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Biomedical subjects

M Knoblauch

Publications and source records attributed to M Knoblauch.

At least 73 records · Page 4Linked to original sources
PubMed1977

[Microcirculation studies on rat small intestine villi in vivo].

A method of observing and studying the microcirculation in the jejunal villus of the living rat is described. It permits measurement of the velocity of plasma gaps and of the diameters of the various vessels, and is based on transillumination of the exposed mucosa. The motility of the gut is overcome by allowing the intestine to adhere to the water-immersion lens. The problems of mucous secretion are resolved by administration of N-acetyl-L-cystein. A direct arteriovenous connection between arterioles and the venous system of the villus is postulated. Plasma gap velocity is 1.78 +/- 0.62 mm/sec in the arterioles and 0.42 +/- 0.08 mm/sec in the capillaries. The measured diameter of the of the erythrocyte column in the vessels is: central artery: 9.14 +/- 1.89 micron; "arcade" arteriole part I, II and III respectively: 5.88 +/- 1.05 micron, 6.69 +/- 1.04 micron, 8.86 +/- 1.63 micron; venule: 13.58 +/- 2.67 micron; capillaries: 4.56 +/- 0.57 micron. The method also allows puncture of the villus vessels.

Acetylcysteine↗
PubMed1977

[Dihydralazine-induced acute hepatitis with IgM deficiency].

Two patients with IgM-deficiency developed acute, recurrent HB3-Ag negative hepatitis with bridging necrosis following ingestion of low daily doses of dihydralazine. The association between the drug and the liver disease appears probable, as recurrence of hepatitis followed each exposure. One patient developed high titers of antimitochondrial antibodies and the other low titers of antibodies against smooth muscles. The relationship between IgM-deficiency and dihydralazine hepatitis is not clear. Investigation of patients with IgM-deficiency for drug hypersensitivity and liver disease may provide additional information.

Acetylation↗
PubMed1977

[Vasculitis in hepatitis B infection].

Personal observations have confirmed the frequent association of HB-infection with certain forms of vasculitis. 4 of 11 patients with polyarteritis nodosa were repeatedly found to be HBs-Ag positive and had chronic hepatitis of varying severity. In patients with giant cell arteritis (polymyalgia rheumatica and temporal arteritis) anti-HBs was found more frequently than in controls, especially when examined within 6 months after onset of symptoms (7 of 20 equal 35% had anti-HBs, versus 6% of controls). Several lines of evidence point to the important role played by circulating HBs-Ag/anti-HBs complexes in the development of HB-associated vasculitis.

Arteritis↗
PubMed1976

[Australia antigenemia and hepatitis after kidney transplantation].

The clinical significance of Australia-antigenemia following kidney transplant has been studied in 18 patients. In 12 of these infection occurred after kidney graft. Sixteen allograft recipients had positive tests for Hbs-AG for 15-89 months. Development of chronic persistent hepatitis was observed in 7 cases; chronic aggressive hepatitis was not seen. Findings in the literature and the practical implications are discussed.

Adult↗
PubMed1976

[Diagnosis of treated and untreated chronic-aggressive hepatitis].

A total of 121 patients with chronic active hepatitis (CAH) of two Zurich hospitals were controlled over a mean time of 5 years and 4 months. All patients of one hospital were consequently treated with corticosteroids and azathioprine, whereas those of the other hospital were not treated unless a severe deterioration occurred. In this case treatment was as short as possible. Results indicate that long - time treatment of CAH results in better prognosis than does no or short - time treatment. Death rate per observed patient - year was 0.079 in the no - therapy group, 0.035 in the short - therapy group and 0.025 in the long - time therapy group.

Adrenal Cortex Hormones↗
PubMed1976

The Mallory-Weiss-syndrome: a clinical study of 20 cases.

This is an account of 20 cases of MWS, representing 8% of a series of 247 consecutive upper GI-bleedings. Men above 40 years and persons with severe concomitant disease are specially at risk. The prognosis is rather good, mortality from bleeding being 10%. Surgery should not be undertaken unless all conservative measures, including vasopressin infusion and even Sengstaken-Blakemore tube have been applied. The typical history, a hiatal hernia and alcohol intake are frequently missing. Neither studies of gastric acid secretion nor esophageal manometry disclosed new pathogenic aspects.

Adult↗
PubMed1975

[Clinical aspects of carcinoma of the liver (author's transl)].

The incidence of epi-cirrhotic liver carcinoma is apparently on the increase. Between 1969 and 1973 there were 84 cases of primary liver carcinoma and 467 of cirrhosis among 10211 autopsies. In 74 (16%) the carcinoma had developed in a cirrhotic liver. Clincally the diagnosis of carcinoma had been made in only 14 cases. The mean survival time after the diagnosis was seven weeks, after onset of the terminal symptoms 13 weeks. Typical clinical features were decompensated, hypertrophic, often coarsely granular, liver cirrhosis. The best diagnostic method was apparently laproscopy and determination of alpha 1-fetoprotein and cholestatic enzymes.

Adult↗
PubMed1975

[Pancreatic carcinoma in chronic pancreatitis].

Chronic pancreatitis and carcinoma of the pancreas are being diagnosed with increasing frequency throughout the world. When both occur together, the question of their causal relationship arises. Secondary chronic pancreatitis following carcinoma of the pancreas is relatively frequent and can be proven histologically in at least 10% of pancreatic cancers. How often primary chronic pancreatitis develops into carcinoma is controversial. So far, there are only a few prospective clinical studies of chronic pancreatitis which cover this problem. We have followed 146 cases of chronic pancreatitis for an average of 8.7 years. Two thirds of our patients show pancreatic calcifications. Our series includes a family with congenital pancreatic insufficiency. So far only one adenocarcinoma of the head of the pancreas has been diagnosed in a 58-year-old male. Another 57-year-old male patient died from a solid metastatic carcinoma, probably of pancreatic origin. Therefore, the incidence of pancreatic cancer in our series is 0.7 and 1.4% respectively. However, 8 more patients suffering from extrapancreatic malignancies have turned up during the follow-up period: 2 cancers of the tongue, 2 colonic carcinomas, 2 bladder papillomas, and 1 bronchial and 1 gastric carcinoma. Our studies indicate that carcinoma of the pancreas probably does not occur more frequently in chronic non-hereditary pancreatitis than in the average population. A review of the literature suggests that there may be a higher incidence of carcinoma in families with hereditary chronic pancreatitis. The frequency of extrapancreatic cancer in our patients is remarkable. As pancreatic carcinoma is rare in chronic pancreatitis there is no reason for early aggressive surgery, e.g. pancreatectomy, in these patients.

Adenocarcinoma↗
PubMed1975

Pancreatitis after renal transplantation.

Pancreatitis is seldom seen as a severe complication of renal transplantation. In a review on 1321 renal transplants, 23 cases with 12 deaths are reported (Johnson and Nabseth, 1970). Single case reports may be added. In our departments pancreatitis has proved to be a fairly frequent complication. It developed in 10 (7 percent) of 147 patients with renal transplantation one week to seven and a half years after transplantation (patients with primary hyperparathyroidism excluded). Three of the eight acute cases had haemorrhagic pancreatitis, in two of them leading to death. Two patients had chronic calcifying pancreatitis. Pancreatitis was complicated in one case by abscess formation and in two by severe haemorrhage into a pseudo-cyst. In two patients the diagnosis was made at necropsy only and death was probably not related to the acute pancreatitis. The exact pathogenesis of pancreatitis after renal transplantation cannot be precisely assessed. Possible contributing factors are treatment with corticosteroids, azathioprin, and L-asparaginase, early hypercalcaemia after transplantation, surgery, infections of bacterial or viral origin, and unknown immunological processes.

Acute Disease↗