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Biomedical subjects

F Vertongen

Publications and source records attributed to F Vertongen.

At least 19 recordsLinked to original sources
PubMed1992

Erythrocyte metabolic alterations in type I diabetes: relationship to metabolic control.

Erythrocytes from young type I diabetic patients (n = 11), incubated in their plasma in anaerobic conditions, exhibited higher glucose consumption than cells from controls (n = 11). This increased metabolic activity is believed to reflect erythrocyte alterations dependent on the degree of metabolic control, as glucose consumption was significantly correlated to glycosylated haemoglobin (HbA1) and to glucose levels (P < 0.05 and P < 0.01 respectively). Red cell hexokinase (HK) and pyruvate kinase (PK) activities were similar in both groups whereas phosphofructokinase (PFK) activity was slightly higher in patients' cells (P < 0.05). No difference was found between patients and controls for red cell ATP and 2.3 diphosphoglycerate (2.3 DPG) levels. However, the concentrations of these glycolytic products seem also closely related to the glucose homeostasis in diabetes. Indeed, within the diabetic group, ATP levels showed a negative relationship with glucose level (P < 0.05) and 2.3 DPG a positive relationship with HbA1 (P < 0.05). In conclusion, higher glycolytic activity is present in young diabetic red cells. This activity as well as ATP and 2.3 DPG levels are related to the degree of short- or long-term diabetic control. These findings stress the importance of a careful metabolic control to avoid haematological disturbances.

Adenosine Triphosphate↗
PubMed1991

Interest of zinc determination in leucocyte fractions for the assessment of marginal zinc status.

In order to test the sensitivity of leucocyte zinc determination in the assessment of zinc status, an isolation procedure of mononuclear (MNC) and polymorphonuclear (PMNC) cell fractions was developed. Zinc concentrations in cells from healthy subjects were (mean +/- SD, in mumol/10(10) cells): 0.81 +/- 0.24 in MNC and 0.55 +/- 0.06 in PMNC. In patients suffering from several diseases known to be associated with a marginal impairment in zinc status (cirrhosis, cancer, obesity, endocrine and rheumatic diseases), these concentrations did not differ from those in controls except in rheumatic patients in whom MNC zinc was increased (1.05 +/- 0.42 mumol/10(10) cells) and correlated with erythrocyte sedimentation rate (r = 0.41, P less than 0.01). This relation was also significant in the whole study population (r = 0.39, P less than 0.01). Leucocyte zinc therefore appears to have a limited value in the assessment of marginally impaired zinc status, except in inflammatory states.

Adult↗
PubMed1991

Domestic endotoxin exposure and clinical severity of asthma.

Endotoxins are potent pro-inflammatory substances present in several natural environments and in commercial house dust extracts. To investigate the possible effect of chronic endotoxin exposure on asthma, 28 patients with perennial chronic asthma (20 allergic to house dust mite and eight intrinsic asthmatics) were evaluated during a 4-month period (lung function, clinical and immunological criteria). At the same time, two house dust samples were collected from each patient's home to determine total house dust weight (mg/m2), endotoxin concentration and house dust mite antigen content (evaluated indirectly by guanine content with HPLC method). The mean (+/- s.d.) endotoxin concentration, as measured by quantitative Limulus assay was 2.59 (+/- 3.41) ng/mg house dust, ranging from 0.12 to 20 ng/mg. The mean guanine content was 0.13 (+/- 0.16) mg/100 mg house dust. There was no correlation between endotoxin and house dust mite concentrations. Patients were compared according to the low or high grade exposure to dust, endotoxins and guanine. Compared with patients with low grade (less than or equal to 5.6 ng/ml) exposure, subjects exposed to high endotoxin concentrations (greater than 5.6 ng/ml) showed a significant increase in dyspnea (median 2.6 vs 3.3; P less than 0.05) and treatment (median 14 vs 44.3; P less than 0.01) scores, oral corticosteroid (median 0.0 vs 13.5 mg/24 hr; P less than 0.01) and beta 2-mimetics (median four vs eight puffs/day; P less than 0.01) intake, and a significant decrease in FEV1/FVC (median 84.5 vs 67% of predicted value; P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Carnitine deficiency with cardiomyopathy presenting as neonatal hydrops: successful response to carnitine therapy.

A small-for-date infant presented at birth with severe non-immune hydrops, cardiac failure, metabolic acidosis and hypoglycaemia. Ultrasonography disclosed a cardiomyopathy. Initial therapy consisting of artificial ventilation, inotropes and diuretics resulted in partial disappearance of oedema without significant improvement in cardiac function. Episodes of hypoglycaemia recurred despite continuous glucose infusions. Total serum carnitine from cord blood was 1.65 nmoles/ml and was undetectable on day 20. Oral DL-carnitine supplements resulted in normoglycaemia, dramatic improvement in cardiac function and restoration of serum carnitine levels to normal values. The infant was thereafter maintained on carnitine therapy. Follow-up over 1 year showed moderate growth retardation and normal developmental milestones. In order to account for such a severe neonatal presentation of carnitine deficiency, a combination of defective pre- and postnatal carnitine supply with an inborn error of carnitine handling is considered. The present case illustrates the need for evaluation of carnitine status in fetuses and neonates presenting with hydrops associated with cardiac failure.

Cardiomyopathies↗
PubMed1989

[Usual values of selenium and glutathione peroxidase in a Belgian population].

Several biological parameters for assessing selenium status have been determined in years 1985-1986 in a large Belgian population group, males and females 0 to 92 years old, representative from Brussels and surroundings. In 145 people, 20 to 79 years old, mean concentrations were: 1.06 +/- 0.15 mumol Se/l plasma, 5.0 +/- 1.1 nmol Se/g Hb in erythrocytes and 7.4 +/- 2.0 mu/g Hb for the selenodependent glutathione peroxidase activity measured in erythrocytes (mean +/- standard deviation). Values for urine selenium have a disymmetric distribution and range from 0.05 to 0.65 mumol Se/g creatinine. No difference was evidenced in this group according to sex and age. Children below 20 years and elderly above 80 years have decreased plasma and erythrocyte selenium concentrations but glutathione peroxidase is not modified. These blood selenium concentrations are lower than those determined in a similar population group in years 1980-1981, suggesting a progressive decrease in selenium intake. The concentrations of the biological parameters are not correlated together except in selenium deficient patients having plasma selenium less than 0.75 mumol/l: a significant correlation is observed between plasma selenium and erythrocyte glutathione peroxidase activity, that becomes more intense with decreasing plasma selenium. Finally, two recent investigations are described where a significant response in platelet glutathione peroxidase was obtained during a 60 days selenium supplementation with 100 to 200 micrograms selenium per day, suggesting that usual selenium intake in Belgium (50 micrograms per day) is marginally deficient.

Adolescent↗
PubMed1988

Selenium supplementation in healthy Belgian adults: response in platelet glutathione peroxidase activity and other blood indices.

Selenium status was explored by investigating effects of a 60-d Se supplementation with DL-selenomethionine (100 micrograms Se/d) in a group of 10 adults (plasma Se levels, 0.76-1.33 mumol/L). Plasma, erythrocyte, and urinary Se and activities of glutathione peroxidase (GSH Px) in plasma, erythrocytes, and platelets were measured before intervention and after 5, 15, 30, 45, and 60 d. A placebo was given to six adults. Plasma and urinary Se were the most sensitive indices to Se exposure. Se in plasma increased steadily during the course of the study whereas urinary Se reached a plateau between 30 and 60 d. By contrast erythrocyte Se did only change after 45 d. Enzyme in plasma and erythrocytes did not respond whereas platelet GSH Px did. The plateau of activity that was observed after 15 d for plasma Se in the range 1.40-1.50 mumol/L could mean that the Se status is insufficient for an optimal function of GSH Px and implies that dietary intake in Belgium (less than 50-60 micrograms Se/d) is not adequate.

Adult↗
PubMed1988

[Sequential development of vitamin D metabolites under isoniazid and rifampicin therapy].

A sequential study of 25-hydroxy vitamin D (25-OH-D), 1.25 dihydroxy vitamin D [1.25 (OH)2-D], PTH, alkaline phosphatase and gammaglutamyl transpeptidase (gamma GT) was undertaken in a series of 46 children with asymptomatic tuberculosis treated by isoniazid (INH) alone or associated with rifampin (RMP). These parameters were measured before treatment, 1 month, 3 months after the onset and at the end of treatment (6 months). In order to reduce the influence of the time of the year on the 25-OH-D levels, 22 patients were selected for whom the whole treatment took place between October and May of the following year. In this group, 13 children were treated by INH and RMP, 9 by INH alone. A statistically significant decrease in 25-OH-D levels could be demonstrated after 3 months of treatment in 13 patients under INH and RMP as well as a significant increase in alkaline phosphatase and gamma GT levels. In 9 patients given INH alone, 1.25 (OH)2-D levels decreased after 3 months without significant changes in 25-OH-D, alkaline phosphatase or gamma GT levels. These results emphasize the need for regular biochemical supervision, even if no sign of rickets is observed in these patients.

Adolescent↗
PubMed1987

Selenium status in relation to clinical variables and corticosteroid treatment in rheumatoid arthritis.

Plasma selenium levels, erythrocyte selenium levels and activity of the selenoenzyme glutathione peroxidase in erythrocytes were determined in patients with rheumatoid arthritis (RA) and acute inflammatory arthritis. Results were compared with those from age and sex matched controls. These variables were not statistically different from controls in patients with inflammatory arthritis and in patients with RA not treated with corticosteroids. No correlation was found in RA between plasma selenium biological variables of inflammation and most clinical indices of disease severity. Therefore, acute or chronic inflammation was not the main factor that accounted for low plasma selenium levels in RA. Corticosteroid treatment, particularly at high doses (20-60 mg prednisolone/day), was significantly related to the depressed plasma selenium levels of some patients with RA. The mechanisms underlying this modification remain poorly understood.

Acute Disease↗
PubMed1986

Deoxythymidine and deoxycytidine incorporation into DNA in B leukemic cells.

Measurements of radioactive DNA after incubation of normal and B leukemic peripheral mononuclear cells, from c-ALL and CLL with labeled deoxythymidine (dTh) and deoxycytidine (dCt) showed that for dTh, incorporation into DNA was similar for normal and c-ALL cells but lower in B-CLL cells and that for dCt, incorporation was highest in c-ALL and lowest in CLL cells. These results contrast with those of dTh and dCt kinase activities; the former has been previously found elevated in c-ALL cells, and the latter is found, in the present study, similar in the three groups tested.

B-Lymphocytes↗
PubMed1986

Influence of the degree of metabolic control on physical fitness in type I diabetic adolescents.

Seventeen type I male diabetic adolescents and 17 control subjects matched for age, height, and weight were submitted to maximal exercise on a bicycle ergometer. The diabetic subjects were divided into two groups according to their degree of metabolic control using total glycosylated hemoglobin (HbA1): group 1, diabetics with HbA1 less than 8.5% (n = 9) and group 2, diabetics with HbA1 greater than 8.5% (n = 8). Oxygen uptake, pulmonary ventilation, and heart rate were recorded at rest and at maximal load. Glucose, lactate, and free fatty acids were determined in blood before and after exercise. Maximal work load and oxygen uptake were significantly lower in the two diabetic groups than in the healthy controls. An inverse relationship was observed between HbA1 concentration and the maximal work load (r = -0.63; P less than 0.01). It can be concluded that diabetic adolescents should obtain the best possible degree of metabolic control to improve their performances.

Adolescent↗
PubMed1986

Generalized unresponsiveness to mineralocorticoid hormones: familial recessive pseudohypoaldosteronism due to aldosterone-receptor deficiency.

The present report describes two sibs--born from consanguineous parents--presenting with severe salt wasting. Generalized pseudohypoaldosteronism (PHA) was diagnosed on the basis of markedly elevated sodium concentration in urine (84 & 63 mmol/L respectively), sweat (181 & 196), saliva (- & 120) and stool (- & 189), hyponatremia (112 & 132) and hyperkalemia (10.7 & 7.3) in the presence of increased plasma aldosterone (greater than 8.5 & 5.4 ng/ml), plasma renin activity (40 & 18.9 ng/ml/hr) and urinary aldosterone (greater than 32 & 11.6 micrograms/day). Both parents investigated under basal conditions (sodium ad libitum) and under sodium restricted diet appeared to be normal. Aldosterone binding studies performed on mononuclear leukocytes showed no type I receptors in the investigated child whereas low amounts were found in both parents (90 sites/cell and 63 sites/cell in the mother and the father, respectively). Isolated renal unresponsiveness to mineralocorticoid hormones is thought to be an autosomal dominant inherited disease. In contrast, the results obtained in these two new cases of generalized PHA, as well as the fact that four of five yet reported cases were born from consanguineous parents, suggest an autosomal recessive mode of inheritance for generalized PHA.

Aldosterone↗
PubMed1985

Selenium deficiency.

Selenium is undoubtedly an essential trace element: its involvement in GPx structure, the presence of deleterious effects of selenium deficiency in animals, and the recognition of deficiency states in man attest to its importance. However, if the consequences of selenium deficiency in man are now widely recognized, the mechanisms underlying these conditions are poorly understood. The definition of the exact role of selenium in human homeostasis has been hampered by the lack of a sensitive parameter, usable in routine investigation, to assess selenium status. Measurements of plasma and urinary levels, although useful in clinical practice, are inadequate indicators. The only true evidence of selenium deficiency lies in a positive response to selenium therapy. Deficiency states have been demonstrated for inhabitants of regions where selenium supply is limited, in protein-energy malnutrition, and in patients maintained on total parenteral nutrition without selenium supplementation. The benefit of selenium supplementation, together with other antioxidant drugs, in non-deficient subjects is still a matter of debate; its protective effect in neoplastic, cardiovascular and neurological degenerative diseases is not yet proven.

Animals↗