The case is reported of a 70 year old man who presented with severe anaemia because of chronic gastrointestinal blood loss. This loss was ascribed to vascular ectasia resembling the gastric antral vascular ectasia syndrome but extended to include the antrum, the duodenum, the jejunum, and, possibly, the cardiac area. This condition was associated with portal hypertension as a result of nodular regenerative hyperplasia. Consecutive treatments including sucralfate, prostaglandin E2, propranolol, organic nitrates, pentoxyphilline, corticosteroids, endoscopic sclerotherapy, portosystemic shunt, total gastrectomy, proved ineffective.

We report on eight children who suffered from cerebrovascular ischemia or stroke at the age of 2 or up to 11 years. Antiphospholipid antibodies (APLA) were detected in two cases during the ischemic event and in six cases during follow-up examinations (after six weeks or within a span of six years). In two patients multiple stenoses of basal cerebral arteries were found; one of them suffered from moyamoya syndrome. The acute hemiplegia in one patient was linked to an asymptomatic mycoplasmal infection and APLA. In three cases, one of the parents was also APLA-positive. Seven patients were treated with acetylsalicylic acid, and in four cases immunoglobulin infusions were given. Transient ischemic attacks subsided after the child with the moyamoya syndrome received immunoglobulins. No effect of medication could be established in the other children. The concept of the antiphospholipid syndrome is still evolving. As none of the common risk factors pertaining to strokes in adults apply to children, pediatric research may offer a suitable platform for specific investigations on the causal, pathogenetic role of APLA. We propose that all children suffering from stroke or transient ischemic attacks should be tested for APLA.

Propafenone, three times 150 mg/d over 33 days and two years later at the same dosage over six days, was administered to an 84-year-old man with ventricular extrasystoles (Lown IVa). Both times intrahepatic biliary stasis occurred, presumably a sign of a drug-allergic hepatitis. All other possible causes in the differential diagnosis were excluded. The lymphocyte transformation test demonstrated in vitro propafenone-sensitive patient-lymphocytes.

In a multicentre single-blind study, ranitidine was compared to cimetidine as prophylactic treatment against stress-induced upper gastrointestinal bleeding in seriously ill patients in the intensive care unit (ICU). 380 patients entered the study. 192 patients were treated with ranitidine 50 mg q.i.d. as i.v. bolus followed by 150 mg orally twice daily. 188 patients received cimetidine 400 mg q.i.d. intravenously and 1,000 mg daily orally in divided doses. Five patients in the ranitidine group (2.6%) and 12 in the cimetidine group (6.4%) developed gastrointestinal bleeding definitely or possibly due to stress lesions. This difference was not significant. The incidence of stress erosions or ulcerations developing during the study was 11.8% for the ranitidine group and 18.3% for the cimetidine group (non-significant difference). Adverse events in the ranitidine group were nausea, tachycardia or vomiting in 4 patients. 5 cimetidine-treated patients developed cholestasis, and 5 additional central nervous system problems. The high degree of efficacy of both drugs compared very favourably with the high incidence of stress ulceration and hemorrhage in similar untreated populations.

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