[Protein-loosing enteropathy: report of four cases and review of etiology, diagnostic work-up and treatment]. / Enteraler Eiweisserlust: Pathophysiologie, Ursachen, Diagnostik und Therapie mit Fallbeispielen.

The protein-loosing enteropathy (PLE) may result from a broad variety of underlying diseases. These conditions are of systemic nature or locally affecting the gastrointestinal tract. Major symptoms are oedema due to low plasma protein levels. Gastrointestinal symptoms are not necessarily present. The diagnosis is confirmed by the finding of increased faecal concentrations of Alpha-1-Antitrypsin (> 320 mg/L). In the majority of cases, in which underlying diseases are present, the etiology is obvious. In unclear cases the differentiation into inflammatory or circulatory disturbances or alterations of the architecture of the basal membrane is helpful. An economic, staged approach is presented. To localize the site of protein loss imaging is required (abdominal ultrasound, CT-scan, endoscopy and Technetium-Scan). If a circumscribed intestinal source of protein loss is suspected which may be amenable to surgery, intraoperative enteroscopy should be considered. If causal treatment is impossible; intravenous replacement of albumin and immunoglobulines in intervals from 1 to 4 weeks will be necessary. The prognosis in patients with isolated PLE is good. Otherwise it depends on the underlying disease.

Active pyrimidine absorption by chicken colon.

Pyrimidine absorption by chicken large intestine was investigated employing the everted sac and flux chamber techniques. 3H-labelled uracil was used as substrate. The small intestine and the colon unlike the caecum, transported uracil from the mucosal to the serosal surface against a concentration gradient in the everted sac experiments. Furthermore, there was a net transport of uracil from the mucosal to the serosal side of the colon and jejunum in the flux chamber experiments. Uracil transport by the everted colon sacs against a concentration gradient was inhibited when the purine hypoxanthine was present in the incubation medium. Uracil transport by the everted colon sacs was also inhibited under anaerobic conditions and when 2,4-dinitrophenol was present in the incubation medium. Replacing the Na+ ions of the incubation medium by Li+ ions also caused an inhibition of uracil transport. It is concluded from these results that uracil (and probably other pyrimidines) are absorbed from the chicken colon by a Na+ ion-dependent active transport process having also an affinity for purines.