In spite of its high incidence, not much is known about the etiology of chronic urticaria. We performed gastroscopic evaluation of 10 patients in whom no cause for chronic urticaria had been found. In 8 of these 10 patients, Helicobacter pylori was identified in the gastric mucosa. The chronic urticarial lesions disappeared within a few days after starting therapy with amoxicillin and omeprazol.

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An 82-year-old patient with untreated chronic lymphatic leukaemia known for 6 years developed large livid red plaques with central blisters and subsequent ulceration of the lower legs. Reactive angioendotheliomatosis was diagnosed based on histological immunohistological and electronmicroscopic examination, since proliferating endothelial cells with intravascular fibrin thrombi were identified. When the leukaemia was treated the skin eruption healed completely.

Sarcoidosis is characterised by the formation of sarcoidal granulomas in all affected organs. Despite intensive research, the cause of the disease in unknown. There are only a few reports suggesting an induction of sarcoidosis by interferons. Three patients are presented in whom sarcoidosis developed during or after interferon alpha therapy. The probability of interferon therapy as cause of sarcoidosis is discussed.

OBJECTIVE: To report a case in which the anticoagulant effectsof warfarinwere attenuatedduring concomitant administration of rifaximin, possibly through induction of CYP3A4 following increased absorption of rifaximin in a patient with smallintestine bacterial overgrowth (5180). CAS E SUMM A RY: A 49-year-old African American female had received effective anticoagulanttherapy for 5 monthswith a target international normalized ratio (INR) of 2.0-3.5on a warfarin regimen of 7.5 mg daily. Five days following initiation of rifaximin 400 mg 3 times daily to treat 5 180, her INR had fallen to 1.2 and remainedsuppressed throughout the durationof her rifaximin regimen despite incremental warfarin dosageincreases (highest dose, 15 mg/day for 2 days, followed by 11.25 mg/day). Twelve days after completion of the rifaximin treatment course, the INR was supratherapeutic at 4.2, requiring titration to her baseline warfarin dosage to achieve an INR within the target range. Similar results wereobtained following rechallenge with rifaximin. DISC USSION: Rifaximin has been shown in vitro to induce the CYP3A4 enzyme for which the R-isomer of warfarin is a known substrate. The lack of in vivo CYP3A4 induction with rifaximin in other patient populations has repeatedly been attributed to its minimal oral bioavailability, while a recent study found that patients with 5180 had a clinically significant increase in intestinal permeability. In this patient population it is plausiblethat rifaximin bioavailability increases enough to induce CYP3A4, leading to clinically significant reductionsin the bioavailability of CYP3A4 substrates, including R-warfBrin. An objectivecausality assessment of this case revealed that a warfarin-rifaximin interaction was probable. No otherdrug dosages were aI1ered during the timeframe in question, and the patienthad an impeccable medication adherence history; we therefore ruledout these potential etiologies. CONCLUSIONS: Toour knowledge, an interaction between warfarin and rifaximin has notbeen previously reported. Whilefurther research needs to be conducted to confirm these results, practitioners should be aware of thispossibilitybecause of the increasi ng useof rifaximin as a first-linechoice in the treatment of 8180.