Given the high prevalence of chronic hepatitis C virus (HCV) infection, its clinical sequelae account for a significant proportion of patients presenting to gastroenterologists and hepatologists. Whereas the hepatic manifestations of hepatitis C are well described, including hepatitis, cirrhosis, and the development of hepatocellular carcinoma, the extrahepatic manifestations, though common, are less well appreciated. Although nonspecific, fatigue and arthralgias are very common in those with chronic hepatitis C. Extrahepatic syndromes have been reported in as much as 36% of HCV patients, but the exact prevalence is not known. Patients with these syndromes can be divided into those with a high degree of association and those with a more moderate or mild association with HCV. The most prevalent extrahepatic diseases with the highest degree of association with HCV are the essential mixed cryoglobulins with skin, neurologic, renal, and rheumatologic complications. Non-cryoglobulin diseases with a less definite relationship to HCV include systemic vasculitis, splenic lymphoma, porphyria cutanea tarda, and the sicca syndromes. This article highlights the pathophysiology and clinical manifestations of these disorders.

Basal gastric secretion of rats with chronic fistulas was studied before and after adrenalectomy or sham operation. A marked exponential fall in concentration and output of free and total acid resulted in virtual anacidity within 3–7 weeks following adrenalectomy. Failure in parietal cell secretion was not accompanied by significant decrease in parietal cell mass. Pepsin concentration and output as well as volume also fell exponentially but more gradually. No significant change in total chloride concentration occurred. Relative influence of concentration in determining output was 30 times greater than volume for free acid, 3 times greater for total acid, and twice as great for pepsin. Volume was responsible for almost all variability in total chloride output. Time after adrenalectomy influenced variability of volume and acid output twice as much as concurrent decrease in body weight.

No abstract

1have clinical significance which is being evaluated currently. Other efforts are being directed toward isolation and identification of the diffusible substance and the plaque material which it produces and an elucidation of the specific substrates involved.The diffusible substance that activates production of the red band differs from the substance that produces the plaque material. This is demonstrated by the fact that whereas all the bloods used for preparation of the media were able to act as substrate for the red band, a few did not act as substrate for production of plaques.Summary. Macroscopically visible lipid plaques were produced on the surface of human blood agar plates and on 10% plasma agar plates when they were inoculated centrally with certain strains of coagulase-positive S. aureus or exposed to active sterile agar segments ( ASA) . Similar lipid plaques covered the surface of liquid media containing plasma when activated sterile agar segments were suspended in the media. Staphylococ-cus antitoxin prevented the appearance of the lipid plaques. The lipid plaques consist primarily of octadecenoic acid, both free and in triglycerides. Lesser amounts of stearic, palmitic and various shorter chain acids are also present. The most likely explanation for the phenomenon is that a lipase released by certain strains of staphylococci acts upon the lipids in human plasma.

N-methyl-N'-nitro-N-nitrosoguanidine (NG) in drinking water (83 mg/l) results in a high incidence of gastric adenocarcinoma in random-bred Wistar rats. When NG was discontinued after 25 weeks, 61% of animals developed cancer and after 52 weeks the incidence was 73%. In a Wistar-Mai-Furth group (39th generation) invasive adenocarcinoma was found in 12% of rats ingesting NG for 25 weeks and in 10% exposed for 52 weeks. No adenocarcinomas and only two sarcomas were found in 50 Buffalo-Mai rats (56th generation) receiving NG for 52 weeks. Varying the dose and frequency of NG administration did not overcome host resistance. Host resistance to gastric adenocarcinogenesis induced by NG may represent a new advantage of this animal model.