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I Transbøl

Publications and source records attributed to I Transbøl.

At least 37 records · Page 2Linked to original sources
PubMed1991

[Basedow's disease and thyroid stimulating hormone producing pituitary adenoma in a patient].

TSH-producing adenomas of the pituitary gland are very rare. Synchronous combinations of TSH-producing adenomas with other causes of hyperthyroidism are certainly extremely rare. We present the second known case, reported in the literature, consisting of observations for 12 years in a woman aged 43 years, who presented with active Graves' disease and an apparently inactive pituitary macro-adenoma. However, after normalisation of serum T3 and serum T4 levels by antithyroid medication for one year, the serum TSH rose inappropriately and continued to rise for the following 11 years. Insidious growth of the adenoma also occurred. After one year of medical treatment, a huge goitre was resected (210 g) leaving the patient euthyroid, clinically and biochemically, for four years. Hereafter, hyperthyroidism developed again this time without Graves' disease. We conclude that the patient experienced hyperthyroidism on two occasions, the first caused by Graves' disease and then caused by a TSH-producing pituitary adenoma.

Adenoma↗
PubMed1991

Lack of relationship between parathyroid hormone and 1,25-dihydroxyvitamin D in chronic renal failure.

In the present study, concentrations of parathyroid hormone (PTH), determined by an intact PTH assay and a midregion/C-terminal PTH assay, 1,25-dihydroxyvitamin D [1,25(OH)2D3], ionized calcium and phosphate were measured in 15 patients with a stable creatinine clearance (Ccr) of 21.2 +/- 14.4 ml/min (mean +/- SD; group 1) and in 10 patients with a Ccr regularly undergoing hemodialysis (group 2, Ccr not measured). In group 1, the mean concentration of 1,25(OH)2D3 was significantly increased compared with the level in group 2, whereas no differences were found concerning the concentrations of intact PTH, midregion/C-terminal PTH, ionized calcium and phosphate. In group 1, the PTH concentration correlated inversely with ionized calcium concentration and Ccr, which in turn, was directly correlated. The concentration of 1,25(OH)2D3 correlated inversely with phosphate concentration, but did not correlate with either PTH or ionized calcium concentrations. In group 2 no correlation was found between any of the biochemical variables. The data demonstrate that in patients with stable renal failure, the concentration of ionized calcium still regulates PTH secretion but other variables such as parathyroid cell mass and setpoint may interfere with the interrelation. The elevated concentration of phosphate in renal failure may override PTH as a regulator of the renal 1,25(OH)2D3 formation. The lack of correlation in the hemodialyzed patients may be attributed to extrarenal production of 1,25(OH)2D3, reduced binding of 1,25(OH)2D3 to parathyroid tissue or the major changes in calcium homeostasis caused by the hemodialysis.

Aged↗
PubMed1991

Awareness of hypercalcaemia in a hospital population?

In a hospital population all patients with hypercalcaemia were registered consecutively during a 6-month period. Fifty per cent of the patients having hypercalcaemia, which was defined as serum calcium concentrations (albumin corrected) above normal mean + 3 standard deviations, had a serum calcium analysis requested. Of these between 14% and 96%, dependent on the clinical diagnosis and the degree of hypercalcaemia, had the hypercalcaemia identified. Since the prevalence of hypercalcaemia was estimated to be 2.6% and only about 1:4 was identified by the clinicians, correct diagnosis of hypercalcaemia seems to be a problem.

Calcium↗
PubMed1990

Diagnostic applicability of intact and midregion/C-terminal parathyroid hormone assays in calcium metabolic disorders.

We compared measurements of parathyroid hormone (PTH) using two assays, in order to detect intact PTH and midregion/C-terminal PTH (M/C-PTH) in a variety of calcium metabolic disorders. The series consisted of a total of 101 patients, including subjects with primary hyperparathyroidism (n = 24), hypoparathyroidism (n = 18), hypercalcaemia of malignancy (n = 10), moderate chronic renal failure (n = 14), chronic renal failure undergoing haemodialysis (n = 19), and small bowel disorders (n = 16). The intact PTH assay was superior to the M/C-PTH assay in reflecting parathyroid function in primary hyperparathyroidism, hypoparathyroidism and hypercalcaemia of malignancy. In patients with chronic renal failure, both assays were indicators of a comparable number of patients with elevated PTH levels. Intact PTH proved most reliable in detecting changes in parathyroid hormone secretion in response to variations in ionized calcium induced by haemodialysis. In patients with extensive intestinal resection, both assays showed increased levels of PTH. It is concluded that measurement of intact PTH is a more reliable index of parathyroid function than measurement of midregion/C-terminal PTH. Thus such an approach should be the one of choice for clinical evaluation of calcium homeostasis.

Calcium Metabolism Disorders↗
PubMed1990

Induced hypocalcaemia controlled by a citrate clamp technique, and the intact parathyroid hormone response obtained.

In order to investigate (1) the possibility of controlled induction and maintenance of hypocalcaemia, and (2) the intact parathyroid hormone (PTH(1-84)) response obtained thereby, 14 healthy individuals were administered an i.v. infusion of trisodiumcitrate. The reproducibility of the method established was assessed in five of the 14 individuals. Aiming at a steady-state level of blood ionized calcium (B-Ca2+) = 1.00 mmol/l, obtained within 30 min and subsequently maintained for 90 min, the infusion was guided by frequent determinations B-Ca2+. The method established was as follows: infusion of 0.85 mmol citrate/kg body weight/h during the first 10 min, followed by 0.44 mmol citrate/kg body wt h 1.26 exp. ((actual B-Ca2(+)--target B-Ca2+)/0.02) mmol/l, until B-Ca2+ = 1.00 mmol/l. In the steady-state period the infusion rate was 0.29 mmol citrate/kg body wt. h 1.26 exp. ((actual B-Ca2(+)--target B-Ca2+)/0.02) mmol/l. The method showed reproducibility by an overall difference in B-Ca2+ measurements of -0.03 mmol/l, which did not statistically differ from zero (p less than 0.05). No severe side effects were observed during a total of 21 infusions. Intact serum parathyroid hormone concentrations (S-PTH(1-84)) obtained during induced hypocalcaemia rose to a peak within 5-10 min, and then declined to a steady-state level about three times the initial. The serum (S) PTH(1-84) response could be caused by a burst of S-PTH(1-84) from a depot source while the steady-state level may indicate a stimulated secretion from parathyroid glands. The S-PTH(1-84) response was shown to be reproducible by an overall difference in S-PTH(1-84) measurements of -0.52 pmol/l, which did not statistically differ from zero (p less than 0.10).

Calcium↗
PubMed1990

Respective roles of 25 hydroxy-vitamin D, PTH, phosphate and renal function for the 1-alpha-hydroxylase activity in primary hyperparathyroidism.

Forty-three women (mean age 67 years, range 34-84 years) with primary hyperparathyroidism were investigated in an effort to examine the regulation of the 1-alpha-hydroxylase. This enzyme catalyzes the 1-hydroxylation of 25-hydroxy-vitamin D [25(OH)vit D] to 1,25-dihydroxy-vitamin D [1,25(OH)2vit D]. Serum 25(OH)vit D, 1,25(OH)2vit D, PTH, ionized calcium, phosphate and the 24-hour clearance of creatinine were measured. Different linear regression models were calculated with 1,25(OH)2vit D as the dependent variable. 25(OH)vit D was found to be definitely important for the regulation. The role of PTH for the 1,25(OH)2vit D production was discussed. Both renal function and phosphate concentration were found to influence the 1-alpha-hydroxylation.

Adult↗
PubMed1990

Adjusted ionized calcium (at pH 7.4) and actual ionized calcium (at actual pH) in capillary blood compared for clinical evaluation of patients with disorders of calcium metabolism.

We report results for adjusted ionized calcium (at pH 7.4) and actual ionized calcium (at actual pH) in capillary blood from 183 patients with disorders of calcium metabolism (primary hyperparathyroidism, secondary hyperparathyroidism of malabsorption, primary hypoparathyroidism, Paget's disease, acromegaly, hypercalcemia of malignancy, osteoporosis, sarcoidosis, idiopathic hypercalciuria, and familial hypocalciuric hypercalcemia). The correlation and the equation for the linear regression between adjusted ionized calcium (y) and actual ionized calcium (x) were y = 1.011x + 0.005 mmol/L, r = 0.992, Sy,x = 0.021 mmol/L. Results were similar within each diagnostic group. Consistent agreement between adjusted and ionized calcium was observed in 96.7% of patients representing a variety of the most frequently encountered disorders of calcium metabolism. Thus we find adjusted ionized calcium to be as useful as actual ionized calcium for evaluation of patients with such disorders. Adjusted ionized calcium may therefore also be a logical choice for establishing agreement between laboratories for reference intervals in healthy adults.

Acromegaly↗
PubMed1989

Amelioration of postmenopausal primary hyperparathyroidism during adjuvant tamoxifen for breast cancer.

The effects of adjuvant treatment with tamoxifen on bone metabolism in a postmenopausal woman with primary hyperparathyroidism is presented. A 69-year-old woman with increased serum ionized calcium, parathyroid hormone, and 1,25-(OH)2 vitamin D levels and a normal bone scan received tamoxifen 10 mg three times daily for 1 year. During treatment bone turnover decreased whereas parathyroid hormone increased further. After cessation of treatment the calcium metabolic variables returned to pretreatment levels. The antiestrogen tamoxifen seems to behave as an estrogen on bone metabolism in primary hyperparathyroidism.

Aged↗
PubMed1989

Ultrasound-guided chemical parathyroidectomy in patients with primary hyperparathyroidism: a prospective study.

Twenty of 31 consecutive ultrasound examined patients with primary hyperparathyroidism were selected for treatment with ultrasound-guided percutaneous injection of ethanol (96%) into biopsy-verified solitary parathyroid tumours following a strict protocol with regard to dose, number of treatments and a minimum of 6 months follow-up. Of 18 patients completing the above protocol, a biochemical improvement was observed in 12, of whom eight became normocalcaemic during the follow-up period of 6 months after the last treatment. An obvious clinical improvement was seen in eight of the patients. In four patients, a unilateral vocal cord paralysis was observed, but was permanent in only one patient. Progressive fibrosis of the parathyroid tumours following injections impeded the intraglandular dissemination of ethanol. Another problem noted was the inability of ultrasound to detect multiglandular involvement. We find ultrasound-guided chemical parathyroidectomy an attractive alternative to surgery in patients who are not well suited for surgical intervention. However, the technique has not been fully developed, and in the present study, possible improvements are indicated.

Adult↗
PubMed1988

Secondary hyperparathyroidism of morbid obesity regresses during weight reduction.

In order to test the relation between obesity and the secondary hyperparathyroidism found in markedly overweight subjects, 24 morbidly obese patients were studied before and after a weight loss of 35.9 kg obtained by a nutritionally adequate, intermittent very-low-calorie diet. Overweight was reduced from 98 +/- 34% to 44 +/- 19%. Serum total calcium did not change, but serum ionized calcium (Ca2+) increased from 1.22 +/- 0.04 mmol/L to 1.25 +/- 0.04 mmol/L (P less than .001). A corresponding fall was observed in serum parathyroid hormone (s-PTH), which decreased from 47.2 +/- 21.7 pmol/L to 35.2 +/- 19.4 pmol/L (P = .01). The change of s-PTH was positively associated with the reduction of body weight (r = .50, P less than .05) and with the reduction of overweight (r = .55, P less than .01). Regarding calcium binding substances, serum albumin remained low. The initially lowered serum phosphate and bicarbonate both rose (P less than .001). Plasma lactate and plasma free fatty acids (FFAs) decreased (P less than .001). The study supports our hypothesis that the change profile of calcium complexing anions in obesity interferes with the tubular reabsorption of calcium, which in turn lowers serum Ca2+, thus promoting hyperparathyroidism. Along with weight loss, concentrations of calcium complexing anions returns towards normal values and the secondary hyperparathyroidism regresses.

Adult↗
PubMed1988

GFR-corrected 24-hour whole body retention of diphosphonate: an improved index of bone metabolism.

The 24-hour whole body retention of diphosphonate (WBR) depends on bone uptake and renal clearance of diphosphonate. To evaluate the influence of glomerular filtration we measured WBR, creatinine clearance (CrCl) and s-alkaline phosphatase (s-AP) in 91 normals and 79 patients with different calcium metabolic disorders. As presumed, a negative correlation between CrCl and WBR exists (r = -0.67, p less than 0.001). By defining CrCl = 100 ml/min as standard, we have introduced a new mathematical model which allows recalculation of the measured WBR to WBR at CrCl = 100 ml/min (WBR100): WBR100 = [(1-WBR) x 100/WBR x CrCl +1]-1 Whole body retention at a clearance of 100 ml/min is demonstrated to be independent of CrCl (r = 0.14, NS). Using this approach we estimate that deviations of CrCl below 70 ml/min and above 150 ml/min lead to more than 25% increase/decrease in WBR. Using s-alkaline phosphatase as a standard, it is shown that WBR overestimates bone formation when CrCl is low. This new model permits the interpretation of WBR measurements in terms of bone turnover in patients with low glomerular filtration rates.

Adult↗
PubMed1988

Simplified protocol for biochemical evaluation of recurrent renal calcium stone disease.

Groups comprising 42 recurrent and 38 single calcium stone formers, and 48 controls underwent a standardized study protocol. During 12 h of fasting along with a standardized water load urine was collected for the last 4 h. One blood sample was drawn midway during urine collection. As compared with controls recurrent stone formers demonstrated significantly raised values of plasma ionized calcium, 1,25-dihydroxyvitamin D [1,25-(OH)2D], urinary ionized calcium, urinary pH, and standardized excretion rate of calcium [ECa(U)]. The tubular reabsorption of sodium and chloride, the maximal tubular reabsorption of phosphate, nephrogenous cyclic AMP (NcAMP), glomerular filtration rate (GFR) and plasma albumin were all significantly depressed. Data from the single stone former group were intermediate between controls and recurrent stone formers. For the pathogenesis of recurrent calcium stone formation these data suggest a general, though variably expressed, defect in the proximal tubular reabsorption of calcium, phosphate, bicarbonate, sodium and chloride leading to hypersecretion of 1,25-(OH)2D, hyperabsorption of calcium from the gut and a modest increase in plasma ionized calcium. Computer analysis of data do not support the concept that stone patients can be classified as either intestinal hyperabsorbers or renal losers. A stepwise discriminant analysis selected plasma albumin, urinary pH, ECa(U), plasma phosphate, GFR and NcAMP as the most important variables contributing to the difference between controls and recurrent stone formers. By this procedure we obtain a sensitivity of 93% and a specificity of 96% respecting proper classification of the recurrent stone former. The analysis may therefore be of value predicting the risk of recurrent stone formation in the single stone former.

Adolescent↗
PubMed1988

Non-invasive evaluation of bone formation: measurements of serum alkaline phosphatase, whole body retention of diphosphonate and serum osteocalcin in metabolic bone disorders and thyroid disease.

Three noninvasive indices of bone formation, serum alkaline phosphatase (s-AP), 24-h whole body retention of diphosphonate (WBR), and serum osteocalcin (s-OC), the two lastnamed clearance-corrected, were compared in 121 patients with various bone disorders and in 50 patients with thyroid disease. In conditions with qualitatively normal matrix formation and mineralization, i.e. thyrotoxicosis, primary hyperparathyroidism, myxoedema and osteoporosis, the three indices deviated from average normal by about the same extent: 134%/128%/200%, 120%/113%/133%, 105%/100%/79% and 89%/86%/69%, respectively. A disproportionately marked deviation of s-AP was observed in states of abnormal matrix formation or mineralization, i.e. osteomalacia and Paget's disease: 430%/145%/282% and 348%/145%/202%, respectively. Furthermore, the formation indices correlate differently with s-calcium in hyper- and hypocalcaemic conditions. In primary hyperparathyroidism the respective r-values were 0.32/0.62/0.68, while an inverse pattern was observed in osteomalacia: -0.60/-0.51/-0.47. As very little is known about the secretion of AP and OC and their role in bone formation and mineralization, the cause(s) for the observed differences remain(s) uncertain.

Adult↗
PubMed1986

Increased parathyroid hormone as a consequence of changed complex binding of plasma calcium in morbid obesity.

To evaluate whether changed plasma calcium binding might lead to a secondary increase of parathyroid hormone in morbid obesity, fasting measurements of serum ionized, ultrafiltrable and total calcium, calcium binding substances, and parathyroid hormone were undertaken in age- and sex-matched groups of obese (n = 44) and normal weight subjects (n = 52). The 24-hour urinary calcium excretion and clearance of creatine were also measured. Calcium binding to proteins was changed. Serum total proteins and protein-bound calcium did not differ, but serum albumin was decreased in obesity. Consequently, obese subjects did not reveal the normal dependency of protein-bound calcium upon albumin. Calcium binding to other substances was also changed. Serum phosphate and bicarbonate were decreased, while the concentrations of citrate, lactate, acetoacetate, 3-hydroxybutyrate, free fatty acids, and urate were all increased, leaving the total concentration of plasma complex-bound calcium unchanged. Nevertheless, these reciprocal changes increase the concentrations of less readily reabsorbable anions in the renal ultrafiltrate. The changed pattern of calcium binding in serum of the obese subjects may serve to explain our findings of increased urinary calcium excretion, lowering of serum ionized calcium and increased parathyroid hormone levels, changes being significantly correlated with degree of overweight.

Adult↗
PubMed1986

Seasonal variations in indices of bone formation precede appropriate bone mineral changes in normal men.

In 10 normal males aged 23-50 years measurements of serum alkaline phosphatase (s-AP) and the 24-h whole body retention of 99mTc-diphosphonate (WBR), as indices of bone formation, and the fasting urinary hydroxyproline:creatinine ratio (OHPr:Cr), as an index of bone resorption, were performed monthly from January 1983 to May 1984. Bone mineral content of the distal forearm (BMC) was measured in the middle of each quarter. From January to May BMC exhibited a reproducible, significant average increase of 2.5%, returning to baseline level between May and August. During the first quarter of both 1983 and 1984 a significant increase in s-AP and WBR was seen. Subsequently, during the second quarter of 1983, these variables fell below the mean of the year. Confirming their interrelationship, the deviations of s-AP and WBR were positively correlated throughout the study period (r = 0.51, P less than 0.05). Since the urinary OHPr:Cr ratio remained constant, the reported seasonal changes in bone mass of normal, adult males appear to result from primary changes in bone formation.

Adult↗