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

Lithium has proved to be a highly effective preventive measure in mood disorders and an increasing number of patients are receiving long-term lithium carbonate therapy. Among other biologically and clinically important effects of lithium, the possible induction of hyperparathyroidism was first suggested in 1973 by Garfinkel et al. About thirty other case reports have since been described, but they could simply have represented the coincidental occurrence of primary hyperparathyroidism and lithium carbonate treatment in the same patients. Eleven cross-sectional studies of calcium metabolism in patients treated with lithium carbonate have been reported. Evidence of a causal relationship of lithium to hyperparathyroidism can lead to a loss of effectiveness of lithium in controlling the affective symptoms. Interestingly, coexistence with hypothyroidism is not uncommon. Low serum phosphate, high serum chloride are also observed. Bone mineral content may decrease. In addition, several studies have shown that lithium treatment increases serum magnesium level. Unusual metabolic features are associated with hyperparathyroidism and long-term lithium treatment: low urinary calcium excretion, absence of nephrolithiasis, and normal urinary cyclic AMP excretion. Lithium inhibition of PTH sensitive adenylcyclase in the kidney would explain these features. In vitro studies suggested that lithium is a potent inhibitor of several hormone responsive adenylcyclase systems. It is possible that the tissue susceptibility to adenylcyclase inhibition in an individual may decide the nature of endocrine dysfunction seen during lithium treatment. Information about the time course with which abnormalities may develop is derived from longitudinal studies. Several months to several years are needed for lithium inducing primary hyperparathyroidism. In vitro studies provide strong evidence that lithium can induce a shift in the set-point for inhibition of PTH secretion by calcium and a direct stimulation of PTH secretion. The extent to which we can extrapolate these data to the clinical situation is discussed. In vivo data from Shen an Seely are compatible with these two mechanisms. These alterations should cause parathyroid hyperplasia. The possibility that a generalized parathyroid stimulus might lead to formation of a single adenima is not proved. Several recommendations regarding parathyroid function in patients receiving lithium have been suggested. Measurement of total calcium and serum proteins or of serum calcium ion values when available should be performed before therapy is begun. If elevated values are obtained, lithium treatment should be deferred and evaluation for hyperparathyroidism performed. Serum calcium should be monitored periodically during lithium treatment. Sustained hypercalcemia or true hyperparathyroidism require parathyroidectomy. If hypercalcemia is mild without complication and psychiatric symptoms well controlled, perhaps surgery should not be employed.
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PMID:[Hyperparathyroidism with lithium]. 808 38

A middle-aged farmer and a female student presented with osteitis fibrosa cystica with nephrocalcinosis in the former and nephrolithiasis in the latter due to primary hyperparathyroidism. Hypercalcaemia was present in both cases and neck exploration revealed a large solitary parathyroid adenoma which was excised. Because primary hyperparathyroidism is less common in tropical countries doctors may be less familiar with the early manifestations of the disease. The number of patients thus undiagnosed and untreated is unknown.
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PMID:Parathyroid adenoma in northern Nigeria. 847 Mar 6

Sarcoidosis has been associated with a wide spectrum of renal manifestations, including disordered calcium metabolism, nephrocalcinosis, nephrolithiasis, granulomatous interstitial nephritis, and glomerulonephritis. In some patients, two or more manifestations of renal sarcoidosis may coexist. The case of a young patient with sarcoidosis who presented with hypercalcemia and acute renal failure is discussed. Despite normalization of the serum calcium with intravenous fluids and corticosteroids, his renal insufficiency persisted. A diagnostic renal biopsy was performed to determine the etiology of his renal failure and was helpful in the selection of optimal medical therapy.
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PMID:The kidney in sarcoidosis. 850 10

Hyperparathyroidism occurs sporadically, in association with multiple endocrine neoplasia (MEN) types I and II, or rarely as familial hyperparathyroidism (FHPT) without other manifestations. We analyzed our experience in 16 FHPT patients from 14 families treated between 1934 and 1991 and reviewed 51 other FHPT patients reported in the literature to determine the clinical course of these patients. Among our 16 patients, 7 (44%) had a serum calcium level >/= 3.75 mmol/L, 5 (31%) presented with hypercalcemic crisis, 3 (19%) had osteitis fibrosa cystica, 5 (31%) had nephrolithiasis, 1 had pancreatitis, 12 (75%) had multiple abnormal parathyroid glands, 3 (19%) had supernumerary glands, and 7 (44%) required reoperation for persistent (n = 4) or recurrent (n = 3) hyperparathyroidism. Three patients (19%) also had papillary thyroid cancer, and 7 (44%) had other coexistent thyroid disorders. Among 51 patients with FHPT reported in the literature, 23 (45%) had serum calcium >/= 3.75 mmol/L, and 23 (45%) had multiple abnormal parathyroid glands; 10 (20%) had recurrent hyperparathyroidism. FHPT without other endocrinopathies is a distinct entity. Patients with FHPT have multiple abnormal parathyroid glands and are prone to both recurrent and persistent hyperparathyroidism. They frequently present with profound hypercalcemia or hypercalcemic crisis, in contrast to patients with MEN-associated hyperparathyroidism or sporadic hyperparathyroidism.
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PMID:Familial hyperparathyroidism without multiple endocrine neoplasia. 894 73

Most cases of primary hyperparathyroidism are due to either a parathyroid adenoma or to parathyroid hyperplasia. Parathyroid carcinoma is a very rare cause of hyperparathyroidism. Although the diagnosis of parathyroid carcinoma is usually established based on pathological criteria of vascular and capsular invasion, some clinical and biochemical features differentiate it from benign forms of hyperparathyroidism. We report the case of a middle-aged woman with a long standing history of nephrolithiasis, who presented with a palpable neck mass, weight loss, severe hypercalcemia and hypophosphatemia, as well as very high serum levels of intact parathyroid hormone. Surgical neck exploration revealed a large tumor that invaded trachea, esophagus, reccurrent laryngeal nerve, right apical pleura and right carotid artery. Pathological examination confirmed the invasive nature of the tumor. Along with the case report, we review the literature and discuss the diagnostic and therapeutic options of this rare condition.
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PMID:Primary hyperparathyroidism due to parathyroid carcinoma. 920 27

Hyperparathyroidism is a common cause of hypercalcemia. The hypercalcemia usually is discovered during a routine serum chemistry profile. Often, there has been no previous suspicion of this disorder. In most patients initially believed to be asymptomatic, previously unrecognized symptoms resolve with surgical correction of the disorder. The symptoms of hyperparathyroidism are vague and often similar to symptoms of depression, irritable bowel syndrome, fibromyalgia or stress reaction. Complications of primary hyperparathyroidism include peptic ulcers, nephrolithiasis, pancreatitis and dehydration. Surgical management is usually indicated. When medical management is used, routine monitoring for clinical deterioration is recommended. Preoperative localization of adenomas with technetium Tc 99m sestamibi scan is possible but may be unnecessary. An experienced surgeon should perform the parathyroidectomy.
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PMID:Hyperparathyroidism. 957 20

The Ca(2+)-sensing receptor (CaR) is a member of the seven-transmembrane domain, G protein-coupled receptor super-family. In the parathyroid gland, it mediates the inhibitory effects of extracellular Ca2+ on the secretion of parathyroid hormone. In the kidney, activation of the CaR causes decreased reabsorption of Ca2+ from the tubular lumen. Mutations in the CaR gene produce abnormalities of Ca2+ homeostasis. Heterozygous loss-of-function mutations cause familial hypocalciuric hypercalcemia. Homozygous loss-of-function mutations cause neonatal severe hyperparathyroidism. In contrast, gain-of-function CaR mutations result in autosomal dominant and sporadic hypoparathyroidism. The resulting hypoparathyroidism and hypocalcemia can range from asymptomatic to life-threatening. Patients with hypocalcemia due to CaR mutations also show disproportionate hypercalciuria that may increase the risk of nephrocalcinosis, nephrolithiasis, and renal insufficiency.
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PMID:Molecular biology and clinical importance of the Ca(2+)-sensing receptor. 975 71

Autosomal dominant hypocalcemia (ADH), caused by activating mutations of the calcium-sensing receptor (CaSR), is characterized by hypocalcemia with an inappropriately low concentration of PTH. Among 11 missense mutations of CaSR reported to date in patients with ADH or sporadic hypocalcemia, functional properties of 8 mutant CaSRs were characterized. Here, we describe a novel mutation of CaSR and its functional property in a family with ADH. The 41-yr-old male proband had asymptomatic hypocalcemia with a history of recurrent nephrolithiasis. His father had asymptomatic hypocalcemia, but his mother was normocalcemic. PCR-single strand conformation polymorphism and sequencing revealed that both the proband and the father had a novel heterozygous mutation in CaSR gene that causes lysine to asparagine substitution at codon 47 (K47N), which is in the extracellular domain of CaSR, like 6 of 11 known activating mutations. Using HEK293 cells transfected with wild-type or K47N CaSR complementary DNA, the intracellular Ca2+ concentration was assessed in response to changes in the extracellular Ca2+ concentration. The EC50 of the mutant CaSR for the extracellular Ca2+ concentration was 2.2 mmol/L and was significantly lower than that of wild-type (3.7 mmol/L). These results confirm that this mutation is responsible for ADH in this family. The fact that several inactivating mutations in familial hypocalciuric hypercalcemia occur in amino acid around K47 suggests the importance of the N-terminal portion of the receptor in extracellular Ca sensing.
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PMID:A novel activating mutation in calcium-sensing receptor gene associated with a family of autosomal dominant hypocalcemia. 992 Jan 8

Parathyroid carcinoma is a rare cause of primary hyperparathyroidism (1-2%). In this paper a case of parathyroid cancer of the right inferior parathyroid gland cyst (5 cm in diameter) localised mostly retrosternally is presented in a patient suffering from severe hypercalcaemia (Ca--3.7 mmol/l, Ca(++)--1.8 mmol/l), severe bone pains and weakness, huge osteoporosis with following L5 compression fracture and recurrent nephrolithiasis. PTH blood level before surgical treatment was 1243 pg/ml (Norm: 10-60 pg/ml). In the preoperative ultrasonography of the neck, a lesion was found, but it was considered to be a cyst in the inferior pole of the right thyroid lobe. In a fine-needle biopsy from the lesion-colloid mass without any cells was found. In a 99mTc-MIBI scintigraphy of the neck a suspicion of focus lesion in the right superior parathyroid gland was made, which was not confirmed intra-operatively. Parathyroid carcinoma was diagnosed intraoperatively in histological examination. 'En block' resection of the retrosternal parathyroid tumor and right thyroid lobe was performed from the jugular incision. Any enlarged jugular lymph nodes were not found. In a postoperative period a transient hypocalcaemia was present, which disappeared after pharmacological treatment. During 32 months of follow-up neither no features of local recurrence nor distant metastases were found. Calcium level in blood was normal, PTH 216.0 pg/ml, severity of bone pains and weakness lessened, osteoporosis in a course of pharmacological treatment--with no further progress.
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PMID:[Retrosternal parathyroid gland cystic neoplasm as a cause of primary hyperparathyroidism]. 1069 86

The introduction of the multichannel autoanalyser made measurement of serum calcium concentrations easier, and led to a dramatic change in clinical presentations. The reliable methods such as computed tomography (CT), ultrasonography (US) and magnetic resonance imaging (MRI) for preoperative localization of abnormal parathyroid glands has long been sought to increase the cure rate of surgical treatment. We report the clinical feature of primary hyperparathyroidism (PHPT). Patients were classified into four stages in chronological order. The early patients (the first stage, 1970-1979) were mainly diagnosed in the treatment of urolithiasis. Approximately 20% of patients in the second stage (1980-1986) were symptom-free, and hypercalcemia was detected by autoanalyzer. Patients in the third stage (1987-1993) underwent preoperative localization studies including CT. scintigraphy, ultrasonography and MRI. The recent patients (the fourth stage, 1993-1999) were mostly treated in the present hospital. In the first stage, PHPT was an uncommon metabolic disorder hat was typically associated with nephrolithiasis and was two to three times more common in men than in women. In the second, third and fourth stages, PHPT is a common and often symptomless endocrine disorder. The ratio of male to female is decreasing, because men are dominant in stone-formers. Four parathyroid glands were searched carefully in the first and second stages, and unilateral cervical exploration was performed in some preoperatively localized parathyroid glands in the third and fourth stages.
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PMID:Clinical features of primary hyperparathyroidism: preoperative localization and parathyroidectory. 1091 95


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