Search PubMed⌕ Search

Biomedical subjects

H W de Valk

Publications and source records attributed to H W de Valk.

At least 19 recordsLinked to original sources

[Pregnancy in women with diabetes mellitus type I: maternal and perinatal complications, in spite of good blood glucose control].

OBJECTIVE: To examine the maternal and neonatal outcome of pregnancies of women with type I diabetes mellitus. DESIGN: Retrospective. METHODS: The medical records of pregnancies (> or = 16 weeks) in women with type I diabetes mellitus between 1986/'97 were studied in University Medical Center Utrecht, Academic Hospital Groningen and Isala Clinics, location 'De Weezenlanden', Zwolle, the Netherlands. RESULTS: During the study period, 172 women had 220 pregnancies: 212 single and 8 twin pregnancies. The mean age was 29.1 years (SD: 4.1), the mean duration of standing of the diabetes was 12 years (range: 1-32) and the mean concentration of glycosylated haemoglobin (HbA1c) was 6.3% at 10 weeks of pregnancy. The incidence of children with congenital malformations was 4 times higher (n = 19; 9.0%) than that in the Dutch population (2%). Macrosomia occurred in 92 children (43.4%) and perinatal mortality in 7 (3.3%). Maternal hypertensive complications occurred in 39 single pregnancies (18.4%), which is 2-3 times more often than in the Dutch population. CONCLUSION: In type I diabetic women maternal complications, perinatal morbidity and mortality are increased, despite near optimal glycaemic control.

Adult↗

[Epilepsy, disturbances of behavior and consciousness in presence of normal thyroxine levels: still, consider the thyroid gland].

Three patients, one man aged 51 years, and two women aged 49 and 52 years, had severe fluctuating and progressive neurological and psychiatric symptoms. All three had normal thyroxine levels but elevated thyroid stimulating hormone levels and positive thyroid antibodies. Based on clinical, laboratory, MRI and EEG findings they were eventually diagnosed with Hashimoto's encephalopathy, associated with Hashimoto thyroiditis. Treatment with prednisone in addition to thyroxine suppletion resulted in a remarkable remission of their neuropsychiatric symptoms. The disease is probably under-recognized.

Autoantibodies↗

[Phenylketonuria: a children's disease in adulthood].

The prognosis for patients with phenylketonuria (PKU) has improved greatly with early institution of treatment after birth. It was assumed that the diet could be terminated after adolescence but there are strong indications that hyperphenylalaninaemia can have detrimental effects in adult patients. Hyperphenylalaninaemia can cause reversible white matter abnormalities, and is also associated with psychiatric illness, which improves with lowering of the plasma phenylalanine level. Even optimally treated patients generally have a decreased performance with neuropsychological tests compared with subjects without PKU. Elevation of the plasma phenylalanine level leads to worsening of neuropsychological performance, lowering of the level leads to improved performance. Strict metabolic control is necessary during pregnancy in women with PKU in view of the increasing frequency of congenital abnormalities with increasing phenylalanine level. The complexity and demanding nature of the diet treatment make specialised facilities for optimal medical and paramedical care mandatory.

Adult↗

High dose of simvastatin normalizes postprandial remnant-like particle response in patients with heterozygous familial hypercholesterolemia.

Familial hypercholesterolemia (FH) and disturbances in postprandial lipoprotein metabolism are both associated with premature atherosclerosis. The effect of beta-hydroxy-beta-methylglutaryl coenzyme A reductase inhibitors on plasma cholesterol levels in patients with FH is well established; however, it is not known whether postprandial lipoproteins are also influenced. In this case-controlled intervention study, we investigated the effects of high-dose simvastatin on postprandial lipoproteins. We used a new method to analyze remnant lipoproteins based on the immunoseparation principle (remnant-like particle cholesterol [RLP-C] assay) and the well-established measurement of retinyl ester (RE) analysis in plasma and in the Svedberg flotation unit (Sf)<1000 fraction. Seven heterozygous FH patients and 7 control subjects matched for sex, age, body mass index, triglycerides, and apolipoprotein E genotype were enrolled in the study. An oral vitamin A (RE) fat-loading test was performed at baseline in both groups and after 3 months of high-dose simvastatin (80 mg/d) treatment in the FH patients. Before treatment, FH patients had significantly higher fasting and postprandial concentrations of lipoprotein remnants (plasma RLP-C 42+/-19 mg/dL and area under the RLP-C curve 415+/-82 mg. L(-1). h(-1), respectively) than did control subjects (7+/-3 mg/dL and 101+/-35 mg. L( -1). h(-1), respectively; P<0.05), suggesting a delayed clearance of chylomicron remnant particles in the FH patients. Treatment with simvastatin significantly reduced fasting and postprandial remnant lipoprotein cholesterol concentrations (13+/-3 mg/dL and 136+/-53 mg. L(-1). h(-1), respectively; P<0.05 for both). Postprandial RE in the Sf<1000 fraction, not total RE in plasma, was also significantly higher in FH patients than in control subjects (24+/-10 versus 6.3+/-5.9 mg. L( -1). h(-1), P<0.05), but treatment with simvastatin did not result in improvement of the postprandial RE response, either in the Sf<1000 fraction or in plasma. It is concluded that heterozygous FH patients have increased fasting and postprandial remnant lipoprotein concentrations. Treatment with simvastatin significantly reduced the fasting and postprandial RLP-C concentrations but did not result in improved postprandial RE response.

Apolipoproteins↗

Magnesium in diabetes mellitus.

A tendency for magnesium deficiency in patients with diabetes mellitus is well-established. Glucosuria-related hypermagnesiuria, nutritional factors and hyperinsulinaemia-related hypermagnesiuria all can contribute. The plasma magnesium level has been shown to be inversely related to insulin sensitivity. Magnesium supplementation improves insulin sensitivity as well as insulin secretion in patients with type 2 diabetes. Nevertheless, no beneficial effects of oral magnesium supplementation has been demonstrated on glycaemic control either in patients with diabetes type 1 or 2. Oral magnesium supplementation reduced the development of type 2 diabetes in predisposed rats. There are some indications that magnesium decreases blood pressure, but negative results have been observed in trials that were, however, not designed to test effect on blood pressure as primary parameter. Patients with (severe) retinopathy have a lower plasma magnesium level compared to patients without retinopathy and a prospective study has shown the plasma magnesium level to be inversely related to occurrence or progression of retinopathy. Further study on magnesium (supplementation) is warranted in the prevention of type 2 and of (progression of) retinopathy as well as a means to reduce high blood pressure.

Animals↗

Oral magnesium supplementation in insulin-requiring Type 2 diabetic patients.

Oral magnesium (Mg) supplementation can improve insulin sensitivity and secretion in patients with Type 2 diabetes mellitus (DM). We studied the effect of Mg supplementation on glycaemic control, blood pressure, and plasma lipids in insulin-requiring patients with Type 2 DM. Fifty moderately controlled patients were randomized to 15 mmol Mg or placebo daily for 3 months. Plasma Mg, glucose, HbA1c, lipids, erythrocyte Mg, Mg and glucose concentrations in 24-h urine, and systolic and diastolic pressure were measured before and after 3 months treatment. Plasma Mg concentration was higher after supplementation than after placebo (0.82 +/- 0.07 vs 0.78 +/- 0.08 mmol l(-1), p < 0.05), as was Mg excretion (5.5 +/- 1.9 vs 3.7 +/- 1.4 mmol 24 h(-1), p = 0.004) but erythrocyte Mg concentrations were similar. No significant differences were found in glycaemic control (glucose: 10.7 +/- 3.8 vs 11.6 +/- 6.2 mmol l(-1), p = 0.8; HbA1c: 8.9 +/- 1.6 vs 9.1 +/- 1.2%, p = 0.8), lipids or blood pressure. On-treatment analysis (34 patients: 18 on Mg, 16 on placebo) yielded similar results. An increase in plasma Mg concentration irrespective of medication was associated with a tendency to a decrease in diastolic pressure (increased plasma Mg vs no increase: -4.0 +/- 10.1 vs +2.5 +/- 12.0 mmHg, p = 0.059). Three months' oral Mg supplementation of insulin-requiring patients with Type 2 DM increased plasma Mg concentration and urinary Mg excretion but had no effect on glycaemic control or plasma lipid concentrations.

Administration, Oral↗

Effect of an increase in the plasma potassium concentration on renal magnesium handling in healthy volunteers.

BACKGROUND: Lower plasma magnesium concentrations are associated with clinical problems such as arrhythmias and hypertension. Plasma magnesium concentration is tightly controlled by the kidney. Modifying renal magnesium threshold may provide a means to increase the plasma magnesium concentration. Since evidence has been presented that potassium deficiency by itself may increase renal magnesium loss, the hypothesis that elevating plasma potassium would result in an increase in plasma magnesium concentration was tested in healthy volunteers. METHODS: Plasma potassium was raised in nine healthy volunteers by oral administration of 20 mg amiloride daily during 3 weeks. Magnesium metabolism was assessed before and after this period by plasma levels, urinary magnesium excretion and fractional magnesium excretion, and magnesium loading test (MLT). This MLT allows calculation of renal retention of a magnesium load. RESULTS: Basal plasma magnesium levels (0.84 +/- 0.07 vs 0.84 +/- 0.05 mmol/l) as well as urinary magnesium excretion (4.37 +/- 1.73 vs 3.67 +/- 1.37 mmol/day) and erythrocyte magnesium levels (1.72 +/- 0.16 vs 1.76 +/- 0.14 mmol Mg/l red blood cells) were similar before and on amiloride. Plasma potassium rose significantly on amiloride (3.64 +/- 0.24 vs 4.07 +/- 0.54 mmol/l, P < 0.05). No change was observed in magnesium retention with the MLT: 22.7 +/- 26.7 vs 29.2 +/- 20.6% (P = 0.5). CONCLUSIONS: Despite an increased plasma potassium concentration, no change was observed in plasma magnesium levels, urinary magnesium excretion or renal magnesium retention of an intravenously administered magnesium load. This indicates that increasing plasma potassium within the normal range does not modify the renal magnesium threshold.

Adult↗

Acute exogenous elevation of plasma free fatty acids does not influence the plasma magnesium concentration.

OBJECTIVE: Plasma non-esterified (free) fatty acid concentrations rise as a consequence of stimulated endogenous lipolysis and are inversely related to the plasma magnesium concentration when plasma adrenaline concentration is increased. The aim of the study was to test whether high plasma non-esterified fatty acid concentration after infusion of non-esterified fatty acids decreases plasma magnesium concentration. METHODS: Twelve healthy subjects received 500 ml Intralipid or saline in a randomised, cross-over, double-blind design. Infusion of Intralipid results in an isolated elevation of plasma non-esterified fatty acid concentration. Plasma magnesium concentration was determined at baseline and every 30 minutes; plasma non-esterified fatty acid and triglyceride concentrations at baseline and after 120 minutes. RESULTS: Initial plasma magnesium, non-esterified fatty acid, and triglyceride concentrations were similar in both groups. A significant increase in plasma non-esterified fatty acids (2.42 +/- 0.96 mmol/l vs 0.58 +/- 0.23 mmol/l, p = 0.00013) and triglyceride (median and 95th percentile 5.36 (7.35) mmol/l vs 1.18 (1.92) mmol/l, p = 0.003) concentrations was seen with Intralipid. Plasma magnesium concentration increased significantly after Intralipid (0.89 +/- 0.09 mmol/l vs 0.81 +/- 0.06 mmol/l, p = 0.007). No significant changes were seen with saline. A positive association was found between the change in plasma magnesium and triglyceride concentrations (r = 0.85, p = 0.001). CONCLUSION: Acute infusion of non-esterified fatty acids from an exogenous source does not result in a fall in plasma magnesium concentration, indicating that the circulating non-esterified fatty acids play no part in a decrease in plasma magnesium concentration. The high circulating non-esterified fatty acid levels and the fall in plasma magnesium concentration are both a consequence of intracellular lipolysis.

Adult↗

Plasma homocysteine as a risk factor for vascular disease. The European Concerted Action Project.

CONTEXT: Elevated plasma homocysteine is a known risk factor for atherosclerotic vascular disease, but the strength of the relationship and the interaction of plasma homocysteine with other risk factors are unclear. OBJECTIVE: To establish the magnitude of the vascular disease risk associated with an increased plasma homocysteine level and to examine interaction effects between elevated plasma homocysteine level and conventional risk factors. DESIGN: Case-control study. SETTING: Nineteen centers in 9 European countries. PATIENTS: A total of 750 cases of atherosclerotic vascular disease (cardiac, cerebral, and peripheral) and 800 controls of both sexes younger than 60 years. MEASUREMENTS: Plasma total homocysteine was measured while subjects were fasting and after a standardized methionine-loading test, which involves the administration of 100 mg of methionine per kilogram and stresses the metabolic pathway responsible for the irreversible degradation of homocysteine. Plasma cobalamin, pyridoxal 5'-phosphate, red blood cell folate, serum cholesterol, smoking, and blood pressure were also measured. RESULTS: The relative risk for vascular disease in the top fifth compared with the bottom four fifths of the control fasting total homocysteine distribution was 2.2 (95% confidence interval, 1.6-2.9). Methionine loading identified an additional 27% of at-risk cases. A dose-response effect was noted between total homocysteine level and risk. The risk was similar to and independent of that of other risk factors, but interaction effects were noted between homocysteine and these risk factors; for both sexes combined, an increased fasting homocysteine level showed a more than multiplicative effect on risk in smokers and in hypertensive subjects. Red blood cell folate, cobalamin, and pyridoxal phosphate, all of which modulate homocysteine metabolism, were inversely related to total homocysteine levels. Compared with nonusers of vitamin supplements, the small number of subjects taking such vitamins appeared to have a substantially lower risk of vascular disease, a proportion of which was attributable to lower plasma homocysteine levels. CONCLUSIONS: An increased plasma total homocysteine level confers an independent risk of vascular disease similar to that of smoking or hyperlipidemia. It powerfully increases the risk associated with smoking and hypertension. It is time to undertake randomized controlled trials of the effect of vitamins that reduce plasma homocysteine levels on vascular disease risk.

Adult↗

Asymptomatic and late-onset ornithine transcarbamylase deficiency caused by a A208T mutation: clinical, biochemical and DNA analyses in a four-generation family.

We describe a 4-generation family in which a previously healthy 10-year-old boy died of late-onset ornithine transcarbamylase (OTC) deficiency. Pedigree analysis and allopurinol loading tests in female relatives were not informative. A missense mutation (A208T) in the OTC gene was detected in the deceased patient and in several clinically healthy male and female relatives, the oldest male being 97 years old. OTC deficiency was established in autopsy liver tissue of the propositus and liver biopsy samples of his sister, mother, and a maternal uncle. The males had 4% and 6% residual activity, respectively, the females 58% and 67%, respectively. The observed relation between the mutation and the decreased OTC activity in liver tissue of these subjects suggests that the mutation is a deleterious one. Late-onset, "mild" OTC deficiency can have a fatal or a favorable outcome. The disease can segregate undetected in families.

Adult↗

Risk factors for bleeding during treatment of acute venous thromboembolism.

OBJECTIVE: Identification of risk factors for bleeding and prospective evaluation of two bleeding risk scores in the treatment of acute venous thromboembolism. DESIGN: Secondary analysis of a prospective, randomized, assessorblind, multicenter clinical trial. SETTING: One university and 2 regional teaching hospitals. PATIENTS: 188 patients treated with heparin or danaparoid for acute venous thromboembolism. MEASUREMENTS: The presenting clinical features, the doses of the drugs, and the anticoagulant responses were analyzed using univariate and multivariate logistic regression analysis in order to evaluate prognostic factors for bleeding. In addition, the recently developed Utrecht bleeding risk score and Landefeld bleeding risk index were evaluated prospectively. RESULTS: Major bleeding occurred in 4 patients (2.1%) and minor bleeding in 101 patients (53.7%). For all (major and minor combined) bleeding, body surface area < or = 2 m2 (odds ratio 2.3, 95% CI 1.2-4.4; p = 0.01), and malignancy (odds ratio 2.4, 95% CI 1.1-4.9; p = 0.02) were confirmed to be independent risk factors. An increased treatment-related risk of bleeding was observed in patients treated with high doses of heparin, independent of the concomitant activated partial thromboplastin time ratios. Both bleeding risk scores had low diagnostic value for bleeding in this sample of mainly minor bleeders. CONCLUSIONS: A small body surface area and malignancy were associated with a higher frequency of bleeding. The bleeding risk scores merely offer the clinician a general estimation of the risk of bleeding. In patients with a small body surface area or in patients with malignancy, it may be of interest to study whether limited dose reduction of the anticoagulant drug may cause less bleeding without affecting efficacy.

Acenocoumarol↗

Comparing subcutaneous danaparoid with intravenous unfractionated heparin for the treatment of venous thromboembolism. A randomized controlled trial.

OBJECTIVE: To compare the efficacy and safety of two subcutaneous doses of danaparoid with that of continuous intravenous administration of unfractionated heparin in the treatment of venous thromboembolism. DESIGN: An open-label, randomized, multicenter clinical trial. SETTING: One university hospital and two university-affiliated hospitals. PATIENTS: 209 patients suspected to have venous thromboembolism. Of these, 188 had a confirmed diagnosis (by ventilation-perfusion lung scan and ultrasonography or contrast venography of the leg) and received study medication. INTERVENTIONS: Patients were randomly assigned to either low-dose danaparoid (intravenous loading dose of 1250 U followed by 1250 U administered subcutaneously twice daily [n = 65]); high-dose danaparoid (intravenous loading dose of 2000 U followed by 2000 U administered subcutaneously twice daily [n = 63]); or unfractionated heparin (intravenous loading dose of 2500 U followed by dose-adjusted continuous infusion [n = 60]). Treatment lasted at least 5 days and was continued until anticoagulation (achieved with acenocoumarol) was adequate. MEASUREMENTS: Efficacy determined clinically and by repeated imaging tests on treatment days 5 to 8; safety determined by daily assessment for bleeding. RESULTS: Two lung scans were done in each of 179 patients; ultrasonography or venography of the leg was done twice in each of 173 patients; and both repeated leg and lung tests were done in 166 patients. A significant reduction in recurrence or extension of venous thromboembolism was seen in patients receiving high-dose danaparoid (8 of 63 [13%]) compared with patients receiving intravenous unfractionated heparin (17 of 60 [28%]; relative risk, 0.45 [95% CI, 0.21 to 0.96]). Four of 61 patients receiving high-dose danaparoid (7%) and 14 of 58 patients receiving unfractionated heparin (24%) had recurrence of pulmonary embolism (relative risk, 0.27 [CI, 0.09 to 0.78]); 3 of 58 patients receiving high-dose danaparoid (5%) and 6 of 54 patients receiving unfractionated heparin (11%) had recurrence of deep venous thrombosis (relative risk, 0.47 [CI, 0.12 to 1.77]). Occurrence of major and minor bleeding was similar in the three groups; major bleeding occurred in 1 patient receiving low-dose danaparoid, 1 patient receiving high-dose danaparoid, and 2 patients receiving heparin. CONCLUSIONS: Our results suggest that high-dose danaparoid is safer and more effective than unfractionated heparin for the treatment of venous thromboembolism.

Adult↗

Impaired fatty acid metabolism in familial combined hyperlipidemia. A mechanism associating hepatic apolipoprotein B overproduction and insulin resistance.

To establish whether insulin resistance and/or postprandial fatty acid metabolism might contribute to familial combined hyperlipidemia (FCH) we have examined parameters of insulin resistance and lipid metabolism in six FCH kindreds. Probands and relatives (n = 56) were divided into three tertiles on the basis of fasting plasma triglycerides (TG). Individuals in the highest tertile (TG > 2.5 mM; n = 14) were older and had increased body mass index, systolic blood pressure, and fasting plasma insulin concentrations compared with individuals in the lowest tertile (n = 24). The former also presented with decreased HDL cholesterol and increased total plasma cholesterol, HDL-TG, and apoprotein B, E, and CIII concentrations. Insulin concentrations were positively correlated with plasma apo B, apo CIII, apo E, and TG, and inversely with HDL cholesterol. Fasting nonesterified fatty acids (NEFA) were elevated in FCH subjects compared to six unrelated controls and five subjects with familial hypertriglyceridemia. Prolonged and exaggerated postprandial plasma NEFA concentrations were found in five hypertriglyceridemic FCH probands. In FCH the X2 minor allele of the AI-CIII-AIV gene cluster was associated with increased fasting plasma TG, apo CIII, apo AI, and NEFA concentrations and decreased postheparin lipolytic activities. The clustering of risk factors associated with insulin resistance in FCH indicates a common metabolic basis for the FCH phenotype and the syndrome of insulin resistance probably mediated by an impaired fatty acid metabolism.

Apolipoproteins B↗

Extracellular and intracellular magnesium concentrations in asthmatic patients.

Magnesium deficiency is associated with increased contractility of smooth muscle cells. Since contractility of bronchial smooth muscle is important in patients with asthma, magnesium deficiency could negatively influence the clinical condition. We wanted to assess whether magnesium deficiency exists in patients with asthma. Extracellular (plasma) and intracellular (erythrocytes and mononuclear leucocytes) concentrations of magnesium were determined in 20 mildly symptomatic patients with asthma and compared to 20 healthy controls. In asthmatic patients, the mean +/- SD magnesium level in plasma was 0.81 +/- 0.05 mmol.l-1, in erythrocytes 0.20 +/- 0.02 fmol.cell-1, and in mononuclear leucocytes 5.10 +/- 2.55 fmol.cell-1; these values did not differ significantly from those of the healthy controls: 0.79 +/- 0.06 mmol.l-1, 0.19 +/- 0.02 fmol.cell-1, and 4.61 +/- 1.75 fmol.cell-1, respectively. No evidence for the existence of a magnesium deficit needing chronic magnesium supplementation was, thus, found in these patients.

Asthma↗