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Biomedical subjects

O Klinge

Publications and source records attributed to O Klinge.

At least 37 records · Page 2Linked to original sources
PubMed1981

Hepatocellular fibrinogen storage in familial hypofibrinogenemia.

In the cytoplasm of hepatocytes of liver biopsy from a 30 year old man, there were proteinaceous inclusions which by use of the peroxidase-antiperoxidase method reacted strongly with antihuman-fibrinogen IgG, but gave a negative reaction with antihuman-alpha-1-antitrypsin IgG and with antihuman-albumin IgG. As shown in the electron microscope, these protein inclusions were composed of densely packed, irregularly arranged tubules of 40 nm diameter. Clinically, the patient and members of his family showed primary hypofibrinogenemia which on the basis of the morphological findings has to be interpreted as the consequence of a disturbance in the secretion of fibrinogen. Besides the well known alpha-1-antitrypsin deficiency, familial hypofibrinogenemia with hepatocellular fibrinogen storage appears to represent another example of a plasma deficiency due to failure of hepatic secretion.

Adult↗
PubMed1981

The significance of serologic, histologic, and immunohistologic findings in the prognosis of 88 asymptomatic carriers of hepatitis B surface antigen.

Eighty-eight asymptomatic carriers of hepatitis B surface antigen (HBsAg) were followed with biochemical, serologic, histologic, and immunohistologic studies over a period of four years. None of the 78 HBsAg carriers with normal or minimally changed liver tissue, antibody to hepatitis B e antigen (HBeAg) in serum, and no intranuclear hepatitis B core antigen (HBcAg) developed a chronic inflammatory liver disease. Four individuals lost circulatory HBsAg, and at least two individuals terminated their HBsAg carrier state. Seven asymptomatic HBsAg carriers with chronic hepatitis were characterized by HBeAg in serum and intranuclear HBcAg. However, three HBsAg carriers with chronic hepatitis and an absence of intrahepatocellular HBcAg were positive for antibody to HBeAg over the observation period. The mechanism that leads to chronic hepatitis in these patients remains to be determined.

Adult↗
PubMed1981

[Hepatic reactions in erythropoietic protoporphyria (author's transl)].

The main hepatic change in erythropoietic protoporphyria is the deposition of protoporphyrin. Brown deposits of this pigment occur in bile canaliculi and ductules, discretely in hepatocytes, and secondarily in macrophages and Kupffer cells. The pigment is deposited in a crystalline form. Under the fluorescence microscope with a mercury maximum pressure burner (HO 50) at a wave length of 380--500 nm, it shows a typical red fluorescence even after paraffin embedding. Its crystalline structure results in a characteristic double refraction under the polarising microscope. Light-microscopically, hepatocellular reactions are characterised mainly by discrete alterations in the ergastoplasm. However, cell damage is indicated by diffusely distributed, hyaline single cell necrosis and by cytolytic piecemeal necrosis at the peripheries of hepatic lobules. Numerous, often disturbed mitoses produce binuclear and multinuclear hepatocytes. The obligatory secretion of protoporphyrin into the bile ducts leads to an alteration in the canalicular and ductular excretion apparatus which involves distinct ductular proliferation and accompanying fibrosis. Piecemeal necrosis is a further consequence of this process. The resulting histological picture is similar to sclerosing cholangitis with which it also has in common the slowly progressive development of hepatic cirrhosis.

Adult↗
PubMed1980

[Types of hepatitis in parenteral opiate addicts (author's transl)].

Fifty drug addicts with parenteral heroin abuse and tentative diagnosis of acute hepatitis were examined by means of biochemical and serological tests and by liver biopsy. Diagnosis of acute hepatitis was confirmed in 23 patients. 12 patients were examined by liver biopsy a second time 2 months to 18 months later, 3 patients underwent liver biopsy three times. In 80% of the patients markers of hepatitis B (HBsAg, anti-HBs and anti-HBc) were found in the sera. There is some evidence of not only hepatitis B, but also hepatitis non-A, non-B in parenteral drug addicts leading to protracted forms of acute hepatitis and chronic hepatitis.

Adolescent↗
PubMed1980

[Drug-induced jaundice].

Cholestasis induced by therapeutic drugs represents only one aspect of the far larger group of post microsomal terminal hepatocellular icterus, which is characterized by alterations of bilirubin excretion as well as of metabolism of bile acids. Drug induced cholestasis represents a special form of facultative toxic hepatosis, the occurrence of which is unpredictable. It is rather unknown where in the system of hepatocellular production and excretion of bile the medicaments in question are inducing lesions. Probably the mechanisms involved are far from being uniform. The possibility of a superordinated genetically caused insufficiency of the hepatocytic apparatus for excretions has to be considered for most cases.

Bile Acids and Salts↗
PubMed1980

Experimental non-A, non-B hepatitis: four types of cytoplasmic alteration in hepatocytes of infected chimpanzees.

On the occasion of an outbreak of non-A, non-B hepatitis in a plasmapheresis centre (81 cases, incubation period: 3--6 weeks) a pool of 12 plasma samples was obtained in the early phase of increasing transaminases. Two chimpanzees were inoculated, each receiving 12 ml of the pooled plasma. After an incubation period of 10--12 weeks a mild non-A, non-B hepatitis developed. Serum transaminases were slightly elevated. Needle biopsies, taken fortnightly, showed a slight activation of Kupffer cells (6--8 weeks), single cell necroses, and infiltration of the portal tracts (10--13 weeks). Electron microscopically four types of cytoplasmic change, were found in hepatocytes and assumed to be specific for the infection, Type I: Sponge-like inclusion (6 weeks after inoculation) composed of a dense matrix and irregularly arranged membranes. Type II: Attaching curved membranes (8 weeks), developing by close apposition of two cisternae of smooth endoplasmic reticulum. Type III: Cylindrical complexes (10 weeks), already described in literature. Type IV: Microtubular aggregates, usually neighbouring type III structures. The findings suggest 1) that the agent of the present infection is, at least in part, identical with that of the long incubation type of experimental non-A, non-B hepatitis, and 2) that ultrastructural alterations may precede manifest hepatitis.

Animals↗
PubMed1976

[The characterization of clinically healthy hepatitis-b-surface-antigen (HBsAg)-carriers. Clinical, biochemical, histiological and immunological investigations in 129 case of a prospective study (author's transl)].

129 blood donors found to be HBsAg-positive on routine testing were studied for evidence of hepatic disease. Twelve had already lost the antigen from the serum when histologically examined. None of these has had clinical or histological evidence of inflammatory liver disease. Two of the 129 patients showed mild icteric hepatitis, cleared the antigen during the follow up and became anti-HBs positive. The remaining 115 patients who appeared clinically healthy and who had no history of previous icteric liver disease remained HBsAg positive during a mean follow up period of 17.3 +/- 3.0 months. Forty patients from these had a normal liver histology and 37 mild to distinct steatosis but no signs of inflammatory liver disease. 11 patients a mild nonspecific mesenchymal activity but no focal necrosis, 16 patients had mild infiltration in portal tracts and a few necrotic parenchymal cells with mesenchymal reaction, 6 patients had chronic persistent hepatitis, 4 chronic aggressive hepatitis, and 1 definite posthepatic cirrhosis.

Adolescent↗
PubMed1976

[Pregnancy induced DNA synthesis in parenchymatous organs of the rat. Autoradiographic investigations following permanent infusion of 3H-thymidine (author's transl)].

Autoradiographic investigations, after permanent infusion of 3H-thymidine during the whole course of pregnancy in 3 to 5 months old white Spraque-Dawley rats of 220-305 g body weight demonstrate an enhanced DNA synthesis in all cell systems tested. 1. In the liver the mean value of the proliferation index in the hepatocytes increases from a control value of 0.7% to 10.4%, in the epithelia of the portal ducts from 6.7% to 42.4% and in the sinus cells from 3.7% to 23.9% at the end of pregnancy. The corresponding values in the pancreas run up to 6.3% (3.4%) in the acinus parenchyma and 19.6% (8.8%) in the islet cells of Langerhans. In the duct epithelia no significant increase of labelled cells can be found. In the kidney, the number of DNA synthesizing tubular cells depends on their localization within the nephron: in the epithelia of the proximal tubulus the proliferation index amounts to 2.7% (0.6%), in that of the distal tubulus to 4.5% (1.4%). The highest percentual increase in comparison with the control animals results in the proximal tubular epithelia of pregnant rats. The cells of the glomerula are practically uninvolved. 2. The enhanced proliferation may rest on the influence of hypophysial or placental hormones--especially of somatotropins--as well as on an intensified function of the organs during pregnancy. Both hormonal and functional stimuli are closely mixed up in their significance for the pregnancy-induced DNA syntheses, accordingly their effect cannot be separated exactly. The hormones seemingly represent the inducing factor for the increased DNA syntheses during pregnancy which is realized in a variable amount within the organs depending on their different functional enhancement. 3. The increase of the proliferation indices ranges considerably from individual to individual, but within one single animal all cellular systems are afflicted in the same way. The individual ranges of the proliferation rates within the organs are directly proportional to the weight of the offsprings and indirectly proportional to the weight of the mother. The only exception of this is in the proximal tubular epithelium of the kidney. The important influence of adaptation drocesses to the enhanced function of an organ during pregnancy is emphasized by this fact.

Animals↗