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Regional Entity.

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Crohn Disease↗

Folic acid absorption in regional enteritis.

The authors have investigated intestinal absorption of folic acid by jejunal perfusion with a triple lumen tube in five subjects with regional enteritis. The subjects' intestinal disabilities ranged from terminal ileitis to short bowel syndrome. Two had steatorrhea and two had low serum folate levels. Absorption of pteroylglutamic acid was normal in all five. This suggests that folic acid deficiency, common in this disorder, is largely caused by malnutrition, not malabsorption.

Adult↗

[Orthopedic aspects of Crohn disease. Examples of extra-intestinal organ manifestations].

Articular changes in Chron's disease represent extraintestinal organic manifestations which generally take the form of so-called enteropathic synovitis. Articular alterations - diagnosed as non-specific arthritis in the great majority of cases--may precede the intestinal disease. In very rare cases it can be shown that the joints display histological changes typical of Morbus Crohn. The etiology and pathophysiological mechanisms of the articular changes are not clear. Probable factors are: autoimmune disease, stimulation of the immunological system by exogenous antigens, induction of a self-sustaining inflammatory process, and demonstrable circulation of antigen-antibody complexes. Genetic factors seem to play a role (familial disposition). A pure "colonic Crohn" (= colitis granulomatosa) leads to a higher degree of articular alteration than a pure "small-intestine Crohn" (= ileitis terminalis). The joints preferentially affected are in the region of the lower extremities (knee and ankle joints). Concomitant Bekhterev's disease (spondylitiis ankylopoietica) is found in 7-10% of cases. Osteomyelitis represents a rare and serious complication: it can appear in the course of chronic Chron's disease (mainly with intestinal fistulas), especially in the region of the pelvic bones. Further aspects of interest from an orthopedic viewpoint are hypertrophic osteoarthropathy with periossal neoformation, granulomatous changes in the bone itself, and aseptic osteonecrosis.

Arthritis↗

Linkage to peroxisome proliferator-activated receptor-gamma in SAMP1/YitFc mice and in human Crohn's disease.

BACKGROUND AND AIMS: Genetic predisposition is implicated strongly in Crohn's disease. Disease-associated mutations in NOD2/CARD15 , the best-studied susceptibility gene in this disorder, explain only a small fraction of the heritability. The SAMP1/YitFc (SAMP1/Fc) mouse strain expresses many features of Crohn's disease in humans. We bred SAMP1/Fc to disease-resistant AKR mice to identify additional susceptibility genes that may play a role in human disease. METHODS: Linkage disequilibrium mapping was performed in an (AKR x SAMP1/Fc) backcross to SAMP1/Fc, followed by sequencing, expression analysis using reverse transcription polymerase chain reaction (PCR) and immunohistochemistry, and functional testing in vivo of the regional candidate gene encoding the peroxisome proliferator-activated receptor gamma ( Pparg ). A cohort-based association study was performed in humans. RESULTS: We show that ileitis is blocked in SAMP1/Fc mice by inheritance of AKR alleles on chromosome 6 in the region of Pparg . Major differences in Ppargamma expression in the parental mouse strains are found specifically in the crypts of the small intestine, and treatment of ileitis-prone mice with a Ppargamma agonist decreased disease severity in susceptible mice expressing low levels of the protein. Rare alleles of PPARG are associated significantly with Crohn's disease in humans. CONCLUSIONS: We have identified Pparg as a susceptibility gene in both the SAMP/Yit mouse and in human Crohn's disease. Similarities between Crohn's disease and the SAMP1/Fc model suggest that the effect of this gene in humans may be mediated through regulation of PPARgamma activity in the crypts of the small intestine.

Adult↗

[17 year old patient with acute abdominal pain, hematochezia and exanthema].

A 17-year old adolescent presented with abdominal pain, petechial lesions, arthralgia, and hematochezia. Abdominal ultrasound showed a suspicious ileocecal region and a lower endoscopy revealed the picture of an ileitis terminalis. The diagnosis of Purpura Henoch Schoenlein was made and confirmed by skin-biopsy showing a leucocytoclastic vasculitis. This case report demonstrates the various clinical symptoms of Purpura Henoch Schoenlein and its clinical course.

Abdominal Pain↗