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In our country liver diseases are frequent and have many different causes. They can often develop into cirrhosis of the liver with mortality beetween 13.5% and 24.5%. Hepatitis B and C-viral infections frequently play a significant role in the recognition of an occupational disease in the case of medical staff, with histological criteria of major importance in this respect. A consequence of cirrhosis of the liver may be the development of hepatoencephalopathia of varying degrees of severity. As it is then likely that a patient will no longer be able to drive motor vehicles, it is important that attending physicians inform their patients accordingly. Liver transplants are an acknowledged method of treatment in the therapy of advanced liver cirrhosis. Rehabilitation shortly after transplantation is highly important to help ensure a speedy return to work. Surprisingly, reintegration is more difficult in patients suffering from alcohol related liver disease than in those with non-alcohol-related liver disease.

Physiology of wound healing especially in its first phase is the basis for understanding application of fibrin sealant. The several components have been reported.

Following single doses of heparin and with continuous heparin infusion the activity of lipase in the serum increases temporarily and can attain pathological values also in healthy persons. Even when the heparin infusion is continued, the lipase values return after at the most 24 hours to the initial value before application of heparin. For a diagnosis of diseases of the pancreas the interpretation of lipase values in serum must consider how long the patient has been treated with heparin.

Heparin is indicated in pulmonary embolism suspicion, in minor and a part of submassive embolism. The dose is 15,000-20,000 U (acute) and 40,000 U/day subsequently. Fibrinolytic therapy with streptokinase or urokinase is indicated in massive embolism. Submassive embolism is treated by fibrinolysis if no contraindications against fibrinolysis are to be registered.

Insulin and C-peptide in venous blood were determined during oral glucose tolerance testing in 59 non-manifest diabetics with histologically established chronic liver disease (fatty degeneration, chronic aggressive hepatitis, cirrhosis). Glucose tolerance was pathologic in 60-80% of patients. When compared to a control group patients with chronic liver disease showed significantly increased values of blood glucose (after glucose intake), of insulin and of C-peptide (fasting and after glucose intake). The C-peptide/insulin ratio, a measure of hepatic insulin degradation, was significantly decreased after glucose uptake. There were no significant differences of blood sugar, insulin and C-peptide among the various liver diseases. In chronic aggressive hepatitis and in cirrhosis the C-peptide/insulin ratio was partly significantly lower than in fatty degeneration. From the increased C-peptide values increased insulin secretion in chronic liver diseases can be deducted. In addition, the decreased C-peptide/insulin ratios show an impairment of insulin degradation in liver cirrhosis and other chronic hepatic diseases. However, in fatty liver degeneration this is clearly less pronounced than in more serious liver diseases.

The radiological and clinical findings of 12 patients with ectopic gastric mucosa in the duodenal bulb are presented. This is a defined disease with characteristic radiological features: multiple small nodular defects of the contrast medium of 1-3 mm diameter. Histology shows complete heterotopia. Pathogenesis and clinical significance are discussed with reference to the literature on this subject.

Disorders of the coagulation system in shock are caused by injuries of the endothelium, influx of thromboplastic material into the blood and stasis. In this way, the intrinsic and the extrinsic system is activated. Fibrin is generated in the blood stream and forms high molecular complexes together with fibrinogen (hypercoagulability). With progress of the shock fibrin can deposit in the small vessels with the consequence of impaired circulation. Finally clotting factors and inhibitors (e.g. antithrombin III) are consumed by disseminated intravascular coagulation. This results in a bleeding tendency (consumption coagulopathy). In this survey particular shock formes (endotoxin induced, cardiogenic, traumatic, hemorrhagic) are discussed with regard to the reflections of the blood coagulation. The therapy of shock-induced disorders of blood coagulation are focused on treatment of primary disease, prevention or elimination of microthrombi, substitution of blood respective plasma components.

In 64 patients suffering from chronic inflammatory liver disease (alcoholic hepatitis, chronic active hepatitis, chronic persistent hepatitis) significantly increased values of blood glucose and insulin, free fatty acids and C-peptide were observed during a 100 g oral glucose load. Fasting values of blood glucose, free fatty acids and C-peptide were also increased, while serum growth hormone remained unchanged. In patients with chronic active hepatitis the C-peptide/insulin-ratio, a measure for hepatic insulin degradation, was significantly lowered after glucose uptake. During oral load there were no discernible differences between the different types of chronic inflammatory liver disease concerning blood glucose, serum insulin and free fatty acids. In normal weight and in overweight patients suffering from liver disease blood glucose and serum insulin values were increased to the same extent. As it is known from the liver cirrhosis chronic inflammatory liver disease lead to an insulin resistance, to which elevated free fatty acid levels contribute. Increased body weight has no influence on the insulin resistance observed in chronic liver inflammation. From the changes of the C-peptide and the C-peptide/insulin-ratio it can be deduced, that the hyperinsulinism in patients with chronic inflammatory liver disease is due to both insulin hypersecretion and diminished hepatic insulin degradation.