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Biomedical subjects

K H Polderman

Publications and source records attributed to K H Polderman.

32 records · Page 2Linked to original sources
PubMed2000

Increased plasma homocysteine after menopause.

Besides genetic defects in the enzymes involved in homocysteine metabolism and nutritional deficiencies in vitamin cofactors, sex steroid hormones may modulate plasma homocysteine levels. The post-menopausal state has been found to be associated with higher plasma homocysteine levels, but data are inconsistent and studies published so far did not adjust for age, which is an important confounding factor in studying the effect of menopause. In the present study total plasma homocysteine levels were measured in a meticulously selected population in which the contrast in estrogen status between pre- and postmenopausal women of the same age was maximized. The study comprised 93 premenopausal and 93 postmenopausal women of similar age (range 43-55 years). Women were selected from respondents to a mailed questionnaire on menopause, which was sent to all women aged 40-60 years in the Dutch town of Zoetermeer (n = 12675). Postmenopausal women who were at least three years after menopause or whose menses had stopped naturally before age 48 were age-matched with premenopausal women with regular menses and without menopausal complaints. Plasma homocysteine levels in the fasting state were related to menopausal status; the age-adjusted geometric mean was 10.7 micromol/l in premenopausal and 11.5 micromol/l in postmenopausal women (difference of 7%, 95% confidence interval 0.3-14%, P = 0.04). Additional adjustment for plasma creatinine, body mass index, smoking habit (yes, no) and alcohol intake did not influence this difference. The results of this population-based study indicate that plasma homocysteine is affected by menopause.

Adult↗
PubMed2000

Modulation of plasma endothelin levels by the menstrual cycle.

Blood pressure varies during the menstrual cycle, but the reason for this is unclear. Administration of (synthetic) sex hormones can influence the level of vasoactive substances such as endothelin (ET). However, it is not known whether short-term variations in sex hormone levels in physiological situations affect ET levels. We assessed the effects of the menstrual cycle on plasma ET-1 in 8 healthy premenopausal women not using oral contraceptives (OCs) and 8 premenopausal women using OCs. ET-1 levels were measured in all subjects on days 1 to 3 (menstrual phase), 9 to 12 (follicular phase), and 20 to 23 (luteal phase) of the menstrual cycle. ET-1 levels remained constant in OC users (2.4 +/- 0.4, 2.6 +/- 0.4, and 2.4 +/- 0.4 pg/mL on days 1 to 3, 9 to 12, and 20 to 23 of the pill cycle). In contrast, ET-1 levels in non-OC users decreased in all women during the follicular and luteal phase of the menstrual cycle compared with the menstrual (low-estrogenic) phase (3.6 +/- 0.5, 2.8 +/- 0.5, and 2.9 +/- 0.3 pg/mL for the menstrual, follicular, and luteal phase, respectively, P < .01 for menstrual vfollicular and P < .01 for menstrual v luteal). The differences between OC users and nonusers were significant in the menstrual phase of the cycle (P < .01). We conclude that ET levels fluctuate during the menstrual cycle. Previously reported effects of the menstrual cycle on blood pressure may be partly explained by the effects of sex hormones on the level of vasoactive mediators. This fluctuation is not present in OC users. Studies on hemodynamic parameters in premenopausal women should account for hormonal variations in the various phases of the menstrual cycle.

Adult↗
PubMed2000

Hypomagnesemia and hypophosphatemia at admission in patients with severe head injury.

OBJECTIVE: Low serum levels of electrolytes such as magnesium (Mg), potassium (K), calcium (Ca), and phosphate (P) can lead to a number of clinical problems in intensive care unit (ICU) patients, including hypertension, coronary vasoconstriction, disturbances in heart rhythm, and muscle weakness. Loss of these electrolytes can be caused, among other things, by increased urinary excretion. Cerebral injury can lead to polyuresis through a variety of mechanisms. We hypothesized that patients with cranial trauma might be at risk for electrolyte loss through increased diuresis. The objective of this study was to assess levels of Mg, P, and K at admission in patients with severe head injury. DESIGN: We measured plasma levels of Mg, P, K, Ca, and sodium at admission in 18 consecutive patients with severe head injury admitted to our ICU (group 1). As controls, we used 19 trauma patients with two or more bone fractures but no significant cranial trauma (group 2). SETTING: University teaching hospital. PATIENTS: Eighteen patients with severe head injury admitted to our surgical ICU (group 1) and 19 controls (trauma patients with no significant cranial trauma; group 2). MAIN RESULTS: Electrolyte levels at admission (group 1 vs. group 2; mean +/- SD, units: mmol/L) were as follows. Mg, 0.57 +/- 0.17 (range, 0.24-0.85) vs. 0.88 +/- 0.21 (range, 0.66-1.42 mmol/L; p < .01). P, 0.56 +/- 0.15 (range, 0.20-0.92) vs. 1.11 +/- 0.15 (range, 0.88-1.44 mmol/L; p < .01). K, 3.54 +/- 0.59 (range, 2.4-4.8) vs. 4.07 +/- 0.45 (range, 3.6-4.8 mmol/L; p < .02). Ca, 2.02 +/- 0.24 (range, 1.45-2.51) vs. 2.14 +/- 0.20 (range, 1.88-2.46; p = NS). In group 1, 12/18 patients had Mg levels <0.70 mmol/L vs. 2/19 patients in group 2 (p < .01); in group 1, 11/18 patients had P levels below 0.60 mmol vs. 0/19 patients in group 2 (p < .01). Moderate hypokalemia (K levels, <3.6 mmol/L) was present in 8/18 patients in group 1 vs. 1/19 patients in group 2 (p < .01). Severe hypokalemia (K levels, < or =3.0) was present in 4/18 patients in group 1 vs. 0/19 patients in group 2 (p < .05). CONCLUSION: We conclude that patients with severe head injury are at high risk for the development of hypomagnesemia, hypophosphatemia, and hypokalemia. One of the causes of low electrolyte levels in these patients may be an increase in the urinary loss of various electrolytes caused by neurologic trauma. Mannitol administration may be a contributing factor. Intensivists should be aware of this potential problem. If necessary, adequate supplementation of Mg, P, K, and Ca should be initiated promptly.

APACHE↗
PubMed1999

Hypernatremia in the intensive care unit: an indicator of quality of care?

OBJECTIVE: To assess the frequency of hypernatremia in patients who were admitted to an intensive care unit (ICU) and to determine the correlation of hypernatremia with the clinical outcomes, durations of the patients' stays in the ICU, and other clinical variables. DESIGN: Retrospective survey. SETTING: University teaching hospital. PATIENTS: All patients (total, 389) who were admitted to the medical ICU of the department of internal medicine during 1 yr. MEASUREMENTS: The database of our hospital's mainframe computer was searched for sodium values > or = 150 mmol/L that were registered in the year 1995. These data were then matched with the registration numbers of all patients who were admitted to our medical ICU between January 1 and December 31, 1995. In this way, we identified all patients in whom hypernatremia was present at admission or those who developed hypernatremia in the course of their stay in our ICU. The prevalence and duration of hypernatremia (defined as a serum sodium concentration of > or = 150 mmol/L or more) were determined; the correlation of hypernatremia with clinical outcome, duration of ICU stay, Acute Physiology and Chronic Health Evaluation II scores, and other clinical variables were evaluated; and changes in fluid administration in response to hypernatremia and fluid regimens in the period preceding hypernatremia were examined. MAIN RESULTS: Of a total of 389 patients who were admitted in 1995, hypernatremia was present at admission in 34 patients (8.9%). The average duration of hypernatremia in these patients was 16.2 (range, 4-56) hrs. A total of 22 patients (5.7%) developed hypernatremia in the course of their stay in the ICU. The average duration of hypernatremia in this group was 34.7 (range, 4-89) hrs. Moderately elevated levels of sodium had been detected in most of these patients (n = 21) in the days before the development of severe hypernatremia; however, adjustments in fluid infusion aimed at preventing the occurrence of hypernatremia were either lacking (n = 7) or inadequate (n = 11). Hospital-acquired hypernatremia vs. hypernatremia present at admission to the ICU was associated with a higher mortality rate (32% vs. 20.3%, respectively; p < .01). CONCLUSIONS: Despite frequent measurement of sodium levels in patients in the ICU, hypernatremia is a relatively common occurrence. Initial treatment of hypernatremia is often inadequate, and sometimes treatment is delayed. The development of hypernatremia is associated with adverse outcomes for patients developing hypernatremia in the ICU. Hypernatremia could potentially be used as an indicator of quality of care in the medical ICU.

APACHE↗
PubMed1999

Associations of C-reactive protein with measures of obesity, insulin resistance, and subclinical atherosclerosis in healthy, middle-aged women.

Obesity, the insulin resistance syndrome, and atherosclerosis are closely linked and may all be determinants of an increased acute-phase response. In this study, we examined the relationship of C-reactive protein (CRP) with measures of obesity, variables of the insulin resistance syndrome, and intima-media thickness of the common carotid arteries in 186 healthy, middle-aged women selected from the general population. Associations were assessed by regression analysis. CRP was strongly associated with body mass index (BMI) and waist circumference. CRP was also associated with other variables of the insulin resistance syndrome, including blood pressure, insulin, high density lipoprotein cholesterol, triglycerides, apolipoprotein A1 (inversely), plasminogen activator inhibitor-1 antigen, and tissue-type plasminogen activator antigen. Associations between CRP and the variables of the insulin resistance syndrome disappeared after controlling for BMI but remained significant for plasminogen activator inhibitor-1 antigen only. The association of CRP with common carotid artery intima-media thickness was weak and limited to ever-smokers. BMI explained 29.7% of the variance of CRP, whereas common carotid artery intima-media thickness explained only 3.7%. The results of this population-based study indicate that adiposity is strongly associated with CRP in healthy, middle-aged women. In this population, BMI accounted for the relationship between CRP and other variables of the insulin resistance syndrome. Further studies should determine whether losing weight ameliorates the inflammatory state.

Adult↗
PubMed1997

Agenesis of the corpus callosum associated with paroxysmal hypothermia: Shapiro's syndrome.

Spontaneous recurrent hypothermia and hyperhidrosis associated with agenesis of the corpus callosum was first described by Shapiro and Plum in 1967. Since then, several cases with similar symptoms (now known as Shapiro's syndrome or spontaneous periodic hypothermia) have been described. We report another case of this syndrome in a 21-year-old-man, and discuss possible pathogenetic mechanisms and therapeutic approaches.

Adult↗
PubMed1996

Effects of insulin infusion on endothelium-derived vasoactive substances.

An association between insulin resistance and hypertension has been reported in several studies. In apparent contradiction, insulin infusion in healthy volunteers is associated with vasodilatation. Furthermore, there is evidence that some insulin effects may differ between the sexes. We performed three-step hyperinsulinaemic-euglycaemic clamp studies in six men and six women to test the hypotheses that: 1) insulin might affect the release of vasoactive substances by the endothelium, and 2): this putative effect on vasoactive substances might differ between men and women. Six other women and six men served as control subjects, receiving 154 mmol/l NaCl (saline) infusion. Plasma levels of insulin, immunoreactive endothelin, L-arginine (precursor of nitric oxide), L-citrulline (by-product of nitric oxide synthesis) and cyclic GMP (second messenger of nitric oxide) were measured during infusion of insulin or 154 mmol/l NaCl (saline), respectively. We also assessed urinary excretion of 6-keto PGF-1 alpha (a degradation product of prostacyclin reflecting prostacyclin production). Blood pressure was monitored in all subjects throughout the experiment. In women plasma levels of immunoreactive endothelin decreased from (mean +/- SD) 2.58 +/- 0.96 to 1.7 +/- 0.72 pmol/l during insulin infusion (p < 0.01), while remaining constant in female control subjects (p < 0.02). No changes in levels of endothelin were observed in men during infusion of insulin or saline. In women levels of cGMP rose and levels of L-arginine decreased significantly during insulin infusion, consistent with an increase in nitric oxide production. Excretion of 6-keto PGF-1 alpha also increased significantly in women during insulin infusion. No such effects were observed in men, or in women during infusion of saline. Blood pressure remained constant in all subjects during hyperinsulinaemia. We conclude that sex differences exist in the effects of insulin on the endothelium. Short-term hyperinsulinaemia in women is associated with a decline in levels of immunoreactive endothelin, and possibly with a rise in production of nitric oxide and prostacyclin. In contrast, levels of vasoactive substances remained constant in men during hyperinsulinaemia. Our findings may partly explain insulin's vasodilatory effects in healthy individuals. It remains to be investigated whether these effects are lost in insulin-resistant states. Our observation that there is a sex difference in insulin effects on the endothelium may help explain why the link between hyperinsulinaemia and cardiovascular disease appears to be clearer in men than in women.

6-Ketoprostaglandin F1 alpha↗
PubMed1995

Effects of gonadal androgens and oestrogens on adrenal androgen levels.

OBJECTIVE: The physiological role of adrenal androgens in humans remains unclear. Furthermore, there are few data on the relation between sex steroids and adrenal androgen production. We have assessed the effects of sex steroid hormone administration on adrenal androgen levels, by studying a large group of transsexual patients. DESIGN: A non-randomized intervention. SETTING: A university teaching hospital. PATIENTS: Thirty-one male-to-female and 22 female-to-male transsexual patients. MEASUREMENTS: Plasma levels of adrenal androgens were measured in a group of male-to-female and female-to-male transsexual patients both before and during cross-gender hormone treatment. This treatment involves administration of testosterone esters to women and of ethinyloestradiol and cyproterone acetate to men. RESULTS: High dose sex steroid administration had marked effects on adrenal androgens levels, which decreased by 27-48% in males treated with ethinyloestradiol and increased by 23-70% in females treated with testosterone. CONCLUSION: We conclude that administration of high doses of testosterone and oestradiol exert opposing effects on adrenal androgen production.

Adolescent↗
PubMed1994

Testosterone administration increases adrenal response to adrenocorticotrophin.

OBJECTIVE: Various studies have demonstrated coexistence of ovarian and adrenal hyperandrogenism in women. This study was designed to determine whether testosterone can increase the response of the adrenal gland to stimulation by adrenocorticotrophin (ACTH). DESIGN: Non-randomized intervention in a university teaching hospital. PATIENTS: Twenty androgen-treated female-to-male transsexual patients (10 ovariectomized and 10 non-ovariectomized) and 10 normal female controls. MEASUREMENTS: ACTH stimulation tests were performed in all subjects. Baseline values and the increase above baseline values after ACTH stimulation were assessed for cortisol and the adrenal androgens androstenedione, dehydroepiandrosterone and dehydroepiandrosterone-sulphate. RESULTS: Increases in levels of cortisol, androstenedione and dehydroepiandrosterone after administration of ACTH were greater in testosterone-treated transsexual patients than controls. CONCLUSION: We conclude that testosterone increases the response of the adrenal gland to stimulation by ACTH.

Adrenal Cortex↗
PubMed1994

Induction of insulin resistance by androgens and estrogens.

Hyperinsulinemia is a common finding in hyperandrogenic women, during pregnancy, and in women using oral contraceptives. To test whether sex hormone treatment can induce insulin resistance in healthy subjects, we studied the effects of administration of testosterone to 13 female to male and of ethinyl estradiol to 18 male to female transsexuals. Utilization and production of glucose and levels of sex steroids were measured during a three-step hyperinsulinemic-euglycemic clamp before and after 4 months of hormone administration. Females were treated with im injections of testosterone esters (250 mg/2 weeks); males were treated with ethinyl estradiol alone (0.1 mg/day, orally) or a combination of ethinyl estradiol and cyproterone acetate (100 mg/day, orally). Similar insulin levels were achieved at each of the three steps of the clamp studies before and during hormone administration. During step 1 of each clamp, with insulin levels in the physiological range, glucose utilization decreased from 3.5 +/- 1.2 to 2.6 +/- 0.9 mmol/kg lean body mass (LBM).h in women treated with testosterone esters (P < 0.001) and from 3.2 +/- 0.7 to 2.5 +/- 0.5 mmol/kg lean body mass.h in men treated with ethinyl estradiol (P < 0.001). The effects of sex steroids during steps 2 and 3 of the clamp at higher (supraphysiological) insulin levels were less clear. Endogenous glucose production (measured by isotope dilution with tritiated glucose) was not affected by hormone administration, indicating that the observed changes in glucose requirement were determined by a diminished peripheral glucose uptake. We conclude that sex hormone administration, i.e. testosterone treatment in females and ethinyl estradiol treatment in males, can induce insulin resistance in healthy subjects.

Adolescent↗
PubMed1993

Influence of sex hormones on plasma endothelin levels.

OBJECTIVE: To determine whether a sex-associated difference in endothelin levels exists and to assess whether this difference is mediated by sex hormones. DESIGN: Initial survey in healthy persons, followed by a nonrandomized intervention. SETTING: A university teaching hospital. PATIENTS: Twenty-three healthy men, 29 healthy women, 20 pregnant women, and 12 male-to-female and 13 female-to-male transsexual patients. MEASUREMENTS: Plasma levels of endothelin were first assessed in healthy men, healthy women, and pregnant women; subsequently, endothelin levels were determined in male-to-female and female-to-male transsexual patients both before and during cross-gender hormone treatment. This treatment involves administration of testosterone esters to women and of ethynylestradiol and cyproterone acetate to men. RESULTS: Endothelin levels were higher in men than in women (5.9 +/- 1.2 compared with 4.17 +/- 0.67 pg/mL; P < 0.01). Endothelin levels were lower in pregnant women than in age- and sex-matched nonpregnant controls (2.19 +/- 0.73 compared with 4.17 +/- 0.67 pg/mL; P < 0.01). In 12 male-to-female transsexuals treated with estradiol and the progestational agent cyproterone acetate, endothelin levels decreased from 8.1 +/- 3.0 to 5.1 +/- 2.0 pg/mL (P < 0.01). In 13 female-to-male transsexuals treated with testosterone, endothelin levels increased from 6.2 +/- 1.1 to 7.8 +/- 1.2 pg/mL (P < 0.01). CONCLUSION: Sex hormones may modulate plasma endothelin levels, with male hormones raising levels and female hormones lowering them. This finding may be important in explaining sex-associated differences in susceptibility to atherosclerotic cardiovascular disease.

Adolescent↗