Liver diseases in pregnancy.

Mild abnormalities of liver function tests are frequently seen in pregnancy but return to normal after delivery. A raised serum alkaline phosphatase is common, along with a decline in the serum albumin, but the aminotransferases remain within normal limits. The physician must interpret abnormal liver function tests in pregnancy with these changes in mind, but most liver diseases in pregnancy result in more marked alterations. Viral hepatitis is the most common cause of jaundice in pregnancy, and the maternal prognosis is generally good. Perinatal transmission of hepatitis B virus is likely when the mother is positive for HBsAg. Concurrent administration of hepatitis B vaccine and HBIG to the infant has an efficacy of 90 per cent in preventing transmission to the infant. ICP is the second most common cause of jaundice in pregnancy. The condition is generally benign, although maternal and fetal mortality occasionally result, probably due to premature delivery and the bleeding tendency of cholestatic patients. Vitamin K administration may correct the coagulopathy, and cholestyramine is effective in controlling pruritus. AFLP is rare but carries a high mortality rate for both the mother and the fetus. Early diagnosis, correction of the coagulopathy, and prompt delivery may improve the outcome significantly. Patients with cirrhosis have reduced fertility, and in those who become pregnant, fetal loss is high. The effect of pregnancy or hepatocellular function is variable, but, when evidence of liver failure is present in the first trimester, termination should be considered. Variceal size and the risk of bleeding may be assessed by endoscopy. Pregnant cirrhotic patients with large esophageal varices and a history of bleeding can undergo shunt surgery. Conservative management may be appropriate for patients with small varices and no history of bleeding.

Autochthonous, allogeneic, and exenogeneic cells as targets for vaccinia immune lymphocyte cytotoxicity.

The cytotoxicity of vaccinia-immune rabbit spleen cells against autochthonous, allogeneic, and xenogeneic vaccinia-infected target cells was studied by using the 51Cr release assay. The results showed that whereas effector cells from rabbit spleen could not lyse the xenogeneic target cells, there was no consistent difference in lysis of autochthonous and allogeneic targets. Antibody-mediated cytotoxicity showed the resistance to cell-mediated lysis in this system not to be the result to reduced virus antigen on the cell surface. The data also showed the established cell line RK13 eas markedly more sensitive to immune spleen cell lysis than short-term rabbit skin fibroblast cultures. The data suggested that it is possible to develop standardized tests to evaluate cell-mediated immunity to virus infections in a noinbred population.

Specific lysis of human colon tumor cells by antibodies to CEA and isoantigen A: dependence on rabbit serum or neuraminidase.

The 51Cr cytotoxicity test was used to measure specific antibody reactions against carcinoembryonic antigen (CEA) and isoantigen A on the surface of human colon tumor cells. When human serum or guinea pig serum was used as a source of complement, no anti-CEA or anti-isoantigen A cytotoxicity was demonstrable despite binding of specific antibodies and activation of complement at least through the C3 component on the cell surface. In contrast, specific anti-CEA and anti-isoantigen A cytotoxicity was demonstrated when rabbit serum was used as a source of complement. Specific antibody-mediated cell lysis was also achieved with guinea pig complement if the cells were treated with neuraminidase before testing. These results support the concept that certain tumor cells have surface properties that render them resistant to immune lysis.

Levels of lysosomal enzymes in tissues of mice infected with Mycoplasma fermentans.

The effects of a toxic dose of Mycoplasma fermentans on levels of lysosomal enzymes in mice were examined. Washed cell suspensions (approximately 10(10) colony-forming units) of a recent isolate of M. fermentans were injected intraperitoneally into 3- to 4-week-old BALB mice, and levels of acid phosphatase and beta-glucuronidase were monitored in liver, spleen, thymus, and serum. Levels of acid phosphatase remained essentially normal, but levels of beta-glucuronidase were markedly evevated in serum and to a lesser extent in liver and thymus. The peak response of serum beta-glucuronidase was noted at 8 h postinjection, with a level of 30 mug of phenolphthalein released per ml per h, representing a six-fold increase over control levels. Pretreatment with BCG did not potentiate the effect as it did with endotoxin. The implication of this increased lysosomal enzyme activity in "lethal toxicity" is that that the increase may be secondary to some other cytotoxic event, or that the affinity of mycoplasmas for biological membranes may be involved. The data suggest that the role of lysosomal enzymes in other models of mycoplasma-induced disease should be evaluated.