PubMed Health⌕ Search

Biomedical subjects

M P Hermans

Publications and source records attributed to M P Hermans.

At least 37 records · Page 2Linked to original sources
PubMed1997

[Treatment and glycemic control of 1200 diabetic patients enrolled at the National Institute of Disease-Disability Insurance diabetes convention].

We have studied the characteristics of insulin therapy and home blood glucose monitoring of 1.200 diabetic patients (590 males, 610 females), mainly type I adults (age: 43 +/- 19 years, mean +/- 1 SD), attending a licensed diabetes center in Belgium which benefits from a National Health Service convention system for providing education and home blood glucose monitoring kits and disposables to diabetic subjects. 50% of these patients were treated with 2 daily insulin injections, while 22% were treated with 3 and 24% with 4 daily injections. 4% of the subjects were treated with a continuous subcutaneous insulin infusion. Patients treated with four daily injections were younger than those treated with other insulin schemes (p < 0.001). Home blood glucose monitoring strip consumption was 2.2 patient-1 day-1. The mean HbA1C level was 8.63 +/- 1.55% [8.54 +/- 1.46 in males and 8.72 +/- 1.62% in females (NS)]. In more than one third of the subjects treated with injections, HbA1C was lower than 8% HbA1C was also below 8% in 50% of patients using 1100-1200 strips year-1.

Adolescent↗
PubMed1997

Clinical aspects of diabetes secondary to idiopathic haemochromatosis in French-speaking Belgium.

Better awareness of the clinical presentation of idiopathic haemochromatosis is a key element for early diagnosis and treatment. We retrospectively analysed the medical records of 105 patients (80 males, 25 females) diagnosed with idiopathic haemochromatosis over the past two decades in the two academic hospitals of Louvain University. Age at diagnosis was 50 +/- 12 years (mean +/- SD). Median ferritin levels were 1,803 micrograms/L-1. Cirrhosis was found at histology in 51%. Ferritin levels were significantly higher in cirrhotic than non-cirrhotic subjects (P < 0.05). Impaired glucose tolerance and diabetes were found at admission in 7 and 40% of all patients. Diabetes was more frequent when cirrhosis was present (53 vs. 25% in cirrhosis-negative patients, P < 0.05). Accordingly, cirrhosis was also more frequent in diabetic than non-diabetic patients (70 vs. 40%, P < 0.05). Diabetic subjects with cirrhosis frequently presented with symptomatic hyperglycaemia at diagnosis, had higher HbA1c levels, and were more insulin-requiring than their non-cirrhotic diabetic counterparts (P < 0.05). There was also a trend towards more frequent chronic complications of diabetes in the former group. Diabetic patients with cirrhosis had slightly higher insulin levels but lower C-peptide values (P < 0.05) than diabetic subjects without cirrhosis. Chronic phlebotomy did not affect subsequent insulin requirements. Thus, diabetes is still a frequent complication of haemochromatosis in Belgium, and its presence and severity are markedly associated with that of cirrhosis at diagnosis of idiopathic haemochromatosis.

Adult↗
PubMed1995

[Nonketotic hyperglycemic coma induced by somatostatin in an AIDS patient].

A 33-year-old woman with AIDS was treated with somatostatin (continuous infusion 6 mg/day) for intractable diarrhoea. Improvement was insufficient and the dose was increased to 12 mg/day 5 days later. Hyperosmolar non-ketotic coma occurred two days later (blood glucose 53 mmol/l, bicarbonate 8 mmol/l, pH of arterial blood 7.2). Search for urinary ketones was negative. Klebsiella pneumonia was isolated in the urine sample. Somatostatin was withdrawn and the patient improved with parenteral nutrition and intravenous insulin. Glucose tolerance was verified after recovery and was normal. Somatostatin is known to impair glucose tolerance and as shown in this case should also be recognized as a cause of hyperosmolar non-ketotic coma. Increasing use of somatostatin, particularly in HIV patients often given other hyperglycaemia inducing drugs such as didanosine, pentamidine, dapsone, and phenytoin should be accompanied with careful monitoring of blood glucose levels.

AIDS-Related Opportunistic Infections↗
PubMed1995

Unexpected borderline malignant and malignant smooth muscle cell tumors of the uterine corpus in women treated with LH-RH analogues.

In this report, two cases of uterine smooth muscle cell tumors, one of uncertain malignant potential and one clearly malignant, are described in women treated for prolonged periods with luteinizing hormone-releasing hormone (LH-RH) analogues. Due to lengthy monitoring of LH-RH therapy, surgical intervention and histologic classification of these tumors was late in the course of disease, resulting in a delay in definite treatment. The risk to these women is discussed. The effects of LH-RH analogue therapy on fibroids is reviewed. Suggestions are put forward for monitoring LH-RH analogue therapy.

Adult↗
PubMed1993

Obstetric characteristics profiles as quality assessment of obstetric care.

In The Netherlands only about 50% of all pregnancies are defined as high risk pregnancies and consequently come into the domain of care of an obstetrician. In order to qualify as a high risk pregnancy, the pregnancy must satisfy certain criteria contained in an officially approved list of indications. Due to varying perceptions of these selection criteria by the selectors, larger differences in the treated population, obstetric interventions and results, respectively, were expected than in other countries. Within the framework of the project 'Obstetric Peer Review' (Verloskundige Onderlinge Kwaliteitsspiegeling, VOKS) the type and the magnitude of the differences of the values of the obstetric characteristics of population, interventions and results, respectively have been investigated. For the high risk pregnancies the data contained in the Perinatal Database of The Netherlands were used for the years 1983-1987, both inclusive. Because the various obstetric departments in The Netherlands had been unaware of these differences, consequently they had to become conscious about these differences and be informed about their own position relative to the others. For an instant comparison a single sheet graphical method has been designed, affording the assessment of one's own obstetric characteristics relative to those of other departments for the above mentioned 5 years for each of the 25 items considered. All departments, which participated in the Perinatal Database of The Netherlands during the years 1983-1987, received their own profiles and were invited to reply. Large differences were observed for the various characteristics considered.(ABSTRACT TRUNCATED AT 250 WORDS)

Databases, Factual↗
PubMed1992

Long-term reduction of microalbuminuria after 3 years of angiotensin-converting enzyme inhibition by perindopril in hypertensive insulin-treated diabetic patients.

We studied the long-term effects of the angiotensin-converting enzyme (ACE) inhibitor perindopril, administered for 36 months on glycemic control, creatinine clearance, and albuminuria in hypertensive insulin-treated diabetics. After 1 month treatment with placebo, 39 patients entered the study and received 4-8 mg perindopril/day. Within the first 3 months, diastolic blood pressure was normalized in 80% of the patients. From these, 23 were followed during a total of 3 years on perindopril therapy, and divided in three groups according to their initial urinary albumin excretion rate (AER): 11 had normal AER (less than 15 mg/24 hours), eight had microalbuminuria (AER 15-150 mg/24 hour), and four had AER greater than 150 mg/24 hours and had overt proteinuria. Long-term (3 years) diastolic blood pressure normalization (less than or equal to 90 mm Hg) was achieved throughout the study. Concomitant with blood pressure reduction, a long-term decrease in AER was observed in normo- and microalbuminuric patients. Macroproteinuria was unaffected by perindopril. Glycemic control and creatinine clearance remained stable during the whole study period. No major side effects were observed. We conclude that perindopril safely produces a long-term normalization of elevated blood pressure in hypertensive insulin-treated diabetics without affecting glycemic control. Blood pressure normalization is associated with long-term AER reduction in normo- and microalbuminuric patients.

Albuminuria↗
PubMed1991

Effects of chloride deficiency on the pancreatic B-cell response to acetylcholine.

Muscarinic stimulation of pancreatic B-cells markedly amplifies insulin secretion through complex mechanisms which involve changes in membrane potential and ionic fluxes. In this study, normal mouse islets were used to evaluate the role of Cl- ions in these effects of acetylcholine (ACh). Whatever the concentration of glucose, the rate of 36Cl- efflux from islet cells was unaffected by ACh. Replacement of Cl- by impermeant isethionate in a medium containing 15 mM glucose did not affect, or only slightly decreased, the ability of ACh to depolarize the B-cell membrane and increase electrical activity, to accelerate 45Ca2+ and 86Rb+ efflux from islet cells, and to amplify insulin release. In the absence of extracellular Ca2+, a high concentration of ACh (100 microM) mobilized intracellular Ca2+ and caused a transient release of insulin and a sustained acceleration of 86Rb+ efflux. None of these effects was affected by Cl- omission or by addition of furosemide, a blocker of the Na+, K+, 2Cl- cotransport. Isethionate substitution for Cl- in a medium containing a nonstimulatory concentration of glucose (3 mM) barely reduced the depolarization of B-cells by ACh, but inhibited the concomitant increase in 86Rb+ efflux. We have no explanation for the latter effect that was not mimicked by furosemide. In conclusion, ACh stimulation of pancreatic B-cells, unlike that of exocrine acinar cells, is largely independent of Cl- and is insensitive to furosemide. The acceleration of ionic fluxes produced by ACh does not involve the Na+, K+, 2Cl- cotransport system.

Acetylcholine↗
PubMed1989

Relative importance of extracellular and intracellular Ca2+ for acetylcholine stimulation of insulin release in mouse islets.

Mouse islets were used to study whether mobilization of intracellular Ca2+ is sufficient to account for acetylcholine (ACh) amplification of glucose-induced insulin release. In the presence of 15 mM glucose, the acceleration of 45Ca efflux and insulin release by 1-100 microM ACh increased with the concentration of extracellular Ca2+ (0.25-2.5 mM). Low concentrations of the Ca2+-channel blockers D 600 (1 microM) or nifedipine (0.1 microM) partially inhibited glucose-induced insulin release and its amplification by ACh. At higher concentrations, D 600 (25 microM) or nifedipine (2 microM) practically abolished the ionic and secretory effects of 1 microM ACh. However, 100 microM ACh still caused a fast, large, but transient acceleration of 45Ca efflux, accompanied by a small, short-lived release of insulin. Similar results were obtained in a Ca2+-free medium, indicating that this peak of 45Ca efflux reflects Ca2+ mobilization. Addition of nifedipine or omission of Ca2+ during ACh stimulation rapidly and strongly inhibited 45Ca efflux and insulin release. Both glucose and ACh-induced 45Ca uptake were inhibited by D 600. Only high concentrations of ACh (100 microM) mobilize enough cellular Ca2+ to trigger a small and transient insulin release when Ca2+ influx is prevented or impossible. A continuous influx of Ca2+ is necessary for low ACh concentrations to increase release and for high concentrations to have a sustained effect. The amplification of release by the neurotransmitter results from a slight enhancement of Ca2+ influx associated with a marked increase in the effectiveness of incoming Ca2+ on the releasing machinery.

Acetylcholine↗
PubMed1988

Glucose-, calcium- and concentration-dependence of acetylcholine stimulation of insulin release and ionic fluxes in mouse islets.

Mouse islets were used to define the glucose-dependence and extracellular Ca2+ requirement of muscarinic stimulation of pancreatic beta-cells. In the presence of a stimulatory concentration of glucose (10 mM) and of Ca2+, acetylcholine (0.1-100 microM) accelerated 3H efflux from islets preloaded with myo-[3H]inositol. It also stimulated 45Ca2+ influx and efflux, 86Rb+ efflux and insulin release. In the absence of Ca2+, only 10-100 microM-acetylcholine mobilized enough intracellular Ca2+ to trigger an early but brief peak of insulin release. At a non-stimulatory concentration of glucose (3 mM), 1 microM- and 100 microM-acetylcholine increased 45Ca2+ and 86Rb+ efflux in the presence and absence of extracellular Ca2+. However, only 100 microM-acetylcholine marginally increased 45Ca2+ influx and caused a small, delayed, stimulation of insulin release, which was abolished by omission of Ca2+. At a maximally effective concentration of glucose (30 mM), 1 microM- and 100 microM-acetylcholine increased 45Ca2+ influx and efflux only slightly, but markedly amplified insulin release. Again, only 100 microM-acetylcholine mobilized enough Ca2+ to trigger a peak of insulin release in the absence of Ca2+. The results thus show that only high concentrations of acetylcholine (greater than or equal to 10 microM) can induce release at low glucose or in a Ca2+-free medium. beta-Cells exhibit their highest sensitivity to acetylcholine in the presence of Ca2+ and stimulatory glucose. Under these physiological conditions, the large amplification of insulin release appears to be the result of combined effects of the neurotransmitter on Ca2+ influx, on intracellular Ca2+ stores and on the efficiency with which Ca2+ activates the releasing machinery.

Acetylcholine↗
PubMed1988

Muscarinic control of pancreatic B cell function involves sodium-dependent depolarization and calcium influx.

Mouse pancreatic islets were used to investigate the mechanisms and functional significance of the B cell membrane depolarization by acetylcholine (ACh). At low glucose (3mM), ACh (20 microM) increased 22Na+ influx, and slightly depolarized the B cell membrane but did not induce electrical activity or stimulate 45Ca2+ influx. ACh also accelerated 86Rb+ and 45Ca2+ efflux and barely affected basal insulin release. At a stimulatory concentration of glucose (10 mM), ACh stimulated 22Na+ influx, depolarized the B cell membrane, increased glucose-induced electrical activity, and stimulated 45Ca2+ influx. ACh also accelerated 86Rb+ and 45Ca2+ efflux and strongly potentiated insulin release. Omission of extracellular Ca2+ did not impair ACh stimulation of 22Na+ influx or 86Rb+ efflux, slightly modified the acceleration of 45Ca2+ efflux, and almost completely suppressed the increase in insulin release. Na+ omission (with N-methyl-D-glucamine as substitute) prevented the B cell membrane depolarization and the stimulation of 45Ca2+ influx, largely inhibited the acceleration of 86Rb+ efflux and insulin release, and suppressed the late phase of 45Ca2+ efflux otherwise produced by ACh. On the other hand, ACh stimulation of 3H efflux from islets prelabeled with myo-[2-3H]inositol was not affected by Na+ omission. All effects of ACh were blocked by atropine and unaffected by nicotinic antagonists. It is concluded that activation of muscarinic receptors depolarized the B cell membrane by increasing its permeability to Na+. When the membrane is already depolarized by glucose, this further depolarization augments Ca2+ influx and, hence, potentiates insulin release.

Acetylcholine↗
PubMed1987

The permissive effect of glucose, tolbutamide and high K+ on arginine stimulation of insulin release in isolated mouse islets.

Mouse islets were used to study how glucose modulates arginine stimulation of insulin release. At 3 mmol/l glucose, arginine (20 mmol/l) decreased the resting membrane potential of B cells by about 10 mV, but did not evoke electrical activity. This depolarisation was accompanied by a slight but rapid acceleration of 86Rb+ efflux and 45Ca2+ influx. However, 45Ca2+ efflux and insulin release increased only weakly and belatedly. When the membrane was depolarised by threshold (7 mmol/l) or stimulatory (10-15 mmol/l) concentrations of glucose, arginine rapidly induced or augmented electrical activity, markedly accelerated 86Rb+ efflux, 45Ca2+ influx and efflux, and triggered a strong and fast increase in insulin release. When glucose-induced depolarisation of the B-cell membrane was prevented by diazoxide, arginine lost all effects but those produced at low glucose. However, the delayed increase in release still exhibited some glucose-dependency. In contrast, depolarisation by tolbutamide, at low glucose, largely mimicked the permissive effect of high glucose. Depolarisation by high K+ also amplified arginine stimulation of insulin release, but did not accelerate it as did glucose or tolbutamide. Omission of extracellular Ca2+ abolished the releasing effect of arginine under all conditions. The results thus show that the permissive action of glucose mainly results from its ability to depolarise the B-cell membrane. It enables the small depolarisation by arginine itself to activate Ca channels more rapidly and efficiently. Changes in the metabolic state of B cells may also contribute to this permissive action by increasing the efficacy of the initiating signal triggered by arginine.

Animals↗
PubMed1987

Modulation of the effect of acetylcholine on insulin release by the membrane potential of B cells.

Mouse islets were used to test the hypothesis that the B cell membrane must be depolarized for acetylcholine to increase insulin release. The resting membrane potential of B cells (at 3 mM glucose) was slightly decreased (5 mV) by acetylcholine, but no electrical activity appeared. This depolarization was accompanied by a Ca-independent acceleration of 86Rb and 45Ca efflux but no insulin release. When the B cell membrane was depolarized by a stimulatory concentration of glucose (10 mM), acetylcholine potentiated electrical activity, accelerated 86Rb and 45Ca efflux, and increased insulin release. This latter effect, but not the acceleration of 45Ca efflux, was totally dependent on extracellular Ca. If glucose-induced depolarization of the B cell membrane was prevented by diazoxide, acetylcholine lost all effects but those produced at low glucose. In contrast, when the B cell membrane was depolarized by leucine or tolbutamide (at 3 mM glucose), acetylcholine triggered a further depolarization with appearance of electrical activity, accelerated 86Rb and 45Ca efflux, and stimulated insulin release. Acetylcholine produced similar effects (except for electrical activity) in the presence of high K or arginine which, unlike the above test agents, depolarize the B cell membrane by a mechanism other than a decrease in K+ permeability. Omission of extracellular Ca abolished the releasing effect of acetylcholine under all conditions but only partially decreased the stimulation of 45Ca efflux. The results show thus that acetylcholine stimulation of insulin release does not result from mobilization of cellular Ca but requires that the B cell membrane be sufficiently depolarized to reach the threshold potential where Ca channels are activated. This may explain why acetylcholine alone does not initiate release but becomes active in the presence of a variety of agents.

Acetylcholine↗