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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

Pancreatic endocrine tumors (PETs) are unusual tumors arising from cells belonging generically to the amine precursor uptake and decarboxylation systems. We present a case of a calcitonin-secreting PET in a 56-year-old female who presented with watery diarrhea, dehydration and hypokalemia. Investigation revealed hypercalcemia, hyperphosphatemia, hypercalcitonemia and a well-defined mass in the head of the pancreas on CT scan. Following a pancreaticoduodenectomy her serum calcitonin levels returned to normal and diarrhea disappeared. The identification of this particularly rare presentation of a calcitonin-secreting PET provides the opportunity to examine this pathological entity within the context of the very few previously reported instances of this disease.
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PMID:Calcitonin-secreting tumor of the pancreas. 1584 74

The authors describe a 9-year-old girl with precursor-B acute lymphoblastic leukemia (ALL) who presented with dehydration and severe hypercalcemia. She had received oral vitamin D and calcium supplementation for 4 days, the last dose 48 hours prior to admission, and required pediatric intensive care unit (PICU) hospitalization for management of the hypercalcemia and safe initiation of induction chemotherapy. Her clinical course was complicated by pancreatitis, disseminated intravascular coagulation, pleural effusion, and focal seizures. Although the exact mechanism of hypercalcemia was not elucidated, it was likely related to the underlying ALL, without dismissing the prior vitamin D and calcium supplementation as a possible contributing factor. The hypercalcemia resolved with specific antileukemic therapy along with supportive care and administration of calcitonin. Hypercalcemia is an uncommon metabolic abnormality in children with ALL, but it can be life-threatening. Children with ALL should be referred to tertiary-care institutions with PICU and subspecialty support because serious metabolic and other complications can occur before or after the administration of chemotherapy.
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PMID:Life-threatening hypercalcemia complicated by pancreatitis in a child with acute lymphoblastic leukemia. 1589 68

We report a case of extreme hypercalcaemia associated with a parathyroid adenoma in a young man. The patient presented with classical symptoms of a hypercalcaemic syndrome, and serum calcium and parathyroid hormone levels were 6.92 mmol L(-1) and 70.2 pmol L(-1) respectively. After stabilizing the patient and reducing the calcium level, a parathyroidectomy was performed. The postoperative course was uneventful with rapidly resolving clinical symptoms. Hypercalcaemic crisis is a rare but life-threatening complication of primary hyperparathyroidism. It should be suspected in acutely ill patients complaining of muscular weakness, gastrointestinal and cerebral symptoms. To reduce mortality, it is essential to correctly diagnose the condition without delay and provide appropriate emergency management correcting hypercalcaemia and dehydration. Successful parathyroidectomy quickly relieves symptoms and prevents recurrence.
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PMID:Surviving extreme hypercalcaemia--a case report and review of the literature. 1595 36

Hypercalcemia associated with malignancies is reported in up to 20 to 30% of patients with cancer during the course of the disease, and points to a poor prognosis. Symptoms related to the central nervous system, as progressive mental impairment, stupor and coma, predominate. Alterations in kidney function (water-concentrating defect leading to polyuria) and gastrointestinal tract (anorexia, nausea, vomiting) corroborate to dehydration and a further increase in serum calcium. Cancer-induced hypercalcemia may be classified as: 1) local osteolytic hypercalcemia (LOH), due to marked increase in osteoclastic bone resorption in areas surrounding the malignant cells within the marrow space; 2) humoral hypercalcemia of malignancy, caused by the secretion of parathyroid hormone-related protein (PTHrP) by the malignant tumor; 3) ectopic hyperparathyroidism; 4) 1,25(OH)2 D-secreting tumors. Adequate control of hypercalcemia is necessary to give the patient time to respond to anti-cancer therapy. Volume expansion with saline will correct dehydration, improve glomerular filtration and increase urinary calcium excretion, which may be further stimulated by loop diuretics. Intravenous bisphosphonates are the most effective agents to control hypercalcemia, as they block osteoclastic osteolysis and also have antitumoral effects, decreasing bone metastases. New approaches to control the skeletal manifestations of malignancies are anti-PTHrP and anti-RANKL antibodies, osteoprotegerin, and also proteasome inhibitors in the case of multiple myeloma.
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PMID:[Hypercalcemia of malignancy: clinical features, diagnosis and treatment]. 1644 66

Transient character of laboratory abnormalities is usually explained as a false result of estimation. Spontaneous disappearance of laboratory abnormalities could be recognized as non-important and contradicting serious disease. Presented case of multiple endocrine neoplasia type 1 (MEN 1) denies these assumptions. Sixty-nine-years old woma was admitted to the internal department because of weakness, fever, dehydration and hypotension--symptom accompanying an upper respiratory infection. Moderate hyponatremia (122.6 mmol/l) was found in a routine laborator examination. All clinical symptoms as well as hyponatremia disappeared during hospitalization. Transient hyponatremi was not ignored. Further laboratory and hormonal investigations were performed. Fasting, morning serum cortisol concentration and 24-hours urinary excretion of free corticosterids were decreased and Synacten stimulation test reveale incomplete cortisol stimulation. Pituitary tumour was found in the CT scan. Moreover blood ionized calcium an parathyroid hormone were elevated. These results revealed secondary adrenal insufficiency, non-functioning pituitary tumor and hyperparathyroidism. Removal of pituitary adenoma was done. Asymptomatic hypercalcemia persists. Presented MEN 1 was atypical because: 1. Usually hyperparathyroidism is the first and most frequent symptom while in our patient the first symptom was transient hyponatremia secondary to the pituitary tumor, 2. was diagnosed in the old age while the majority of MEN 1 patients are younger, 3. asymptomatic course of hypercalcemia indicates that in some of elder patients removal of the parathyroid glands might not be necessary.
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PMID:[Transient hyponatremia the first symptome of multiple endocrine neoplasia type 1 (MEN 1)--case report]. 1680 15

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

Multiple mycloma causes a disproportionate amount of the malignancy-related renal insufficiency. Acute renal insufficiency in myeloma patients can occur due to dehydration, hypercalcemia, side effects of medications (NSAIDs) or tumor lysis syndrome in addition to cast nephropathy, amyloidosis and light chain deposition disease. Patients on hemodialysis have traditionally been excluded from antineoplastic therapy due to fear of side effects and lack of studies addressing benefit. Melphalan is the most effective chemotherapeutic agent in myeloma and its PK (pharmacokinetics) are not adversely affected by impaired renal function. Because of more pronounced toxicity of Melphalan 200 mg/m2 conditioning regimen, Melphalan 140 mg/m2 has become the standard of care. 24% of patients become dialysis-independent at a median of 4 months after autotransplantation. Favorable factors for becoming dialysis independent were duration of dialysis <or=6 months and pretransplant creatinine clearance >10 ml/min. While no good data are available on the use of thalidomide in the presence of renal failure, it is our experience that severe neuropathy, constipation, lethargy and bradycardia are more frequent in patients with creatinine >or=3 mg/dl. It has become apparent that bisphosphanates-zoledronic acid more than pamidronate-cause renal dysfunction. If patients remain dialysis-dependent after autotransplantation, we recommend to delay considering a renal transplant until at least 3 years after the first transplant.
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PMID:High-dose therapy in patients with plasma cell dyscrasias and renal dysfunction. 1707 30

Nephrogenic diabetes insipidus which can be inherited or acquired, is characterized by an inability to concentrate urine despite normal or elevated plasma concentrations of the antidiuretic hormone, arginine-vasopressine (AVP). Polyuria, with hyposthenuria and polydipsia are the cardinal clinical manifestations of the disease. Hypercalcemia, hypokaliemia, lithium administration and chronic renal failure are the principal causes of acquired nephrogenic diabetes insipidus. About 90 percent of patients with congenital nephrogenic diabetes insipidus are males with X-linked recessive nephrogenic diabetes insipidus who have mutations in the arginine-vasopressin receptor 2 (AVPR2) gene that codes for the vasopressin V2 receptor. The gene is located in chromosome region Xq28. In about 10 percent of the families studied, congenital nephrogenic diabetes insipidus has an autosomal recessive or autosomal dominant mode of inheritance. In these cases, mutations have been identified in the aquaporin-2 gene (AQP2), which is located in chromosome region 12q13 and codes for the vasopressin-sensitive water channel. Other inherited disorders with mild, moderate or severe inability to concentrate urine include Bartter's syndrome and Cystinosis. Identification of the molecular defect underlying congenital nephrogenic diabetes insipidus is of immediate clinical significance because early diagnosis and treatment of affected infants can avert the physical and mental retardation associated with episodes of dehydration.
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PMID:[Nephrogenic diabetes insipidus]. 1708 61

Tumor-induced hypercalcemia is a frequent complication of advanced cancers, but it has been rarely reported in patients with sarcoma. We report a 16 year-old boy presenting with polyuria, polydipsia and severe dehydration. Laboratory examination revealed severe hypercalcemia (serum calcium 23 mg/dl) which caused emaciation and was accompanied by low serum phosphorus and suppressed parathyroid hormone. Diagnostic imaging revealed a huge anterior mediastinal mass. Hypercalcemia was successfully treated with pamidronate, a bisphosphonate, and the patient underwent surgical resection. Pathological and immunohistochemical analyses confirmed a diagnosis of biphasic synovial sarcoma. To our knowledge, this is the first case of mediastinal synovial sarcoma presenting with hypercalcemia.
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PMID:Tumor induced hypercalcemia in a patient with mediastinal synovial sarcoma. 1784 48


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