[Alcoholic fatty liver, alcoholic hepatitis and alcoholic cirrhosis. Drinking behavior and incidence of clinical, clinico-chemical and histological findings in 282 patients]. / Alkoholfettleber, Alkoholhepatitis und Alkoholzirrhose. Trinkverhalten und Häufigkeit klinischer, klinisch-chemischer und histologischer Befunde bei 282 Patienten.

Drinking pattern as well as clinical, biochemical and histological findings were recorded of 282 males with alcohol-induced liver disease (fatty liver in 103, hepatitis in 61, cirrhosis in 118). The proportion of persons under 50 years of age was significantly greater with alcoholic hepatitis (70%) than cirrhosis (46%). Mean daily alcohol consumption was clearly lower among those with fatty liver than hepatitis or cirrhosis (P less than 0.02). Duration of alcohol abuse was on average shorter in patients with fatty liver and hepatitis than with cirrhosis (excessive consumption of less than 15 years was 61% and 62%, respectively, in the former, 28% in the latter (P less than 0.02). Symptoms and clinical and biochemical findings did not help in differentiating between hepatitis without cirrhotic change and cirrhosis. The most marked differences between cirrhosis and hepatitis, on one hand, and fatty liver, on the other, related to the frequency of certain signs and symptoms: upper abdominal pain, hard consistency of the liver, generalized jaundice, bleeding from esophageal varices and ascites; among biochemical findings they were: elevation of serum-bilirubin concentration above 34 mumol/l (2 mg/dl), lowering of the Quick values and of albumin concentration. Mortality rate during hospital stay was lower among patients with hepatitis but no cirrhotic change (6.6%) than among those with cirrhotic change (31.4%). While the prognosis under abstinence was relatively more favourable in patients with mild or moderately severe hepatitis, nonicteric forms require closer attention than has been given them so far.

Jejunal microflora in patients with chronic alcohol abuse.

The types and numbers of bacteria were examined in aspirates from the jejunums of 27 chronic alcoholics and 13 hospitalized control patients of comparable age distribution without alcohol abuse or diseases of the liver. Samples of jejunal juice were aspirated in the fasting state. The mean number of microorganisms obtained during anaerobic incubation was distinctly higher in the alcoholics (log10, mean +/- SD: alcoholics 4.9 +/- 2.2, controls 3.2 +/- 1.5, p less than 0.025). A similar difference was found for the number of aerobic bacteria (alcoholics 4.7 +/- 1.9, controls 3.3 +/- 2.1, p less than 0.05). Significant counts (greater than 10(5)/ml) of bacteria obtained during anaerobic incubation were more frequent in the alcoholics (48.1%) than in the controls (7.6%, p less than 0.001). Coliform microorganisms were cultured much more frequently from the jejunal fluid of the alcoholics (alcoholics 55.6%, controls 15.4%, p less than 0.025). In addition the incidence of Gram-negative anaerobic bacteria and endospore-forming rods was higher in the aspirates from alcoholics (p less than 0.05). In both groups the number of microorganisms in jejunal fluid correlated closely with the pH found in the gastric juice. No correlation was found between the numbers or types of microorganisms in the jejunum and the type or degree of liver disease in the alcoholics. It is concluded that bacterial overgrowth might contribute to functional and/or morphological abnormalities of the small intestine commonly found in patients with chronic alcohol abuse.

[Liver fibrosis. 2]. / Die Leberfibrose Teil 2.

The mortality of liver cirrhosis has doubled during the past two decades and is still increasing in most of the European countries. One important feature and precursor of liver cirrhosis is liver fibrosis. Its aetiology includes a wide spectrum of well known causes, in Europe most frequently alcohol, virus infection, and chemical agents. The pathomechanism of liver fibrosis is unknown. Diagnostic and therapeutic approaches for early detection and treatment have been recently developed applying the results of pathobiochemical, cellular and clinical research. The composition of the excess hepatic connective tissue suggests the involvement of myofibroblasts and shows similarities to atherosclerotic plaques and lung fibrosis. The isolation, purification and cultivation of cells from liver biopsies offers new avenues for the study of fibroplastic cells. Clinical studies are now facilitated, since products of the collagen synthetic pathway - procollagen peptides - can be measured in serum with a sensitive radioimmunoassay. Further prospective studies including additional parameters of fibroplasia, such as N-acetyl-beta-D-glucosaminidase, lysyl-oxidase and prolyl-hydroxylase will have to demonstrate the diagnostic value of such methods. Even today, they should be applied in therapeutic trials of chronic fibrotic liver diseases. Better knowledge of the molecular regulation of connective tissue and the use of new animal models and cellular systems support a successful search for new therapeutic tools. Above all, limitation of alcohol consumption, vaccination for viral hepatitis and elimination of chemical agents offer the prevention of fibrosis, which calls for major efforts on a nation-wide scale.

[Liver fibrosis. 1 (author's transl)]. / Die Leberfibrose Teil 1.

The mortality of liver cirrhosis has doubled during the past two decades and is still increasing in most of the European countries. One important feature and precursor of liver cirrhosis is liver fibrosis. Its aetiology includes a wide spectrum of well known causes, in Europe most frequently alcohol, virus infection, and chemical agents. The pathomechanism of liver fibrosis is unknown. Diagnostic and therapeutic approaches for early detection and treatment have been recently developed applying the results of pathobiochemical, cellular and clinical research. The composition of the increased hepatic connective tissue suggests the involvement of myofibroblasts and shows similarities to atherosclerotic plaques and lung fibrosis. The isolation, purification and cultivation of cells from liver biopsies offers new avenues for the study of fibroplastic cells. Clinical studies are now facilitated, since products of the collagen synthetic pathway -- procollagen peptides--can be measured in serum with a sensitive radioimmunoassay. Further prospective studies including additional parameters of fibroplasia, such as N-acetyl-beta-D-glucosaminidase, lysyloxidase and prolylhydroxylase will have to demonstrate the diagnostic value of such methods. Even today, they should be applied in therapeutic trials of chronic fibrotic liver diseases. Better knowledge of the molecular regulation of connective tissue, and the use of new animal models and cellular system support a successful search for new therapeutic tools. Above all, limitation of alcohol consumption, vaccination for viral hepatitis and elimination of chemical agents offer the prevention of fibrosis, which calls for major efforts on a nation-wide scale.

[Prenatal diagnosis of alpha-1-antitrypsin phenotype. Case record and prognosis in severe alpha-antitrypsin deficiency Pi ZZ (author's transl)]. / Pränataler Ausschluss eines Alpha-1-antitrypsinmangels. Kasuistik und Prognose bei Phänotyp Pi Z.

A mother had a child with cirrhosis of the liver and alpha-1-antitrypsin deficiency. In a subsequent pregnancy the fetal phenotype Pi MZ was detected by isoelectrofocusing in the amniotic fluid. Quantitative assay of alpha-1-antitrypsin gave results in the normal range. Umbilical vein blood analysis confirmed the antenatal findings. In this case it has been possible to rule out the disease before birth. In this context the clinical importance of alpha-1-antitrypsin deficiency is stressed, its frequency in the European and North-American population and the prognosis with phenotype Pi Z.

Adaptative changes of activity of enzymes involved in fructose metabolism in the liver and jejunal mucosa of rats following fructose feeding.

The adaptative response of a diet containing 60% fructose on the activity of those enzymes which are involved in the metabolism of fructose was measured in the liver and in the jejunal mucosa of rats over a period of 12 days. Control animals received isocaloric amounts of glucose or starch. Under fructose feeding there was a marked increase in the activity of fructose-1-phosphate aldolase (3-fold), ketohexokinase (2--3-fold), and triokinase (3-fold) in the jejunal mucosa. In the liver, however, a significant increase in enzyme activity could only be seen for triokinase (2--3-fold), whereas the activity of the other enzymes measured were only slightly or not at all altered. The activity of the three enzymes mentioned above were elevated to a maximum within 3 days after feeding the fructose diet. In the following time of observation no major further changes occurred. The results show that fructose feeding in comparison to a glucose or starch containing diet leads to a marked adaptative increase in the activity of those enzymes, which are involved in the breakdown of fructose, only in the jejunal mucosa.