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Biomedical subjects

M Bahnsen

Publications and source records attributed to M Bahnsen.

At least 19 recordsLinked to original sources
PubMed1988

Prevalence of microalbuminuria, arterial hypertension, retinopathy and neuropathy in patients with insulin dependent diabetes.

Diabetic nephropathy is the main cause of the increased morbidity and mortality in patients with insulin dependent diabetes. The prevalence of microalbuminuria was determined in adults with insulin dependent diabetes of five or more years' duration that had started before the age of 41. All eligible patients (n = 982) attending a diabetes clinic were asked to collect a 24 hour urine sample for analysis of albumin excretion by radioimmunoassay; 957 patients complied. Normoalbuminuria was defined as urinary albumin excretion of less than or equal to 30 mg/24 h (n = 562), microalbuminuria as 31-299 mg/24 h (n = 215), and macroalbuminuria as greater than or equal to 300 mg/24 h (n = 180). The prevalence of microalbuminuria and macroalbuminuria was significantly higher in patients whose diabetes had developed before rather than after the age of 20. The prevalence of arterial hypertension increased with increased albuminuria, being 19%, 30%, and 65% in patients with normoalbuminuria, microalbuminuria, and macroalbuminuria respectively. The prevalence of proliferative retinopathy and blindness rose with increasing albuminuria, being 12% and 1.4%, respectively, in patients with normoalbuminuria, 28% and 5.6% in those with microalbuminuria and 58% and 10.6% in those with macroalbuminuria. An abnormal vibratory perception threshold was more common in patients with microalbuminuria (31%) and macroalbuminuria (50%) than in those with normoalbuminuria (21%). This study found a high prevalence (22%) of microalbuminuria, which is predictive of the later development of diabetic nephropathy. Microalbuminuria is also characterised by an increased prevalence of arterial hypertension, proliferative retinopathy, blindness, and peripheral neuropathy. Thus, urinary excretion of albumin should be monitored routinely in patients with insulin dependent diabetes.

Adult↗
PubMed1987

The relationship of secretin and somatostatin levels in plasma to glucose administration and acid secretion during fasting.

The concentrations of secretin and somatostatin in plasma were measured in 10 healthy subjects during a 4-day fast. The fast induced increased concentrations of plasma secretin (from 1.2 +/- 0.5 to 9.5 +/- 2.3 pmol/l) and somatostatin (from 5.2 +/- 1.5 to 8.6 +/- 1.7 pmol/l). Gastric aspiration for 1 h suppressed the high concentrations of secretin by 46% and somatostatin by 27%. The intravenous infusion of glucose reduced the plasma secretin even further by 88%; the decrease in somatostatin was not statistically significant. The study shows that gastric aspiration and/or glucose infusion suppressed the high plasma concentration of secretin and that factors other than hyperchlorhydria must be involved in the hypersecretinemia seen during starvation. The elevated plasma somatostatin concentration seen during starvation may be a consequence of increased acid secretion.

Adult↗
PubMed1986

Acute reduction of arterial blood pressure reduces urinary albumin excretion in type 1 (insulin-dependent) diabetic patients with incipient nephropathy.

The effect of an acute reduction in arterial blood pressure upon kidney function was studied in 12 patients with Type 1 (insulin-dependent) diabetes and incipient nephropathy (persistent microalbuminuria). Renal function was assessed by measurement of the glomerular filtration rate (single bolus 51Cr-EDTA technique) and by the urinary albumin excretion rate (radioimmunoassay). The study was performed twice within 2 weeks, with the patients receiving a slow intravenous injection of either clonidine (225 micrograms) or saline (154 mmol/l) in random order. Clonidine reduced arterial blood pressure from 125/79 +/- 13/8 to 104/68 +/- 9/7 mmHg (p less than 0.01), urinary albumin excretion rate from 68 (31-369) to 46 (6-200) micrograms/min (median and range) (p less than 0.01), and fractional clearance of albumin in all patients (median 29%) (p less than 0.01). Glomerular filtration rate was 110 +/- 11 before and 106 +/- 13 ml/min/1.73 m2 after clonidine injection. The blood glucose concentration was 15 +/- 4 mmol/l before and 14 +/- 5 mmol/l after clonidine injection. In agreement with findings in animal studies, our results suggest that microalbuminuria is to a large extent pressure-dependent, probably because of glomerular hypertension, and that autoregulation of glomerular filtration rate is normal in most patients with incipient diabetic nephropathy.

Adult↗
PubMed1984

Mechanisms of catecholamine effects on ketogenesis.

Ketogenesis may be controlled at several sites. Lipolysis with release of plasma nonesterified fatty acid (NEFA) substrate is the first step. Plasma NEFA are taken up by the liver in a concentration-dependent fashion and, after conversion to the acyl-CoA derivative, may either be reesterified or enter the mitochondria via the carnitine shuttle. After beta-oxidation the resultant acetyl-CoA may either be converted to ketone bodies that are then released into the circulation or be condensed with oxaloacetate and enter the tricarboxylic acid cycle, the third potential control point. In humans, infusion of epinephrine causes a transient two- to threefold increase in fatty acids, glycerol, and ketone bodies. Insulin levels show a small absolute increase. Norepinephrine has similar effects, although insulin levels tend to be suppressed and glucagon levels rise somewhat. If somatostatin is added simultaneously, the lipolytic and ketogenic effects are accentuated and prolonged. Dopamine, in a high dose, has no effect on ketone bodies alone but shows small increases in NEFA and ketone bodies in the presence of somatostatin and may play a modulatory role in ketogenesis. The ketogenic effect of catecholamines could thus be in the adipocyte or in the liver. Studies with perfused liver or hepatocytes showed only trivial effects on ketogenesis even with supraphysiological doses of catecholamines. Furthermore infusion studies in rats showed decreased rather than increased ketogenesis with no change in NEFA levels. The data suggest that a) there are species differences, and b) in humans epinephrine- and norepinephrine-induced increases in ketogenesis are secondary to increases in NEFA substrate supply.

Animals↗
PubMed1984

Cholecystokinin-stimulated and postprandial serum concentrations of bile acids in alcoholic liver cirrhosis.

This investigation was undertaken to examine the alterations in serum bile acid concentration after intravenous administration of cholecystokinin and a standard meal in 13 patients with alcoholic cirrhosis. Total 3 alpha-hydroxy bile acids in serum (SBA) were monitored for 2 h after injection of cholecystokinin and for 3 h after the standard meal. The median fasting value of SBA was 39.9 mumol/l (range, 3.2-148 mumol/l). The increase in SBA after cholecystokinin started earlier and lasted shorter than after standard meal stimulation (median, 30 min and 120 min, respectively). The appropriate relative peak levels of SBA were 173% and 212% of the fasting value. The increments were significant (P less than 0.01) within groups but insignificant between groups. Day-to-day variation of postprandial SBA was more pronounced than after cholecystokinin stimulation. The difference, however, was insignificant. An inverse correlation was detected between both fasting and stimulated peak levels of SBA and P-coagulation factors 2, 7, and 10.

Adult↗
PubMed1984

Prediction of fatality in fulminant hepatic failure.

Thirty-three consecutive patients admitted to the intensive care liver unit of Rigshospitalet with acute hepatic encephalopathy induced by viral hepatitis, drugs, or pregnancy were studied. All were treated with a standard anticoma regime. The 20 patients (61%) who died had a higher bilirubin level and lower total cholic acid conjugation and glycine cholic acid conjugation (p less than 0.05) than the surviving patients. Antipyrin clearance and galactose elimination capacity tended to be lower in the non-survival group than in the survival group (p = 0.09 and 0.11, respectively). Of single variables a bilirubin level of greater than 384 mumol/l gave the best prediction of non-survival (sensitivity, 0.80; specificity, 0.69; PVpos, 0.80; PVneg, 0.69; kappa, 0.49). However, a discriminant score based on combination of variables distinguished completely between non-survivors and survivors when validated by an unbiased method in which each patient is classified on the basis of the other patients' data. It is suggested that the discriminant score is used to select patients with very low probability of survival for liver transplantation or liver assistance procedures of unknown value.

Adult↗
PubMed1983

Diagnostic values of fasting and postprandial concentrations in serum of 3 alpha-hydroxy-bile acids and gamma-glutamyl transferase in hepatobiliary disease.

Fasting and postprandial concentrations in serum of 3 alpha-hydroxy-bile acids and gamma-glutamyl transferase were measured in 138 consecutive patients, 62 with (D) and 76 without (D) hepatobiliary disease. The maximum efficiencies of the three tests--that is, the fractions of patients allocated correctly to the D or D group at the optimum discrimination values--were 0.85, 0.84, and 0.83, respectively. Furthermore, the predictive values and nosographic sensitivities and specificities were rather similar. When the three tests were combined, the nosographic sensitivity increased significantly to a value of 0.84, and the corresponding specificity was 0.91. The diagnostic value of the absolute postprandial increase in serum bile acid concentration was slightly inferior to the diagnostic values of the fasting and postprandial serum bile acid concentrations and, finally, the relative postprandial serum bile acid increase was of no diagnostic value at all.

Adolescent↗
PubMed1983

Oral testosterone load related to liver function in men with alcoholic liver cirrhosis.

The relation between liver function and an oral testosterone load was examined in 42 consecutive patients with alcoholic liver cirrhosis. Administration of an oral load of 400 mg micronized free testosterone increased the serum concentration of testosterone (range, 31.9-694.4 nmol/l; median, 140.8 nmol/l) in male patients with alcoholic liver cirrhosis to significantly (P less than 0.01) higher levels than in male subjects without liver disease (range, 25.4-106.6 nmol/l; median, 61.5 nmol/l). The increase of testosterone after the load (log delta testosterone) in patients correlated inversely with galactose elimination capacity (r = 0.54; P less than 0.001), serum albumin (r = -0.53; P less than 0.001), plasma factor II + VII + X (r = 0.62; P less than 0.001), indocyanine green clearance (r = -0.71; P less than 0.001), and hepatic blood flow (r = -0.61; P less than 0.01) and correlated directly with wedged-to-free hepatic vein pressure (r = +0.54; P less than 0.01). The increase of testosterone after the load did not correlate significantly with sex hormone-binding globulin (r = +0.35; P greater than 0.05). It is concluded that the hepatic extraction of testosterone is significantly decreased in patients with alcoholic cirrhosis. This decrease seems to be due to decreased liver function, decreasing hepatic blood flow, and increased portosystemic shunting. Oral testosterone loading may therefore be of prognostic significance in patients with alcoholic liver cirrhosis.

Administration, Oral↗
PubMed1983

Cholic acid conjugation test and quantitative liver function in acute liver failure.

In 33 patients with acute hepatic encephalopathy due to toxic or viral hepatitis the following analyses were performed: (24-14C)cholic acid conjugation and sulfation, plasma phenazone clearance, galactose elimination capacity, and concentrations of glycocholic acid and glycolithocholic acid sulfate in plasma. The (24-14C)cholic acid conjugation in patients with viral hepatitis was significantly lower in fatal cases than in patients who survived (p less than 0.002). In these patients the galactose elimination capacity and the plasma phenazone clearance were insignificantly lower. Tauro-(24-14C)cholic acid was the predominant metabolite of (24-14C)cholic acid in six patients, but in four patients with toxic hepatitis this metabolite was only found in trace amounts. Sulfation after 3 h of (24-14C)cholic acid accounted for 0-8.2% of the administered dose. The sulfate of glycolithocholic acid was found in the plasma of all patients. No survival limit with regard to the capacity for the (24-14C)cholic acid conjugation could be defined.

Acute Disease↗
PubMed1983

Hypothalamic-pituitary-gonadal function in relation to liver function in men with alcoholic cirrhosis.

Serum concentrations of oestrone, oestradiol, follicle-stimulating hormone (FSH), luteinizing hormone (LH), and sex hormone-binding globulin (SHBG) were significantly (P less than 0.01) raised in men with alcoholic liver cirrhosis (no. = 42) compared with age-matched controls (no. = 20). No significant difference was observed when comparing serum testosterone concentrations. Patients were divided into three groups in accordance with the severity of liver cirrhosis, using biochemical and clinical criteria. Patients with the best-preserved liver function (no. = 11) and patients with moderately affected liver function (no. = 18) had significantly (P less than 0.05) raised serum concentrations of testosterone, FSH, and LH when compared with both controls and patients with severely affected liver function (no. = 13). Serum concentrations of testosterone, FSH, and LH in the latter group showed no significant differences from the controls. Serum concentrations of oestrone and oestradiol were significantly (P less than 0.05) increased in all patient groups, and serum oestrone increased with decreasing liver function. No significant differences were observed concerning SHBG concentrations in the three groups of patients. Dexamethasone suppression did not change the concentration of testosterone significantly, but oestrone and oestradiol concentrations decreased significantly (P less than 0.01) in controls and patients. In patients, but not in controls, a significant (P less than 0.01) increase in FSH and LH concentrations was observed after dexamethasone suppression. The mean percentage increase of FSH and LH was higher the greater the severity of liver cirrhosis.

Adult↗
PubMed1983

Fasting plasma somatostatin in alcoholic liver disease.

Fasting level of somatostatin-like immunoreactivity (SLI) in plasma was measured by a highly sensitive radioimmunoassay in 36 patients with alcoholic liver disease verified by histopathology (10 patients with steatosis and 26 with cirrhosis of the liver). The median value of SLI was markedly elevated in patients with steatosis of the liver as compared to normal subjects, P less than 0.01, while the median value of SLI in the cirrhotic group was even higher, P less than 0.05, as compared to the steatotic group. Correlations of SLI to se-bilirubin and p-coagulation factors 2, 7 and 10 were significant, P less than 0.001 and P less than 0.01, respectively, whereas no correlation to plasma insulin could be elicited. These results suggest that in alcoholic liver disease fasting plasma somatostatin is correlated to the degree of hepatic failure and indicate that the liver is an important site for clearance of portal vein somatostatin.

Adult↗
PubMed1981

Pituitary-testicular function in patients with alcoholic cirrhosis of the liver.

In forty-two patients with alcoholic liver cirrhosis and without recent alcohol ingestion the pituitary-testicular function was studied in an effort to relate the endocrine abnormalities with the degree of liver cell dysfunction, evaluated on a quantitative basis. Compared with values in twenty-one healthy controls, we found significantly elevated serum oestrone, oestradiol, follicle-stimulating hormone, luteinizing hormone and prolactin (P less than 0.01). Serum dehydro-epiandrosterone and dehydroepiandrosterone sulphate were significantly reduced in the cirrhotics (P less than 0.01), whereas serum testosterone was not significantly different from that in the controls. Raised levels of sex-hormone binding globulin were found in 71% (22/31) of the patients (median 8 x 10(-18) mol/l, range 3-17 x 10(-8) mol/l). The incidence of gynaecomastia (38%), cutaneous spiders (67%), testicular atrophy (24%) and reduced axillary hair (71%) was without significant relation to raised levels of sex-hormone binding globulin or progressively reduced liver function. In the presence of clinical or hormonal hypo-gonadism we found evidence of a state of primary hypogonadism together with an inadequate secretion of gonadotropins. The state of hyperoestrogenaemia and the concentration of gonadotropins were significantly correlated to the hepatic synthesis of coagulation factors.

Adult↗
PubMed1981

Autoantibodies, histocompatibility antigens and testosterone in males with alcoholic liver cirrhosis.

Titres and immunoglobulin classes of autoantibodies were examined in 69 male patients with alcoholic liver cirrhosis and the findings were related to particular human leucocyte antigens and serum concentration of testosterone. Both anti-nuclear antibodies (ANA) and smooth muscle antibodies (SMA) were significantly more prevalent in patients with cirrhosis than in sex- and age-matched controls. Antimitochondrial antibodies and liver cell membrane antibody were found in 4% of the patients, and in none of the controls, but this difference was not significant. Patients with HLA-B8 and/or HLA-B12 had higher titres of ANA (n.s.) and SMA (P less than 0.05) than patients without these HLA antigens. Serum concentrations of testosterone were significantly lower in ANA-positive patients than in those negative (P less than 0.05), and a similar tendency was found in SMA-positive patients. With increasing titres of ANA the concentration of testosterone fell. Serum concentration of testosterone correlated inversely (P less than 0.05) with plasma immunoglobulin G and A. It is concluded that both genetic and hormonal factors may influence the humoral immune response in these patients.

Adult↗
PubMed1979

Histological changes in testicular biopsies from chronic alcoholics with and without liver disease.

Testicular and liver biopsies were obtained from thirty consecutive patients at the age of 30 and 64 years with chronic alcoholism (daily consumption of 72 g of alcohol or more for at least five years). The spermatogenesis was normal in 12 patients (40 per cent), moderately reduced in 15 patients (50 per cent) and severely reduced in 3 patients (10 per cent). No relation between the presence of liver disease as assessed by histological examination of the liver biopsy and the impairment in the spermatogenesis could be demonstrated.

Adult↗
PubMed1978

Pituitary-testicular function in patients with chronic alcoholism.

Testis and liver histology, and pituitary-testicular function were studied in thirty chronic alcoholics. Severe reduction of spermatogenesis was found in 30% and in these patients serum follicle stimulating hormone and prolactin concentrations were significantly higher. There was no correlation between abnormalities in the liver and testis. The serum testosterone was normal in most cases. Sexual dysfunction and testicular atrophy occurred in more than half of the patients and were not related to liver disease. Testicular disorder in chronic alcoholism may be independent of liver disease.

Alcoholism↗
PubMed1978

Sex steroids and sex-hormone binding globulin in males with chronic alcoholism.

Thirty men with chronic alcoholism were studied. Biopsies of the liver and testis were performed in all. Serum concentrations of total and non-protein bound (free) testosterone and oestradiol, dihydrotestosterone and sex-hormone binding globulin (SHBG) were determined. Testosterone and dihydrotestosterone concentrations were normal in most patients, whereas oestradiol and free oestradiol were above normal in approximately 50% of the patients. None of the hormones measured differed significantly between patients with and without cirrhosis. SGBG was significantly higher in men with severely reduced spermatogenesis compared to those with intact germinal epithelium, but there was no difference between men with and without cirrhosis. No relation could be demonstrated between clinical signs of hypogonadism and any of the hormones measured. The results support the view that hormonal and sexual disturbances may occur in chronic alcoholism independent of the presence of liver disease.

Adult↗