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Biomedical subjects

R Lesch

Publications and source records attributed to R Lesch.

At least 19 recordsLinked to original sources
PubMed1990

Immunohistochemical localization of thromboxane synthase in human tissues.

Thromboxane A2 is formed mainly in platelets where we have isolated thromboxane synthase as a cytochrome P450-like haemoprotein. A rabbit antiserum prepared against this enzyme was monospecific according to Western blot analysis and was used for immunostaining of human tissues. In liver the Kupffer cells were clearly stained and in the connective tissue, histiocytes and monocytic cells were positive. In lung, alveolar macrophages contained most of the enzyme, whereas Type I and II cells were negative. Kidney mesangial cells were stained and in lymphatic tissue dendritic reticular cells as well as invading macrophages were positive. These were also seen in the crypts of tonsils and surprisingly also the epithelium. Placenta again showed staining of the Hofbauer cells and of the endothelial lining of the vessels. Umbilical cord and uterus only contained weak antigenicity in dendritic cells.

Female↗
PubMed1984

Budd-Chiari-Stuart-Bras syndrome: clinical, sonographic, radiological reexaminations in occlusive diseases of hepatic veins.

Ten patients with clinically and histologically verified Budd-Chiari-Stuart-Bras Syndrome (i.e. occlusive disease of small or large efferent hepatic veins) were re-examined, the examination also including combined ultrasonography and computed tomography. These non-invasive methods help to establish a quick diagnosis by locating and defining the most severe changes, by helping to select the most appropriate invasive diagnostic procedure, and by defining their topographical target. They thus facilitate immediate, optimal therapy. The disease process often starts in the right dorsal lobe of the liver and may cause extreme hyperplasia of the left or middle lobes, causing gross changes in the shape of the liver and considerably displacing the gallbladder in some cases. Thrombosis of the portal vein and pulmonary embolism seem to be most frequent complications or accompanying diseases. We therefore suggest immediate long-term anticoagulation, provided portal hypertension is not too severe; patients with severe portal hypertension should undergo a shunt operation. Our patients were followed up for periods ranging from 3 to 8 years. The very variable prognosis includes complete cure and good compensation over a long period and appears to be much better than has been reported by some authors.

Adult↗
PubMed1982

Follow-up of treated adult celiac disease: clinical and morphological studies.

A follow-up study of 18 patients with celiac disease is reported. Adherence to the diet, blood chemistry and serum amino acid concentration were investigated in all patients. In addition, HLA blood group typing was performed. Ten patients agreed to undergo jejunal biopsy, xylose test and X-ray of the small intestine. The jejunal mucosa showed no complete restitution even in patients on a strict diet and function tests were abnormal, too. In this study HLA typing demonstrated an association with HLA-B8, HLA-DR3, and HLA-DR7. The results of the follow-up study are discussed with special reference to therapeutic aim and definition of therapeutic success of the gluten-free diet. In addition, a case of jejunal adenocarcinoma complicating celiac disease is presented.

Adenocarcinoma↗
PubMed1980

[Non-tropical sprue discrepancy between clinical and biopsy findings. Five years' observation of a case (author's transl)].

After doagnosis and establishment of an appropriate diet a 51-year-old female patient with coeliac disease, who was critically ill in the beginning, became symptomless; nevertheless, a five year follow-up study with mucosa biopsies reveals a persisting villous atrophy with hyperplastic crypts ("flat mucosa"). This discrepancy between clinical and histological findings is discussed and it is emphasized that for coeliac patients a strict adherence to a gluten-free diet and bioptic supervision of therapy are essential. Treatment aimed solely at abolishing the clinical symptoms obviously bears the risk of a persisting symptomless illness and the danger of late complications.

Biopsy↗
PubMed1980

[Oral contraceptives and benign tumorous conditions of the liver (author's transl)].

Tumorous lesions of the liver were diagnosed by means of angiography, sonography and laparoscopy in six patients on oral contraceptives for a long time. These lesions were identified as liver cell adenoma (1), focal nodular hyperplasia (4) and cavernous hemangioma (1). The relationship between oral contraceptives and liver disorders is well-known. All cases of focal nodular hyperplasia show vascular alterations which may be important in the discussion of oral contraceptives being responsible. In contrast to liver cell adenoma and hemangioma, focal nodular hyperplasia may be considered as a nodular reparative regeneration of the parenchyma following focal parenchymal necrosis due to segmental vascular occlusion (i. e. thrombosis or fibrotic intimal obliteration). This lesions can therefore not be defined as a true neoplasm. The clinical findings are uncharacteristic, whereas selective hepatic artery angiography, shows typical features that distinguish liver cell adenoma from focal nodular hyperplasia. Regular medical examinations are recommended for women on continuous oral contraceptives for more than five years, because this group of patients is threatened by serious sequelae including intrahepatic and abdominal hemorrhage.

Adenoma↗
PubMed1979

Consequences of recurrent phosphate trapping induced by repeated injections of 2-deoxy-D-galactose. Biochemical and morphological studies in rats.

2-Deoxy-D-galactose, in a dose of 3 mmol/kg, was administered intraperitoneally twice daily to young rats for periods up to 12 weeks. This dosage schedule resulted in recurrent phosphate trapping predominantly in liver. UTP deficiency was excluded by simultaneous uridine injections. Phosphate trapping was caused by the rapid accumulation of 2-deoxy-D-galactose 1-phosphate and was most pronounced in liver but also demonstrated in small intestine, brain, spleen, and thymus. The marked, although transient, drop in the hepatic content of inorganic phosphate triggered the catabolism of adenine nucleotides and a loss of ATP. Other metabolic pathways affected by phosphate deficiency include glycogenolysis and glycolysis. Increasing with time, repeated doses of the galactose analog led to retardation and arrest of growth, hepatomegaly, and splenomegaly. The average relative liver and spleen weights were elevated 2.5- and 4.5-fold, respectively, after 12 weeks of treatment. Liver damage was indicated by hyperbilirubinaemia and a progressive rise in the activity in plasma of sorbitol dehydrogenase, alkaline phosphatase, and gamma-glutamyltransferase. Examination by light and electron microscopy showed increasing numbers of vacuoles, surrounded by a single membrane, in hepatocytes, sinusoidal endothelial cells, and Kupffer cells. Focal cytoplasmic degeneration in hepatocytes was occasionally indicated by formation of autophagic vacuoles and finger print lysosomes. Hepatocytes of 2-deoxy-D-galactose-treated rats showed a dissociation and fragmentation of the rough endoplasmic reticulum. Sinusoidal endothelial cells and Kupffer cells were markedly enlarged, the latter contained a PAS-positive but amylase resistant substance. Extrahepatic changes included an increased occurrence of vacuolated cells in thymus. Phosphate trapping and its metabolic consequences are common phenomena in the experimental injury induced b 2-deoxy-D-galactose and in some hereditary diseases such as uridylyltransferase deficiency galactosaemia, fructose intolerance and glucose-6-phosphatase deficiency.

Animals↗
PubMed1979

Histochemical studies on carbohydrate metabolism in rat liver after galactosamine administration.

The development of hepatitis, induced in 48 rats by the administration of galactosamine (GalN) in varying doses, was studied with the use of substrate and enzyme histochemical techniques. The so-called atypical glycogen, which is at first highly resistant to diastase, was shown to be digestible after deamination. The increasing accumulation of atypical glycogen during the course of GalN-hepatitis conceals the loss of normal glycogen when the PAS-reaction is used. Nevertheless glycogenolysis could also be demonstrated by the increasing activity of phosphorylase. The acid phosphatase activity was progressively diminished, which was interpreted as signifying early lysosomal damage. G6Pase activity remained nearly constant but SDH showed a decrease in activity after 12 h. These histochemical results are considered to provide deeper insight into the pathological mechanism of GalN-hepatitis.

Acid Phosphatase↗
PubMed1979

[Hypernephroma in a pelvic kidney. Diagnostic problems during angiography (author's transl)].

A hypernephroma in a pelvic kidney of a 54-year-old patient is described, which could not be demonstrated angiographically. This is explained by marked compression of the kidney because of the limited available space and the pressure of the surrounding organs. There was also histological proof of advanced intimal fibrosis in the artery and extensive obstruction of the vein by tumour, leading to diminished circulation of blood. The extreme rarity of hypernephromas in pelvic kidneys is stressed; this is barely mentioned in the literature.

Adenocarcinoma↗