Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Monozygotic male twins with DiGeorge's syndrome had facial dysmorphism, cardiovascular abnormalities, hypocalcemia, and immunodeficiency; however, they showed differences in several aspects of this developmental complex. An early gestational insult, rather than a mutation, may be one cause of this heterogenous disorder. One twin had clinically appreciable hypoparathyroidism and had received calcitriol since early infancy. Despite close monitoring of therapy, he experienced two episodes of unexpected and prolonged hypercalcemia. Following the first episode, he was eucalcemic for nine weeks without therapy, attesting to the prolonged biological effects of calcitriol when used in the treatment of hypoparathyroidism.
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PMID:DiGeorge's syndrome in monozygotic twins. Treatment with calcitriol. 668 80

A 22-year-old woman developed hypoparathyroidism in 1970, 10 months after treatment of hyperthyroidism with I-131. The hypocalcemia was corrected with Vitamin D2 and oral calcium and she remained normocalcemic for 8 yr. In 1979 hypercalcemia was found and Vitamin D2/calcium was discontinued. Because she remained normocalcemic without therapy for 3 yr, we measured the levels of immunoreactive and bioactive PTH in plasma stored since 1970 and in plasma obtained in 1982 to determine whether there had been restoration of parathyroid function. Indeed, PTH levels in 1970 while the patient was hypocalcemic were low. The bioactive PTH was 0.26 pg/ml (normal 1.5-30), whereas--COOH terminal immunoreactive PTH was 620 pg/ml (normal 600-1500) and midmolecule immunoreactive PTH was 433 pg/ml (normal 300-900). In 1982 while normocalcemic the bioactive PTH and immunoreactive PTH were normal (5.18 pg/ml;--COOH, 970 pg/ml; midmolecule, 789 pg/ml, respectively). Thus, an unusual case of hypoparathyroidism after I-131 therapy with return of parathyroid function is documented by measurements of both immunoreactive and bioactive PTH.
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PMID:Hypoparathyroidism after I-131 therapy with subsequent return of parathyroid function. 686 81

Familial hypocalciuric hypercalcemia (FHH) is an autosomal dominant trait comprising hypercalcemia, hypophosphatemia, parathyroid hyperplasia, and unusually low renal clearance of calcium. We evaluated the role of parathyroid hormone in the relative hypocalciuria of FHH and characterized the renal transport of calcium in this disorder using three previously hypercalcemic FHH patients with surgical hypoparathyroidism and three controls with surgical hypoparathyroidism. Intravenous infusion of calcium chloride in two patients with FHH and in three controls increased serum calcium from a mean basal of 5.0 to a mean peak of 6.8 meq/liter in two FHH patients and from 4.2 to 5.7 in three control subjects. Urinary calcium in a third FHH patient was studied without calcium infusion during recovery from hypercalcemia of vitamin D intoxication. At all serum concentrations of calcium, calcium clearance was lower in FHH than in controls; at base-line serum calcium, the ratio of calcium clearance to inulin clearance (C(Ca)/C(IN)) in FHH subjects was 32% of that in controls and decreased to 19% during hypercalcemia. Calcium infusion increased the ratio of sodium clearance to inulin clearance in controls from a base line of 0.020 to 0.053 at peak concentrations of calcium in serum, but did not affect this parameter in FHH (0.017 at base-line serum calcium vs. 0.019 at peak). When calcium infusion studies were performed (in two patients with FHH and one control) during administration of acetazolamide, a drug whose principal renal action causes inhibition of proximal transport of solute, C(Ca)/C(IN) in the patients with FHH was 29 and 7% of that of the control at base-line and peak serum calcium, respectively. In contrast, ethacrynic acid, a diuretic that acts in the ascending limb of the loop of Henle, increased C(Ca)/C(IN) more in the FHH patients than in the control subject; C(Ca)/C(IN) was 65% at base-line and 47% at peak serum calcium, compared with that of the control subject. The greater calciuric response to ethacrynic acid than to acetazolamide or calcium infusion alone in FHH indicates that a major renal locus of abnormal calcium transport in this disorder may be the ascending limb of the loop of Henle.Decreased clearance of calcium in patients with FHH and hypoparathyroidism when compared with hypoparathyroid controls indicates that relative hypocalciuria in FHH is not dependent on hyperparathyroidism. Since the parathyroid glands in FHH are not appropriately suppressed by calcium, this implies that FHH represents a disorder of abnormal transport of, and/or response to, extracellular calcium in at least two organs, parathyroid gland and kidney.
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PMID:Urinary calcium excretion in familial hypocalciuric hypercalcemia. Persistence of relative hypocalciuria after induction of hypoparathyroidism. 687 59

Although hypercalcemia is a well-known complication of malignant diseases, hypocalcemia seems to be a rather rare one. A 34-yr-old woman with advanced breast cancer who presented hypocalcemia is described. She had generalized multiple osteolytic bone metastases which were progressive in spite of chemo-endocrine and radiation therapy. She was admitted because of severe bone pain and dyspnea caused by bilateral pleural effusion. Laboratory examination on admission showed that the serum calcium was 9.6 mg/dl, serum total protein 5.9 g/dl, serum inorganic phosphorus 4.6 mg/dl, and serum alkaline phosphatase 29.6 King-Armstrong units. The serum calcium gradually fell to 7.0 mg/dl on the 45th hospital day when the serum total protein was 6.8 g/dl and she complained of paresthesia in the extremities. On the 58th day, severe tachycardia and hypotension developed and she died of congestive heart failure on the 67th hospital day. At that time the serum calcium was 5.4 mg/dl. During her hospital course, the plasma parathyroid hormone levels were examined repeatedly and were 0.4, 0.6, 0.6 and 0.7 ng/ml (normal; less than 0.5 ng/ml). Autopsy revealed that cancer invaded the space between the thyroid and the trachea and no parathyroid glands could be found even in the mediastinum. Microscopically the parathyroid glands were replaced completely by the cancer cells. These observations indicate that metastasis of breast cancer to the parathyroid glands caused relative hypoparathyroidism, resulting in hypocalcemia. In addition, congestive heart failure which was refractory to digitalis and diuretics might have been caused by impaired contractility of the myocardium associated with hypocalcemia.
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PMID:A case of advanced breast cancer associated with hypocalcemia. 688 61

Mineral retention was measured during 39 metabolic balance studies in 34 patients with nutritional osteomalacia or late rickets; they were divided into 5 treatment groups consisting of oral vitamin D, artificial ultra-violet irradiation, 25-hydroxycholecalciferol (calcifediol), 1 alpha-hydroxycholecalciferol (alfacalcidol) and 1 alpha, 25-hydroxycholecalciferol (calcitriol). With the 1 alpha-hydroxylated derivatives, initial dosage of 2 to 6 micrograms daily was required to achieve optimal healing rates by comparison with other responses. Mineral retention was markedly enhanced by supplementation with microcrystalline hydroxyapatite compound (MCHC); untreated X-linked hypophosphataemic rickets healed in 7 weeks on 10 micrograms alfacalcidol daily and 6 grams MCHC daily without developing hypercalcaemia. By contrast, adult-presenting hypophosphataemic osteomalacia developed early hypercalcaemia on the same treatment; additional phosphate supplementation, without changing other treatment, abolished hypercalcaemia and improved calcium retention. A long-term crossover trial of the vitamins D in 6 patients with hypoparathyroidism suggested that relative potencies were as follows (assigning to vitamin D an arbitrary potency of l): vitamin D2 (or D3) l: dihydrotachysterol (DHT) 3: calcifediol 10: alfacalcidol 750: calcitriol 1500. The two-fold superiority of calcitriol over alfacalcidol was evident. Calcifediol and vitamin D controlled plasma calcium at comparable levels of circulating 25-hydroxyvitamin D (25-OH-D), elevated 25-OH-D persisting at least 1 to 2 years after discontinuing long-term (greater than 4 years) vitamin D. In 2 patients with myositis ossificans progressiva treated with 10 to 20 micrograms calcitriol daily, hypercalcaemia was minimized by a low-calcium diet supplemented with cellulose phosphate, suggesting that bone resorption did not play a major role in vitamin D intoxication. Net mineral loss was documented in a young male patient but not in a menopausal female, suggesting that calcitriol treatment was not likely to produce post-menopausal osteoporosis.
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PMID:Calcitriol dosage in osteomalacia, hypoparathyroidism and attempted treatment of myositis ossificans progressiva. 689 16

Eleven subjects aged four to 76 years with primary hypoparathyroidism have been treated with 1,25-dihydroxycholecalciferol (1,25-D3). Five subjects were not on vitamin D analogues before starting this drug. 1,25-D3 was found to be an effective treatment and a rapid biochemical response to dose adjustments was observed. In two subjects hypercalcaemia and reversible renal failure occurred. Thiazide-type diuretics necessitated dose reductions in a further two subjects. A scheme for starting hypoparathyroid subjects on this treatment is suggested. The need for regular biochemical assessment and awareness of possible drug interactions is emphasised. It is felt that 1,25-vitamin D3 has practical advantages over traditional forms of vitamin D in the treatment of hypoparathyroidism.
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PMID:1,25-dihydroxy-vitamin D3: a new treatment for hypoparathyroidism. 693 21

Clinical aspects of two patients with hypoparathyroidism are presented. In a post-surgical case the diagnosis was delayed for 46 years yet few of the recognised complications of hypoparathyroidism occurred. A patient with primary hypoparathyroidism received toxic doses of vitamin D3 and developed paroxysmal atrial tachycardia. Later, when the serum calcium fell, he had an epileptic fit. Alternative forms of therapy of hypoparathyroidism and hypercalcaemia are discussed.
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PMID:Aspects of hypoparathyroidism: late diagnosis and toxic effects of therapy. 693 64

The physiological mechanisms involved in the alterations in calcium homeostasis during pregnancy are complex. The fetal acquisition of calcium, for skeletal growth, is obtained by an increase in intestinal calcium absorption in the mother with transplacental calcium transfer to the fetus. The regulation of calcium homeostasis during the transition from the intrauterine to the extrauterine environment is complex and poorly understood. Within the first few hours of life the serum calcium concentrations begins to fall progressively reaching a "trough" value by the second or third day of life and then increases to normal values by the tenth day of life. In some neonates the fall in calcium concentration is sufficient to be associated with either tetany or convulsions. Hypocalcemia is probably the commonest disturbance of calcium homeostasis that occurs in the neonate and can be subdivided into three main groups on the basis of the etiological mechanism involved. Other disorders of calcium homeostasis that may affect the neonate include hypoparathyroidism, either congenital or acquired, pseudohypoparathyroidism, and vitamin D deficiency. Hypercalcemia may occur, but is a relatively rare occurrence in the neonate.
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PMID:Disorders of calcium homeostasis in the fetus and neonate. 704 84

In view of our last 100 patients operated on for hyperparathyroidism we found the following: 1. The operation is safe, with no mortality and a 2 per cent morbidity from transient hypoparathyroidism. 2. The operation is effective (99 per cent in our series) with removal of only clinically enlarged glands. 3. Most patients have symptomatic hypercalcemia (73 per cent in our series) and are improved with parathyroidectomy.
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PMID:Symptomatic hyperparathyroidism. 707 90

Thirty-five patients with primary or radiation-induced hyperparathyroidism underwent autotransplantation with fresh diseased parathyroid tissue. Due to previous neck surgery (34 percent), concomitant thyroid surgery (66 percent), and a high proportion of multiglandular parathyroid disease (43 percent), all patients ran a high risk of becoming hypoparathyroid, At follow-up , a mean of 28 months after operation, 32 patients had normal parathyroid function, 2 had hyper- and 1 had hypoparathyroid function. The amount of tissue used for transplantation was individually chosen by relating the serum calcium level to the total parathyroid mass. In patients with water-clear cell hyperplasia and thus low endocrine activity on a weight basis, large grafts were needed, whereas less than 120 mg was used in most other cases. In two of our three failures we did not follow these tactics. Our results show that autografting fresh diseased parathyroid tissue can minimize the occurrence of postoperative hypoparathyroidism in patients at high risk of this complication. In no case has recurrent or progressive hypercalcemia developed.
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PMID:Autotransplantation of fresh diseased parathyroid tissue in primary and radiation-induced hyperparathyroidism. 708 72


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