Crohn Disease: Siegmund B

Hoffmann JC, Preiss JC, Autschbach F, Buhr HJ, Häuser W, Herrlinger K, Höhne W, Koletzko S, Krieglstein CF, Kruis W, Matthes H, Moser G, Reinshagen M, Rogler G, Schreiber S, Schreyer AG, Sido B, Siegmund B, Stallmach A, Bokemeyer B, Stange EF, Zeitz M. · Medizinische Klinik I, St. Marienkrankenhaus, Ludwigshafen. · Z Gastroenterol. · Pubmed #18810679 No free full text.

This publication has no abstract.

Hoffmann JC, Autschbach F, Bokemeyer B, Buhr HJ, Herrlinger K, Höhne W, Krieglstein C, Kruis W, Moser G, Preiss JC, Reinshagen M, Rogler G, Schreiber S, Schreyer AG, Siegmund B, Stallmach A, Stange EF, Zeitz M. · Medizinische Klinik I, St. Marienkrankenhaus Ludwigshafen. · Dtsch Med Wochenschr. · Pubmed #18788069 No free full text.

This publication has no abstract.

Siegmund B, Zeitz M. · Medizinische Klinik I, Charité Universitätsmedizin Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, 12200 Berlin, Germany. · Langenbecks Arch Surg. · Pubmed #15449064 No free full text.

Abstract: Crohn's disease is a condition of chronic inflammation potentially involving any location of the alimentary tract from mouth to anus but with a propensity for the distal small bowel and proximal large bowel. Frequent complications include stricture and fistula. Numerous extra-intestinal manifestations may also be present. The aetiology of Crohn's disease is incompletely understood, and therapy, although generally effective in alleviating the symptoms, is not curative. Due to the heterogeneity of the disease a major need for the therapeutic approach is the ability to define subgroups with distinct characteristics. However, with regard to the heterogeneity of demographic, anatomic and disease behaviour characteristics, distillation of the numerous possible phenotypes in simple categories is a formidable task. In the present review the focus will be on clinically relevant situations providing therapeutic algorithms according to international guidelines.

Schumann M, Preiss JC, Loddenkemper C, Günther U, Somasundaram R, Siegmund B, Zeitz M. · Klinik für Gastroenterologie, Infektiologie und Rheumatologie, Charité Universitätsmedizin Berlin. · Dtsch Med Wochenschr. · Pubmed #18788068 No free full text.

Abstract: HISTORY: A 48-year-old patient with Crohn's disease was admitted to our hospital with fatigue, icterus, hepatosplenomegaly and ascites. INVESTIGARTIOS: The whole blood count revealed a pancytopenia, hyperbilirubinemia and slightly elevated transaminases. Examination of the liver histology showed areas of enlarged hyperplastic hepatocytes adjacent to areas of atrophic hepatocytes and dilated sinusoids. DIAGNOSIS, TREATMENT AND COURSE: Pancytopenia was most likely azathioprine-related. Analysis of the liver histology was highly suggestive of an azathioprine-related, nodular regenerative hyperplasia (NRH). After discontinuation of azathioprine the patient's condition improved substantially. CONCLUSIONS: NRH is a rare but potentially serious complication of azathioprine therapy. Other causes include various rheumatological, vascular and myeloproliferative diseases. When azathioprine is prescribed it must be borne in mind that it can cause NRH as a potential adverse effect, and liver enzymes should be measured at regular follow-up examinations.

Ludwiczek O, Vannier E, Borggraefe I, Kaser A, Siegmund B, Dinarello CA, Tilg H. · Department of Medicine, University Hospital Innsbruck, Innsbruck, Austria. · Clin Exp Immunol. · Pubmed #15498044 links to  free full text

Abstract: Interleukin (IL)-1 is a key mediator in the pathogenesis of inflammatory bowel disease (IBD). Naturally occurring IL-1 modulators include IL-1 receptor antagonist (IL-1Ra), IL-1 soluble receptor Type I (IL-1sRI), IL-1sRII and IL-1 receptor accessory protein (AcP). Systemic and mucosal levels of IL-1 soluble receptors remain unknown in IBD. Plasma or colonic tissues were obtained from 185 consecutive unselected patients with Crohn's disease (CD) or ulcerative colitis (UC) and from 52 control subjects. Plasma and colonic explant culture supernatants were assessed for IL-1alpha, IL-1beta, IL-1Ra, IL-1sRI and IL-1sRII. Plasma IL-1Ra levels were higher in UC (+93%) than in healthy subjects. IL-1alpha and IL-1beta were not detected. IL-1sRII levels were marginally lower in CD (-10%) and UC (-9%), whereas IL-1sRI levels were elevated in CD (+28%) only. Plasma IL-1sRI levels correlated positively (P < 0.01) with Crohn's disease activity index (r = 0.53), C-reactive protein (r = 0.46) and alpha1-acid glycoprotein (r = 0.42). In colonic explant cultures, IL-1alpha and IL-1Ra levels were elevated in non-lesional (+233% and +185% respectively) and lesional CD (+353% and +1069%), lesional UC (+604% and +1138%), but not in non-lesional UC. IL-1beta was elevated in lesional UC (+152%) and CD (+128%). In contrast, IL-1sRII levels were elevated in non-lesional CD (+65%), but remained unchanged in lesional CD, non-lesional and lesional UC. IL-1sRI levels did not differ between patient and control groups. These results indicate that (i) the proinflammatory moiety IL-1sRI is a systemic marker of inflammation and activity in CD and (ii) local shedding of the functional antagonist IL-1sRII may dampen colonic inflammation in CD, but not in UC.