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H Wernze

Publications and source records attributed to H Wernze.

At least 19 recordsLinked to original sources
PubMed1992

[Angioneurotic edema caused by angiotensin-converting enzyme inhibitors].

Inhibition of angiotensin converting enzyme (ACE) may cause angioneurotic oedema. In order to define the clinical spectrum of this important adverse effect, we analysed data on 60 patients with angioneurotic oedema notified to the Drug Commission of the German Medical Association, after taking captopril (n = 24), enalapril (n = 25) or lisinopril (n = 11). In 48 cases the oedema affected the face, tongue and pharynx, while swelling of the extremities (n = 4), the trunk (n = 2) or the genitalia (n = 1) was observed less frequently. While oedema appeared most often after 1 to 21 days, it started within an hour in one patient, and only after 6 months of therapy in five patients. After discontinuation of the ACE inhibitor, the angioneurotic oedema resolved within 72 hours; additional therapeutic measures (glucocorticoids, antihistamines, adrenaline, C1 inhibitors) did not shorten the recovery time. In view of the increasing use of ACE inhibitors, the features of this unusual adverse reaction need to be widely recognized, since angioneurotic oedema of the larynx is potentially life-threatening.

Angioedema↗
PubMed1991

Response of gonadotropins to pituitary stimulation with luteinizing hormone releasing hormone is a more specific than sensitive parameter for the polycystic ovary syndrome.

Gonadotropin response to exogenous luteinizing hormone-releasing hormone (LHRH) was studied in two groups of patients with the polycystic ovary syndrome (PCOS). Group I (n = 44) was diagnosed as 'overt PCOS' based on clinical and endocrine abnormalities, and the typical ultrasonic picture of multicystic changes in an increased amount of ovarian stroma. Group II patients (n = 34), with similar clinical and hormonal changes, were classified as 'borderline PCOS' because endosonography of the ovaries was not conclusive. Serum gonadotropins were followed 15, 30, 45 and 60 min after administration of 100 micrograms LHRH intravenously. Plasma LH and the peak ratio of luteinizing hormone to follicle stimulating hormone (LH/FSH peak) after LHRH were significantly higher in Group I and II patients (p less than 0.001) than in controls (n = 11). There was a significant positive correlation between LH (r = 0.73 and 0.68, p less than 0.05) and LH/FSH ratio peaks (r = 0.61 and 0.68, p less than 0.05) after LHRH, and the basal values in each group. However, hyperreactivity of LH and the LH/FSH ratio after LHRH (defined as values exceeding the 95th percentile of control values) was only present in Group I in 38.6 and 56.8%, and in Group II in 47.1 and 73.5% of patients. It is concluded that: exaggerated LH release after LHRH is a typical yet not unique feature of PCOS and its sensitivity is inferior to its specificity; a higher rate for sensitivity is achieved when the LH/FSH ratio after LHRH (instead of LH release alone) is used; and that hyperreactivity of LH after LHRH is neither correlated with the plasma concentrations of total testosterone, free plasma testosterone or androstenedione, nor with the ultrasonic picture of the ovaries as significantly higher (p less than 0.05) LH and LH/FSH ratio peaks were found in borderline PCOS patients. While the heterogeneity of gonadotropin response to LHRH clearly limits its routine diagnostic use, the FSH and LH response is useful in patients with inconsistent clinical and ultrasonic features suggestive of PCOS.

Adolescent↗
PubMed1990

Hepatic efflux and renal extraction of plasma glutathione: marked differences between healthy subjects and the rat.

Hepatic efflux of glutathione accounts for almost 85% of the plasma level in the rat. However, the expected high concentration in the hepatic vein in man has not been demonstrated as yet. Our findings in ten patients without liver dysfunction reveal that substantial translocation of glutathione from the liver to the plasma does not occur. The removal rate of circulating glutathione by the kidney is far lower in man than in the rat (49.5% vs 84.6%). Moreover, the inferior vena cava in man contains more circulating glutathione than the artery, which is not consistent with the results obtained in the rat. Furthermore, the plasma concentration in man is about one tenth of that in the animals. These results clearly indicate that species-specific differences in the overall biosynthesis and metabolism of the tripeptide occur, resulting in marked variations in its plasma concentration.

Adult↗
PubMed1989

Atrial natriuretic factor and renin-aldosterone in volume regulation of patients with cirrhosis.

The role of the atrial natriuretic factor and of the main counteracting sodium-retaining principle, the renin-aldosterone system, in acute volume regulation of cirrhosis of the liver has been investigated. Central volume stimulation was achieved in 21 patients with cirrhosis, 11 without and 10 with ascites, and 25 healthy controls by 1-hr head-out water immersion. Immersion prompted a highly significant (p less than 0.001) increase of atrial natriuretic factor plasma concentrations in cirrhotic patients without ascites from 8.5 +/- 1.3 fmoles per ml to 16.5 +/- 2.6 fmoles per ml, comparable to the stimulation in control subjects (6.0 +/- 0.6 fmoles per ml to 13.6 +/- 2.6 fmoles per ml). In cirrhotic patients with ascites, atrial natriuretic factor increase (from 7.7 +/- 1.3 fmoles per ml to 11.4 +/- 2.3 fmoles per ml) was blunted (p less than 0.05). Plasma renin activity and plasma aldosterone concentration were elevated in cirrhotic patients, especially in the presence of ascites. Following immersion, plasma renin activity and plasma aldosterone concentration were reduced similarly in all groups. Water immersion induced a more pronounced natriuresis and diuresis in control subjects than in cirrhotic patients. Neither atrial natriuretic factor nor plasma renin activity nor plasma aldosterone concentration alone correlated to sodium excretion. However, atrial natriuretic factor to plasma aldosterone concentration ratios were closely correlated to basal and stimulated natriuresis in cirrhotic patients, particularly in those with ascites. These data suggest that atrial natriuretic factor and the renin-aldosterone system influence volume regulation in patients with cirrhosis.

Adult↗
PubMed1989

Increased bioavailability of enzymes of eicosanoid synthesis in hepatic and extrahepatic tissues after portacaval shunting.

Metabolites of arachidonic acid have been attributed to severe circulatory, metabolic and hormonal alterations in patients with chronic liver disease. In order to study changes of the tissue-specific availability of enzymes of eicosanoid synthesis, we used portacaval-shunted rats, as this model exhibits many clinical and biochemical similarities to patients suffering from cirrhosis of the liver. Microsomal mass and maximal velocity of prostaglandin H synthase, the initial enzyme of prostaglandin synthesis, were markedly and permanently increased after shunting in both hepatic and extrahepatic tissues as compared to those of sham-operated rats. Maximal velocity of thromboxane synthase and prostacyclin synthase, two more peripheral enzymes of the arachidonic acid cascade, were tissue-specifically enhanced, whereas the apparent affinities (Km) remained unchanged. Determination of 5-lipoxygenase activity in tissue preparations disclosed a preferential increase in the liver, lung and renal cortex after portacaval shunting. Furthermore, exposure to endotoxin closely mimicked the shunting-induced changes. These results suggest that after portacaval shunting and possibly in patients with advanced liver disease, profound abnormalities at the level of local enzyme expression might play a pathophysiologically important role in the control of eicosanoid synthesis.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Improved sexual function in hemodialysis patients on recombinant erythropoietin: a possible role for prolactin.

As it was reported that correction of anemia in long-term hemodialysis patients by recombinant human erythropoietin (r-HuEPO) is associated with improved sexual function, we conducted the present study to further delineate the mechanism(s) by which this is brought about. Serum prolactin, testosterone, and parathyroid hormone (PTH) levels were followed during 4 months of r-HuEPO therapy. Within 4 months of treatment with r-HuEPO, hematocrit values rose from 23.7 +/- 1.2 to 35.7 +/- 0.2% and hemoglobin increased from 7.3 +/- 0.3 to 11.3 +/- 0.4 g/100 ml. In parallel, serum prolactin values decreased significantly from 66.9 +/- 9.3 to 9.6 +/- 2.6 ng/ml in females and from 39.5 +/- 10.5 to 10.3 +/- 1.0 ng/ml in male dialysis patients. Testosterone concentrations were low in male patients and remained unchanged during r-HuEPO therapy. Baseline PTH values were elevated (1,880 +/- 220 pg/ml) in patients of both sexes and declined to 1,410 +/- 180 pg/ml during treatment with r-HuEPO. However, this difference did not reach statistical significance. Sexual function improved in 4 out of 7 males and 5 out of 9 female patients began to menstruate regularly again. It appears that treatment of anemia in end-stage renal disease by r-HuEPO improves sexual function via normalization of elevated serum prolactin concentrations.

Adult↗
PubMed1988

Role of atrial natriuretic factor, cyclic GMP and the renin-aldosterone system in acute volume regulation of healthy human subjects.

The role of the atrial natriuretic factor (ANF), its second messenger cyclic guanosine monophosphate (cGMP), and the counteracting renin-aldosterone system in acute volume regulation was investigated in 25 healthy human subjects. Central volume stimulation by 1-h head-out water immersion (WI) into a thermoneutral water-bath increased plasma levels of ANF (mean +/- SEM) from 6.0 +/- 0.6 to 13.6 +/- 2.6 fmol ml-1. This was paralleled by a rise of plasma cGMP levels from 1.9 +/- 0.2 to 2.8 +/- 0.4 pmol ml-1, and an increase of urinary cGMP excretion from 340 +/- 64 to 692 +/- 103 pmol min-1. Water immersion reduced plasma aldosterone concentration (PAC) from 13.0 +/- 1.7 to 6.5 +/- 0.8 ng 100 ml-1 and plasma renin activity (PRA) from 5.3 +/- 0.9 to 2.4 +/- 0.3 ng AI ml-1 h-1. Volume stimulation markedly increased diuresis and natriuresis. Whereas the plasma cGMP increase correlated with plasma ANF stimulation, neither ANF nor PRA or PAC correlated with basal or stimulated renal parameters. Water immersion-induced changes in natriuresis and urinary cGMP excretion were correlated. These data suggest a role of ANF and cGMP in acute volume regulation of healthy human subjects.

Adult↗
PubMed1988

Interrelationship between atrial natriuretic peptide and plasma renin, aldosterone and catecholamines in hepatic cirrhosis: the effect of passive leg rising.

To assess the role of atrial natriuretic peptide (ANP) in relation to the sympathoadrenal and renin-angiotensin-aldosterone system, and sodium excretion, 88 cirrhotic patients (mean age 52 years; 28 compensated, 28 decompensated with ascites, and 32 decompensated and treated with diuretics) and 26 control subjects were investigated. Basal ANP levels were not different between any group of cirrhotics and controls. Circulating ANP was not related to elevated plasma noradrenaline and adrenaline, and enhanced plasma renin/aldosterone levels in ascitic patients. Furthermore, ANP was not related to urinary sodium excretion, blood pressure, and heart rate. In 30 cirrhotic patients (12 compensated, 18 decompensated with ascites including eight on diuretic therapy) and nine controls, a passive leg rising procedure for 1 h was performed in order to augment central blood volume and atrial pressure physiologically. Ascitic patients (with and without diuretic treatment) experienced a slight but significant increase in plasma ANP indicating preserved responsiveness of ANP release in cirrhosis. Plasma aldosterone was markedly depressed. The data support the underfilling concept of ascitic formation in advanced stages of cirrhosis. The failure of enhanced ANP release under basal conditions may be due to the diminished effective blood volume, resulting in insufficient atrial stretching.

Adult↗
PubMed1988

Renin-angiotensin system, blood pressure homeostasis and renal function in galactosamine-induced fulminant hepatic failure in the guinea pig.

Arterial blood pressure, renal function and plasma concentrations of renin and renin substrate (angiotensinogen) were investigated in guinea pigs subjected to galactosamine-induced (1 g/kg i.v.) liver cell necrosis. Blood pressure declined continuously by 50% during a follow-up period of 72 h which was associated with a decrease in diuresis and natriuresis to 36 and 31%, respectively. Simultaneously, plasma renin concentration increased 30-fold indicating marked reduction of renal perfusion, while plasma renin substrate concentration fell to 6% of the baseline level. There was microscopic evidence of oligemic circulatory renal damage characterized by acute proximal tubular necrosis with concomitant tubular dilatation. Short-term infusion of homologous renin substrate-enriched plasma, derived from nephrectomized animals, was followed by marked increase in mean arterial blood pressure from 34 +/- 9 to 77 +/- 7 mm Hg accompanied by marked diuresis and natriuresis. Renin substrate depletion following galactosamine-induced fulminant liver failure may represent impaired hepatic biosynthesis as well as increased renin substrate consumption due to excessive renin secretion. Angiotensinogen repletion has a beneficial effect on both renal function and blood pressure probably due to marked generation of the potent vasoconstrictor angiotensin II which consequently inhibits renin secretion. These observations strongly support the suggestion that the renin-angiotensin system is of major importance to cardiovascular homeostasis in acute liver failure.

Angiotensinogen↗
PubMed1986

Atrial natriuretic peptide in hepatic cirrhosis: relation to stage of disease, sympathoadrenal system and renin-aldosterone axis.

58 patients (mean age 51 years) with cirrhosis of the liver were studied. 16 patients were compensated, 18 decompensated with ascites, and 24 decompensated and treated with diuretics. Basal plasma levels of atrial natriuretic peptide were not different between any groups of cirrhotic patients and 17 control subjects (mean age 43 years). In contrast, the sympathoadrenal system (plasma noradrenaline, plasma adrenaline) and renin/aldosterone were significantly activated in decompensated cirrhotics. Circulating ANP was not related to plasma noradrenaline and adrenaline, plasma renin activity, plasma aldosterone, blood pressure, heart rate, or urinary sodium/potassium excretion in any cirrhotic group. Despite established sodium and volume retention in decompensated cirrhosis, the results indicate that diminished effective blood volume fails to release atrial natriuretic peptide in a larger amount due to insufficient atrial stretching. After insertion of a peritoneovenous shunt in one patient for treatment of refractory ascites, plasma atrial natriuretic peptide, urinary volume and sodium excretion increased, whereas elevated plasma levels of noradrenaline, renin activity and aldosterone decreased markedly.

Adult↗
PubMed1979

Plasma renin, renin substrate and angiotensin II changes following experimental endotoxinaemia.

The effect of a single dose of endotoxin (B. coli, 1.5 mg/kg intravenously) on plasma renin concentration (PRC), renin substrate (PRSC), and angiotensin II (AT II) was studied in rats over a period of 48 hours. All determinations were performed by specific radioimmunoassay. Six and nine hours following endotoxin administration, renin secretion was decreased, whereas at 48 hours a slight increase in the PRC was found. In contrast, a three-fold elevation of the PRSC occurred during the first 24 hour period, attributable to a stimulation of the hepatic biosynthesis as result of corticosterone oversecretion. According to the observed changes in PRC and PRSC, AT II remains unchanged after six and nine hours, whereas a significant increase was detected after 24 and 48 hours. Based on the actual AT II level, the findings emphasize that in the rat the RAS does participate in the later stages of endotoxin stress only.

Angiotensin II↗
PubMed1979

Changes of serum angiotensin I converting enzyme in patients with viral hepatitis and liver cirrhosis.

Serum angiotensin I converting enzyme, identical with kininase II, was measured fluorometrically in patients with acute viral hepatitis (n=18), liver cirrhosis without (n=44) and with (n=19) ascites. In all groups of patients the enzyme was significantly elevated as compared to 44 healthy controls (p less than 0.001). No correlation could be found between angiotensin I converting enzyme activity and liver function tests (serum glutamic oxalacetic transaminase, serum glutamic pyruvic transaminase, total protein, albumin, bilirubin) or other parameters (serum potassium, serum sodium). High serum converting enzyme activity in chronic liver diseases might originate primarily from an altered pulmonary circulation and indicates higher conversion rate of angiotensin I by passage through the lungs as well as increased bradykinin degradation. The reason for the enzyme liberation in acute viral hepatitis is as yet uncertain.

Adult↗
PubMed1978

Studies on the activity of the renin-angiotensin-aldosterone system (RAAS) in patients with cirrhosis of the liver.

Plasma renin activity (PRA), plasma renin concentration (PRC), angiotensinogen, angiotensin II (AT II) and plasma aldosterone were determined by radioimmunoassay in 77 patients with cirrhosis of the liver [group I: with ascites, untreated (n=23); group II: patients with ascites during treatment (n=32); group III: after removal of fluids, but under further spironolactone therapy (n=10); group IV: untreated subjects without ascites (n=12)]. With the exception of decreased angiotensinogen values in all groups ranging between 39% (group IV) and 73% (group III) no significant changes of the other parameters of the RAAS were found in untreated patients. A highly significant increase of PRA, PRC, AT II and plasma aldosterone was observed in treated cirrhotics with (group II) or without (group III) ascites. In the total series of patients AT II was closely related to PRA, PRC and aldosterone emphasizing aldosterone secretion. Plasma sodium was inversely correlated to PRA, PRC, AT II and aldosterone, but no relationship was detected between these parameters of the RAAS and plasma potassium. Our results indicate that hyperaldosteronism in cirrhosis appears unlikely to be the major determinant of avid renal sodium retention and ascites formation. An increased activity of the RAAS is most often initiated by therapeutic factors and/or markedly altered electrolyte metabolism. Therefore, basal conditions of the patients to be studied must be well defined to exclude any artificially induced stimulation of the RAAS.

Adult↗