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)

A 68-year-old woman was admitted in March 1997 because of lumbago, fever, vomiting, and general malaise. Laboratory data disclosed anemia and severe hypercalcemia (7.7 mEq/l). Multiple osteolytic lesions were detected in the patient's vertebra, pelvis, and bilateral tibia by x-ray films and 99mTc bone scintigrams. Bone marrow aspiration sample was not obtained due to dry tap. Marked myelofibrosis and proliferation of lymphoid cells were revealed by a bone marrow biopsy specimen. Immunohistochemical analysis showed that cells in the biopsy specimen were positive for L-26 and LCA, but not for UCHL-1. Gastrointestinal endoscopic examination found multiple polypoid lesions in the stomach; biopsy specimens of the lesion tissue disclosed invasion by B lymphoid cells. A diagnosis of diffuse large B cell lymphoma was thus made. THP-COP chemotherapy was performed, but only minimal response was obtained. Lymphoma cells subsequently invaded the brain stem, and the patient eventually died of respiratory failure.
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PMID:[Extranodal non-Hodgkin's lymphoma associated with systemic bone metastasis and secondary myelofibrosis]. 1002 51

Patients with end-stage renal disease commonly develop secondary hyperparathyroidism. Calcitriol may be administered to such patients to decrease the synthesis and secretion of parathyroid hormone (PTH) and to help maintain calcium and phosphorus homeostasis. However, the doses of calcitriol required to suppress serum PTH concentrations can lead to hypercalcemia or hyperphosphatemia in many patients undergoing hemodialysis. Paricalcitol is a new vitamin D analogue that is safe and effective in suppressing elevated concentrations of PTH in patients with established hyperparathyroidism who are maintained on chronic hemodialysis. As with vitamin D, the biologic action of paricalcitol is mediated through activation of the vitamin D receptor (VDR). The VDR functions as a ligand-induced transcription factor regulating the rate of expression of genes that are involved in controlling not only calcium homeostasis and bone remodeling but also hormone secretion, inhibition of cell growth, and induction of cell differentiation. In vitro studies have shown that paricalcitol inhibits PTH secretion from bovine parathyroid cells in a dose-dependent manner. Studies in renally insufficient rats demonstrated that paricalcitol caused approximately 10 times less elevation of serum calcium concentrations than calcitriol. In clinical studies, paricalcitol effectively decreased PTH by about 60% over a 12-week period. Mean serum concentrations of calcium were significantly increased but remained within the normal range. There were occasional (5/414 determinations) transient elevations in serum calcium above the upper limit of normal in some (5/401) patients. Serum phosphorus values did not change significantly compared with baseline, although they tended to be slightly higher in the paricalcitol-treated group than in the group receiving placebo. Elevations of the calcium-times-phosphorus product were relatively few but occurred more often in the paricalcitol than in the placebo group. The terminal half-life of paricalcitol was 5 to 7 hours in healthy subjects; in patients undergoing hemodialysis, it was 14 hours. Adverse events associated with paricalcitol use included, among others, chills, feeling unwell, fever, sepsis, palpitations, dry mouth, gastrointestinal bleeding, nausea, vomiting, edema, light-headedness, and pneumonia. Paricalcitol should be considered as an alternative to calcitriol in the treatment of patients who are undergoing maintenance hemodialysis for end-stage renal disease, as it has a decreased potential to induce hypercalcemia and hyperphosphatemia. Additional studies are required to determine the long-term effects of therapy.
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PMID:Paricalcitol, a new agent for the management of secondary hyperparathyroidism in patients undergoing chronic renal dialysis. 1032 13

A 59-years-old male patient was admitted to our Service because of acute renal failure with maintained diuresis (creatinine at admittance 6.2 mg/dl), preceded by malaise and weight loss. Clinical examination was normal and no investigation lead to a sure differential diagnosis of acute renal failure. The only abnormal laboratory investigations were: marked hypercalcaemia (12.7 mg/dl), slightly depressed parathormone (10 pg/ml) and anemia (Hb 11.2 g/dl). Also instrumental investigations performed were inexpressive. The abrupt appearance of an unilateral 7th cranial nerve paralysis lead to start a steroid therapy followed, in some days, by the normalization of calcium level and by a partial improvement of renal function. A renal biopsy was finally performed which permitted the diagnosis of interstitial granulomatous nephritis according to a sarcoidosis disease. Steroid therapy was continued allowing to a progressive, although not complete, recovery of renal function. The case peculiarity consists of isolated renal lesions with a severe expression of renal disease. The absence of classical disease criteria (pulmonary involvement firstly), in our case total body Gallium-67 scintigraphy was normal, should not exclude the diagnosis of sarcoidosis. The authors underline the importance of renal biopsy in detecting interstitial renal lesions potentially leading to uremia.
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PMID:[Isolated acute renal failure secondary to sarcoidosis. Apropos of a case]. 1102 Nov 66

Hypercalcaemia is a well-recognised feature of hypoadrenalism. The adrenal glands are often involved with metastatic disease subclinically although full hypoadrenal crisis is not uncommon. Ill patients with known malignancy should generate a high degree of clinical suspicion for the possibility of adrenal involvement. This case highlights the need to look beyond confirmed bone metastases as the cause of hypercalcaemia in patients with widespread carcinomatosis.
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PMID:Hypercalcaemia of hypoadrenal crisis mistaken for hypercalcaemia of malignancy in a patient with known bone metastases: a case report. 1111 62

Mesenteric panniculitis is a rare disease of the bowel mesentery, characterized by tumor-like infiltration by chronic inflammatory cells, fat necrosis, and fibrosis. Reported cases cited clinical presentation ranging from abdominal pain to fever of unknown origin, the majority of which were idiopathic and associated with a benign prognosis. We report the case of a 43-yr-old male who presented with malaise, weight loss, microcytic anemia, and a high erythrocyte sedimentation rate. Radiographic and histological investigations revealed typical features of mesenteric panniculitis. Initial treatment with high-dose oral prednisolone led to rapid and complete resolution of symptomatology, radiographic, and laboratory anomalies. Within 6 months, the patient presented again with anemia, renal failure, and hypercalcemia. A diagnosis of IgA kappa chain myeloma was made. Despite chemotherapy and restoration of normocalcemia, he died from refractory pulmonary edema. This is the first report of a hematological malignancy initially presenting with features of mesenteric panniculitis culminating in an aggressive course and a fatal outcome.
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PMID:Aggressive multiple myeloma presenting as mesenteric panniculitis. 1119 60

A 76-year-old man presented with a subacute history of weight loss, malaise and anorexia. Laboratory investigations revealed serially increasing hypercalcaemia, correlating with deterioration in his clinical status. He was subsequently shown to have hypocortisolaemia, which improved with the administration of intravenous steroids. Subsequent biochemical testing revealed the endocrinological defect to be one of isolated ACTH deficiency, which, unlike Addison's disease, does not classically include hypercalcaemia in its presentation.
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PMID:A case of isolated ACTH deficiency presenting with hypercalcaemia. 1122 Sep 94

The files were studied of 300 patients operated for primary hyperparathyroidism for the first time. Their median age was 60 years. The female/male ratio was 3/1, but in the younger patients males and females were about equally present. Preoperatively, one third was considered as asymptomatic with respect to hyperparathyroidism. In this subgroup the hypercalcemia was detected coincidentally and the mean parathyroid hormone level was lower than in the others. Another third of the patients had nephrolithiasis, they were on the average younger and there were more males. Finally one third showed other symptoms as gastrointestinal disease, bone disease or general malaise. Intraoperatively, we found a solitary adenoma in 90% of the cases, a double adenoma in 5% (on each side of the neck in half of the cases) and hyperplasia in 4%. The adenomas had a tendency to occur more often in the upper parathyroid glands, but the difference was not important enough to influence the surgical technique. Hyperplasia patients were, on the average, younger and double adenoma patients older. The female/male ratio was 1/1 for hyperplasia and 15/1 for double adenoma.
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PMID:Pre- and intra-operative findings in primary hyperparathyroidism. 1144 71

A first-trimester primigravid patient presented with hyperemesis and malaise. Work-up was consistent with primary hyperparathryoidism. During acute treatment, she developed generalized motor seizures considered to be secondary to hypercalcemia. Evaluation and treatment of women with primary hyperparathyroidism and hypercalcemia are reviewed, and the pathogenesis of seizures associated with hypercalcemia is discussed.
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PMID:Primary hyperparathyroidism, hypercalcemic crisis and subsequent seizures occurring during pregnancy: a case report. 1260 69

The management of metastasis from parathyroid carcinoma (PC) is an unusual challenge. Systemic therapy has minimal effect on the course of the disease and its associated hypercalcemia. Resection of isolated pulmonary metastases is an attractive option in the setting of recurrent hypercalcemia. We report a case of a patient who underwent resection of multiple functional PC pulmonary metastases almost 20 years after the original neck resection. The patient originally presented in 1982 with what was thought to be hyperparathyroidism secondary to a parathyroid adenoma. Surgical exploration revealed the presence of a well differentiated PC. The patient was transiently normocalcemic, but underwent surgical exploration in 1993 and 1996 for recurrent PC in the neck. The patient again improved, but presented in 2001 with diffuse arthralgia, fatigue, malaise, weight loss, and decreased appetite. She was found to have a serum calcium of 12.7 mg/dL and an intact parathyroid hormone of 1542 pmol/L. Computed tomography identified the presence of two right-sided and two left-sided pulmonary masses. Sternotomy with bilateral pulmonary metastectomy was performed. Functional PC metastasis was confirmed on pathological examination. One year following metastectomy the patient is hypocalcemic, requiring oral calcium and vitamin D supplementation. Functional pulmonary metastasis from PC is a rare cause of hypercalcemia. Complete resection of isolated pulmonary metastases can provide effective palliation with long-term survival.
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PMID:Resection of pulmonary metastasis from parathyroid carcinoma. 1450 26

Parathyroid hormone-related protein (PTHrP) plays a central role in humoral hypercalcemia of malignancy (HHM), which is one of the most frequent paraneoplastic syndromes. PTHrP produced by the tumor acts through a common PTH/PTHrP receptor to promote bone resorption, inhibit calcium excretion from the kidney, and induce hypercalcemia. Patients with HHM often develop cachexia associated with typical symptoms such as anorexia, malaise, nausea, constipation, polyuria, polydipsia, and confusion. The etiology of the cachexia is not fully understood but is thought to be caused by hypercalcemia and various cytokines such as interleukin-6, tumor necrosis factor-alpha, leukemia inhibitory factor, and others. In this study, we investigated the role of PTHrP in hypercalcemia and cachexia in HHM by using humanized anti-PTHrP antibody. A mouse monoclonal antibody that binds to PTHrP amino acid sequence 1-34 and inhibits PTHrP function has been humanized to create a specific and potent agent for the treatment of patients with HHM. The mouse monoclonal antibody has been shown to have antihypercalcemic activity against nude mice bearing human tumors. Because a mouse antibody is highly immunogenic in human patients, the complementarity-determining regions from the mouse antibody were grafted into a human antibody. The resulting humanized antibody specifically recognizes PTHrP(1-34) and neutralizes PTHrP functions in vitro and in vivo. The humanized anti-PTHrP antibody was administered intravenously to HHM model animals bearing tumors such as LC-6 human lung carcinoma. These animals showed symptoms similar to those of patients with HHM (eg, hypercalcemia and cachexia). The humanized anti-PTHrP antibody-treated animals responded with normalization of blood ionized calcium level through an improvement of bone metabolism and calcium excretion. Moreover, the treated animals also showed an improvement in body weight, ultromotivity, metabolic alkalosis, food consumption, water intake, serum phosphorus, and renal function. Consequently, the humanized antibody-treated animals experienced complete resolution of hypercalcemia and cachexia. These results suggest that the humanized antibody would be an effective and beneficial agent for patients with HHM, and that PTHrP is a major pathogenetic factor of hypercalcemia and cachexia in patients with HHM.
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PMID:Treatment of malignancy-associated hypercalcemia and cachexia with humanized anti-parathyroid hormone-related protein antibody. 1461 38


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