Maternal and cord blood complement activity: relationship to premature rupture of the membranes.

Human complement levels are known to reflect the presence of clinical infection, with low levels indicative of increased utilization in the body's immune response. Premature rupture of the membranes (PRM) is associated with an increased maternal-fetal infectious morbidity, yet histopathologic and bacteriologic parameters often do not reflect this. In this prospective study maternal and cord serum total hemolytic complement activity (CH50) was measured in 102 patients without evidence of infection, with and without PRM, to determine if there exists within the maternal-fetal unit an immunologic response to this event. It was found that maternal serum CH50, regardless of length of gestation, is similar to that of the nonpregnant adult population, except in cases of PRM greater than 12 hours in which it is significantly lower. The CH50 in term newborn infants was significantly lower than that of matched maternal samples and dropped with decreasing gestational age. CH50 in cord serum from babies of mothers with PRM failed to show a significant decrease when compared to those of mothers without PRM.

Kinetics of haemolysis by complement. ii.--Development of new equations.

A new quantitative equation was developed by a process of trial and error. This equation, more complex than the classic Von Krogh equation, nevertheless gives a better account of percentages of haemolysis versus quantities of complement. A basic biological unit independent of red corpuscles quantity and sensitivity can be calculated. In addition, variations of the slope coefficient are of interest in pathology. However, the present paper is devoted to "normal" complement kinetics. Time-kinetics were found to follow the rules of general chemistry and could be derived mathematically.

Antibodies to single-stranded DNA: an aid in diagnosis of viral hepatitis.

In clinical and subclinical viral hepatitis a significant increase of antibodies to single-stranded DNA revealed by the prepatent stage of the disease before any elevation of serum transaminases. In type A hepatitis, a rise in anti-DNA titers was detectable one to two weeks before onset of clinical and biochemical signs; in type B hepatitis, the rise of anti-DNA coincided with or preceded the appearance of HBSAg, several weeks before the onset of clinical illness. In both hepatitis types anti-DNA titers reached a peak (640--2,560) at onset and dropped shortly after serum transaminases returned to normal at the end of acute illness. The anti-DNA response in non-A/non-B hepatitis was of similar magnitude. Anti-DNA elevation was the only positive sign found in most silent infections of either type that later showed specific seroconversion. Anti-DNA levels in noninfected contacts were in the same range as those found in a group of health individuals. The anti-DNA test is useful for early diagnosis of viral hepatitis and should be a valuable addition to current epidemiological and clinical procedures.