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I Transbøl

Publications and source records attributed to I Transbøl.

At least 73 records · Page 4Linked to original sources

Renal hypomagnesaemia in human diabetes mellitus: its relation to glucose homeostasis.

Interrelations between magnesium and glucose metabolism were studied in 215 insulin-treated diabetic out-patients aged 7-70 years. All had normal serum creatinine concentrations (below 115 mumol/l) and none had other diseases or received drugs known to interfere with mineral metabolism. A definite hypomagnesaemia (less than normal mean - 2 SD) and hypermagnesiuria (greater than normal mean + 2 SD) occurred in 38.6% and 55% of the patients. In the presence of hypermagnesiuria the serum magnesium concentration was inversely correlated to the urinary magnesium excretion rate (R = -0.23, P less than 0.02). Serum magnesium correlated inversely with both fasting blood glucose (R = -0.32, P less than 0.001) and the urinary glucose excretion rate (R = -0.22, P less than 0.005). The urinary magnesium excretion rate correlated directly with the same variables (R = 0.27, P less than 0.001 and R = 0.58, P less than 0.001, respectively). These data indicate that the net tubular reabsorption of magnesium is decreased in diabetic patients in presence of hyperglycaemia, leading to hypermagnesiuria and hypomagnesaemia.

Adolescent↗

Bone mineral homeostasis, bone growth, and mineralisation during years of pubertal growth: a unifying concept.

Serum calcium, magnesium proteins, phosphate, and immunoparathyroid hormone were measured in 338 normal children and adolescents aged between 7 and 20 years and in 123 normal adults aged between 21 and 50 years. Protein corrected serum calcium and magnesium remained stable throughout the study. Despite hyperphosphataemia protein corrected calcium exceeded the concentrations of normal adults. Serum phosphate and the Ca X P product greatly exceeded adult values and fell rather slowly towards adult levels after the pubertal growth spurt. Serum immunoparathyroid hormone tended to exceed normal adult values and was judged high for the level of serum calcium. Similarities between mineral metabolism in childhood an adolescence and in acromegaly were striking. On this basis in the light of studies demonstrating stimulatory actions of gonadal hormones on growth hormone and of growth hormone on the secretion of parathyroid hormone and 1,25-dihydroxyvitamin D3, a unifying concept is developed. This concept places growth hormone in the unique position of being the main driver and co-ordinator during childhood and adolescence of bone growth an mineralisation on the one hand, and of blood mineral homeostasis on the other. Gonadal hormones probably express some of their actions through stimulation of growth hormone secretion and others by different mechanisms. According to this concept growth hormone is maintaining th Ca X P product at a suitable high level as long as growth hormone and gonadal hormones deliver bone matrix for mineralisation at a high rate.

Adolescent↗

Effects of two years' estrogen-gestagen replacement on climacteric symptoms and gonadotropins in the early postmenopausal period.

The effects of estrogen/gestagen (e/g) treatment given in a 28-day cycle (Trisequens forteR, Novo) on menopausal symptoms and plasma concentrations of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were studied in a placebo trial. 119 normal women in the early postmenopausal period with mild to moderate climacteric complaints were included. At 3-month intervals for 2 years the participants were examined and filled in questionnaires containing the 11 symptoms of the Kupperman index (10). For each symptom a score was given. In the e/g group 77% (43/56) completed the trial compared with 83% (54/63) in the control group. A total of 61% of the women complained of hot flushes and from 9% to 44% complained of the remaining 10 Kupperman symptoms. At all eight examinations e/g treatment was found to have reduced the symptom score as well as the proportion of women with hot flushes, paresthesia, insomnia, nervousness, vertigo and formication. The symptom score of hot flushes and insomnia declined significantly (p less than 0.01). In the 24 women with hot flushes and in the 19 without, e/g caused similar reduction in the mean score of the other 10 symptoms. No placebo effect was seen. E/g caused a significant (p less than 0.01) fall in the elevated plasma concentrations of FSH and LH. Vaginal bleeding was regular in 38/43 and irregular in 4/43 women during hormone treatment. No serious side effects were attributed to e/g therapy. It is concluded that e/g treatment, in addition to its beneficial effects on hot flushes and insomnia, also alleviates several other climacteric symptoms.

Bendroflumethiazide↗

1,25(OH)2D3 and renal function. A controlled clinical study in normal elderly women.

A controlled study of the effect of 1,25(OH)2D3 was performed in 58 normal 70-year-old Danish women. After 6 months; observation of the spontaneous course the participants were randomized to treatment with either 1,25(OH)2D3 (0.5 micrograms daily) or placebo. Both groups received 500 mg calcium daily. Seven out of 20 participants treated with 1,25(OH)2D3 developed slight hypercalcaemia which disappeared after dose adjustment. One participant in the placebo group developed slight hypercalcaemia. A highly significant increase in serum creatinine was observed in the 1,25(OH)2D3 group when compared with the initial value and with the change in the placebo group. Serum creatinine remained elevated throughout the study despite normalization of serum calcium. It is concluded that 1,25(OH)2D3 treatment in normal, elderly women has a negative effect on the renal function as estimated from serum creatinine.

Aged↗

Epidemiology of postmenopausal spinal and long bone fractures. A unifying approach to postmenopausal osteoporosis.

The incidence of spontaneous postmenopausal fractures and their relationship to menopausal age and bone mass were determined in a representative sample of 70-year-old Danish women. Two hundred and eighty-five women (1.2% of all women in that age group) were examined by case history, by 125I photon absorptiometry in both forearms (BMC), by metacarpal index (CA/TA), and by lateral radiographs of the spine. Twenty-four per cent of the participants had sustained single fractures, and 20% multiple fractures. Nineteen per cent had fractures of the lower forearm, 5% of the proximal humerus, 4% of the hip, and 5% crush fractures of the spine. These comprise Group I fractures, the most definite expressions of osteoporosis. The remaining other long bone fractures (7%) and spinal wedge fractures (18%) comprise Group II fractures. Group I cases were characterized by an earlier onset of the menopause and a definite decrease in bone mass, as judged from BMC and CA/TA, as compared with the nonfracture group. Group II cases did not display this distinction. Of Group I cases, those with multifractures differed from those with single fractures by having a five-year earlier occurrence of first fracture, a further decrease in bone mass, and a slightly raised serum alkaline phosphatase level. Serum calcium and phosphate levels were the same in all groups.

Age Factors↗

Fracture frequency and bone preservation in postmenopausal women treated with estrogen.

Two hundred eighty-five normal 70-year-old Danish women were divided according to postmenopausal use of gonadal hormones into 3 groups: 1 virtually untreated (3 months or less, N = 231), 1 treated over a short term (4 months to 6 years, N = 36), and 1 treated over a long term (6 years or more, N = 18). The 3 groups had been treated for a median of 0, 6, and 70%, respectively, of their postmenopausal years. The degree of bone loss varied inversely with the duration of postmenopausal hormone treatment. Bone mineral content was 11.8% higher in the long-term treated group than in the untreated group (P less than .05). Likewise, the metacarpal bone mass was 8.5% greater (P less than .01). The number of women with postmenopausal fractures was 13% lower in the long-term treated group than in the untreated group (Difference not significant). Data from this retrospective study present evidence that estrogen protects bones in elderly women.

Aged↗

Bone mass in postmenopausal women after withdrawal of oestrogen/gestagen replacement therapy.

The effect on forearm bone mineral content (BMC) of initiation and withdrawal of oestrogen/gestagen treatment was studied in a randomised trial in 94 healthy female volunteers six months to three years after the menopause. BMC was measured every three months for three years. BMC increased by 3.7% (p less than 0.001) during three years' hormone treatment and decreased by 5.7% (p less than 0.001) during three years' placebo treatment. The annual rate of bone loss after discontinuation of hormone therapy was identical with the bone loss in the placebo group. The present study indicates that even temporary hormone replacement therapy after the menopause will have a lasting beneficial effect on bone mass.

Bone and Bones↗

Normalization of bone mineral content to height, weight, and lean body mass: implications for clinical use.

The main object of the present study was to reduce the large biological variation in forearm bone mineral content (BMC) by correction for individual variation in gross morphology. In 315 normal females aged 45--54 years, determinations of height, weight, and 24-h urinary creatinine excretion rates were performed, and lean body mass was calculated, BMC was measured by photon absorptiometry on both forearms. BMC was correlated to height (r = 0.19, P less than 0.01), to weight (r = 0.09, P greater than 0.05), to lean body mass (r = 0.15, P less than 0.05), and to creatinine excretion rate (r = 0.29, P less than 0.001). The biological variation in BMC of the 315 females was for raw BMC 15.8%; after correction of BMC for height 15.5%, for weight 15.8%, for lean body mass 15.6%, and for creatinine excretion rate 15.2%. Regression analysis with two independent variables (creatinine excretion and height or weight) increased in both cases the correlation coefficient to 0.32 and decreased the interindividual coefficient of variation of BMC to 15.0%. For diagnostic purposes BMC must be corrected for age and sex, but further corrections seem of minimal benefit.

Body Composition↗

Influence of calcium infusion on urinary cyclic AMP and phosphate in hyperparathyroidism.

Urinary cyclic AMP (cAMP) and phosphate were measured before and after calcium infusion in 12 patients with operatively verified primary hyperparathyroidism (PHP) and in 12 healthy persons. In normal subjects infusion of calcium caused a reduction in urinary cAMP directly correlated to the preinfusion values and inversely correlated to the serum calcium concentration determined as albumin-corrected serum calcium. In normal subjects with high normal albumin-corrected serum calcium the infusion of calcium caused no or only a small depression in the urinary excretion of cAMP. Changes in phosphate excretion were not correlated to the calcium concentration. Four of the 12 hyperparathyroid patients showed normal relative suppression in urinary cAMP after the infusion of calcium, and 5 had normal suppression of phosphate excretion. It is concluded that some patients with PHP retain calcium-sensitive secretion of PTH, and that the classical calcium infusion test is of doubtful value in the diagnosis of PHP.

Adolescent↗

Practical clinical value of the C-peptide response to glucagon stimulation in the choice of treatment in diabetes mellitus.

In order to discriminate between insulin-dependent and non-insulin-dependent patients, serum C-peptide concentration was determined using antiserum M1230 in the fasting state and 6 min after an i.v. injection of 1 mg glucagon in 215 patients treated with insulin and 53 treated with diet and oral antidiabetics. A patient was considered well controlled without insulin when fasting blood glucose was below 8 mmol/l and when glucosuria was absent. After re-evaluation of therapy in hospital it was found that the majority of patients with a post-stimulatory serum C-peptide concentration above 0.60 pmol/ml appeared to have non-insulin-dependent diabetes mellitus. When fasting C-peptide was used, a great overlap was found between the two treatment groups. During evaluation of therapy in hospital, 6 previously insulin-treated patients could be well treated with diet and tablets and 6 diet- and tablet-treated patients required insulin. The glucagon test seems to be of value in the outpatient clinic to discriminate non-insulin-dependent from insulin-dependent patients.

Adult↗

Development of bone mineral loss in insulin-treated diabetes: a 1 1/2 years follow-up study in sixty patients.

The change in bone mass during 1 1/2 years was determined in a longitudinal study of sixty adult insulin-treated diabetic out-patients. During the study period the mean bone mass decreased by 1.30 +/- 0.28 (SEM)% (P less than 0.001), to a mean value of 91.0 +/- 1.7% of normal (P less than 0.001). The rate of bone loss was significantly higher in patients with 1-6 years of diabetes (n = 29, bone loss: 1.96 +/- 0.32%/1 1/2 years) than in patients with longer duration of the disease (n = 31, bone loss: 0.61 +/- 0.44%/1 1/2 years, P less than 0.02). The endogenous insulin secretion estimated with the glucagon-stimulated serum C-peptide concentration decreased during the observation period in 58.6% of the patients with 1-6 years of diabetes compared to 16.1% among patients with 7-11 years of diabetes (P less than 0.002). The rate of bone mineral loss was almost 3 times higher in the twenty-two patients in whom endogenous insulin secretion had deteriorated (2.12 +/- 0.30%/1 1/2 years) than in the thirty-eight patients without as well as with unchanged or increased insulin secretion (0.78 +/- 0.39%/1 1/2 years, P less than 0.01). In twenty patients with an increased insulin dose during the study period the mean bone mineral loss was 2.05 +/- 0.36%/1 1/2 years compared to a mean bone mineral loss of 0.91 +/- 0.38%/1 1/2 years in the forty patients with unchanged or decreased insulin dosage (P less than 0.05). This longitudinal study further supports the hypothesis that the bone mineral loss in insulin-treated diabetic patients begins with the onset of clinical diabetes and that its development is associated with the deterioration of the beta-cell function and with the increment in insulin dosage. The rate of bone mineral loss is high during the first few years of clinical diabetes, but levels off with increasing duration of the disease.

Adult↗

Effect of 1,25-dihydroxy-vitamin D3 in itself or combined with hormone treatment in preventing postmenopausal osteoporosis.

Eighty-four normal women, 2.5--5 years after their natural menopause, participated in a controlled double-blind trial. The effect of various therapeutic regimens on postmenopausal bone mineral loss was measured by photonabsorptiometric determination of the bone mineral content of both forearms. The women were randomized into four treatment groups: 1,25-dihydroxycholecalciferol (1,25(OH)2D3) alone in a daily dose of 0.25 micrograms, oestrogens/gestagen alone or combined with 1,25(OH)2D3, and placebo. The groups treated with oestrogens/gestagen (without and with 1,25(OH)2D3) showed a similar increase in bone mineral content of about 1% during one year of treatment. In contrast, both the placebo group and the 1,25(OH)2D3 group demonstrated a decrease of 1.9% and 2.1%, respectively, within the same period of time. While 1,25(OH)2D3 did not alter the rate of bone loss, it caused the characteristic and pronounced increase in urinary calcium excretion (15%). It is concluded that 1,25 (OH)2D3 neither serves as an alternative nor as an additive to gonadal hormones in the prevention of postmenopausal osteoporosis.

Bone and Bones↗