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Biomedical subjects

W Hummerich

Publications and source records attributed to W Hummerich.

At least 37 records · Page 2Linked to original sources
PubMed1980

[Kaposi's sarcoma (author's transl)].

Kaposi's sarcoma of the skin and an aplastic syndrome occurred together in a 51-year-old patient. Macroscopically livid papules and nodules were observed. Histomorphologically endotheliomatous cell proliferation with signs of infiltrative growth was found. Because of the aplastic pancytopenia cytostatic treatment of the Kaposi sarcoma was contraindicated. The patient finally died of vascular failure with haemorrhagic diathesis being manifest. Syntropy of Kaposi's sarcoma with malignant haematological diseases is known. However, association with aplastic anaemia has not been observed so far. The pathogenesis of Kaposi's sarcoma is unknown.

Anemia, Aplastic↗
PubMed1980

[Sézary syndrome (author's transl)].

Morphological demonstration of the typical Sézary cell in peripheral blood confirmed the diagnosis of Sézary syndrome in a 64-year-old patient with generalized erythrodermia and typical histopathological skin changes. Enzymes and immunocytological membrane characteristics of Sézary cells changed in the course of the disease after cytostatic therapy. Polychemotherapy clinically led to transitory complete regression of skin changes. Reviewing the few published investigations it is found that the morphologically sufficiently defined Sézary cells are apparently not uniform cytochemically and immunocytologically in different patients.

Autopsy↗
PubMed1980

Extrarenal prorenin and renin in anephric patients.

Active renin was detected in 6 of 7 anephric patients (mean value: 0.72 +/- 0.27 microU/ml, n = 7; normals: 19.7 +/- 2.4 microU/ml, n = 10), using an assay method without intrinsic acid- or cryoactivation. Prorenin, measured as the difference between plasma renin concentration (PRC) before and after acid-activation in vitro, was present in considerable amounts in all patients (32.4 +/- 3.5 microU/ml; normals: 80.7 +/- 9.7 microU/ml). PRC after cryoactivation at--5 degrees C during 1 week was insignificantly lower than after acid-activation in the patients. There was a linear correlation between PRC after either activation procedure (p less than 0.01). Supine or upright posture did not influence active or inactive renin in the anephric subjects. Our studies show that low but significant levels of active renin and a considerable amount of prorenin are detectable in anephric patients. The data suggest that prorenin in normal subjects in a significant proportion is of extrarenal origin. Orthostasis has no effect on extrarenal active or inactive renin.

Adult↗
PubMed1980

The renin--kallikrein--prostaglandin system: plasma active and inactive renin and urinary kallikrein during prostacyclin infusion in man.

Renal prostaglandins are integrated with the kallikrein-kinin and renin-angiotension systems in a vasoactive hormone complex. Prostacyclin potently stimulates renin release from rabbit cortical slices and plasma renin activity rises in response to prostacyclin infusion in man. Prostaglandins also stimulate the production of kallikrein, a potential activator of renin in vivo. To investigate the mechanism of prostacyclin induced renin release, human volunteers were infused with prostacyclin 8ngKg-1min-1 and vehicle alone in random order. Despite a marked increase in plasma active renin during prostacyclin both plasma inactive renin and urinary kallikrein failed to alter from control values. Urinary sodium and volume were increased by prostacyclin. The stimulation of renin by intravenous prostacyclin is not mediated by activation of the kallikrein system.

Adult↗
PubMed1980

Sodium-potassium-dependent ATPase activity in erythrocyte ghosts of patients with primary and secondary hypertension.

1. We have investigated the function of the Na+-K+ pump in the erythrocytes of patients with various types of hypertension by measuring the activity of ouabain-sensitive Na+-K+-dependent ATPase and ouabain-insensitive ATPase in the erythrocyte ghosts of these patients. 2. Mean Na+-K+-ATPase activity was increased threefold in six patients with Cushing's syndrome and hypertension (0.985 +/- SD 0.288 mumol of phosphate h-1 mg-1) compared with that in 49 control subjects (0.334 +/- 0.147 mumol of phosphate h-1 mg-1) (P < 0.0025), but not in four patients with primary aldosteronism (0.278 +/- 0.108 mumol of phosphate h-1 mg-1). 3. Na+-K+-ATPase activity slightly exceeded the control range in 57 patients with primary hypertension (0.410 +/- 0.245 mumol of phosphate h-1 mg-1; P < 0.025) and in 12 patients with renal hypertension (0.475 +/- 0.250 mumol of phosphate h-1 mg-1) (P < 0.025). 4. There was no difference in ouabain-insensitive ATPase between the controls and the different types of hypertension. 5. The data support the hypothesis of an activation of the Na+ pump in patients with glucocorticoid excess. This helps to explain previous observations of a redistribution of sodium and water to the extracellular compartment in experimental glucocorticoid-induced hypertension.

Adult↗
PubMed1980

Sézary syndrome: immunocytological and cytochemical variability of Sézary cells.

The characteristic large cells in the blood of a patient with Sézary syndrome underwent immunocytological and cytochemical changes during polychemotherapy, which caused transient regression of skin lesions. Tartrate-resistant acid phosphatase was demonstrable in a few cells only after chemotherapy; initially, only 2% T cells and 26% B cells could be demonstrated in the blood by immunocytological methods; after cytostatic therapy, 35% T cells but no B cells were detected.

Acid Phosphatase↗
PubMed1979

Acid- and cryoactivation of renin in human plasma.

Inactive renin in normal human plasma was activated in vitro either by cryoactivation (incubation at 0 degrees C/-5 degrees C up to 3 months) or acid-activation (dialysis to pH 3.0 for 48 h followed by diaylsis to pH 7.5). Plasma-renin-concentration was similar after either activation procedure (96 +/- 50 microU/ml vs 100 +/- 43 microU/ml). There was no further significant acid-activable renin after cryoactivation. These data suggest that conversion of inactive to active renin by optimized procedures is complete. The term "total renin" for activation results under these conditions seems to be valid.

Dialysis↗
PubMed1979

[The saralasin test in the diagnosis of hypertension (author's transl)].

The saralasin test was performed in 68 hypertensives. A clear-cut dependence of the test results on initial plasma-renin concentration and particular sodium balance was demonstrated. Because of this dependence the saralasin test should be performed only under constant conditions. A mild stimulation of the renin-angiotension system by salt restriction to a mean sodium excretion of 50 mmol daily and 80 mg furosemide by mouth 12 hours before the test seems best. In this way essential and renovascular hypertension could be distinguished with considerable reliability (P less than 0.001). Among patients with essential hypertension one could clearly separate those with high plasma-renin concentration from those with a normal or low one. Among patients with renovascular hypertension those with haemodynamically significant renal artery stenosis could with high probability be distinguished from those with non-effective stenosis. A positive saralasin test without testing the function of the normal contralateral kidney does not provide an indication for operation.

Adult↗
PubMed1979

[Sodium-potassium-adenosine triphosphatase-activity in red cell ghosts of patients with essential hypertension (author's transl)].

Increased sodium concentration and high influx of Na22 are reported in erythrocytes of patients with essential hypertension. It was speculated, that these findings are due to a disturbed transport for sodium across red cell membranes. We found a significantly increased activity of the ouabainsensitive Na-K-ATP'ase in red cell ghosts of 27 patients with essential hypertension compaired with 32 normotensive controls. There existed no difference in Mg-ATP'ase-activity between the two groups. These findings suggest an increased activity of the Na-pump in red cell membranes of patients with essential hypertension.

Erythrocyte Membrane↗
PubMed1979

[Improved interpretation of renal-vein-renin-ratio by simultaneous determination of renal 131I-hippuric-acid-clearance-ratio in patients with renovascular hypertension (author's transl)].

In patients with unilateral vascular kidney disease and hypertension, ratio of renal-vein-renin was compared with 131I-Hippuric-acid clearance and change in blood pressure during Saralasininfusion. The ratio of renal-vein-renin was positively correlated with the ratio in renal plasma flow between the kidneys in all patients studied. The ratio of renins therefore is a result of two factors: The difference in renin secretion and the difference in blood flow in the two kidneys. In patients with angiotensin independent hypertension renin-ratios up to 2.0 were found without relevance to elevated blood pressure. When the difference in renal blood flow between both kidneys was small, even a slight difference in renal vein renin indicated hypertension related to increased renin secretion. Renin-ratios in the critical range between 1.5 and 2.5 should only be interpreted in respect to a similar ratio in renal blood flow.

Adult↗
PubMed1979

Renin-activation by kallikrein: evidence for alkaline-activation of plasma renin.

Porcine pancreatic kallikrein leads to a significant activation of human plasma renin when incubated at pH 8.2. 'Endogenous' activation of plasma renin can be seen by incubation of plasmas at the same pH. Both 'endogenous' alkaline- and kallikrein-activation of plasma renin can be inhibited by aprotinin. Both, kallikrein- and 'endogenous' alkaline activation of plasma renin are significantly correlated to cryo- and acid-activation. We suggest that kallikrein-and 'endogenous' alkaline-activiation come close to the in vivo activation process.

Animals↗
PubMed1975

Improvement of renin determination in human plasma using a commonly available renin standard in a radioimmunological method.

UNLABELLED: A new method for the measurement of renin in human plasma is described. The method is based on the introduction of the internationally available renin standard of the Medical Research Council (MRC) London, as a calibration system. Thus, some principal disadvantages of methods expressing results in renin reaction velocity (angiotensin generation rate) only are avoided. Both renins, unknown and standard, react with a sheep substrate preparation and are handled identically throughout the whole procedure including the angiotensin I radioimmunoassay (RIA). The plasma renin concentration (PRC) is given in 10(-6) MRC-renin units (muM/ml). RESULTS: the renin standard is free of angiotensin, angiotensinases, and angiotensinogen; it is stable on storage. Identical enzyme kinetics are shown for both renins. An interference between endogenous and exogenous substrate could be avoided. The potentially harmful influences of proteins from the enzyme incubation mixture of the RIA dose response curve are shown. The use of an angiotensin I calibration system could be omitted. Using a standard renin dilution from 250-0.9 muU/ml also the full biological range is covered. When giving an unrestricted diet the preliminary normal values of PRC are 21.9 +/- 12.6 muU/ml in recumbent and 40.1 +/- 19.8 muU/ml in upright position (n = 16,x +/- s, age 20-35 years). Earlier findings of age-dependency of PRC were confirmed.

Adult↗