Molsidomine, a long acting vasodilator with antianginal properties, has been shown to decrease porto-hepatic pressure gradient in patients with cirrhosis. The present study aimed at assessing the effects of molsidomine, propranolol and of the association of these two drugs on portal vein blood flow as measured using Doppler and B-mode sonography. In 10 patients without liver disease (group 1), portal flow time average mean velocity (TAV) and portal vein bloodflow (PVBF) were measured under basal conditions, 1 hour then 2 hours after ingestion of 4 mg of molsidomine. The same measurements were performed in 15 patients with cirrhosis (group 2) under basal conditions, 1 then 2 hours after double-blind administration of either molsidomine (10 patients) or placebo (5 patients). Fifteen further patients with cirrhosis (group 3) were studied after the double blind administration of 80 mg of propranolol and two hours later of 4 mg of molsidomine (10 patients) or placebo (5 patients); TAV and PVBF were measured under basal conditions, two hours after propranolol ingestion or placebo, then one and two hours after molsidomine or placebo ingestion. TAV and PVBF remained unchanged in patients treated with placebo. Molsidomine reduced TAV by 23.8 +/- 19.5% in group 1 (P < 0.01) and by 25.6 +/- 21.4% in group 2 (P < 0.01). In group 3, a 10% decrease was observed after propranolol (NS). When molsidomine was added, TAV was further decreased (-17.6 +/- 13.3% vs baseline, P < 0.01). PVBF remained unchanged in the three groups of patients. Considering the absence of changes in TAV and PVBF in placebo treated patients, Doppler and B-mode sonography were found to give reproducible results. The significant decrease of TAV in patients treated with molsidomine suggests that this atraumatic method could be used for evaluating vasoactive drugs in portal hypertension.

We report a case of jaundice, fever, weight loss and pancytopenia occurring in a 61-year-old man after transurethral administration of bacillus Calmette-Guerin. Liver and bone marrow biopsies both found disseminated granulomas but no organisms were identified in these tissues. The patient was successfully treated with isoniazid and rifampicin for 8 months.

Percutaneous endoscopic gastrostomy, a recent nutritional support was indicated in 97 patients, most of whom had deglutition problems or dysphagia. Assistance was possible in all but one cases, with difficulty in 5 cases. These were 2 important complications and no mortality reliable to the procedure. 19 benign complications occured during follow up but did not necessitate the removal of the tube. The follow up of patients showed good tolerance Our experience suggests that PEG deserves a prime place as a nutritional aid for selected cases.

Endocarditis occurring in the course of a psittacosis is a rare but serious event. We describe the case of a 79-year-old woman dead in 50 days because of intractable cardiac failure in spite of a precocious and appropriate antibiotic therapy.

Organic nitrates were reported to reduce portohepatic venous pressure gradient in patients with cirrhosis. However, these drugs lower arterial pressure and are well known to induce tolerace. The aim of the present study was to assess the hemodynamic effects of molsidomine, an antianginal agent, which does not induce tolerance and has little effect on arterial pressure in patients with normal liver, in 13 patients with alcoholic cirrhosis. Wedged hepatic vein pressure (−11%, p < 0.01), portohepatic venous pressure gradient (−15%, p < 0.005), hepatic blood flow (−17.4%, p < 0.005), mean arterial pressure (−13.5%, p < 0.01) and cardiac output (−17%, p < 0.001) were significantly reduced by molsidomine. Free hepatic vein pressure, intrinsic hepatic clearance indocyanin green, heart rate and systemic vascular resistances were not significantly modified. There was no correlation between the decrease in portohepatic venous pressure gradient and the reduction in mean arterial pressure on one hand and the decrease in cardiac output on the other hand. We therefore conclude that in patients with cirrhosis, molsidomine has effects similar to nitrates on systemic and splanchnic hemodynamics.

Molsidomine, a long acting vasodilator with antianginal properties, has been shown to decrease porto-hepatic pressure gradient in patients with cirrhosis. The present study aimed at assessing the effects of molsidomine, propranolol and of the association of these two drugs on portal vein blood flow as measured using Doppler and B-mode sonography. In 10 patients without liver disease (group 1), portal flow time average mean velocity (TAV) and portal vein blood flow (PVBF) were measured under basal conditions, 1 hour then 2 hours after ingestion of 4 mg of molsidomine. The same measurements were performed in 15 patients with cirrhosis (group 2) under basal conditions, 1 then 2 hours after double-blind administration of either molsidomine (10 patients) or placebo (5 patients). Fifteen further patients with cirrhosis (group 3) were studied after the double blind administration of 80 mg of propranolol and two hours later of 4 mg of molsidomine (10 patients) or placebo (5 patients); TAV and PVBF were measured under basal conditions, two hours after propranolol ingestion or placebo, then one and two hours after molsidomine or placebo ingestion. TAV and PVBF remained unchanged in patients treated with placebo. Molsidomine reduced TAV by 23.8 +/- 19.5% in group 1 (P < 0.01) and by 25.6 +/- 21.4% in group 2 (P < 0.01). In group 3, a 10% decrease was observed after propranolol (NS). When molsidomine was added, TAV was further decreased (-17.6 +/- 13.3% vs baseline, P < 0.01). PVBF remained unchanged in the three groups of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

The slipping rib syndrome is characterized by upper abdominal pain due to irritation of the intercostal nerve by incomplete dislocation of the costal cartilage of the 8th, 9th, or 10th ribs. Twenty-three new cases are reported and the literature is reviewed. Diagnosis is only clinical. The pain is precipitated by movement and certain postures; it is faithfully reproduced by pressure on one particular point of the costal margin and is relieved by local injection of an anaesthetic. Pain from a slipping rib is usually attributed to visceral causes, which is a source of diagnostic errors.