Search PubMed⌕ Search

Biomedical subjects

H K Koch

Publications and source records attributed to H K Koch.

At least 37 records · Page 2Linked to original sources
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

Electron microscopic studies on the small intestinal mucosa of rats after mechanical intestinal obstruction and ischemia.

Ultrastructural changes in the small intestine during the early phase following mechanical obstruction were compared with those after vascular ligation. In both experiments (the early phase of mechanical ileus and ischemia) intestinal epithelial cells at the tips of villi showed common features. One of the most significant changes was an alteration in microvilli, with fragmentation into vesicles, narrowing of apical microvilli and decrease in number. The other change was fatty degeneration of the epithelial cells, which was accompanied by vesiculation of smooth endoplasmic reticulum beneath the terminal webs, fat deposition and dilated Golgi complex containing fat. These observations suggest that in the early phase of mechanical ileus, ischemic damage plays an important role.

Animals↗
PubMed1980

[Lymphangioleiomyomatosis. Problems in differential diagnosis, etiology and prognosis (author's transl)].

Four different cases (diffuse interstitial lung fibrosis with leiomyomatosis, Lymphangioleiomyomatosis of the lung, fibroleiomyoma of the lung and adenomyofibroma of the lung) are presented and the differential diagnostic criteria are discussed. On survey of the literature on Lymphangioleiomyomatosis it is concluded that so far this diagnosis seems ill defined. As it cannot be excluded that the cases described so far represent an assortment of various diseases with different etiology, the authors believe that it is impossible to give a reliable statement on prognosis either for the condition in general or for an individual case.

Adult↗
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

Electron microscopic studies on the small intestine of rats after mechanical intestinal obstruction.

The morphologic changes of the small intestine after the mechanical obstruction were studied by light and electron microscopy. After the ligation of the upper small intestine, segments of jejunum, both proximal and distal to the site of obstruction, were removed at intervals varying from 45 min to 24 h. The essential changes were found in the epithelial cells of the tips of villi, and few morphologic differences were recognized between samples proximal and distal to the site of obstruction. The most remarkable changes in the mucosa were the pseudopodlike extension of the cytoplasm, vacuolar alteration of the villus epithelial cells, desquamation of these degenerated cells, and the dilatation of the epithelial intercellular spaces. A few epithelial cells showed hypertrophy of the smooth endoplasmic reticulum. In the submucosa, vascular stasis and edema were observed throughout the course. The mechanism of fluid loss into the intestinal lumen was discussed briefly.

Animals↗
PubMed1978

Adaptive changes of rat liver cells induced by repeated intraperitoneal injections of d-galactosamine. III-Light- and electron-microscopic investigations of hepatocellular cytoplasmic changes.

In rats hepatocellular cytoplasmic changes after daily repeated D-galactosamine (GalN) intoxication--i.e. subacute GalN intoxication--were studied by light and electron microscopy. The number of GalN injections--and thus the days of survival--was between one and 30. The rats were killed six hours after the last GalN injection. Less degenerative changes were found after repeated GalN injections. An increased formation of atypical dense bodies (ADB), a temporary pronounced lipid accumulation and changes of the rough and smooth endoplasmic reticulum were prominent features of subacute GalN intoxication. The implications with respect to a modified GalN action in subacute GalN intoxication are discussed with special reference to biochemical data obtained in the same experimental model (Schuchhardt et al., 1977).

Adaptation, Physiological↗
PubMed1977

Adaptive changes of the rat liver cells induced by repeated intraperitoneal injections of d-galactosamine. II. Light and electron microscopic investigations of hepatocellular nucleolar alterations.

The effects of repeated d-galactosamine (GalN) administration - i.e. subacute GalN intoxication - on rat liver cell nucleoli were examined. After an initial intraperitoneal injection of 375 mg GalN/kg body weight the rats were treated with 250 mg GalN/kg body weight daily at intervals between 24 h and 30 days. The rats were sacrificed six h after the last injection by decapitation. Specimens of liver were studied by light and electron microscopy. According to the nucleolar size three stages were to be distinguished. Stage I: decreased nucleolar size after one injection, stage II: increased and maximal nucleolar size after two to five injections, stage III: slightly increased relatively stable nucleolar size after six and more injections. Fine structural observations suggest a nucleolar hyperfunction in subacute GalN intoxication as well as a minor disturbance of the transcription and the transfer of the nucleolar RNA.

Adaptation, Biological↗