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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperparathyroidism is a disease characterized by hypercalcemia with hypophosphoremia resulting from increased secretion of parathyroid hormone (PTH). The disease may be divided into 3 forms: a) primary, b) secondary, c) tertiary (secondary refractory form). Primary hyperparathyroidism is rare in children; hyperplasia is more frequent during the early years of life (neonates and infants) and is difficult to distinguish from adenoma in children. The disease may be asymptomatic; elevated calcemia levels (>12 <13.5 mg/dl) are accompanied by anorexia, asthenia and persistent stipsis; severely elevated concentrations (>13.5 mg/dl) are accompanied by nausea, vomiting, polyuria due to osmosis, with dehydration and progressive onset of lethargy, stupor and coma. Osteopenia or osteitis fibrosa cystica may be present due to augmented bone resorption. Height and weight increases are altered due to anorexia and dehydration. Differential diagnosis includes iatrogenic causes of hypercalcemia (excessive vitamin D intake, prolonged immobilization, etc.) and idiopathic familial hypercalcemia. Emergency treatment is required in cases of extremely elevated hypercalcemia (Ca >13.5-14 mg/dl), due to risk of injury to the heart, the central nervous system, the gastrointestinal tract and the kidneys. The 4 cardinal points of treatment are: hydration, calciuresis, inhibition of bone calcium resorption, treatment of the cause underlying hyperparathyroidism. Secondary hyperparathyroidism is found in cases where chronic hypocalcemia is present, particularly in chronic renal failure, untreated deficiency rickets, chronic intestinal malabsorption, hepatobiliary disease, types I and II vitamin D-dependent rickets, tubular acidosis or Fanconi's syndrome. The tertiary form is distinguished by the autonomous nature of the parathyroid glands which have become hypertrophic/hyperplastic due to uncontrollable, chronic severe renal failure. It can also be of iatrogenic origin due to excessive intake of inorganic phosphates in familial hypophosphatemic rickets or chronic vitamin D deficiency.
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PMID:Hyperparathyroidism. 1524 24

Brown tumor is a rare clinical entity complicating hyperparathyroidism. It may occur in the head and neck, with the mandible being the most frequent site. Hyperparathyroidism is usually associated with hypercalcemia. We report a case of madibular Brown tumor secondary to primary hyperparathyroidism. In this case in spite of hyperparathyroidism and the bony lesion the serum calcium level was within normal range. The case managed by surgical excision of the mandibular tumor with an en-bloc hemithyroidectomy with inclusion of the diseased parathyroid gland. This case demonstrates that in osteolytic bony lesions a hyperparathyroid complication can be expected even with normal serum calcium level. The presence of normocalcemia in primary hyperparathyroidism should prompt the physician to look for vitamin D deficiency.
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PMID:Normocalcemic hyperparathyroidism presented with mandibular brown tumor: report of a case. 1536 68

Because the chronic renal failure state basically means the active vitamin D deficiency, the minimum physiological daily dose of active vitamin D should be supplemented in all of the patients. But few informations about the frequency of vitamin D supplementation or treatment are available in European countries and in the USA. Only the Japanese Society for Dialysis Therapy presented the frequency of it in 2002, which was about 40 % of the dialysis patients, unexpectedly as same as that in Shinraku-En Hospital in 1985. Hypercalcemia, uncontrollable hyperphosphatemia, low ALP, and low PTH might impair the vitamin D introduction.
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PMID:[The present state of vitamin D supplementation or treatment among chronic dialysis patients]. 1557 51

Hypercalcemia has been described in patients with a number of granulomatous diseases, including sarcoidosis and mycobacterial infection. Disordered vitamin D metabolism is the root cause for the elevated serum calcium levels. A similar mechanism of abnormal vitamin D metabolism explained the hypercalcemia occurring in patients with lymphoma. Crohn's disease is a granulomatous disorder that is more commonly associated with hypocalcemia caused by poor calcium intake and decreased intestinal calcium absorption related to vitamin D deficiency as a consequence of malabsorption. A man with Crohn's disease who presented with hypercalcemia and acute renal failure is described. Biochemical parameters showed an elevated 1,25-dihydroxyvitamin D level, with a low-normal 25-hydroxyvitamin D level and decreased parathyroid hormone level. Inflammatory bowel disease had been clinically active during the preceding 2 months. With resolution of gastrointestinal symptoms, serum calcium, vitamin D, and parathyroid hormone levels returned to normal. Serum creatinine levels decreased toward normal. Angiotensin-converting enzyme (ACE) levels have been reported to be elevated in patients with sarcoidosis, particularly in the setting of active disease with hypercalcemia. Controversy exists about ACE levels in the face of active Crohn's disease: 1 report noted elevated levels, whereas other publications reported depressed levels. Our patient had an elevated ACE level in the setting of active bowel disease and hypercalcemia, and ACE levels returned to normal with resolution of gastrointestinal symptoms.
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PMID:Hypercalcemia due to excess 1,25-dihydroxyvitamin D in Crohn's disease. 1569 36

Primary hyperparathyroidism (PHP) is associated with impaired GH secretion. Whether this effect is due to hypercalcemia or to increased serum PTH concentration is unclear. However, patients with familial hypocalciuric hypercalcemia (FHH), who have normal PTH and increased serum calcium concentrations, also have an impaired GH secretion, suggesting that calcium rather than PTH is responsable for this effect on GH secretion. To further investigate this issue, 10 consecutive patients with secondary hyperparathyroidism (SHP) due to vitamin D deficiency were evaluated by the GH response to GHRH+arginine (Arg) test. A group of 60 consecutive untreated PHP patients served as controls. Mean GH response to GHRH+Arg test was 15.8+/-14 microg/l and 37.5+/-16 microg/l (p<0.001) in PHP and in SHP patients, respectively. Forty-two out of 60 (70%) PHP patients had a suppressed or blunted GH response, whereas all SHP patients had normal GH response. The results of the present study confirm and extend our previous observations that PHP is associated with an impaired GH secretion in the majority of cases, and indicate that SHP patients have no abnormality of GH secretion. Thus, hypercalcemia rather than increased serum PTH is responsible for the abnormality of GH secretion.
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PMID:Growth hormone secretion in primary and secondary hyperparathyroidism. 1588 55

Rickets is seen in association with vitamin D deficiency and in several genetic disorders associated with abnormal mineral ion homeostasis. Studies in vitamin D receptor (VDR)-null mice have demonstrated that expansion of the late hypertrophic chondrocyte layer, characteristic of rickets, is secondary to impaired apoptosis of these cells. The observation that normalization of mineral ion homeostasis in the VDR-null mice prevents rachitic changes suggests that rickets is secondary to hypocalcemia, hypophosphatemia, or hyperparathyroidism, rather than impaired VDR action. To determine which of these abnormalities is responsible for impaired chondrocyte apoptosis and subsequent rachitic changes, two additional models were examined: diet-induced hypophosphatemia/hypercalcemia and hypophosphatemia secondary to mutations in the Phex gene. The former model is associated with suppressed parathyroid hormone levels as a consequence of hypercalcemia. The latter model demonstrates normal calcium and parathyroid hormone levels, but 1,25-dihydroxyvitamin D levels that are inappropriately low for the degree of hypophosphatemia. Our studies demonstrate that normal phosphorus levels are required for growth plate maturation and implicate a critical role for phosphate-regulated apoptosis of hypertrophic chondrocytes via activation of the caspase-9-mediated mitochondrial pathway.
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PMID:Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes. 1597 27

Hypocalcaemia not associated with hypoalbuminaemia or 25(OH)-Vitamin D deficiency is rare and should be referred to a specialist clinic. 25(OH)-Vitamin D deficiency can often be treated safely by GPs, unless it is associated with renal impairment and secondary hyperparathyroidism, in which case a nephrology referral is required. An endocrine referral is required if deficiency is associated with pregnancy, co-existent primary hyperparathyroidism or the patient is receiving warfarin. The key role of the GP in managing hypercalcaemia is to distinguish between malignant and parathyroid causes in order to make the appropriate specialist referral (oncology, endocrine or renal). Severe hypercalcaemia (greater than 3.5 mmol/L or hypercalcaemia with dehydration, abdominal pain or reduced consciousness is a medical emergency.
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PMID:Disorders of calcium metabolism. 1703 12

Although approximately half of patients undergoing hemodialysis receive activated forms of Vitamin D, the primary reason to initiate this therapy has rested solely on the management of secondary hyperparathyroidism. Secondary hyperparathyroidism is likely one of several consequences of Vitamin D deficiency, and only now have other consequences of Vitamin D deficiency emerged. Although previously viewed as a contributor to hypercalcemia and hyperphosphatemia, recent studies suggest Vitamin D may improve cardiovascular structure and function, improve vascular compliance, and reduce pro-inflammatory cytokines, all of which may contribute to the improved survival observed in retrospective studies examining the outcome of patients treated with activated Vitamin D compared to those who were not. The current review examines two recent large-scale studies of hemodialysis patients: one that demonstrated a survival advantage of paricalcitol over calcitriol, and a second that demonstrated a significant survival advantage of any intravenous Vitamin D formulation versus none. In both studies, the findings were independent of mineral and parathyroid hormone levels, suggesting "non-traditional" actions of Vitamin D contributed to the observed survival advantage. Potential steps moving forward in light of these observational studies are subsequently discussed.
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PMID:Vitamin D in patients with renal failure: a summary of observational mortality studies and steps moving forward. 1719 69

Primary hyperparathyroidism is an endocrine disorder with variable clinical expression, frequently presenting as asymptomatic hypercalcemia in Western countries but still predominantly as a symptomatic disease in developing countries. The objective of this retrospective study was to describe the diagnostic presentation profile, parathyroidectomy indication and post-surgical bone mineral density follow-up of patients with primary hyperparathyroidism seen at a university hospital. We found 115 patients (92 women, median age 56 years) with primary hyperparathyroidism diagnosed during the last 20 years. We defined symptomatic patients based on the presence of any classical symptom affecting bone, kidney or the neuromuscular system. Surgical criteria followed the guidelines of the National Institutes of Health regarding asymptomatic primary hyperparathyroidism. Symptomatic patients and patients meeting surgical criteria for parathyroidectomy were 66 and 93% of the sample, respectively. Median calcium and parathyroid hormone values were 11.9 mg/dL and 189 pg/mL, respectively. After surgical treatment, 97% of patients were cured, with increases in bone mineral density of 19.4% in the lumbar spine and 15.7% in the femoral neck 3 years after surgery. Greater bone mass increases were detected in pre-menopausal women, men, and in symptomatic and younger patients, both in the lumbar spine and femoral neck. Our results support the previous findings of a predominantly symptomatic disease with a presentation profile that could be mainly related to a delayed diagnosis. Nevertheless, genetic and racial backgrounds, and nutritional factors such as calcium and vitamin D deficiency may play a role in the clinical presentation of primary hyperparathyroidism of Brazilian patients.
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PMID:Analysis of the diagnostic presentation profile, parathyroidectomy indication and bone mineral density follow-up of Brazilian patients with primary hyperparathyroidism. 1740 95

A 71-year-old man presented with acute pulmonary edema related to new onset of severe left ventricular dysfunction (ejection fraction, 30%). His symptoms did not improve with emergency therapy with diuretics and dobutamine. He was noted to be severely hypocalcemic (5.5 mg/dL) and subsequently showed dramatic improvement in symptoms and ejection fraction (58%) with correction of hypocalcemia with intravenous calcium and calcitriol replacement. Hypocalcemia was related to surgically induced hypoparathyroidism. The patient had been instructed to decrease calcium supplements and to discontinue calcitriol 3 months previously due to hypercalcemia. Additional factors that may have contributed to hypocalcemia included vitamin D deficiency, alendronate therapy for osteoporosis, and chronic kidney disease. We concluded that the patient's congestive heart failure was precipitated by severe hypocalcemia and resolved with correction of hypocalcemia. Hypocalcemia is a rare cause of reversible congestive heart failure that should be in the differential diagnosis in any patient presenting with heart failure and not responding to traditional therapy.
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PMID:Reversible congestive heart failure related to profound hypocalcemia secondary to hypoparathyroidism. 1743 16


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