriatic arthritis. A Department of Veterans Affairs Cooperative Study. Arthritis Rheum. 39, 2013–2020 (1996). Helliwell, P. S. et al. Development of an assessment tool for dactylitis in patients with psoriatic arthritis. J. Rheumatol. 32, 1745–1750 (2005). Healy, P. J. & Helliwell, P. S. Measuring dactylitis in clinical trials: which is the best instrument to use? J. Rheumatol. 34, 1302–1306 (2007). Chandran, V. et al. International multicenter psoriasis and psoriatic arthritis reliability trial for the assessment of skin, joints, nails, and dactylitis. Arthritis Rheum. 61, 1235–1242 (2009).Mease, P. et al. Effect of certolizumab pegol on signs and symptoms in patients with psoriatic arthritis: 24-week results of a phase 3 double-blind randomised placebo-controlled study (RAPID-PsA). Ann. Rheum. Dis. 73, 48–55 (2014). Fournie, B. et al. Extrasynovial ultrasound abnormalities in the psoriatic finger. Prospective comparative power-doppler study versus rheumatoid arthritis. Joint Bone Spine 73, 527–531 (2006). Benjamin, M. & McGonagle, D. The anatomical basis for disease localisation in seronegative spondyloarthropathy at entheses and related sites. J. Anat. 199, 503–526 (2001). Kane, D., Greaney, T., Bresnihan, B., Gibney, R. & FitzGerald, O. Ultrasonography in the diagnosis and management of psoriatic dactylitis. J. Rheumatol. 26, 1746–1751 (1999). Tinazzi, I. et al. Comprehensive evaluation of finger flexor tendon entheseal soft tissue and bone changes by ultrasound can differentiate psoriatic arthritis and rheumatoid arthritis. Clin. Exp. Rheumatol. 36, 785–790 (2018). McGonagle, D., Gibbon, W. & Emery, P. Classification of inflammatory arthritis by enthesitis. Lancet 352, 1137–1140 (1998). Olivieri, I. et al. Dactylitis in patients with seronegative spondylarthropathy. Assessment by ultrasonography and magnetic resonance imaging. Arthritis Rheum. 39, 1524–1528 (1996).Olivieri, I. et al. Toe dactylitis in patients with spondyloarthropathy: assessment by magnetic resonance imaging. J. Rheumatol. 24, 926–930 (1997). Olivieri, I. et al. Fast spin echo-T2-weighted sequences with fat saturation in dactylitis of spondylarthritis. No evidence of entheseal involvement of the flexor digitorum tendons. Arthritis Rheum. 46, 2964–2967 (2002). Healy, P. J., Groves, C., Chandramohan, M. & Helliwell, P. S. MRI changes in psoriatic dactylitis extent of pathology, relationship to tenderness and correlation with clinical indices. Rheumatology 47, 92–95 (2008). Tan, A. L. et al. High-resolution MRI assessment of dactylitis in psoriatic arthritis shows flexor tendon pulley and sheath-related enthesitis. Ann. Rheum. Dis. 74, 185–189 (2015). FitzGerald, O., Haroon, M., Giles, J. T. & Winchester, R. Concepts of pathogenesis in psoriatic arthritis: genotype determines clinical phenotype. Arthritis Res. Ther. 17, 115 (2015). McHugh, K. & Bowness, P. The link between HLA-B27 and SpA—new ideas on an old problem. Rheumatology 51, 1529–1539 (2012). Ritchlin, C. T. et al. Treatment recommendations for psoriatic arthritis. Ann. Rheum. Dis. 68, 1387–1394 (2009). Coates, L. C. et al. Group for Research and Assessment of Psoriasis and Psoriatic Arthritis 2015 treatment recommendations for psoriatic arthritis. Arthritis Rheum. 68, 1060–1071 (2016). Gossec, L. et al. European League Against Rheumatism (EULAR) recommendations for the management of psoriatic arthritis with pharmacological therapies: 2015 update. Ann. Rheum. Dis. 75, 499–510 (2016). Coates, L. & Helliwell, P. S. Methotrexate efficacy in the Tight Control in Psoriatic Arthritis study. J. Rheum. 43, 356–361 (2016). Rose, S., Toloza, S., Bautista-Molano, W. & Helliwell, P. S. Comprehensive treatment of dactylitis in psoriatic arthritis. J. Rheumatol. 41, 2295–2300 (2014). Kavanaugh, A. et al. Efficacy and safety of ustekinumab in psoriatic arthritis patients with peripheral arthritis and physician-reported spondylitis: post-hoc analyses from two phase III, multicentre, double-blind, placebo-controlled studies (PSUMMIT-1/PSUMMIT-2). Ann. Rheum. Dis. 75, 1984–1988 (2016). Mease, P. et al. Tofacitinib or adalimumab versus placebo for psoriatic arthritis. N. Engl. J. Med. 377, 1537–1550 (2017). Kavanaugh, A. et al. Golimumab in psoriatic arthritis: one-year clinical efficacy, radiographic, and safety results from a phase III, randomized, placebo-controlled trial. Arthritis Rheum. 64, 2504–2517 (2012). Kavanaugh, A. & Mease, P. Treatment of psoriatic arthritis with tumor necrosis factor inhibitors: longer-term outcomes including enthesitis and dactylitis with golimumab treatment in the Longterm Extension of a Randomized, Placebo-controlled Study (GO-REVEAL). J. Rheumatol. Suppl. 89, 90–93 (2012). Antoni, C. E. et al. Two-year efficacy and safety of infliximab treatment in patients with active psoriatic arthritis: findings of the Infliximab Multinational Psoriatic Arthritis Controlled Trial (IMPACT). J. Rheumatol. 35, 869–876 (2008). Kavanaugh, A. et al. Infliximab maintains a high degree of clinical response in patients with active psoriatic arthritis through 1 year of treatment: results from the IMPACT 2 trial. Ann. Rheum. Dis. 66, 498–505 (2007). Baranauskaite, A. et al. Infliximab plus methotrexate is superior to methotrexate alone in the treatment of psoriatic arthritis in methotrexate-naive patients: the RESPOND study. Ann. Rheum. Dis. 71, 541–548 (2012). Carron, P. et al. Scintigraphic detection of TNF-driven inflammation by radiolabelled certolizumab pegol in patients with rheumatoid arthritis and spondyloarthritis. RMD Open 2, e000265 (2016). Nash, P. et al. Efficacy and safety of secukinumab administration by autoinjector in patients with psoriatic arthritis: results from a randomized, placebo-controlled trial (FUTURE 3). Arthritis Res. Ther. 20, 47 (2018). Mease, P. et al. Secukinumab improves active psoriatic arthritis symptoms and inhibits radiographic progression: primary results from the randomised, double-blind, phase III FUTURE 5 study. Ann. Rheum. Dis. 77, 890–897 (2018). Mease, P. J. et al. Ixekizumab, an interleukin-17A specific monoclonal antibody, for the treatment of biologic-naive patients with active psoriatic arthritis: results from the 24-week randomised, double-blind, placebo-controlled and active (adalimumab)-controlled period of the phase III trial SPIRIT-P1. Ann. Rheum. Dis. 76, 79–87 (2017). Wells, A. F. et al. Apremilast monotherapy in DMARD-naive psoriatic arthritis patients: results of the randomized, placebo-controlled PALACE 4 trial. Rheumatology 57, 1253–1263 (2018). Gladman, D. et al. Tofacitinib for psoriatic arthritis in patients with an inadequate response to TNF inhibitors. N. Engl. J. Med. 377, 1525–1536 (2017). Mease, P. J. et al. Efficacy and safety of abatacept, a T cell modulator, in a randomised, double-blind, placebo-controlled, phase III study in psoriatic arthritis. Ann. Rheum. Dis. 76, 1550–1558 (2017). Genovese Mark, C. et al. Apremilast in patients with active rheumatoid arthritis: a phase II, multicenter, randomized, double-blind, placebo-controlled, parallel-group study. Arthritis Rheum. 67, 1703–1710 (2015). Smolen, J. S. et al. A randomised phase II study evaluating the efficacy and safety of subcutaneously administered ustekinumab and guselkumab in patients with active rheumatoid arthritis despite treatment with methotrexate. Ann. Rheum. Dis. 76, 831–839 (2017). Kavanaugh, A. et al. Treatment of psoriatic arthritis in a phase 3 randomised, placebo-controlled trial with apremilast, an oral phosphodiesterase 4 inhibitor. Ann. Rheum. Dis. 73, 1020–1026 (2014). Kunwar, S., Dahal, K. & Sharma, S. Anti-IL-17 therapy in treatment of rheumatoid arthritis: a systematic literature review and meta-analysis of randomized controlled trials. Rheumatol. Int. 36, 1065–1075 (2016). da Silva Junior, G. B., Daher Ede, F. & da Rocha, F. A. Osteoarticular involvement in sickle cell disease. Rev. Bras. Hematol. Hemoter. 34, 156–164 (2012). Braum, L. S. et al. Characterisation of hand small joints arthropathy using high-resolution MRI — limited discrimination between osteoarthritis and psoriatic arthritis. Eur. Radiol. 23, 1686–1693 (2013). Tan, A. L., Grainger, A. J., Tanner, S. F., Emery, P. & McGonagle, D. A high-resolution magnetic resonance imaging study of distal interphalangeal joint arthropathy in psoriatic arthritis and osteoarthritis: are they the same? Arthritis Rheum. 54, 1328–1333 (2006). Tuttle, K. S., Vargas, S. O., Callahan, M. J., Bae, D. S. & Nigrovic, P. A. Enthesitis as a component of dactylitis in psoriatic juvenile idiopathic arthritis: histology of an established clinical entity. Pediatr. Rheumatol. Online J. 13, 7 (2015). Nash, P. et al. Ixekizumab for the treatment of patients with active psoriatic arthritis and an inadequate response to tumour necrosis factor inhibitors: results from the 24-week randomised, double-blind, placebo-controlled period of the SPIRIT-P2 phase 3 trial. Lancet 389, 2317–2327 (2017).Jeong, H. et al. Spondyloarthritis features in zymosan-induced SKG mice. Joint Bone Spine 85, 583–591 (2018). 

In this episode I cover ankylosing spondylitis.If you want to follow along with written notes on ankylosing spondylitis go to https://zerotofinals.com/medicine/rheumatology/ankylosingspondylitis/ or the rheumatology section in the Zero to Finals medicine book.This episode covers the definitions, presentation, associations, investigations and management of ankylosing spondylitis. The audio in the episode was expertly edited by Harry Watchman.

(Cápsula 011) Generalidades de las espondiloartritis. Comentamos sobre los diferentes tipos (espondilitis anquilosante, artritis reactiva, artritis psoriásica, artritis enteropática), utilidad del HLA-B27 y radiografía de sacroiliacas.

This week, we discuss anterior uveitis, especially HLA B27 related disease. Next week, we'll discuss the other causes of anterior uveitis, as well as treatment and management.   Also, we are doing a survey to assess the impact of the podcast. If you'd like to support us, take this 4 minute survey: bit.ly/2VpPRND  

SHR # 2287 :: RLRx: Connecting The Dots: Human Leukocyte Antigen B27, Autoimmunity and Vitamin C :: Adam Lamb - Human Leukocyte Antigen B27 (HLA-B27) is a genetic marker of autoimmunity that leads to horrific life-derailing disorders. Almost all effect a degrading of chondrocytes and soft tissue that causes immense pain and disability. A few of the disorders caused by HLA-B27 is ankylosing spondylitis, inflammation of the eyes, several forms of joint pain and arthritis, joint stiffness, skin lesions, and much more. The standard of care is biologics that weaken the immune system that carry a host of negative side effects. But what if a simple vitamin could actually eliminate the pain and symptoms better than dangerous biologics? Could it be that the medical orthodoxy doesn't know about this? Or are they just ignoring it? ::

SHR # 2287 :: RLRx: Connecting The Dots: Human Leukocyte Antigen B27, Autoimmunity and Vitamin C :: Adam Lamb - Human Leukocyte Antigen B27 (HLA-B27) is a genetic marker of autoimmunity that leads to horrific life-derailing disorders. Almost all effect a degrading of chondrocytes and soft tissue that causes immense pain and disability. A few of the disorders caused by HLA-B27 is ankylosing spondylitis, inflammation of the eyes, several forms of joint pain and arthritis, joint stiffness, skin lesions, and much more. The standard of care is biologics that weaken the immune system that carry a host of negative side effects. But what if a simple vitamin could actually eliminate the pain and symptoms better than dangerous biologics? Could it be that the medical orthodoxy doesn't know about this? Or are they just ignoring it? ::

HIV-1 is a chimpanzee virus which was transmitted to humans by several zoonotic events resulting in infection with HIV-1 groups M P, and in parallel transmission events from sooty mangabey monkey viruses leading to infections with HIV-2 groups A H. Both viruses have circulated in the human population for about 80 years. In the infected patient, HIV mutates, and by elimination of some of the viruses by the action of the immune system individual quasispecies are formed. Along with the selection of the fittest viruses, mutation and recombination after superinfection with HIV from different groups or subtypes have resulted in the diversity of their patterns of geographic distribution. Despite the high variability observed, some essential parts of the HIV genome are highly conserved. Viral diversity is further facilitated in some parts of the HIV genome by drug selection pressure and may also be enhanced by different genetic factors, including HLA in patients from different regions of the world. Viral and human genetic factors influence pathogenesis. Viral genetic factors are proteins such as Tat, Vif and Rev. Human genetic factors associated with a better clinical outcome are proteins such as APOBEC, langerin, tetherin and chemokine receptor 5 (CCR5) and HLA B27, B57, DRB1{*}1303, KIR and PARD3B. Copyright (C) 2012 S. Karger AG, Basel

Dr Paul Bowness tells us about his work on spondyloarthritis. Dr Paul Bownessis works on Ankylosing Spondylitis, the commonest form of spondyloarthritis. This rheumatic disease seems to be caused by an overacting immune system. It has a major genetic component: at least 5-10 genes are known to contribute the disease, with HLA-B27 being by far the most important. Dr Bowness studies how these genes work in the immune systems of both healthy people and patients with arthritis.

Professor Paul Bowness tells us about his work on spondyloarthritis. Professor Paul Bowness works on Ankylosing Spondylitis, the commonest form of spondyloarthritis. This rheumatic disease is caused by an overacting immune system. It has a major genetic component: at least five to ten genes are known to contribute the disease, with HLA-B27 being by far the most important. Professor Bowness is investigating interactions between these genes and the immune system, for both healthy people and patients with arthritis, to better understand Ankylosing Spondylitis and how to manage it.

Professor Paul Bowness tells us about his work on spondyloarthritis. Professor Paul Bowness works on Ankylosing Spondylitis, the commonest form of spondyloarthritis. This rheumatic disease is caused by an overacting immune system. It has a major genetic component: at least five to ten genes are known to contribute the disease, with HLA-B27 being by far the most important. Professor Bowness is investigating interactions between these genes and the immune system, for both healthy people and patients with arthritis, to better understand Ankylosing Spondylitis and how to manage it.

Dr Paul Bowness tells us about his work on spondyloarthritis. Dr Paul Bownessis works on Ankylosing Spondylitis, the commonest form of spondyloarthritis. This rheumatic disease seems to be caused by an overacting immune system. It has a major genetic component: at least 5-10 genes are known to contribute the disease, with HLA-B27 being by far the most important. Dr Bowness studies how these genes work in the immune systems of both healthy people and patients with arthritis.

Thu, 20 Jan 2011 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/12691/ https://edoc.ub.uni-muenchen.de/12691/1/Mathavan_Ernest.pdf Mathavan, Ernest ddc:610, ddc:600, Medizinische Fakultät

In der vorliegenden Arbeit wurden therapeutische und immunmodulatorische Effekte einer TNF-Blockade bei Patienten mit aktiver Spondylitis ankylosans untersucht. Hierzu wurde an 10 Patienten während einer 60wöchigen Infliximabtherapie eine Evaluation von Therapiewirksamkeit und -sicherheit, sowie eine durchflusszytometrische Analyse der HLA-Oberflächenexpression auf Lymphozyten vorgenommen. Von 8 Patienten wurde die Therapie ohne ernste Nebenwirkungen gut vertragen und führte zur raschen und dauerhaften Verbesserung der klinischen, laborchemischen und radiologischen Verlaufsparameter. Ein Patient entwickelte nach initialer Wirksamkeit ein sekundäres Therapieversagen, bei einem weiteren Patienten wurde die Therapie unter dem Verdacht eines medikamentös induzierten Lupus-Syndroms abgebrochen. Gegen Mitte des Behandlungszeitraumes konnte ein am deutlichsten auf den B-Lymphozyten ausgeprägter Anstieg der HLA-B27- und MHC-Klasse-I-Expression beobachtet werden. Die Expressionszunahme ist möglicherweise Ausdruck immunmodulatorischer Effekte, die mit der langfristigen Therapiewirksamkeit assoziiert sind. Für die Zunahme der Oberflächenexpression kommen folgende Mechanismen in Frage: 1. eine vermehrte intravasale Kompartimentierung primär hoch exprimierender Zellen oder 2. eine durch die TNF-Suppression induzierte Hochregulation einer zuvor niedrigeren HLA-B27-Oberflächenexpression. Angesichts unserer Ergebnisse und der aktuell in der Literatur verfügbaren Daten halten wir letzteren Mechanismus für wahrscheinlicher. Innerhalb dieses Erklärungsmodells ist die bei Therapiebeginn niedrigere HLA-B27-Expression bedingt durch die Expression einer verminderten Anzahl von HLA-B27-Molekülen oder aberranter β2m-freier Varianten, die durch die von uns verwendeten konformationsabhängigen Antikörpern nicht detektierbar sind. Unter Hemmung des TNF-Einflusses kommt es schließlich zur schrittweisen Wiederherstellung der physiologischen Prozessierung trimolekularer HLA-B27-Oberflächenantigene mit konsekutiv vermehrter AK-Bindung. Eine verminderte oder aberrante HLA-B27-Expression ist möglicherweise mit immunmodulatorischen Effekten im Sinne einer erhöhten Zelldepletion assoziiert. Durch die Reexpression trimolekularer HLA-B27-Moleküle wird die Interaktion zwischen immunkompetenten Zellen und HLA-B27-positiven Zellen beeinflusst, wodurch das Zellüberleben begünstigt wird. Dieser Erklärungsansatz ist vereinbar mit dem gegenwärtig favorisierten pathogenetischen Modell der fehlerhaften HLA-B27-Prozessierung und der derzeit diskutierten Beteiligung von TNF bei der Manifestation der AS.

Das nicht polymorphe HLA-Klasse-I-Antigen HLA-G wird hauptsächlich in der Plazenta exprimiert, wo es vermutlich den semiallogenen Fötus vor Angriff des mütterlichen Immunsystems schützt. Eine Besonderheit von HLA-G ist das Auftreten von mehreren verkürzten Isoformen, die von alternativ gespleißten Transkripten translatiert werden. Neben dem kompletten membranständigen HLA-G1 mit den extrazellulären Domänen a1, a2 und a3 existieren die verkürzten Isoformen HLA-G2 (∆a2), HLA-G3 (∆a2, ∆a3) und HLA-G4 (∆a3). Außerdem wurden die löslichen Isoformen HLA-G5 (HLA-G1s), HLA-G6 (HLA-G2s, ∆a2) und HLA-G7 (HLA-G3s, ∆a2, ∆a3) beschrieben. Um die Expression und Funktion einzelner Isoformen getrennt voneinander und ohne Beeinflussung durch andere MHC-Klasse-I-Moleküle untersuchen zu können, wurden Transfektanten für die Isoformen HLA-G1, HLA-G2, HLA-G4 und HLA-G5 in der HLA-Klasse-I-negativen humanen Zellinie K-562 generiert. HLA-G kann mit inhibitorischen und aktivierenden Rezeptoren auf NK- und T-Zellen in Wechselwirkung treten und so Effektorfunktionen beeinflussen. Die Expression von HLA-G kann außerdem indirekt über HLA-E auf die Zytotoxizität von NK-Zellen und T-Zellen einwirken. Die HLA-E-Expression ist abhängig von Peptiden aus den Signalsequenzen von HLA-Klasse-I-schweren Ketten. Zum Ausschluß der Koexpression des HLA-Klasse-I-Antigens HLA-E auf der Zelloberfläche wurden HLA-G1mut- und HLA-G4mut-cDNA-Vektoren eingesetzt, deren Exon 1 so verändert ist, daß kein Ligand für HLA-E zur Verfügung gestellt wird. Während in der Zellinie K-562 HLA-G1 und HLA-G5 auf der Zelloberfläche exprimiert bzw. sezerniert werden, waren die verkürzten Isoformen HLA-G2 und HLA-G4 mittels FACS-Analyse mit einer Reihe HLA-Klasse-I- und HLA-G-spezifischer Ak nicht auf der Zelloberfläche nachweisbar. Diese Ergebnisse korrelieren mit der Sensitivität dieser verkürzten Isoformen gegenüber Endo H. Aus der fehlenden Resistenz der HLA-G2- und HLA-G4-Polypeptide gegenüber Endo H ergibt sich kein Hinweis auf ihren Transport zur Zelloberfläche. Diese fehlende Oberflächenexpression von HLA-G2 und HLA-G4 könnte auf einer gestörten Assoziation mit b2m oder Bestandteilen der MHC-Klasse-I-Prozessierungsmaschinerie beruhen. Kopräzipitationsexperimente ergaben, daß nur die HLA-G1-schwere Kette mit b2m und TAP assoziiert ist. HLA-G2 ließ sich zwar mit TAP, jedoch nicht mit b2m kopräzipitieren und HLA-G4 ließ sich weder in Assoziation mit b2m noch mit TAP nachweisen, so daß diesen Isoformen ein wichtiger Bestandteil der vollständigen HLA-I-Komplexe fehlt und bei HLA-G4 außerdem die Beladung mit Peptiden gestört ist. Diese Daten sprechen gegen eine Zelloberflächenexpression der verkürzten HLA-G-Isoformen. Im Unterschied zu HLA-G1 war HLA-G5 nicht in Kopräzipitaten mit TAP zu finden. Daher scheint für diese Isoform eine stabile Assoziation mit TAP für die Peptidbeladung nicht essentiell zu sein. Zum funktionellen Nachweis von HLA-G wurden Zytotoxizitätstests mit der Zellinie NKL sowie mit PBL, NK-Zellen und LAK-Zellen aus dem peripheren Blut mehrerer Donoren durchgeführt. Dabei zeigte sich, daß die Expression der verkürzten Isoformen HLA-G2 und HLA-G4 die Zytotoxizität der verschiedenen Effektorzellen nicht beeinflußte. HLA-G1 inhibierte die Lyse von K-562 in Abhängigkeit von der HLA-G1-Expressionsstärke und wirkte sich weniger deutlich als eine entsprechende HLA-E-Expression auf die Zytotoxizität aus. Neben der Plazenta wird HLA-G auch in zahlreichen anderen Geweben exprimiert und kann in Tumoren induziert oder hochreguliert werden. Da bei verschiedenen Tumoren die MHC-Klasse-I-Expression aufgrund von Mutationen im b2m-Gen gestört ist, wurden HLA-G1-Transfektanten in der b2m-negativen humanen Zellinie Daudi etabliert. Daudi HLA-G1-Transfektanten weisen gegenüber K-562 HLA-G1-Transfektanten eine reduzierte HLA-G-Proteinmenge auf. In Abwesenheit von b2m ist HLA-G1 außerdem nicht resistent gegenüber Endo H und kann auch nach Inkubation der Zellen bei niedrigen Temperaturen und Zugabe von b2m oder Ligand nicht auf der Zelloberfläche nachgewiesen werden. Da von HLA-B27 bekannt war, daß b2m-freie Homodimere auf der Zelloberfläche exprimiert werden können und eine Dimerisierung von HLA-G über ungepaarte Cysteinreste möglich ist, wurden die Daudi HLA-G1-Transfektanten auf Anwesenheit von HLA-G1-Dimeren untersucht. In Abwesenheit von b2m waren jedoch keine Dimere nachweisbar. Auch in funktionellen Experimenten mit LAK oder gd T-Zellen hatte die HLA-G-Expression in Daudi HLA?G1-Transfektanten keine Auswirkung auf die Zytotoxizität oder Proliferation der Effektorzellen. Die HLA-G1-Expression in b2m-negativen Tumoren trägt daher nicht zur Tumorprogression bei. Eine Analyse der Unterschiede in der Expression und der Auswirkungen der HLA-G-Isoformen in verschiedenen Zellinien könnte Hinweise auf die Regulation und die Funktion der HLA-G-Expression liefern.

Aims: An association between inflammatory bowel disease (IBD) and spondyloarthropathies (SpA) has repeatedly been reported. The aim of the present study was to investigate whether serologic markers of IBD, e. g. antibodies against Saccharomyces cerevisiae (ASCA), antibodies against exocrine pancreas (PAB) and perinuclear antineutrophil cytoplasmic antibodies (pANCA) are present in HLA-B27-associated SpA. Methods: 87 patients with HLA-B27-positive SpA and 145 controls were tested for ASCA, PAB and pANCA employing ELISA or indirect immunofluorescence, respectively. Antibody-positive patients were interviewed regarding IBD-related symptoms using a standardized questionnaire. Results/Conclusion: When compared to the controls, ASCA IgA but not ASCA IgG levels were significantly increased in patients with SpA, in particular in ankylosing spondylitis (AS) and undifferentiated SpA (uSpA). pANCA were found in increased frequency in patients with SpA whereas PAB were not detected. The existence of autoantibodies was not associated with gastrointestinal symptoms but sustains the presence of a pathophysiological link between bowel inflammation and SpA. Copyright (C) 2004 S. Karger AG, Basel.

The assembly of the classical, polymorphic major histocompatibility complex class I molecules in the endoplasmic reticulum requires the presence of peptide ligands and ~2-microglobulin (~2m). Formation of this trimolecular complex is a prerequisite for e~cient transport to the cell surface, where presented peptides are scanned by T lymphocytes. The function of the other class I molecules is in dispute. The human, nonclassical class I gene, HLA-E, was found to be ubiquitously transcribed, whereas cell surface expression was dif~cult to detect upon transfection. Pulse chase experiments revealed that the HLA-E heavy chain in transfectants, obtained with the murine myeloma cell line P3X63-Ag8.653 (X63), displays a significant reduction in oligosaccharide maturation and intracellular transport compared with HLA-B27 in corresponding transfectants. The accordingly low HLA-E cell surface expression could be significantly enhanced by either reducing the culture temperature or by supplementing the medium with human ~2m, suggesting inefficient binding of endogenous peptides to HLA-E. To analyze whether HLA-E binds peptides and to identify the corresponding ligands, fractions of acid-extracted material from HLA-E/X63 transfectants were separated by reverse phase HPLC and were tested for their ability to enhance HLA-E cell surface expression. Two fractions specifically increased the HLA class I expression on the HLA-E transfectant clone.

Sun, 1 Jan 1989 12:00:00 +0100 http://epub.ub.uni-muenchen.de/3079/ http://epub.ub.uni-muenchen.de/3079/1/3079.pdf Wildner, G.; Weiß, Elisabeth; Szöts, Hannelore; Riethmüller, Gert; Schendel, Dolores J. Wildner, G.; Weiß, Elisabeth; Szöts, Hannelore; Riethmüller, Gert und Schendel, Dolores J. (1989): The use of fusion proteins to study HLA-B27-specific allorecognition. In: Molecular Immunology, Vol. 26: pp. 33-40. Biologie

Sun, 1 Jan 1989 12:00:00 +0100 http://epub.ub.uni-muenchen.de/3071/ http://epub.ub.uni-muenchen.de/3071/1/3071.pdf Thureau, S. R.; Wildner, G.; Kuon, W.; Weiß, Elisabeth; Riethmüller, Gert Thureau, S. R.; Wildner, G.; Kuon, W.; Weiß, Elisabeth und Riethmüller, Gert (1989): Expression and immmunogenicity of HLA-B27 in high-transfection recipient P815:. a new method to induce monoclonal antibodies directed against HLA-B27. In: Tissue Antigens, Vol. 33: pp. 511-519. B

Fri, 1 Jan 1988 12:00:00 +0100 http://epub.ub.uni-muenchen.de/3085/ http://epub.ub.uni-muenchen.de/3085/1/3085.pdf Weiß, Elisabeth; Bloemer, Katharina; Doerner, C.; Kuon, W.; Lang, M.; Pohla, Heike; Schattenkirchner, M.; Riethmüller, Gert Weiß, Elisabeth; Bloemer, Katharina; Doerner, C.; Kuon, W.; Lang, M.; Pohla, Heike; Schattenkirchner, M. und Riethmüller, Gert (1988): Molecular biology of the HLA-B27 locus. In: British Journal of Rheumatology, Vol. 27, Nr. 2: pp. 12-18. Biologie

Antigen HLA-B27 is a high-risk genetic factor with respect to a group of rheumatoid disorders, especially ankylosing spondylitis. A cDNA library was constructed from an autozygous B-cell line expressing HLA-B27, HLA-Cw1, and the previously cloned HLA-A2 antigen. Clones detected with an HLA probe' were isolated and sorted into homology groups by differential hybridization and restriction maps. Nucleotide sequencing allowed the unambiguous assignment of cDNAs to HL4-A, -B, and -C loci. The HLA-B27 mRNA has the structural features and the codon variability typical of an HLA class I transcript but it specifies two uncommon amino acid replacements: a cysteine in position 67 and a serine in position 131. The latter substitution may have functional consequences, because it occurs in a conserved region and at a position invariably occupied by a species-specific arginine in humans and lysine in mice. The availability of the complete sequence of HLA-B27 and of the partial sequence of HLA-Cw1 allows the recognition of locus-specific sequence markers, particularly, but not exclusively, in the transmembrane and cytoplasmic domains.

Tue, 1 Jan 1985 12:00:00 +0100 http://epub.ub.uni-muenchen.de/3099/ http://epub.ub.uni-muenchen.de/3099/1/3099.pdf Weiß, Elisabeth; Kuon, W.; Doerner, C.; Lang, M.; Riethmüller, Gert Weiß, Elisabeth; Kuon, W.; Doerner, C.; Lang, M. und Riethmüller, Gert (1985): Organization, sequence and expression of the HLA-B27 gene. a molecular approach to analyze HLA and disease associations. In: Immunobiology, Vol. 170: pp. 367-380. Biologie