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Two cases of right hepatic hydrothorax occurring in the absence of clinical ascites are reported. Diagnosis was confirmed by the intraperitoneal and intrapleural injection of radioisotope 99mTc-sulfur colloid that demonstrated the one-way transdiaphragmatic flow of fluid from the peritoneal to pleural cavities. In contrast, radioisotope injected into the peritoneal cavity of 5 patients with pleural effusions secondary to pulmonary or cardiac disease failed to traverse the diaphragm and localize in the pleural space. Medical therapy with salt and water restriction and diuretics resulted in both of the patients with hepatic hydrothorax developing signs of intravascular volume depletion without significant mobilization of the pleural fluid. Thoracotomy allowed identification of the diaphragmatic defects that were repaired by chemical and traumatic pleurodesis followed by postoperative peritoneal and pleural drainage. This therapy resulted in complete resolution of the pleural effusions, which have not recurred despite the subsequent development of clinical ascites in both patients.

To identifiy causative factors responsible for the disseminated intravascular coagulation complicating peritoneovenous (LeVeen) shunts, the ascitic fluid from 12 patients with alcoholic liver disease or peritoneal malignancy was examined for its effects on human platelets. In all patients, concentrated ascitic fluid caused irreversible platelet aggregation. Properties of the aggregating factor suggested that it is collagen, and subsequently, the presence of collagen in ascitic fluid was confirmed. This finding, together with the known effects of collagen on platelets and contact clotting factors, would be sufficient to explain the development of disseminated intravascular coagulation following this procedure. Aspirin by inhibiting collagen-induced aggregation may have a therapeutic role in the management of this problem.

To be maximally effective, antiulcer medications should relieve ulcer symptoms rapidly and promote rapid healing of an ulcer crater; after the cessation of a course of treatment the ulcer should not recur. A wide variety of agents is available. These are of similar efficiency in the control of ulcer symptoms and in the acceleration of the healing of the ulcer crater. However, evidence exists of differences in the rate of the recurrence of duodenal ulcers on the cessation of these drugs. Surface-active agents (bismuth complexes, sucralfate, prostaglandins and carbenoxolone) are consistently superior to H2-histamine receptor antagonist drugs (cimetidine and ranitidine). A high relapse rate produces more patients with active disease at any one time, hence more patients will be exposed to the complications of the disease, and will require active investigation and therapy. Because of the increased rate of relapse, the use of H2-receptor antagonist drugs as first-line intermittent healing therapy can be shown to be associated with an eight-fold (800%) increase in cost of pharmaceutical agents as compared with first-line treatment with bismuth salts; a four-fold increase compared with the cost of using antacid drugs; and a two-fold increase compared with the cost of using sucralfate. When maintenance therapy with H2-receptor antagonist agents is given instead of intermittent therapy with bismuth complexes, a 14-fold increase in pharmaceutical costs is incurred, with inferior results that have already been demonstrated under the conditions of a controlled clinical trial. These considerations of efficacy and cost suggest that H2-receptor antagonist drugs ought not to be first-line therapy for duodenal ulcers; rather, surface-active agents such as colloidal bismuth or sucralfate should be prescribed initially.

Serum C(3) (beta(1C)/beta(1A)) has been measured in normal individuals and the range found is in agreement with findings of other authors (85-370 mg/100 ml). In 18 patients with acute hepatitis and massive necrosis serum C(3) was consistently reduced to below 50% of normal. In other patients with acute hepatitis the serum C(3) concentration was normal. In the majority of the 150 patients with chronic liver disease serum C(3) concentration was normal. However, 10 patients (six with active chronic hepatitis, four with cryptogenic cirrhosis) had hypocomplementaemia. The reason for the depression is not clear but could reflect either decreased synthesis or increased consumption, or a combination of the two.