Biomedical subjects

H P Volkmann

Publications and source records attributed to H P Volkmann.

6 recordsLinked to original sources

PubMed1990

Transfer from animal insulins to semisynthetic human insulin: a study in four centres.

The effects of transfer from animal insulin to semisynthetic human insulin on glycaemic control, insulin dose and anti-insulin antibodies were investigated in a total of 108 patients at four centres in a double-blind controlled study of eight months duration. Six months after transfer from porcine to human insulin there was a mean (+/- SE) increase in pre-breakfast blood glucose of 1.1 +/- 0.6 mmol l-1 (vs a reduction of 1.6 +/- 0.7 mmol l-1 in controls) (p less than 0.01), and a mean increase of pre-lunch blood glucose of 0.9 +/- 0.7 mmol l-1 (vs a reduction of 1.14 +/- 0.7 mmol l-1 in controls) (p less than 0.05). Six months after transfer from bovine to human insulin, there were no significant changes in blood glucose. Glycated haemoglobin showed no significant change six months after transfer from either bovine or porcine to human insulin. Hypoglycaemic symptoms, the total daily insulin dose, and the ratio of short- to intermediate-acting insulin did not change significantly after transfer from either bovine or porcine to human insulin. Transfer from bovine to human insulin resulted in a significant decline in anti-human insulin antibodies (mean (range): 50.5(14.8-125)% of initial levels), vs controls (113(43.4-234)% of initial levels; p = 0.034), and a non-significant decline in anti-bovine insulin antibodies (52.2(25.8-111)% vs 81.7(42.5-128)%; p = 0.082).

Adult↗

PubMed1989

Therapeutic value of calcium antagonists in autonomous hyperaldosteronism.

The chronic effect of the calcium antagonist nitrendipine was investigated on blood pressure (BP), plasma aldosterone concentration (PAC), plasma renin activity (PRA), and serum potassium in six patients with primary aldosteronism, either due to an (unilateral) aldosterone-producing adenoma (APA; n = 3; age, 44 +/- 4 years; PAC, 312 +/- 96 pg/ml; PRA, less than 0.1 ng/l.h; serum potassium, 2.8 +/- 0.3 mmol/l) or to bilateral idiopathic hyperaldosteronism (IHA; n = 3; age, 49 +/- 1 years; PAC, 212 +/- 32 pg/ml; PRA, 0.1 +/- 0.1 ng/l.h; serum potassium, 3.3 +/- 0.2 mmol/l). After withdrawal of antihypertensive medications at least 3 weeks prior to the study, nitrendipine was given orally in a daily dosage of 40 to 60 mg. BP, PAC, PRA, and serum potassium were determined before (see data above) and after 4 weeks of nitrendipine therapy. After 4 weeks, BP was significantly reduced (178 +/- 10 to 165 +/- 6 mmHg systolic, 109 +/- 7 to 101 +/- 6 mmHg diastolic) in three patients with APA and in two with IHA. No significant changes of PAC, PRA, and serum potassium were observed in these patients. However, one patient with clinical characteristics of IHA and a long-term history of diuretic therapy showed a complete normalization of BP, PAC, PRA, and serum potassium, suggesting that the etiology of autonomous hyperaldosteronism in this patient might differ from typical primary aldosteronism. From these findings we conclude that calcium antagonists may be helpful in lowering BP in those patients with primary aldosteronism who develop intolerable side effects under treatment with spironolactone or trilostane.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗

PubMed1988

[Diagnostic significance of the clonidine suppression test in suspected pheochromocytoma].

A clonidine suppression test and the measurement of the catecholamine (noradrenaline and adrenaline) concentration in 24-hour urine were undertaken on 13 patients with benign phaeochromocytoma (PCC), 30 patients with benign hypertension (BHT) and ten healthy, normotensive volunteers. In 11 patients with PCC (85%) the clonidine suppression test gave true-positive results (no significant suppression of initially raised plasma-catecholamine concentration after oral intake of 300 micrograms clonidine). Continuous fall in plasma-catecholamine level after clonidine occurred in two patients with PCC and only moderately elevated initial levels (false-negative results, 15%), as well as in all patients with BHT and all normal controls (true-positive, 100% each). A false-negative result for catecholamine concentration in 24-hour urine was obtained in only one patient (8%). In all others there were either true-positive results (urine concentration greater than 200 micrograms/24 h in 12 patients with PCC, 92%) or true-negative results (urine concentration less than 150 micrograms/24 h in all patients with BHT, 100% each). Compared with direct catecholamine measurement in 24-hour urine, the clonidine suppression test did not fulfil the criteria for further investigations in those patients who had moderately raised plasma-catecholamine levels.

Adrenal Cortex Function Tests↗

PubMed1987

Chlorpropamide alcohol flushing: a normal response?

The relationship between chlorpropamide alcohol flushing and non-insulin dependent diabetes remains uncertain. It is known, however, that the frequency of facial flushing with alcohol and the temperature response depend upon both the plasma level of chlorpropamide and the starting facial temperature [10]. We tested 23 young adult non-diabetic subjects with 8 g of ethanol after a dose of chlorpropamide 250 mg twice daily for 2 days or a placebo, in a double blind, cross-over manner. Previously, nine other subjects had participated in a pilot study to assess the safety of the chlorpropamide dose and to ensure that adequate plasma chlorpropamide levels were achieved. No subject was negative for chlorpropamide alcohol flushing, as defined by the following criteria: facial temperature rise of 35% or more of maximum possible rise, observer assessment or subject assessment. In 26 of the total 32 subjects, all three criteria were fulfilled. Thus, among young, healthy non-diabetic adults chlorpropamide alcohol flushing would appear to be a normal phenomenon.

Adult↗

PubMed1986

Metabolic abnormalities in children of non-insulin dependent diabetics.

Non-insulin dependent diabetes appears to be an inherited condition. A study of young offspring of non-insulin dependent diabetics was conducted to determine whether metabolic abnormalities could be found at a young age before clinical diabetes developed. Thirteen patients with non-insulin dependent diabetes were selected who fulfilled the following criteria: they had a sibling who also had non-insulin dependent diabetes, their spouse was non-diabetic, and the offspring were aged between 12 and 45 years, not diabetic, and available for study. All 32 offspring had a 75 g oral glucose tolerance test, and results in 13 of them, one randomly selected from each family, were compared with 13 controls of similar age, sex, and weight. The offspring had significantly higher fasting concentrations of glucose, higher proportions of haemoglobin A1, and higher concentrations of insulin, C peptide, and glucagon. After glucose challenge the increases in both glucose and C peptide concentrations were significantly greater in the offspring. These differences were maintained in all 32 offspring when compared with 18 controls of similar age, sex, and weight; seven of the 32 offspring had impaired glucose tolerance. These results indicate that young offspring of selected non-insulin dependent diabetics can show extensive metabolic changes including impaired glucose tolerance. These changes are associated with hyperinsulinaemia and hyperglucagonaemia.

Adolescent↗

PubMed1986

Renal vessel changes in diabetic KK-mice.

Glomerular hyperfiltration is thought to be of pathogenic importance in the structural abnormalities seen in diabetic nephropathy but its cause is not known. It has been suggested that the changes in the preglomerular vascular system may lead to a disturbance of glomerular blood flow in diabetes. We therefore examined the potential role of changes in the vascular system supplying the glomerulus in diabetic mice. The kidneys of 15 diabetic KK-mice (aged 2, 5 and 12 months) were studied and compared with those of 15 non-diabetic NMRI-mice. We determined vessel cross-sectional, wall and lumen areas of 408 small intrarenal arteries, 5,140 arterioles and 518 preglomerular afferent arterioles using a morphometric method. At 2 months, diabetic arteries and arterioles were considerably smaller than the controls, while preglomerular afferent arterioles were the same size. At 12 months, however, all diabetic vessels measured were much larger than the controls. This was chiefly due to an excessive increase in lumen area: in the diabetic arteries the mean (+/- SEM) lumen area at 12 months was 1,057 +/- 142 vs 616 +/- 72 sq mu in controls (P less than 0.001), in arterioles 176 +/- 7 vs 115 +/- 4 sq mu (P less than 0.001) and in preglomerular afferent arterioles (at 5 months) 131 +/- 8 vs 95 +/- 7 sq mu (P less than 0.001). The dilatation of small intrarenal arteries and arterioles in diabetic mice may result from progressive impairment of vasoconstriction and may be a cause of the glomerular hyperfiltration in diabetes.

Animals↗