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Inflammatory cartilage destruction in chronic arthritides is usually regarded as the process owing to chondrocytic chondrolysis or ingrowth of pannus tissue. Besides these two mechanisms a third one-cartilage degradation directly mediated by polymorphonuclear granulocytes (PMN's) of the synovial fluid-seems to be underestimated. There is growing evidence that PMN's are involved in several non-bacterial organ destructions (e.g., alcoholic hepatitis); thus, two case reports are presented demonstrating cartilage destruction by PMN's via the synovial fluid. It is shown by light and electron microscopy that in florid rheumatoid arthritis, PMN's from the inflamed synovial fluid can gain access to the cartilaginous surface. The adherence of PMN's to the superficial matrix, eventually mediated by immunocomplexes, may activate these cells with the subsequent secretion of destructive enzymes as well as reactive oxygen species. Cartilage degradation may be the consequence. From the morphological findings it is deduced that this mechanism may have important implications for inflammatory cartilage loss.

Alcoholic hepatitis is defined by histological findings, i.e. Mallory bodies, necrosis and polynuclear infiltration. It may be accompanied by steatosis and more or less advanced fibrosis. The clinical picture is variable, ranging from a total absence of symptoms to high fever, jaundice and encephalopathy. Laboratory findings reveal high polynuclear white cell counts, SGOT (but not SGPT) and glutamate dehydrogenase levels. The prognosis varies according to the series studied. The pathogenesis is unclear but cellular and humoral immunity mechanisms may play a role. Therapeutic possibilities are limited, corticosteroids only being useful in very serious cases. Alcoholic hepatitis is not a nosological entity but an acute inflammatory reaction of the liver due to cell necrosis caused by alcohol, and can therefore occur at any stage of alcoholic liver.

The study Hepatitis-B-virus infection was performed in the population of chronic alcoholics (224 persons). Among this population the HBs-antigenemia was proved in 42%. The immunoglobulin dysproteinemia and coexistence of autoantibodies can indicate a symptomatic Hepatitis-B-virus infection.

Serum interferon activity was measured in 40 patients with acute viral hepatitis A, B and non-A-non-B during the acute stage of the disease and correlated with the severity, the long-term outcome and the viral etiology of the disease. Patients with alcoholic hepatitis, patients with an influenza-like illness and healthy volunteers served as controls. 80% of all patients with virus hepatitis revealed no measureable or only borderline interferon activity in their serum. No correlation was found with severity and long-term outcome of the disease, but patients with virus hepatitis A showed a stronger interferon induction than patients with hepatitis B and non-A-non-B. Further investigations of the interferon system in patients with virus hepatitis might help to improve our understanding of the different forms of the disease. The data presently available, however, do not permit as yet to define the value of interferon in the treatment of severe forms of acute virus hepatitis.

Acetaldehyde in non-toxic doses (15.6 micrograms per start) causes in the inhibition test of the migration of leucocytes an inhibition of the migration in 6/13 of the patients with alcoholic hepatitis, a stimulation of the migration in 6/11 of alcohol cirrhoses. Healthy (n = 16) persons, patients with alcoholic fatty degeneration of the liver (n = 3) as well as non-alcoholic liver diseases (chronic persisting hepatitis, n = 11; chronic active hepatitis, n = 8, cirrhosis, n = 7) did not show this cellular immune reagibility. The inhibition of the migration and the stimulation of the migration, respectively, might develop by hapten autoantigen complexes (altered cytoskeleton?) with release of the factors of inhibition of migration and stimulation of migration, in which case the role of a hapten belongs to acetaldehyde. The results of the tests did not correlate with functional and histological findings of the liver, with the actual consumption of alcohol and also not with haptoglobin phaenotypes. When it is postulated that by acetaldehyde also the release of further lymphokines is mediated, origin and progression of alcoholic hepatitis and alcoholic cirrhosis might be explained immunopathogenetically.