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Biomedical subjects

M D Nielsen

Publications and source records attributed to M D Nielsen.

At least 37 records · Page 2Linked to original sources
PubMed1989

Autoimmune involvement in Cushing syndrome due to primary adrenocortical nodular dysplasia.

Cushing syndrome due to primary adrenocortical nodular dysplasia was diagnosed in two patients, aged 3 years 9 months and 9.5 years. Subsequently, adrenalectomy was performed and followed by steroid replacement. In both cases, the adrenals were normal or only slightly enlarged and showed adrenocortical nodular dysplasia histologically. Small lymphocytic infiltrates consisting of T-cells and class II MHC positive macrophages were present in adrenal specimens of both the patients. Samples of protein A sepharose purified serum immunoglobulins from both children stimulated adrenocortical DNA synthesis and cortisol production in cultured guinea-pig adrenal segments in vitro in a dose dependent fashion. Adrenal stimulating immunoglobulins were also demonstrated in serum specimens of both patients' mothers. However, none of them had overt signs of adrenal disease. Our data support the view that autoimmune mechanisms may be involved in primary adrenocortical nodular dysplasia.

Adrenal Cortex↗
PubMed1989

Removing a retained placenta by oxytocin--a controlled study.

No increase in maternal plasma oxytocin concentration was detected after administration of 100 IU oxytocin into the umbilical veins of seven women immediately after delivery. The delivery of the placenta was accelerated after umbilical vein injection of 100 IU oxytocin in a placebo-controlled study of 40 women: 12 minutes (4 to 40) in the oxytocin group versus 40 minutes (29 to 40) in the placebo group (median and interquartile ranges), p less than 0.05.

Clinical Trials as Topic↗
PubMed1989

Plasma concentrations of adrenaline, noradrenaline and dopamine during forearm dynamic exercise.

In six healthy volunteers plasma concentrations of adrenaline, noradrenaline and dopamine were measured at rest and during dynamic forearm exercise at submaximal and maximal intensities. Arterial and venous concentrations of adrenaline and noradrenaline increased with forearm exercise at all workloads. Dopamine concentrations did not change. The increases in adrenaline and noradrenaline were almost linearly related to the increase in heart rate with no levelling off at maximal exercise intensities. It is concluded that dynamic exercise with the forearm muscle group causes a small but significant activation of the sympatho-adrenal system as reflected by increases in plasma concentrations of adrenaline and noradrenaline.

Adult↗
PubMed1989

On the pathogenesis of arterial blood pressure elevation early in the course of diabetic nephropathy.

We measured plasma- and extracellular fluid volume (125I-albumin, 51Cr-EDTA), plasma concentrations of renin, angiotensin I and II, aldosterone and atrial natriuretic peptide by radio-immunoassays in insulin-dependent diabetic (IDDM) patients with (n=28) and without (n=11) nephropathy and in 14 normal control subjects matched for sex and age. Glomerular filtration rate (GFR) (ml/min/1.73 m2, single intravenous bolus 51Cr-EDTA technique) was within normal range in all nephropathic patients; 107 (range 78-134). Mean arterial blood pressure (mmHg) was elevated 102 +/- 13 (+/- S.D.) compared to the diabetic and normal control group, 92 +/- 8 and 87 +/- 5, respectively (p less than 0.01). Plasma volume was identical in all three groups while extracellular volume (1/1.73 m2) was expanded in nephropathic patients, 14.5 +/- 1.5 vs 13.1 +/- 0.9 and 12.4 +/- 1.3 in the diabetic and non-diabetic control groups, respectively (p less than 0.05). A significant correlation between extracellular fluid volume and mean arterial blood pressure was found (n=53, r=0.49, p less than 0.001). Active renin was significantly increased in patients with diabetic nephropathy compared with the normal control subjects, while all the remaining hormones were about the same in the three groups. Our study suggests that fluid retention plays a dominant role in the initiation and maintenance of arterial blood pressure elevation early in the course of diabetic nephropathy.

Adult↗
PubMed1989

Changed cyclic guanosine monophosphate atrial natriuretic factor relationship in hypertensive man.

Plasma concentrations of atrial natriuretic factor (ANF) and cyclic guanosine monophosphate (cGMP) were measured in 10 patients with essential hypertension and 10 normotensive controls on the fifth day of a low (50 mmol/day), a medium (180 mmol/day) and a high (380 mmol/day) dietary sodium intake. Plasma ANF and cGMP concentrations were less on the low than on the high sodium intake. Values for ANF on the medium sodium intake were intermediate. In normotensive subjects cGMP concentrations did not differ significantly on the low and the medium sodium intake. As compared with the controls plasma concentrations of cGMP were significantly increased in hypertensive patients on all three levels of sodium intake, while ANF concentrations were identical in the two groups. Since cGMP is a second messenger to ANF the data suggest an increased cellular response to ANF in patients with essential hypertension.

Adult↗
PubMed1988

Male pseudohermaphroditism due to 5 alpha-reductase deficiency in a Swedish family.

Three sibs with an inherited form of male pseudohermaphroditism are described. They were all born with ambiguous external genitalia but no diagnosis of a possible enzyme defect was made during childhood. First seen at the ages of 16, 14 and 10 years respectively, they were investigated in order to establish the pathogenetic nature of the disorder. Serum concentrations of testosterone and dihydrotestosterone before and after stimulation with human chorionic gonadotropin suggested 5 alpha-reductase deficiency. Measurement of steroid metabolites in urine confirmed this diagnosis. It is essential to recognize this condition in order to decide the sex of rearing of the children.

Adolescent↗
PubMed1987

Central role for sodium in the pathogenesis of blood pressure changes independent of angiotensin, aldosterone and catecholamines in type 1 (insulin-dependent) diabetes mellitus.

We studied 73 Type 1 (insulin-dependent) diabetic patients, 18 to 50 years of age, with a diabetes duration of more than five years. Group 1: normal urinary albumin excretion below 30 mg per 24 h (n = 19); group 2: microalbuminuria, 30-300 mg per 24 h (n = 36); and group 3: diabetic nephropathy, above 300 mg per 24 h (n = 18). Fifteen nondiabetic persons matched for sex and age served as control subjects. The sodium intake evaluated on the basis of 24-h urine sodium excretion was similar in patients and control subjects. Blood pressure in groups 1 and 2 and control subjects was below 160/95 mmHg. The blood pressure was increased in group 3 as compared with the other groups (systolic/diastolic 161 +/- 22/101 +/- 9 mmHg vs 131 +/- 13/84 +/- 10, mean +/- SD, p less than 0.0001). Exchangeable sodium was increased in patients (p less than 0.01) and correlated to the mean blood pressure (n = 70, r = 0.41, p less than 0.01). Extracellular volume was increased in patients (p less than 0.05), whereas plasma volume was normal. Supine serum angiotensin II was suppressed in the patients (p less than 0.001). A negative correlation was found between mean blood pressure and supine serum aldosterone (n = 68, r = -0.24, p less than 0.05), and exchangeable sodium and aldosterone (n = 66, r = -0.36, p less than 0.002) in all patients. The catecholamine levels were also suppressed or normal in the patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

A highly sensitive and reproducible immunoradiometric assay for total human renin using monoclonal antibodies, iodogen labelling and polystyrene star tubes.

A two-site immunoradiometric assay for total renin concentration in human plasma is described. A new type of polystyrene tubes with a special bottom geometry, so-called Star Tubes were used. The lower limit of detection was 2 microIU per ml and the working range from 2 to 2000 microIU per ml. The variation for duplicate determinations on standards and plasma samples was 2.7% and the day to day variation was 4.8%. No significant interferences or cross reactivities were identified. EDTA-plasma was analyzed after dilution with a phosphate buffer. Plasma samples from different patient categories were analyzed. The results were compared with those obtained by our substrate enrichment method after acid activation of the samples had taken place. A linear correlation (r = 0.990) between the results obtained with the two methods was found.

Antibodies, Monoclonal↗
PubMed1986

Effects of combined therapy with amiloride and hydrochlorothiazide on plasma and total body potassium, blood pressure, and the renin-angiotensin-aldosterone system in hypertensive patients.

After a run-in period of 8 weeks on a regimen of hydrochlorothiazide (HCT, median dosage 75 mg/day), patients with essential hypertension were randomly allocated to continued hydrochlorothiazide therapy (Group I) or additional treatment with amiloride (Group II, median dosage 15 mg/day, or 5 mg per 25 mg hydrochlorothiazide) for the following 12 weeks. Thereafter all the patients were changed to treatment with a fixed combination tablet containing 5 mg amiloride and 50 mg hydrochlorothiazide (Moduretic), keeping the thiazide dosage unchanged for an additional 12 weeks. In Group I patients there was no change in plasma potassium, total body potassium content or the renin-angiotensin-aldosterone system during the 12 weeks on HCT. When the treatment was changed to Moduretic, significant increases were found of 10% in plasma potassium and 3% in total body potassium content. No important stimulation of the renin-angiotensin-aldosterone system was found. In Group II patients addition of an average of 15 mg amiloride to the hydrochlorothiazide treatment led to significant increases in plasma potassium and total body potassium content of approximately 15% and 4%, respectively. There was also a significant increase in the plasma concentrations of renin, angiotensin II and aldosterone. Reducing the average dose of amiloride to 7.5 mg/day by use of Moduretic did not lead to decrease in plasma potassium or total body potassium content. Plasma concentrations of renin, angiotensin II, and aldosterone were decreased, but the individual changes varied markedly and no significant overall change was found.

Adult↗
PubMed1986

Lack of effect of nifedipine on counterregulatory mechanisms in essential hypertension.

The influence of long-term nifedipine treatment on body fluid compartments, renal function, the renin-angiotensin system, and the adrenergic system was studied in 18 patients with essential hypertension. A placebo period of 4 weeks was followed by a 6-week dose-titration period. Thereafter, the dose was kept constant for an additional 6 weeks (mean dose, 51 mg/day). As compared with placebo values, diastolic blood pressure decreased approximately 12% during nifedipine treatment. Plasma volume, extracellular fluid volume, and the ratio of plasma to interstitial fluid volume did not change significantly, either in the group as a whole or in a subgroup in which pedal edema developed. Plasma concentrations of epinephrine and norepinephrine increased slightly after 2 weeks of treatment, but they returned to control values after 6 weeks of therapy. Plasma concentrations of renin, angiotensin II, and aldosterone did not change significantly. Glomerular filtration rate and renal clearances of sodium and potassium were unchanged as well. These results indicate that long-term nifedipine treatment does not lead to activation of counterregulatory mechanisms, such as fluid retention or the renin-angiotensin or adrenergic systems. This may well be of importance for the antihypertensive efficacy of nifedipine treatment.

Adult↗
PubMed1985

The influence of nifedipine treatment on counter-regulatory mechanisms in essential hypertension.

The influence of nifedipine treatment on plasma (PV) and extracellular fluid volume (ECV), the ratio of plasma volume to interstitial fluid volume (PV:IF), glomerular filtration rate (GFR), renal clearances of Na+ and K+, plasma concentrations of renin (PRC), angiotensin II (pANG II), aldosterone (pAldo), adrenaline (PA) and noradrenaline (PNA) were studied in 18 consecutive patients with essential hypertension. A 4-week placebo period was followed by a 6-week dose-titration period (period A). Thereafter the dose was kept constant for an additional 6 weeks (period B), the mean dose being 51 mg/day. As compared with placebo, diastolic blood pressure (DBP) decreased from 105 +/- 7 to 93 +/- 9 mmHg at the end of period B. Extracellular fluid volume, PV, and PV:IF were not significantly changed at the end of period A or B, neither in the group as a whole nor in a subgroup, who developed pedal oedema. After 2 weeks on nifedipine, PA as well as PNA increased slightly but returned to control values after 6 weeks of therapy. Plasma renin concentration, pANG II, pAldo and GFR did not change significantly. Renal sodium handling was also unchanged. It is concluded that long-term nifedipine therapy (exceeding 6 weeks) does not lead to activation of counter-regulatory mechanisms such as fluid retention, activation of the renin-angiotensin system and the adrenergic system. Renal function is unaffected by nifedipine.

Adult↗
PubMed1984

Testosterone treatment and arginine-induced growth hormone stimulation in male delayed puberty: effects on serum calcium, phosphate and vitamin D metabolites.

Hormonal changes after arginine-induced growth hormone stimulation and subsequent testosterone treatment were examined in 5 patients classified as having male delayed puberty. All the patients responded well to growth hormone stimulation and a significant negative correlation was found between the delay in height age and the maximal growth hormone response, r = 0.80, P less than 0.05. The testosterone treatment did not alter this pattern. Changes in PTH, 25OHD, 24.25(OH)2D, and 1.25(OH)2D were examined at 24 h after the infusion. The results showed significant reductions in PTH (P less than 0.05) and 24.25 (OH)2D (P less than 0.05) and a possible increase in 1.25(OH)2D, whereas 25OHD remained unchanged. These results may support the conception of growth hormone as a common denominator of growth and bone metabolism.

Adolescent↗
PubMed1984

The influence of ACE-inhibition by captopril on renal formation and metabolism of angiotensins I and II in patients with renovascular hypertension.

Fourteen patients with hypertension of presumed renovascular etiology were studied by renal vein catheterization. Unilateral renin secretion was found in 8 patients. In 4 of these patients a positive veno-arterial difference of plasma angiotensin I concentration (PAI) across the affected kidney increased markedly after a single dose of captopril. Across the contralateral kidney the net veno-arterial PAI difference changed from about zero before captopril to clearly negative values after captopril. The PAI values in the remaining 4 patients, who were already on captopril before the catheterization, were similar to those observed after a single dose of captopril. In patients with bilateral renin secretion the renal veno-arterial PAI differences across the kidneys were positive or close to zero before captopril. After captopril both positive and negative veno-arterial differences of PAI were observed. The plasma angiotensin II concentrations decreased after captopril to low values. These low values together with extremely high PAI values demonstrate effective ACE-inhibition. A high generation rate of angiotensin I in the affected kidney in patients with unilateral renin secretion after captopril is probably explained by activation of the local renin secretion. The angiotensin I "consumption" in the contralateral kidney after captopril in spite of no angiotensin II formation suggests the presence of alternative degradation processes for angiotensin I in the human kidney.

Adult↗
PubMed1984

Placental steroid sulfatase deficiency: biochemical diagnosis and clinical review.

Twenty-three cases of placental steroid sulfatase deficiency are reported. All children were boys who later acquired ichthyosis of the recessive X-linked type. The steroid sulfatase deficiency was present in placental tissue, umbilical cord leucocytes, and cultured skin fibroblasts of affected boys. An antepartum diagnosis can be obtained either by detecting the enzyme deficiency in cultured amniotic fluid cells or by finding an elevated total excretion of androstenetriol , 16 alpha-hydroxy-dehydroepiandrosterone, and 16 alpha-hydroxy-pregnenolone in maternal third-trimester urine. Vaginal delivery was accomplished in 16 patients (70%). No conspicuous pregnancy complications or neonatal problems were noted. However, birth weights tended to be relatively low. Intervention is unnecessary unless other obstetric indications require it. The incidence of this disorder appears to be approximately one per 2000 male births.

17-alpha-Hydroxypregnenolone↗
PubMed1984

Group I pepsinogens in serum. I. Normal range, age and sex relation, diurnal rhythm, seasonal variation, and distribution in ABO blood groups.

The concentration of group I pepsinogens (PG I) in serum was determined in 235 healthy persons and hospital controls. The concentration was significantly higher in males. Correction of PG I with regard to body weight or lean body mass eliminated the sex difference but not the weak correlation with age. The normal range was 0.60-3.3 ng PG I/ml serum/kg body weight. For comparison with other PG I studies another normal range, 46-211 ng PG I/ml serum, was calculated as the 95% interpercentile range of the present PG I concentrations. In a study of diurnal rhythm and in a 6-month study of seasonal variation, no significant variation of PG I in serum was found. Serious non-gastric surgical disease did not influence the PG I level in serum. The PG I levels in blood groups O, A, and B did not differ significantly.

ABO Blood-Group System↗
PubMed1983

Effects of amiloride on plasma and total body potassium, blood pressure, and the renin-angiotensin-aldosterone system in thiazide-treated hypertensive patients.

Total body potassium content, plasma potassium concentration, blood pressure, and plasma concentrations of renin, angiotensin II, and aldosterone were measured in patients with essential hypertension after a run-in period of 8 wk on a regimen of hydrochlorothiazide (median dosage 75 mg/day). Patients were then randomly assigned to continued hydrochlorothiazide therapy (group I) or to receive adjunctive treatment with amiloride (group II, median dosage 15 mg/day or 5 mg per 25 mg hydrochlorothiazide) for the following 3 mo. There were no changes in group I patients during 3 mo on hydrochlorothiazide in plasma potassium, total body potassium content, or the renin-angiotensin-aldosterone system. Blood pressure was also unchanged. In group II patients addition of amiloride to hydrochlorothiazide induced a rise in plasma and total body potassium of approximately 15% and 4%. The potassium-retaining effect was maintained throughout the 12-wk period, although the maximal changes were observed after 8 wk of treatment. Supine blood pressure did not change, but there was a significant decrease in standing systolic blood pressure. There was a marked rise in plasma concentrations of renin, angiotensin II, and aldosterone.

Adult↗