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Clinical Journal Club https://www.mdc-berlin.de/de/veroeffentlichungstypen/clinical- journal-club Als gemeinsame Einrichtung von MDC und Charité fördert das Experimental and Clinical Research Center die Zusammenarbeit zwischen Grundlagenwissenschaftlern und klinischen Forschern. Hier werden neue Ansätze für Diagnose, Prävention und Therapie von Herz-Kreislauf- und Stoffwechselerkrankungen, Krebs sowie neurologischen Erkrankungen entwickelt und zeitnah am Patienten eingesetzt. Sie sind eingelanden, um uns beizutreten. Bewerben Sie sich! A 46-year-old woman presented to the clinic with a 3- month history of walking difficulty due to worsening knee pain. She had received a diagnosis of rheumatoid arthritis 12 years earlier but had received treatment inconsistently. On physical examination, she had nodular swelling and outward bowing of both knees. She had limited range of motion in her left shoulder and in both wrists and both knees. Anteroposterior radiograph of the knees is shown. What is the diagnosis? Synovial chondromatosis Synovial chondrosarcoma Osteochondritis dissecans Pigmented villonodular synovitis Disseminated tuberculosis Correct! The findings are consistent with synovial chondromatosis, a disorder of the synovium that is characterized by the development of loose cartilaginous bodies. Die Synoviale Chondromatose ist eine seltene Erkrankung der Synovialis großer Gelenke. Es handelt sich um eine knorpelbildende Metaplasie (Chondromatose). Die ersten Kasuistiken stammen von Paul Friedrich Reichel, Melvin Starkey Henderson (1918) und Hugh Toland Jones (1924). Die Ursache ist nach wie vor unklar. Pathologisch-anatomisch handelt es sich um eine Metaplasie mesenchymaler Zellen in umschriebene Knorpelareale. Bei Männern kommt das seltene Krankheitsbild etwa doppelt so häufig wie bei Frauen vor, bei Kindern nur vereinzelt. „Häufig“ befallen sind Knie-, Hüft-, Schulter- und Ellbogengelenk. Auch das Kiefergelenk kann betroffen sein. Die meisten Patienten sind lange relativ beschwerdefrei. Schließlich erfordern Einklemmungserscheinungen, Bewegungsbehinderung oder Schmerzen durch freie Gelenkkörper und synoviale Chondrome, sowie die mögliche Schädigung von Gelenkstrukturen durch Abrieb (Sekundärarthrose) eine Abklärung. Die synoviale Chondromatose ist eine radiologische Blickdiagnose. Als gefürchtete Komplikation ist die Entstehung eines sekundären Chondrosarkoms zu sehen. In einer größeren Studie mit 53 Fällen in 30 Jahren wurden drei Chondrosarkome diagnostiziert. Bei dieser Unterform verschmelzen viele einzelne Chondrome, so dass sich ein solider Tumor bis zu einem Durchmesser von 20 cm ausbilden kann. Auch eine entsprechende Vergrößerung eines einzelnen Chondroms wird für möglich erachtet. Histologisch und radiologisch ist die Abgrenzung von einem Chondrosarkom schwierig. Die Osteochondrosis dissecans, kurz OD, ist eine aseptische, meist traumatisch bedingte Knochennekrose eines umschriebenen Gelenkflächenareals, die mit der Abstoßung eines Gelenkflächenfragmentes einhergehen kann. Die Osteochondrosis dissecans wird im ICD10 den Chondropathien zugeordnet. Alle Gelenke des menschlichen Körpers können betroffen sein, am häufigsten ist jedoch das Kniegelenk in der Wachstumsphase erkrankt. Die Ätiologie ist oftmals unbekannt. Mögliche Ursachen können Mikro- oder Makrotraumata sowie Ischämie oder Störungen der Schilddrüsenfunktion sein. Dauer- und Überbelastung der Gelenkflächen bei Sportlern erhöht vermutlich das Risiko. Eine subchondrale Vaskularisationsstörung führt zur Demarkierung des betroffenen Knochenareals und zur anschließenden Osteolyse oder Sklerosierung an der Gelenkfläche. Der sich darauf befindende Knorpelbereich verfärbt sich anfangs gelb und zeigt erste degenerative Veränderungen. Im weiteren Verlauf löst sich das geschädigte Knorpel-Knochenareal als Dissekat (sogenannte Gelenkmaus) aus der Gelenkoberfläche und hinterlässt eine Defektstelle. Der Gelenkflächendefekt wird später mit fibrösem Gewebe ausgekleidet. Die Colitis Ulcerosa (CU, englisch ulcerative colitis) gehört zur Gruppe der chronisch-entzündlichen Darmerkrankungen. Sie ist durch einen entzündlichen Befall des Dickdarms bzw. des Colons gekennzeichnet. Im Gegensatz zum Morbus Crohn ist von der Entzündung nur der Dickdarm kontinuierlich betroffen und diese ist auf die Darmschleimhaut (Mukosa und Submukosa) beschränkt. Die Ursache der Erkrankung ist unbekannt. Ähnlich wie beim Morbus Crohn nimmt man eine genetisch prädisponierte, krankhaft gesteigerte Immunreaktion gegen die Darmflora an. Es konnten mehrere Genmutationen identifiziert werden, die mit dem Auftreten von chronisch-entzündlichen Darmerkrankungen in Verbindung stehen. Wie bei Morbus Crohn steht der NF-κB-Transkriptionsfaktor im Verdacht, durchgängig aktiv zu sein. Umweltfaktoren wie Hygienestandard und Ernährung sollen eine ebenso wichtige Rolle spielen. Stress und Belastungen können wesentlich zu einem schwierigen Verlauf beitragen und aktive Schübe der Krankheit auslösen. Colitis ulcerosa wurde über einen langen Zeitraum ähnlich wie Morbus Crohn zu den psychosomatischen Krankheiten gezählt, sie gehört zu den Holy Seven. Mittlerweile ist allerdings klar, dass die Colitis ulcerosa durch die genannten organischen Ursachen hervorgerufen wird, und dass die Psychosomatik allenfalls Begleit- und Folgeerscheinungen beeinflusst Ustekinumab ist ein Arzneistoff, der in der Behandlung der Psoriasis eingesetzt wird. Ustekinumab ist ein humaner monoklonaler Antikörper gegen die Zytokine Interleukin-12 (IL- 12) und Interleukin-23 (IL-23). Ustekinumab ist für die Behandlung der mittelschweren bis schweren Plaque-Psoriasis bei Erwachsenen und Jugendlichen ab dem 12. Lebensjahr zugelassen, bei denen andere Therapien nicht angesprochen haben, kontraindiziert sind oder nicht vertragen wurden.[ Zu den häufigsten Nebenwirkungen unter Ustekinumab zählen Infektionen, insbesondere der oberen Atemwege (> 10 %). Häufig (1–10 %) treten auch Depressionen, Schwindel, Kopfschmerz, Durchfall, Juckreiz, Rücken- und Muskelschmerz und Müdigkeit auf. Darüber hinaus können Reaktionen an der Injektionsstelle beobachtet werden. Es gibt auch Hinweise auf mögliche kardiovaskuläre Risiken. Interleukin-23 (IL-23) is a heterodimeric cytokine composed of an IL12B (IL-12p40) subunit (that is shared with IL12) and the IL23A (IL-23p19) subunit.[1] A functional receptor for IL-23 (the IL-23 receptor) has been identified and is composed of IL-12R β1 and IL- 23R. IL-23 is a proinflammatory cytokine. IL-23 has been shown to be a key cytokine for Th17 maintenance and expansion. Th17 are polarised by IL-6 and TGF-β which activate Th17 transcription factor RORγt. IL-23 stabilises RORγt and thus enables Th17 to properly function and release their effector cytokines such as IL- 17, IL-21, IL-22 and GM-CSF which mediate protection against extracellular parasites (fungi and bacteria) and participate in barrier immunity. Similar effects as IL-23 has on Th17 cells were described on type 3 innate lymphoid cells which actively secrete Th17 cytokines upon IL-23 stimulation. NK cells express IL-23 receptor too. They respond with increased IFN-γ secretion and enhanced antibody-dependent cellular cytotoxicity. IL- 23 also induces proliferation of CD4 memory T cells (not naïve cells). Along with mentioned proinflammatory effects IL-23 promotes angiogenesis. IL-23 heterodimer binds the receptor complex - p19 subunit binds IL-23R while p40 subunit binds IL-12RB1 which leads to recruitment of Janus kinase 2 and Tyrosine kinase 2 kinases. Janus kinase 2 and Tyrosine kinase 2 transduce the signal and phosphorylate STAT3 and STAT4. STATs dimerise and activate transcription of target genes in nucleus. STAT3 is responsible for key Th17 development attributes like RORγt expression or transcription of Th17 cytokines.[ Ustekinumab as Induction and Maintenance Therapy for Ulcerative Colitis The efficacy of ustekinumab, an antagonist of the p40 subunit of interleukin-12 and interleukin-23, as induction and maintenance therapy in patients with ulcerative colitis is unknown. We evaluated ustekinumab as 8-week induction therapy and 44-week maintenance therapy in patients with moderate-to-severe ulcerative colitis. A total of 961 patients were randomly assigned to receive an intravenous induction dose of ustekinumab (either 130 mg [320 patients] or a weight- range–based dose that approximated 6 mg per kilogram of body weight [322]) or placebo (319). Patients who had a response to induction therapy 8 weeks after administration of intravenous ustekinumab were randomly assigned again to receive subcutaneous maintenance injections of 90 mg of ustekinumab (either every 12 weeks [172 patients] or every 8 weeks [176]) or placebo (175). The primary end point in the induction trial (week 8) and the maintenance trial (week 44) was clinical remission (defined as a total score of ≤2 on the Mayo scale [range, 0 to 12, with higher scores indicating more severe disease] and no subscore >1 [range, 0 to 3] on any of the four Mayo scale components). Patients with Clinical Remission, Endoscopic Improvement, Clinical Response, or Histo-Endoscopic Mucosal Healing at Week 8 in the Induction Trial. Weight-range–based doses of ustekinumab approximating 6 mg per kilogram were as follows: 260 mg (weight, ≤55 kg), 390 mg (weight, >55 kg and ≤85 kg), and 520 mg (weight, >85 kg). Patients who had a prohibited change in concomitant medication for ulcerative colitis or who had undergone an ostomy or colectomy before week 8 were considered not to have met the end point. Clinical remission was defined as a total score of
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