Background/Aims: Strongyloidiasis, which is caused by Strongyloides stercoralis, is one of the prevalent infections in the tropical and subtropical regions worldwide. The larvae mainly infect the small intestine and cause serious disseminated strongyloidiasis. Although upper gastrointestinal features in strongyloidiasis are well known, colonoscopic evaluation has not been established yet. The aim of this study is to clarify the characteristic findings on colonic lesions in strongyloidiasis. Method: From January 2005 to December 2009, 10 cases with strongyloidiasis underwent colonoscopy at a single center on an endemic island of Japan. The clinical and colonoscopic findings were analyzed retrospectively. Results: Six (60%) cases had an immunocompromised condition, including human T lymphotropic virus type 1 infection, corticosteroids, and chemotherapy. Hyperinfection or disseminated strongyloidiasis was not presented. Endoscopic features included yellowish-white nodules, erythema, and loss of vascular pattern, which were mainly observed in the right colon. Pathological examination revealed the filariform Strongyloides larvae and the eosinophilic infiltration of the lamina propria. Conclusion: This study demonstrates that colonoscopic observation and biopsies are very useful to diagnose strongyloidiasis. Asymptomatic cases with strongyloidiasis can have colonic involvement. Yellowish-white nodules may be a characteristic finding of colonic lesions in strongyloidiasis and can be a cautious marker to prevent fatal disseminated strongyloidiasis in endemic regions.

A 36-year-old womanwith ulcerative colitis presented with fever, chest and back pain, and fatigue sensation of the arm. Her upper limb pulses were absent. Angiography showed multiple aneurysms of the aorta and its branches, consistent with Takayasu's arteritis. She showed HLA-B35but no B52, which is the typical haplotype among the coexistence cases of both diseases. Prednisolone was effective. The possible pathogenic association of the disorders is discussed. (Internal Medicine 42: 897-898, 2003)

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Background and aims: Barrier dysfunction is an important feature contributing to inflammation and diarrhoea in Crohn's disease (CD). Recently, tumour necrosis factor a (TNF-a) antibodies were recognised as effective in steroid refractory CD. The aim of this study was to characterise the effects of this therapy on the epithelial barrier. Patients and methods: Forceps biopsies were obtained from the sigmoid colon before and 14 days after TNF-a antibody therapy in 11 patients treated for chronic active CD (Crohn's disease activity index .150). Epithelial apoptoses were measured after terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate nick end labelling (TUNEL) and 49,6-diamidino-2-phenylindole staining. Epithelial resistance was determined by alternating current impedance analysis in miniaturised Ussing chambers. Occludin, claudin 1, and claudin 4 expression was quantified in immunoblots. Results: The epithelial apoptotic ratio was 2.1 (0.2)% in controls and increased to 5.3 (1.0)% in CD. TNF-a antibody therapy decreased the apoptotic ratio to 2.9 (1.0)% (normalised in 10 of 11 patients). In parallel, epithelial resistance was lower in CD than in controls (24 (3) v 42 (3) V6cm2 ) and improved to 34 (3) V6cm 2 after therapy. Occludin, claudin 1, and claudin 4 were not affected by TNF-a antibody therapy. In support of a functional role of epithelial apoptoses in CD, a similar decrease in resistance of 240% was observed when the apoptotic rate was selectively upregulated from 2.6% to 5.4% with camptothecin in HT-29/B6 cells. Conclusions: Epithelial apoptoses were upregulated in the colon in CD and restored to normal in 10 of 11 patients by TNF-a antibody therapy. This is the structural correlate of epithelial barrier dysfunction measured as epithelial resistance while expression of tight junction proteins did not contribute to this therapeutic effect.