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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of primary hyperparathyroidism and coincidental Cushing's syndrome of hypothalamic-hypophyseal origin is reported. The hyperparathyroidism was based on an adenoma of the parathyroid glands and produced a severe hypercalcaemia (4.5 mmol/l) and calcinosis of kidneys and lungs. The Cushing's syndrome was caused by a hyperplasiogenic ACTH cell-adenoma of the pituitary which had induced a regulative hyperplasia of the ACTH-dependent zones of the adrenal cortex. The ultrastructure of the zona fasciculata and reticularis showed a conspicuous activation of the steroid hormone-producing organelles. The two endocrine diseases added together in skeleton, heart, duodenum, and pancreas. As a sign of hyperparathyroidism the osteoclastic absorption of the bone was strongly increased, whereas the bone formation was reduced due to the hypercortisolism. The pancreas showed a severe acute recurrence of chronic pancreatitis which was induced by a parathyrotoxic crisis. This was the immediate cause of death.
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PMID:[Simultaneous occurrence of primary hyperparathyroidism and pituitary Cushing's syndrome (author's transl)]. 19 Dec 34

The diangosis, clinical manifestations and management of 11 children with nephrocalcinosis encountered in a 20-year period are presented. Renal tubular acidosis, primary hyperoxaluria, primary hyperparathyroidism, exogenous hyperadrenocorticism and idiopathic hypercalcemia of infancy were the principal causes of nephrocalcinosis in this series. In the presence of normal or near-normal renal function, a 55 per cent or better cure rate can be expected. Children with significantly diminished renal function have a poor prognosis and should be considered for renal transplantation.
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PMID:Nephrocalcinosis in infancy and childhood. 109 88

Alkaline phosphatase, osteocalcin and hydroxyproline levels were evaluated in patients with the following conditions: primary hyperparathyroidism, renal dialysis, hyperthyroidism, Cushing's syndrome, long term corticosteroid therapy, Paget's disease, osteoblastic metastases, osteolytic or mixed metastases, and nutritional osteomalacia. In all cases the levels of the three substances were increased, with the following exceptions: a) in endogenous or exogenous hypercortisolism states osteocalcin level was reduced and those of alkaline phosphatase and hydroxyproline were unchanged; and b) in blastic or lytic metastases osteocalcin level was unchanged. In general, alkaline phosphatase and hydroxyproline levels had a higher sensitivity than those of osteocalcin in structural bone disease (Paget's disease, blastic or lytic metastases), whereas the converse was true for endocrine bone disease (the remaining conditions except osteomalacia, which is mixed, both structural and endocrine; in this syndrome, the three substances showed the same sensitivity.
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PMID:[Different behavior of bone turnover markers in endocrine (extrinsic) and structural (intrinsic) osteopathies]. 234 91

The aim of the present study was to determine the diurnal secretion of melatonin, cortisol, prolactin, and calcitonin during chronic parathyroid hormone-dependent hypercalcemia. Eight women, aged 40-76 years, with primary hyperparathyroidism (PHPT) were studied before and after surgical removal of a parathyroid adenoma. The hormone concentrations in blood were determined at 08, 12, 16, 22, 02, 04, and 06 h. Concomitantly, the excretion of melatonin and cortisol in urine between 07-19 h and 19-07 h, and the clearance of calcium and creatinine were measured. Nyctohemeral serum prolactin and calcitonin were unaffected by moderate parathyroid hormone-dependent hypercalcemia. In contrast, serum cortisol and melatonin were significantly higher during active disease than after surgical cure. Mean 24-h variation of serum cortisol was 349 +/- 34 nmol/liter vs. 223 +/- 17 nmol/liter and mean serum melatonin was 0.13 +/- 0.04 nmol/liter vs. 0.06 +/- 0.02 nmol/liter. Endogenous creatinine clearance was similar before and after surgery, while the clearance of melatonin and cortisol significantly increased after surgery, indicating an increased tubular reabsorption of both hormones during active disease. Fasting morning glucose concentrations were also significantly decreased after successful surgery, 6.1 +/- 0.6 vs. 5.2 +/- 0.5 mmol/liter. It is suggested that the relative hypercortisolism may be the cause of the glucose intolerance in primary hyperparathyroidism. Three to 4 months after surgical cure the serum melatonin levels were significantly lower than those seen in age-matched controls, indicating a melatonin insufficiency in patients successfully treated for PHPT. The meaning of this finding is not yet understood but might be of importance in the development of primary hyperparathyroidism.
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PMID:Melatonin, cortisol, prolactin, and calcitonin secretion in primary hyperparathyroidism before and after surgery. 362 59

In 100 patients with various types of endocrine dysfunction, we measured bone mineral density (BMD) at the midradius (greater than 95% cortical bone) and distal radius (75% cortical and 25% trabecular bone) by single photon absorptiometry and at the lumbar spine (greater than 66% trabecular bone) using the new technique of dual photon absorptiometry. BMD in each endocrine disorder deviated in at least one site from the sex-specific age regression of 187 normal subjects. For patients with primary hyperparathyroidism, hypercortisolism, and hyperthyroidism this deviation was negative (suggesting bone loss), whereas for patients with secondary hyperparathyroidism due to chronic renal failure, acromegaly, and postsurgical hypoparathyroidism it was positive (suggesting bone gain). When all six states of endocrine dysfunction were compared concomitantly by multivariate analysis of variance, the profile of the changes in BMD differed significantly (P less than 0.001), indicating a nonuniform response of bone to the various hormonal alterations. When values for BMD at each of the three scanning sites were compared the midradius and distal radius did not differ significantly; either of the radius measurements, however, differed significantly (P less than 0.001) from the lumbar spine. Thus, the BMD of the axial skeleton cannot be reliably predicted from measurements made in the appendicular skeleton. We conclude that the effects of endocrine dysfunction on bone density are complex and are both disease and site specific.
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PMID:Differential effects of endocrine dysfunction on the axial and the appendicular skeleton. 708 76

Bone is a living tissue; throughout life, new bone formation coexists with bone resorption. Although a large number of hormones and cytokines modulate osteoblast and osteoclast function, osteoporosis results from any disorder in which bone formation becomes uncoupled from bone resorption. Many disorders are associated with the uncoupling of bone formation and resorption. The most common is loss of gonadal steroid action on bone, as occurs in menopause or in male and female hypogonadism not associated with menopause. Other relatively common causes include primary hyperparathyroidism and endogenous or exogenous hypercortisolism and thyrotoxicosis. A large number of other, less frequent disorders also cause osteoporosis. Treatment of osteoporosis consists first of removing the cause if possible, for example, abolishing hypercortisolism, thyrotoxicosis, or hyperparathyroidism. In menopausal women or hypogonadal men or women, replacement of estrogens or androgens represents effective therapy. Estrogens and androgens given to hypogonadal subjects strikingly reduce bone resorption. For patients with established osteoporosis who either cannot take gonadal steroids or who are not hypogonadal, calcitonin decreases bone resorption and may stabilize bone mass. Estrogen replacement and calcitonin are approved by the Food and Drug Administration for treatment of osteoporosis. Experimental therapies presently include 1,25-dihydroxyvitamin D (calcitriol), bisphosphonates in intermittent treatment regimes, and fluoride in lower dosages than were used in previous studies. The use of fluoride is controversial, and to some extent it has fallen into disrepute. Effective use of any treatment is predicated on understanding the pathophysiology in any particular disease setting.
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PMID:Osteoporosis: pathophysiology, prevention, diagnosis, and treatment. 822 93

Uroliths composed predominantly of calcium phosphates have been infrequently identified in dogs. Factors incriminated in the etiopathogenesis of calcium phosphate urolithiasis include an alkaline urine pH, hypercalciuria, decreased urine concentrations of crystallization inhibitors, and increased urine concentrations of crystallization promoters. Disorders associated with calcium phosphate urolith formation in dogs include primary hyperparathyroidism, hyperadrenocorticism, and idiopathic hypercalciuria. Medical therapy of patients with recurring calcium phosphate uroliths should be directed at removing or minimizing factors contributing to urine supersaturation with calcium phosphate.
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PMID:Canine calcium phosphate uroliths. Etiopathogenesis, diagnosis, and management. 1002 56

The frequency of hypercalciuria is increasing in western countries with an incidence of nephrolithiasis which can reach 13%. Hypercalciuria appears as an alteration of the calcium transport system (kidney, bowel, bone) which is regulated by calcitriol and parathormone. The aim of this review was to screen etiologies of hypercalciuria taking into account recent genetic advances (calcium epithelial channel and calcium sensing receptor). Hypercalciuria may be favored by nutritional causes (diet rich in calcium, sodium, carbohydrates, proteins, poor in phosphates and potassium). It may also be related to an increase in calcium absorption (vitamin D excess, primary hyperparathyroidism, sarcoidosis, lymphoma, estrogens, and certain genetic causes), an increase in osteoresorption (bone metastasis, myeloma, Paget, hyperthyroidism, immobilization, hypercortisolism and corticosteroid therapy), or a decrease of kidney tubular resorption (diuretics, Cacci and Ricci, acromegally, Bartter, familial dominant hypocalcemia, Fanconi, Dent, familial hypomagnesemia-hypercalciuria syndrome, type 1 distal tubular acidosis, pseudohypoaldosteronism, diabetes). If no cause is identified, persistence of hypercalciuria after instituting a correct diet is defined as idiopathic hypercalciuria. Treatment of the cause is essential in secondary hypercalciuria, in addition to diet (low sodium intake, normocalcic diet, hydration), associated with thiazide diuretics and biphosphonates if necessary.
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PMID:[Hypercalciuria]. 1635 16

Changes in sensitivity to insulin occur in the course of a number of endocrine disorders. Most of the hormones through their antagonistic action to insulin lead to increased hepatic glucose output and its decreased utilisation in peripheral tissues. Carbohydrate disorders observed in endocrine diseases result from the phenomenon of insulin resistance, and in some cases also a reduction in insulin secretion is present. Abnormalities of glucose metabolism are observed in acromegaly, but also in growth hormone deficiency, hypercortisolism in the course of Cushing's syndrome, hyper- or hypothyroidism, primary hyperparathyroidism, aldosteronism, pheochromocytoma, congenital hypertrophy of the adrenal glands, polycystic ovaries syndrome, hypogonadism, or other hormonally active neuroendocrine tumours. They are of a secondary nature in relation to impaired hormonal balance. Hyperglycaemia is therefore often reversible, and the most effective method of treatment of impaired insulin sensitivity is successful therapy of specific endocrinopathies. Insulin sensitisers, also with a good effect, are used. Most experiences to date can be attributed to metformin therapy. Attempts have been made at treatment with other agents that are also effective in reducing insulin resistance as incretins or glitazones. In the presented paper, the authors reviewed endocrine diseases in which there is a clinically significant change in insulin sensitivity. Moreover, methods of therapy of concomitant disturbed glucose metabolism were presented.
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PMID:Insulin resistance in endocrine disorders - treatment options. 2866 Sep 91

An underlying disease affecting bone health is present in up to 40% and 60% of osteoporotic post-menopausal women and men respectively. Among the disorders leading to a secondary form of osteoporosis, the endocrine diseases are highly represented. A frequent finding in patients affected with an endocrine-related forms of bone disease is that the skeletal fragility is partially independent of the bone density, since the fracture risk in these patients is related more to a reduction of bone quality than to a decrease of bone mass. As a consequence, bone mineral density evaluation by dual-X-ray Absorptiometry may be inadequate for establishing the risk of fracture in the setting of the endocrine-related forms of osteoporosis. In the recent years several attempts to non-invasively estimating bone quality have been done. Nowadys, some new tools are available in the clinical practice for optimizing the fracture risk estimation in patients with endocrine disorders. The aim of this review is to summarise the evidences regarding the role of the different imaging tools for evaluating bone density and bone quality in the most frequent forms of endocrine-related osteoporosis, such as obesity, diabetes, acromegaly, thyrotoxicosis, primary hyperparathyroidism, hypercortisolism and hypogonadism. For each of these disorders, data regarding both the current available tools and the future possible new techniques for assessing bone fragility in patients with endocrine diseases are reported.
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PMID:DIAGNOSIS OF ENDOCRINE DISEASE: Evaluation of bone fragility in endocrine disorders. 3104 75


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