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Biomedical subjects

I Transbøl

Publications and source records attributed to I Transbøl.

At least 55 records · Page 3Linked to original sources
PubMed1984

Bone mass as referent for urinary hydroxyproline excretion: age and sex-related changes in 125 normals and in primary hyperparathyroidism.

Fasting urinary hydroxyproline: creatinine ratio (OHPr:Cr) and bone mineral content of the forearm (BMC) were measured in 125 normals, 67 females and 58 males, aged 20-79 years, and in 15 patients with primary hyperparathyroidism. In normals, both variables were significantly correlated to age and sex. The interrelation of OHPr:Cr and BMC was studied in subgroups of normals who were supposedly in metabolic balance, that is, females aged 20-39 years (n = 24) and males aged 20-49 years (n = 29). In both sexes OHPr:Cr and BMC were positively correlated: r = 0.60 and 0.58, respectively (P less than 0.001). On this basis, BMC correction of all OHPr:Cr values was undertaken now revealing a stable increased level of bone resorption per unit of bone mass in postmenopausal females. In males OHPr:Cr per unit of BMC remained unaltered throughout life. In primary hyperparathyroidism, in which increased bone resorption is inherent, the discriminatory power of OHPr:Cr was significantly improved when calculated per unit of BMC (P less than 0.001). These observations suggest that estimation of bone resorption by use of OHPr:Cr requires adjustment for differences in bone mass.

Adult↗
PubMed1984

Low-risk lipoprotein pattern in post-menopausal women on sequential oestrogen/progestogen treatment.

Female hormones are known in influence serum lipoproteins. In post-menopausal women oestrogens decrease the concentration of low-density lipoprotein (LDL) and increase that of high-density lipoprotein (HDL), while progestogens may have the opposite effect. The risk of coronary heart disease (CHD) should consequently be decreased by oestrogens and increased by progestogens. We report here the changes observed in serum total cholesterol, triglycerides, and lipoproteins in post-menopausal women during sequential oestrogen/progestogen treatment. Oestriol and 17 beta-oestradiol were given alone for the first 12 days, in combination with norethisterone acetate (1 mg/day) for the next 10 days, and then in reduced amounts for the last 6 days of the 28-day cycle. Three different doses of the oestrogens were investigated (high, medium and low). A total of 177 normal post-menopausal women volunteered for random allocation to treatment or placebo groups. Blood samples were taken every 3 mth during the progestogen phase of the cycle. Serum total cholesterol was found to be 10-13% lower over a 3-yr period on the high oestrogen dose and 5 and 3% lower on the medium and low doses, respectively. No significant changes were seen in serum triglycerides. Determination of lipoprotein fractions showed that the reduction in total cholesterol was due to reduced LDL-cholesterol, the HDL-cholesterol levels remaining virtually unchanged.

Adult↗
PubMed1984

Measurements of whole body retention of diphosphonate and other indices of bone metabolism in 125 normals: dependency on age, sex and glomerular filtration.

Measurements of 24-h whole body retention of 99m-Tc-MDP (WBR) has been performed in 125 normal volunteers, together with determinations of serum alkaline phosphatase, urinary hydroxyproline excretion and creatinine clearance. WBR decreased slightly from the 3rd to the 4th decade, after which it increased gradually in the older age-groups. Serum alkaline phosphatase followed an identical pattern, while the urinary hydroxyproline excretion demonstrated a marked but temporary rise in the post-menopausal age-groups. Finally, the creatinine clearance decreased gradually in the older age groups. Analysis of variance demonstrated that WBR varied independently with serum alkaline phosphatase and creatinine clearance, while no relationship between WBR and the hydroxyproline excretion was found. It seems likely that the increasing retention of diphosphonate in elderly persons reflects rising osteoblastic activity as well as decreasing glomerular filtration.

Adult↗
PubMed1984

Testosterone treatment and arginine-induced growth hormone stimulation in male delayed puberty: effects on serum calcium, phosphate and vitamin D metabolites.

Hormonal changes after arginine-induced growth hormone stimulation and subsequent testosterone treatment were examined in 5 patients classified as having male delayed puberty. All the patients responded well to growth hormone stimulation and a significant negative correlation was found between the delay in height age and the maximal growth hormone response, r = 0.80, P less than 0.05. The testosterone treatment did not alter this pattern. Changes in PTH, 25OHD, 24.25(OH)2D, and 1.25(OH)2D were examined at 24 h after the infusion. The results showed significant reductions in PTH (P less than 0.05) and 24.25 (OH)2D (P less than 0.05) and a possible increase in 1.25(OH)2D, whereas 25OHD remained unchanged. These results may support the conception of growth hormone as a common denominator of growth and bone metabolism.

Adolescent↗
PubMed1984

Urinary 99m-Tc-diphosphonate excretion as a simple method to quantify bone metabolism.

Twenty-four-hour whole-body retention (WBR) of 99m-Tc-methylene-diphosphonate (an index of bone turnover) was determined by whole-body counting (WBRs) and complementarily by urine counting (WBRu) in nineteen subjects with normal to highly increased bone turnover. WBRs and WBRu correlated well (r = 0.94, P less than 0.001), and gave almost the same results. Both WBRs correlated equally well with serum alkaline phosphatase and urine hydroxyproline/creatinine (r = 0.82-0.93). Coefficient of variation in WBRu was 7.0%, determined by duplicate measurements in sixteen normals. The injected dose of diphosphonate did not influence WBRu. However, since almost 50% of the diphosphonate excreted in urine appeared during the first few hours after the i.v. injection, the method of WBRu requires careful urine collection. Thus, the simple WBRu determination provides the same information on bone metabolism as does the more cumbersome and expensive WBRs technique.

Adult↗
PubMed1984

Calcium homeostasis in morbid obesity.

Calcium homeostasis in morbidly obese subjects has attracted little attention. Prompted by reports of elevated serum levels of parathyroid hormone in such patients, calcium homeostasis was investigated in 36 patients with morbid obesity and in 44 normal weight controls. Concerning serum immunoreactive parathyroid hormone (C-terminal), serum ionized calcium (Ca++) and serum albumin corrected magnesium no significant differences between the groups were detected. When albumin corrected, serum total calcium turned out to be significantly elevated (p less than 0.0001) in the obese subjects. Also, serum alkaline phosphatase activity was significantly raised in the obese state. The results demonstrate that calcium homeostasis, as expressed by the metabolically active serum Ca++, is normal in morbid obesity. But the results also point towards an abnormal calcium binding due to either an increased calcium binding to albumin or to calcium complexing small anions.

Adult↗
PubMed1984

Effect of menopause and estrogen substitutional therapy on magnesium metabolism.

Magnesium homeostasis was determined in 48 healthy premenopausal women and in 54 early postmenopausal women. After an initial examination, the 54 postmenopausal women were randomly allocated to two groups with 33 receiving placebo treatment and 21 receiving estrogen substitutional therapy for 2 years. The 24-hour mean urinary excretion rates of magnesium were increased in the 54 postmenopausal women compared with the premenopausal women, namely: 467 +/- 20 (SEM) versus 355 +/- 13 mmol/mol creatinine (p less than 0.001) or 33.9 +/- 1.2 versus 24.3 +/- 1.0 mumol/l glomerular filtration (p less than 0.001). The same pattern was observed when the excretion rates were determined on fasting 1-hour morning urinary collections. This postmenopausal hypermagnesiuria was reduced to the premenopausal level during 2 years of estrogen substitutional therapy (p less than 0.001). As no evidence of hypomagnesemia was found, postmenopausal hypermagnesiuria probably originates from increased intestinal magnesium absorption, somehow induced by estrogen deficiency.

Adult↗
PubMed1983

Effect of natural oestrogen/gestagen therapy on uric acid metabolism in post-menopausal women.

Uric acid metabolism was studied in groups of early post-menopausal women before and during long-term administration of natural oestrogen/gestagen (n = 21), bendroflumethiazide (n = 19) or placebo (n = 34). Serum uric acid rose definitely, by 13.0% during thiazide, and decreased slightly, by 4.9%, during hormone treatment. The latter deviation did not differ significantly from that of -2.9% seen in the placebo group. The urinary excretion rates of uric acid observed during thiazide and hormone treatment did not differ significantly from that of the placebo group. It is concluded, that within the present design of study, which readily permits detection of the well-known hyperuricaemic action of thiazide, oestrogen/gestagen hardly affects uric acid metabolism.

Adult↗
PubMed1983

Relationship between bone mineral content and frequency of postmenopausal fractures.

To elucidate the relationship between bone mineral content (BMC) and the frequency of postmenopausal fractures, we performed an epidemiologic investigation in a representative sample of 70-year-old women. Anamnestic data concerning postmenopausal fractures due to minor trauma were recorded and lateral X-rays of the spine were taken for evaluation of spinal fractures. BMC was measured by 125I photon absorptiometry. The 285 women studied were allocated into quintiles according to their BMC value. In 77 women, there were 131 definite osteoporotic fractures (i.e., spinal crush, and fracture of the hip, proximal humerus, and distal forearm), and in 48 women, there were 162 other non-violent fractures (i.e., spinal wedge and other long bone fractures). The frequencies of osteoporotic fractures varied inversely with the mean BMC values for each quintile (r = 0.959, p less than 0.01). The difference in frequency of osteoporotic fractures between the first and fifth quintiles was highly significant (p less than 0.001). In contrast, other non-violent fractures appeared to be unrelated to BMC. It is concluded that low BMC levels predispose to osteoporotic fractures.

Aged↗
PubMed1983

Effect of thiazides on the urinary calcium oxalate stone-forming potential in normal males.

We studied the effect of bendroflumethiazide on a risk factor index, COSP, reflecting the stone-forming potential of urinary calcium oxalate. This index includes the concentrations of three stone promotors: calcium, oxalate, and uric acid in its numerator, and two stone inhibitors: magnesium and citrate, in its denominator. These risk factors were measured in 4-hour and 24-hour urinary specimens obtained under fixed conditions of food and fluid intake. Eight normal males were studied before and after two and four weeks of continued thiazide treatment. Thiazide 2.5 mg b.i.d. was given for two weeks, followed by 2.5 mg t.i.d. for another two weeks. Before treatment COSP exhibited a pronounced diurnal variation with peaks between 8 a.m. and noon, and 8 p.m. and midnight. After four weeks of thiazide treatment suppression of two stone promotors, calcium (p less than 0.01) and uric acid (p less than 0.02), and reduced COSP by 36 to 95% in each subject (median: -71%, p less than 0.01). Moreover, thiazide abolished the diurnal variation of COSP. After the initial two weeks of thiazide 2.5 mg b.i.d., almost identical effects were observed. Nearly all the changes in COSP were explained by the effects on urinary calcium. This marked suppression of COSP supports the theory that thiazides may be useful in the prevention of renal calcium oxalate stone formation.

Adult↗
PubMed1982

Dose-response evaluation of cyclic estrogen/gestagen in postmenopausal women: placebo-controlled trial of its gynecologic and metabolic actions.

In order to study dose-response relationships of estrogen in normal postmenopausal women, 100 volunteers were randomized to 12 months' treatment with placebo or one of three different doses (high, medium, or low) of natural estrogens (17 beta-estradiol and estriol), sequentially combined with norethisterone acetate for 10 of the 28 cycle days. A total of 87 women completed the trial with examinations every 3 months. Relief of climacteric symptoms was dose related, being 70%, 56%, and 33% in the high, medium, and low estrogen groups and unchanged in the placebo group. Regular vaginal bleeding occurred in 78% receiving high-dose in 64% receiving medium-dose, and in 40% receiving low-dose estrogen. Bone mass increased in the high and medium groups, was unchanged in the low group, and declined in the placebo group. Dose-related decreases in serum cholesterol of 10%, 5%, and 3% occurred in the three respective estrogen groups. Serum triglyceride levels, blood pressure, and body weight remained unchanged in all groups.

Adult↗
PubMed1982

Renal hypouricaemia in insulin treated diabetes mellitus.

Uric acid metabolism was investigated in 69 insulin-treated male diabetic outpatients and in 23 healthy male subjects, because of a reported coincidence between diabetes and gout. All subjects had normal serum creatinine concentrations and none received diuretic treatments. Compared with normal, the diabetics had significantly lower mean serum uric acid concentrations (0.34 +/- 0.08 (SD) mmol/l versus 0.23 +/- 0.06 mmol/l, p less than 0.001). 17% of the diabetic patients had serum concentrations below the normal mean--2 SD. In contrast, the diabetic patients had a 42% increase in renal uric acid excretion rate (p less than 0.01), and an 83% increase in the ratio of uric acid clearance/creatinine clearance (p less than 0.001). These indices of renal uric acid excretion were both positively correlated to fasting blood glucose levels (r=0.57, p less than 0.001, and r=0.50, p less than 0.001, respectively), to the degree of glycosuria (r=0.73, p less than 0.001, and r=0.63, p less than 0.001, respectively), and to the magnitude of water diuresis (r=0.60, p less than 0.001, and r=0.39, p less than 0.01, respectively). The hypouricaemia observed in these insulin-dependent diabetic male subjects may probably be caused by the increased renal excretion of uric acid in the presence of hyperglycaemia. The study gave no evidence of increased serum uric acid concentrations in insulin-dependent diabetics. It is therefore likely that any coincidence between gout and diabetes derives from other coexisting serum uric acid raising factors.

Adult↗
PubMed1982

Hyponatremia and hyperkalemia in relation to hyperglycemia in insulin-treated diabetic out-patients.

Interrelations between glucose and electrolyte homeostasis were evaluated in 193 insulin-treated diabetic out-patients. All had normal serum creatinine and were studied during their everyday metabolic control. Although the patients were selected to be without proteinuria and ketonuria, they exhibited wide ranges of blood glucose values (2.5-29.5 mmol/l) and urine glucose excretions (0-301 mmol/mmol creatinine). Patients with blood glucose values within 2.5-10 mmol/l (n = 80) had entirely normal levels of serum sodium (140.6 +/- 2.7 (SD) versus 141.0 +/- 2.6 mmol/l) and potassium (4.35 +/- 0.38 versus 4.40 +/- 0.38 mmol/l) as compared with normals (n = 371). In contrast, diabetics with higher blood glucose concentrations (n = 113) showed hyponatremia (137.7 +/- 2.6 mmol/l, p less than 0.001) and a moderate increase of serum potassium (4.60 +/- 0.39 mmol/l, p less than 0.001). On stratification into classes of blood glucose, serum sodium declined from 142 to 135 mmol/l (r = -0.61, p less than 0.001), whereas serum potassium rose from 4.33 to 4.87 mmol/l (r = 0.37, p less than 0.001). Despite these reciprocal changes the urinary excretion rates relative to creatinine of sodium potassium and water rose with rising degrees of glycosuria (r = 0.24, p less than 0.001; r = 0.28, p less than 0.001; and r = 0.63, p less than 0.001, respectively). The decline in serum sodium represents a well-known osmoregulatory response to hyperglycemia. However, the rising level of serum potassium in virtual absence of renal failure and ketonuria suggests an abnormality in potassium homeostasis. Diabetic dysregulation, or rather insulin deficiency may be its cause.

Cross-Sectional Studies↗
PubMed1982

Thiazide for the postponement of postmenopausal bone loss.

The effect of thiazide on bone mineral loss in normal postmenopausal women was examined during a 3 yr placebo-controlled clinical trial. Sixty-three healthy women in their early menopause were randomized to treatment with bendroflumethiazide 5 mg/day or placebo for 2 yr, while both groups received placebo for the third year of the trial. Calcium supplement 0.5 g/day was given throughout the 36 mo to all participants. Bone mineral content (BMC) determined by 125I-photon absorptiometry of the forearms decreased 2% per year in the placebo group (p less than 0.001). In the thiazide group no fall in BMC was seen during the first 6 mo. whereafter BMC declined with the same rats as in the placebo group. At the end of the 3 yr trial BMC averaged 94.1% in the placebo group and 95.2% in the thiazide group (p greater than 0.05). Despite a daily supplement of 0.5 g calcium, thiazide induced a persistent fall in the urinary calcium excretion of 25% (p less than 0.001), whereas the calcium supplement in the placebo group caused a significant increase in mean urine calcium of 10%-20% (p less than .001). At stop of thiazide medication a rebound effect caused a marked rise in urine calcium. One month after withdrawal of the calcium supplement the urinary calcium excretion had returned to the initial level in both groups. It is concluded that despite a sustained urine calcium lowering action the effect of thiazide upon postmenopausal bone loss is shortlived.

Alkaline Phosphatase↗
PubMed1982

Is cigarette smoking a promotor of the menopause?

All women (n = 11,809) aged 44-53 years from a representative district of Denmark were asked by questionnaire about their date of birth, date of latest menstrual bleeding, possible gynaecological operations, smoking habits, and use of medications. A total of 9,411 (80%) questionnaires were returned. After exclusions because of incomplete information (n = 275), possible surgical menopause (n = 1,270), and treatment with gonadal hormones (n = 2,221), 5,645 women remained suitable for to study. The reproducibility of the information given by these women was excellent as judged by personal interviews of 315 participants. The study population was divided into five 2-year age groups, and the proportion of postmenopausal women among non-smokers and heavy smokers was calculated. Differences in respect to the menopausal status were not observable in the oldest and the youngest two age groups comprising just a few per cent of post-menopausal women. However, heavy smokers in the other two age groups had passed the menopause earlier than the non-smokers (p less than 0.001). This finding suggests cigarette smoking as a promotor of the menopause.

Adult↗
PubMed1982

Treatment of post menopausal osteoporosis. A controlled therapeutic trial comparing oestrogen/gestagen, 1,25-dihydroxy-vitamin D3 and calcium.

A controlled therapeutic trial on seventy-four 70-year-old women was carried out with the purpose of finding the optimal treatment for post menopausal osteoporosis. The bone mineral content (BMC) was measured by I-photonabsorptiometry at two sites in the distal part of the forearms, where the trabecular/cortical ratio is 0.25 and 1.5, respectively. Radiographs were done on the right hand to measure the metacarpal bone mass (cortical area/total area=CA/TA. After observing the spontaneous course of bone loss for 6 months the participants were allocated at random to 12 months' treatment with 1,25-dihydroxycholecalciferol [1,25(OH)2D3] and oestrogen/gestagen, alone or in combination, and calcium. The groups treated with oestrogen/gestagen [with or without 1,25(OH)2D3] showed a highly significant increase in BMC. In contrast bone mineral remained unchanged or decreased in both the calcium and the 1,25(OH)2D3 groups with a tendency towards more pronounced negative bone balance in the 1,25-(OH)2D3 group. Seven out of nineteen patients of 1,25(OH)2D3 developed hypercalcaemia, which necessitated a reduction in dosage. It is concluded that the new vitamin D metabolite, 1,25(OH)2D3, given in clinically acceptable doses, is without value in the treatment of post menopausal osteoporosis.

Aged↗