25-hydroxyvitamin-d-2 and Hyperparathyroidism

Topics: 25-Hydroxyvitamin D 2; Animals; Calcifediol; Calcitriol; Calcium; Cyclic AMP; Ergocalciferols; Glomerular Filtration Rate; Humans; Hyperparathyroidism; Hyperparathyroidism, Secondary; Hypoparathyroidism; Mathematics; Methods; Parathyroid Diseases; Parathyroid Hormone

The relationship between 25 hydroxyvitamin D (25(OH)D), parathyroid hormone (PTH) and metabolic traits appear to differ among ethnicities and may be influenced by obesity. The aim of the study was to examine the association of serum 25(OH)D or PTH with metabolic syndrome (MetS) while controlling for adiposity in black women. Using a cross-sectional study design, 209 urban black women aged ≥ 43 years from the North West Province, South Africa, were included. Multiple regression models were used to explore the relationship between 25(OH)D or PTH and body composition. To explore the association between 25(OH)D or PTH and MetS, a separate variable was created including at least 3 of the MetS criteria, but excluding elevated waist circumference as a diagnostic criterion in a logistic regression model. The majority of the women (69.9%) were overweight or obese and 65.5% of the women had excessive adiposity using the age-specific cut-off points for body fat percentage. All body composition variables were positively associated with PTH, whereas body mass index and waist circumference, but not body fat percentage, had negative associations with 25(OH)D also after adjusting for confounders. Before and after adjusting for age, body fat, habitual physical activity, tobacco use, season of data collection, and estimated glomerular filtration rate, neither 25(OH)D nor PTH showed significant associations with MetS. Although PTH was positively associated and 25(OH)D was negatively associated with adiposity in black women, there was no association between either 25(OH)D or PTH and MetS in this study population, nor did adiposity influence these relationships.

Topics: 25-Hydroxyvitamin D 2; Adiposity; Black People; Body Mass Index; Calcifediol; Confounding Factors, Epidemiologic; Cross-Sectional Studies; Female; Follow-Up Studies; Humans; Hyperparathyroidism; Insulin Resistance; Metabolic Syndrome; Middle Aged; Obesity; Overweight; Parathyroid Hormone; Prevalence; Prospective Studies; Risk; South America; Urban Health; Vitamin D Deficiency

Vitamin D deficiency was assessed previously on the basis of rickets and osteomalacia, which represent an extreme end of the spectrum. As a result of this, many clinically-asymptomatic patients go undetected. As vitamin D deficiency results in secondary hyperparathyroidism, we propose to use the normalisation of intact parathyroid hormone (iPTH) as a surrogate marker for assessing the adequacy of vitamin D nutrition.. A descriptive study was undertaken on 195 premenopausal Pakistani women. 25-hydroxy-cholecalciferol and iPTH levels were measured by standard laboratory techniques.. The minimum level of vitamin D required to keep iPTH below 53 pg/dL was found to be 16 ng/ml with a 95 percent confidence interval of 13.8 and 18.2. Existing normal range is 9-36 ng/ml.. Normalisation of iPTH if taken as a criterion for judging vitamin D deficiency can lead to detection of clinically asymptomatic patients. The simplicity, low cost of correction, and the potential beneficial skeletal and non-skeletal consequences of doing so makes it essential that this criterion be used to redefine the optimal vitamin D levels. This should be internationally standardised and made available to clinicians.

Topics: 25-Hydroxyvitamin D 2; Adolescent; Adult; Age Distribution; Female; Humans; Hyperparathyroidism; Middle Aged; Parathyroid Hormone; Seasons

Although abnormalities of calcium and vitamin D metabolism are recognized in children with nephrotic syndrome, longitudinal observations are not available in these patients during periods of relapse and remission. We report observations in 58 children (mean age 10.1 years) with nephrotic syndrome and normal glomerular filtration rate. Hypocalcemia, modest hyperparathyroidism, and strikingly low calcidiol levels were identified during episodes of relapse. Most alterations were transient, and normalized on remission. The plasma concentration of calcitriol, the most active metabolite of vitamin D, was found to be normal in both relapse and remission. In the presence of hypocalcemia and hyperparathyroidism, however, normal plasma calcitriol levels in relapse may be inappropriately low and reflect a state of relative deficiency. Concurrent glucocorticoid therapy did not modify the results. A corollary of our observations is that children with relapsing or protracted nephrotic syndrome are at risk of developing metabolic bone disease, even without impairment of glomerular filtration rate.

Topics: 25-Hydroxyvitamin D 2; Adolescent; Adult; Calcium; Child; Child, Preschool; Ergocalciferols; Glomerular Filtration Rate; Humans; Hyperparathyroidism; Hypocalcemia; Nephrotic Syndrome; Parathyroid Hormone; Recurrence; Vitamin D

Despite great interest in the elevated circulating levels of calcitriol (1,25-[OH]2D) associated with the clinical syndrome of human primary hyperparathyroidism, the relative potencies of known and potential stimuli/suppressors of long-term calcitriol levels have not been evaluated in either clinical or experimentally induced hyperparathyroid states. Based on reports that aparathyroid animals exhibit suppressed plasma calcitriol concentration and that acute administration of parathyroid hormone (PTH) to both humans and experimental animals or to renal slices in vitro results in increased plasma calcitriol concentration/production rate, it might be predicted that a chronic experimental model of either hypercalcemic primary hyperparathyroidism or hypocalcemic secondary hyperparathyroidism would show increased plasma calcitriol concentration. Chronic alterations in plasma calcium concentration have not been implicated as modulating calcitriol levels in any species. Accordingly, we investigated the long-term response of plasma calcitriol concentration in states of sustained experimental primary and secondary hyperparathyroidism. Intact dogs (group I) undergoing continuous intravenous PTH infusion for 12 d developed sustained hypercalcemia and hypophosphatemia, and plasma calcitriol concentration decreased from 23 +/- 3 to 14 +/- 3 pg/ml (P less than 0.01). Subsequent chelator (EGTA)-induced chronic normalization of hypercalcemia during ongoing PTH infusion resulted in a large and sustained increase in plasma calcitriol concentration to supernormal levels, reversible during subsequent cessation of chelator infusion. In additional intact dogs (group II), chronic chelator-induced hypocalcemic secondary hyperparathyroidism resulted in a sustained increase in plasma calcitriol concentration despite hyperphosphatemia. In normal human subjects undergoing a 12-13-d continuous intravenous PTH infusion to result in sustained moderate hypercalcemia (12.0 +/- 0.2 mg/100 ml) and hypophosphatemia, plasma calcitriol concentration decreased significantly (P less than 0.01) as in group I dogs and was followed by reversal to normal levels in a recovery period. The present results provide strong evidence in both humans and dogs that during experimentally induced chronic PTH excess, alterations in plasma calcium concentration dictate the directional response of circulating calcitriol concentrations. The long-term potency of plasma calcium concentration as a modulator of calcitri

Topics: 25-Hydroxyvitamin D 2; Animals; Calcitriol; Calcium; Cattle; Dogs; Egtazic Acid; Ergocalciferols; Humans; Hyperparathyroidism; Parathyroid Hormone; Phosphates; Sodium Chloride; Thyroidectomy; Vitamin D

Serum 25-hydroxyvitamin D and immunoreactive parathyroid hormone concentrations were measured in normal elderly subjects living at home and in sick elderly patients in hospital. Normal old people tended to have high 25-hydroxyvitamin D and low parathyroid hormone concentrations; in the sick elderly this pattern was reversed. The raised serum parathyroid hormone concentrations in the sick elderly were not due to poor renal function and may have been a response to vitamin D deficiency. A high serum parathyroid hormone concentration in an elderly patient must be interpreted in the light of the patient's general health and nutritional state. Caution is needed in diagnosing primary hyperparathyroidism in this age group.

Topics: 25-Hydroxyvitamin D 2; Aged; Alkaline Phosphatase; Ergocalciferols; Female; Humans; Hyperparathyroidism; Kidney Diseases; Male; Middle Aged; Parathyroid Hormone

Serum parathyroid hormone and 25 hydroxyvitamin D were measured in 124 normal subjects aged from 20 to 90 years. There was a significant progressive increase in serum parathyroid levels with age associated with a progressive decrease in total serum calcium. After the sixth decade there was a significant reduction of 25 hydroxyvitamin D serum levels. In each age group, there were no significant differences between men and women in all parameters measured. In normal elderly subjects there is an age-related decline of calcium absorption associated with reduced calcium intake and sun exposure leading to secondary hyperparathyroidism. These results emphasize the importance of calcium and vitamin D supplementation in elderly European population, not only in long-stay patients but in ambulatory normal people after 60 years.

Topics: 25-Hydroxyvitamin D 2; Adult; Aged; Aging; Calcium; Ergocalciferols; Female; Fractures, Bone; Humans; Hyperparathyroidism; Male; Middle Aged; Parathyroid Hormone

A 48-year-old woman underwent jejunoileal bypass surgery for obesity while hypercalcemic. Three years later, she developed symptomatic osteomalacia impairing her daily activities. Bone biopsy confirmed the clinical diagnosis of osteomalacia, and treatment with 8000 U daily of vitamin D and milk resulted in striking improvement of clinical symptoms and resolution of her osteomalacia both chemically and histologically. The patient, however, again became hypercalcemic and a parathyroid adenoma was subsequently removed with restoration of serum calcium values to normal. Neither the occurrence and successful treatment of gross symptomatic osteomalacia consequent to jejunoileal bypass surgery, nor the obscuration of primary hyperparathyroidism by osteomalacia has been hitherto well documented in the United States.

Topics: 25-Hydroxyvitamin D 2; Biopsy; Bone and Bones; Dihydroxycholecalciferols; Ergocalciferols; Female; Humans; Hyperparathyroidism; Ileum; Jejunum; Middle Aged; Obesity; Osteomalacia; Postoperative Complications; Vitamin D

Oral administration of prednisone (30 mg/day for 9 days) to six normal individuals induced a significant rise in the concentration of serum 1,25-dihydroxyvitamin D [1,25-(OH)2D] within 2 days. In four patients with primary hyperparathyroidism a larger increase of 1,25-(OH)-2D was observed within 3 days. In these patients the 1,25-(OH)-2D concentration remained elevated during the whole period of prednisone administration (10 days) whereas in the control group it had returned to basal levels or below after 9 days of prednisone administration. This response appeared dependent upon parathyroid hormone (PTH) as we found no change in the (basally low) 1,25-(OH)2D concentrations in five patients with hypoparathyroidism during 3-4 days of prednisone administration (30 mg/day). In these patients vitamin D medication had been interrupted 3-5 days before the administration of prednisone, whereafter serum calcium was kept between 2.10 and 2.30 mmol/1 by means of calcium infusion. The response of 1,25-(OH)2D to prednisone is best explained by a stimulatory action of glucocorticoids upon PTH secretion or by the induction of increased PTH sensitivity.

Topics: 24,25-Dihydroxyvitamin D 3; 25-Hydroxyvitamin D 2; Adult; Aged; Calcitriol; Dihydroxycholecalciferols; Ergocalciferols; Female; Humans; Hyperparathyroidism; Hypoparathyroidism; Male; Middle Aged; Prednisone

Vitamin D appears to influence parathyroid function indirectly through its effects on calcium metabolism rather than by a direct action of its metabolites on the parathyroid glands. In states of both secondary and primary hyperparathyroidism, the quantitative production of 1,25-(OH)2D may be determined by the prevailing concentration of serum 25-(OH)D but there appears to be some constraint that limits the formation of 1,25-0(OH)2D when the provision of its precursor exceeds the physiological. From the absence of this constraint in 'type 2 vitamin D dependency' it is inferred that it may operate through 'self-inhibition' of the renal production of 1,25-(OH)2D. It is shown that the level of serum 25-(OH)D may always exert some influence on the production of 1,25-(OH)2D and that this effect is facilitated by hyperparathyroidism. In developing vitamin D deficiency the reactive secondary hyperparathyroidism may thus function as an adaptive mechanism that sustains the level of serum 1,25-(OH)2D in the face of a diminishing serum 25-(OH)D. Failure of this adaptation and the development of a critical deficiency of 1,25-(OH)2D is regarded as the direct cause of defective mineralisation of bone. This concept would explain the absence of osteomalacia in some patients with very low levels of serum 25-(OH)D and the occurrence of defective osseous mineralisation in hypoparathyroidism.

Topics: 25-Hydroxyvitamin D 2; Calcitriol; Ergocalciferols; Humans; Hyperparathyroidism; Hyperparathyroidism, Secondary; Hypocalcemia; Osteomalacia; Parathyroid Hormone; Vitamin D; Vitamin D Deficiency