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We evaluated liver function and coagulation parameters in 117 patients with spontaneous intracerebral hemorrhage (68 men and 49 women) admitted to our clinic within 24 hours after onset. Liver dysfunction was more common among men than women due to differences in alcohol consumption. Number of thrombocytes and fibrinogen concentrations were lower, especially among men with elevated concentrations of glutamic oxaloacetic transaminase or glutamic pyruvic transaminase and/or elevated gamma-globulin fraction. Five of the 78 patients undergoing stereotactic hematoma aspiration and one of the 39 treated nonsurgically rebled. All six of the patients who rebled were men, heavy alcohol consumers with liver dysfunction. Fibrinogen concentration was abnormally low in four of the six and at the lower end of the normal range in one. Two showed thrombocytopenia and one case showed prolonged prothrombin time. These facts suggest that liver disorders produce a state in which hemorrhage occurs more readily and that this hemorrhagic tendency may be one of the causal factors of spontaneous intracerebral hemorrhage.

In a retrospective study, we review here the clinical presentation of patients with the biphasic form of hepatitis A, a variant of viral hepatitis characterised by an increase in ALAT levels after an initial recovery in clinical condition and laboratory tests. Twenty-one patients were diagnosed as having a biphasic form; they represent about 10% of a selected population of hepatitis A cases. Six patients were asymptomatic. Eleven patients were jaundiced, nine of them showing a "cholestatic" pattern. The second phase of the disease had a more protracted course and displayed higher ALAT levels than the first phase. The total duration of the disease was 120 +/- 28 (mean +/- SD) days, and its course was benign.

Two types of gammaG4 proteins, termed 4a and 4b, were characterized through antigenic studies of myeloma proteins. Both were recognized by specific antigens on the Fc fragment which were shared with other gammaG classes. The distinctive antigen of the common 4a type was shared with all gammaG1 and gammaG3 proteins but missing in those of the gammaG2 class; that for the rarer 4b type was selectively found in proteins of the gammaG2 class. Analyses on gammaG4 fractions isolated from normal sera showed that either the 4a or the 4b or a mixture of the two types was present in each serum. Evidence was obtained that these differences were on a genetic basis and that allelic genes linked to those of the Gm system were involved. Such a reciprocal occurrence in other classes of gammaG globulin of the antigenic markers distinguishing genetic variants has not been observed previously. A number of questions regarding the evolutionary development of the genes responsible are discussed. The possibility is raised that those for the gammaG4 class arose relatively early and preceded the development of those for the other gammaG classes.

Experiments were done to investigate mechanisms of appearance of both 7 S and 11 S IgA in nasal secretions. Three IgA preparations, (a) 11 S IgA from nasal secretions, (b) 7 S IgA from homologous serum, and (c) 7 S IgA from autologous serum, were isolated, labeled, and injected intravenously into volunteers. The rate of disappearance from plasma and the extent and nature of their appearance in nasal secretions were examined in detail. After intravenous injection, 11 S IgA from nasal secretions disappeared rapidly from plasma. However, only negligible amounts of 11 S IgA were detected in nasal secretion, which suggested that rapid selective secretion of circulating 11 S IgA does not occur as a mechanism of IgA accumulation in nasal secretions. Both the homologous and autologous 7 S IgA preparations disappeared from plasma at a normal rate, and both appeared in nasal secretions unchanged in sedimentation behavior. The specific activity of IgA in nasal secretions, when related to the total IgA concentration, was about 30-fold less than that in serum. When related to only the 7 S IgA concentration of nasal secretions, the specific activity was about one-half that of serum. These studies are consistent with the following hypotheses: (a) circulating 7 S IgA is a source of part of the 7 S IgA found in nasal secretions. The remainder of the nasal secretion 7 S IgA may be synthesized locally in the tissues of the upper respiratory tract; (b) 11 S IgA in nasal secretions is not assembled from serum 7 S IgA components; and (c) 11 S IgA in nasal secretions is synthesized de novo in the tissues of the upper respiratory tract.