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Biomedical subjects

H K Koch

Publications and source records attributed to H K Koch.

At least 19 recordsLinked to original sources
PubMed1992

Serodiagnosis of Helicobacter pylori infections with an enzyme immunoassay using the chromatographically purified 120 kilodalton protein.

A membrane-associated 120 kDa protein of Helicobacter pylori with known species-specificity was isolated and used in an enzyme immunoassay (EIA) for the detection of Helicobacter pylori-specific IgG antibodies in patient sera. The EIA was compared with two other methods used for serodiagnosis of Helicobacter pylori infections: an EIA using sonicated whole Helicobacter pylori cell antigen and Western immunoblot. In a prospective study 127 unselected patients (76 patients with antrum gastritis, 51 patients without gastritis) who underwent gastroscopy were studied histologically and serologically. The EIA using the purified 120 kDa protein had the highest specificity (92%) compared with the EIA using a whole cell sonicate of a single Helicobacter pylori strain as antigen (60.7%) and the immunoblot (90.2%). The sensitivity was 96%, 100% and 92%, respectively. Sera of three control patients reacted strongly in all three methods, indicating possible Helicobacter pylori infection with negative histological findings. The EIA using the 120 kDa protein as antigen was shown to be a specific and sensitive technique for the serodiagnosis of Helicobacter pylori infections.

Adult↗
PubMed1991

A simple and rapid method for the detection of RNA in formalin-fixed, paraffin-embedded tissues by PCR amplification.

A simple and rapid method for the extraction, reverse transcription and PCR amplification of RNA from formalin-fixed, paraffin-embedded tissue is described. The procedure can be completed within 24 hours. In a first application of this method we detect human albumin mRNA in liver tissue, demonstrating the feasibility to retrospectively analyze gene expression and RNA viruses in fixed tissue.

Albumins↗
PubMed1990

An evaluation of gastric dysplasia in the years 1986 and 1987.

Since the fate and significance of gastric mucosal dysplasia is still largely unknown we have started a follow-up study for patients with dysplasia in the years 1986 and 1987. In this paper the short term results are reported. Dysplasia grade II was found in 2% of all patients and dysplasia grade III in 0.5%. The following results suggest a close-possibly sequential relationship of dysplasia and gastric cancer: dysplasia and gastric cancer are preferentially located in distal parts of the stomach; sex distribution of dysplasia and gastric cancer (especially intestinal type) are similar; considering the mean age of patients with dysplasia or gastric cancer we have observed that patients with dysplasia II were younger than patients with dysplasia III and both were younger than patients with gastric cancer of the intestinal type; during the short term follow-up (12-24 months) 4-8% of patients with dysplasia II and 18-20% of patients with dysplasia III showed a progression; of 26 carcinomas detected by follow-up of patients with dysplasia III 10 were early gastric cancer, 11 resectable with curative intent, 2 were metastatic and 3 without sufficient information for staging. We conclude therefore that gastric dysplasia is probably a true precancerous lesion that helps to identify high risk patients and thus contributes to the objective of an early diagnosis of gastric cancer.

Aged↗
PubMed1990

Malignant pleural mesothelioma: some aspects of epidemiology, differential diagnosis and prognosis. Histological and immunohistochemical evaluation and follow-up of mesotheliomas diagnosed from 1964 to January 1985.

64 diffuse pleural mesotheliomas diagnosed between 1964 and January 1985 at the Institute of Pathology of the University of Freiburg were analyzed. Since 1980 an increase from one case to 10 cases per year has been observed. The tumor was 3 to 4 times more frequent in men than in women. The age distribution showed a peak between the age of 50 and 60. In 26 cases evidence of exposure to asbestos was detected. In one patient radiotherapy of Hodgkin's disease may have been of etiological significance. The median survival time was 13 months. The five-year survival rate was only 4%. Histologic reevaluation was only possible in cases diagnosed after 1975. Of 43 cases thus evaluated 26 were pure mesothelial, 15 biphasic and 2 of the spindle-cell subtype. A median survival time of 23 months for pure mesothelial mesothelioma in comparison to 13 months for the biphasic mesothelioma indicated a better prognosis for pure mesothelial mesothelioma. Although no other primary tumors were detected, in 10 cases the differential diagnosis of adenocarcinoma had to be considered, and in 3 cases tumors of non-epithelial origin had to be excluded. 35 of 43 mesothelioma were CEA-negative, 38 out of 43 cytokeratin-positive, and 33 out of 43 were EMA-positive. Factor-VIII-related antigen was not demonstrated. 12 of 43 mesotheliomas showed PAS-positive staining, 29 of 43 were stained with Alcian blue. 7 of these 29 showed a positive digestion with hyaluronidase. Although CEA may not be negative in every mesothelioma, this marker seems to be a valid tool for the differential diagnosis of adenocarcinoma. In order to safeguard against a mistaken diagnosis of pleural mesothelioma, the exclusion of other tumors is always indispensable.

Adult↗
PubMed1990

Prevalence of Campylobacter pylori as demonstrated by histology or CLO-test in different types of gastritis. A study in 5 clinically predefined groups of patients.

The prevalence of Campylobacter pylori infection as detected by histology was studied in 5 predefined groups of patients. The associated histologic and endoscopic findings were registered. Validity of CLO-test was tested against the histologic detection. The following groups of patients were studied: A) Non-ulcer dyspepsia (defined by one or all of three symptoms: heartburn, nausea/inappetence, halitosis/belching) B) control group (no specific symptoms, no ulcer, no history of gastric surgery) C) Duodenal ulcer D) Gastric ulcer E) Billroth I or II resection of the stomach. 200 patients were recruited for group A-C, in group D 134 patients and in group E 113 patients were studied. A mean prevalence of 60% was observed. Prevalence was highest in patients with duodenal ulcer (86%). In group D a prevalence of 65%, in A and E a prevalence of 54%, and in B of 40% were seen. The overall test sensitivity of the CLO-test compared against the histologic detection rate was 75%, the specificity 81%. Sensitivity was reduced in group A (69%) and E (53%) and in patients with inactive chronic gastritis (67%). In all groups patients with active forms of gastritis showed the highest prevalence of C. pylori infection. The specificity of the CLO-test was reduced in patients with duodenal ulcer (46%) and gastric ulcer (48%). Decreased specificity observed after therapy with histamin receptor (H2) blockers may explain this finding. The relationship of C. pylori infection with active types of gastritis or gastro-duodenal ulcer hints at a causal relation but is no definite proof of its etiologic role. The validity of the CLO-test seems questionable in patients with gastroduodenal ulcer or operated stomach.

Antacids↗
PubMed1986

Benign circumscribed lesions of the liver diagnosed by ultrasonically guided fine-needle biopsy.

Cytologic evaluation of aspirates obtained by ultrasonically guided puncture of circumscribed lesions leads to the diagnosis of a malignant lesion when tumor cells are detected. In the absence of tumor cells, it remains uncertain whether the focus had been biopsied correctly, since the histologic diagnosis of a benign focal lesion can only occasionally be made by means of cytologic smears. Cases are presented showing circumscribed lesions of the liver. With a cut-biopsy fine needle, small cylinders of tissue were obtained under ultrasonic guidance and examined after histologic preparation. In each case, a benign focal lesion could be diagnosed, proving that the observed lesion had been correctly biopsied.

Adult↗
PubMed1985

Drug-induced liver injury in liver biopsies of the years 1981 and 1983, their prevalence and type of presentation.

Based on the histological picture of liver biopsies examined in the years 1981 and 1983, drug-induced liver injury has been suspected in 131 and 170 cases. In relation to the total number of the examined liver biopsies this accounted for 6 and 9.6%, respectively. In only 20 (i.e. 15%), respectively 17 (i.e. 10%) of the cases, a drug-induced injury could be clinically excluded. However, a drug-induced injury was doubtlessly secured in 21 (16%) and 28 (16.5%) of the cases. The histological phenotype seen in association with the incriminated drug is presented. In 90 (68.7%) and 125 (73.5%) of the cases it was neither possible to secure nor to exclude the drug as cause of this damage, either because in 32/72 cases the clinical work-up was incomplete or because the drug-induced damage was clinically suspected, but not sufficiently documented by follow-up examinations after drug-withdrawal.

Adolescent↗
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↗