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)

Brown tumor is a focal lesion of the bone caused by primary or, less commonly, secondary or tertiary hyperparathyroidism (HPT). While the mandible is the most frequently involved bone in the head and neck region, atypical involvement of the cranium in the area of the sphenoid sinus is exceedingly rare. In the literature, a unique case of brown tumor of the sphenoid sinus was reported in a patient with primary HPT. We present a case of sphenoid sinus and occipital bone brown tumor associated with primary HPT. A 47-yr-old woman presented a 2-yr history of headaches, dizziness, diffuse body and articular pain, fatigue, and a 6-month history of intermittent nausea and vomiting, polydipsia, and polyuria. Magnetic resonance imaging (MRI) demonstrated an expansive mass lesion in the sphenoid sinus with erosion of the sellar floor and medial wall of the right orbit, and expansion in the medulla of bone. Examination of biopsy specimens obtained from sphenoid sinus mass confirmed the diagnosis of brown tumor. The biochemical laboratory studies showed elevation of parathyroid hormone and confirmed the diagnosis of primary HPT. Excision of a parathyroid adenoma affected the metabolic status into normalizing. At the follow-up of 12 months postoperatively, the size of sphenoid sinus brown tumor decreased and the mass of occipital bone disappeared. In conclusion, this is a first report of primary HPT masquerading as a destructive fibrous sphenoid sinus brown tumor associated with a mass lesion of occipital bone and hypercalcemia in the literature.
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PMID:Sphenoid sinus brown tumor, a mass lesion of occipital bone and hypercalcemia: an unusual presentation of primary hyperparathyroidism. 1523 58

Uncorrected hypercalcemia can cause clinical signs such as polyuria, polydipsia, vomiting, diarrhea, lethargy, and depression and contributes to the development of primary renal failure and soft tissue mineralization. Treatment of hypercalcemia includes diagnosis and treatment of the underlying disease process and some combination of excracellular fluid volume expansion by administration of fluids intravenously and administration of glococorticosteroids, salmon calcitonin, and furosemide. Bisphosphonates such as pamidronate disodium also may be safe and effective in the treatment of hypercalcemia. The purpose of our study was to characterize the efficacy and safety of pamidronate in the treatment of hypercalcemia attritutable to several different disease processes in the dog and cat. Seven dogs and 2 cats were administered pamidronate at a dose of 1.05-2.0 mg/kg IV for a variety of disease processes, including neoplasia (n = 4), calcipotriene toxicity (n = 3), nocardiosis (n = 1), and idiopathic hypercalcemia with chronic renal failure (n = 1). In all the animals, IV pamidronate administration rapidly decreased serum calcium concentrations without evident toxicosis. Two animals received pamidronate several times without obvious toxicosis. On the basis of the findings in our retrospective study, pamidronate may be a safe and effective drug with which to lower both serum total and ionized calcium concentrations in patients with hypercalcemia arising from a wide variety of underlying disease processes.
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PMID:Uses and effectiveness of pamidronate disodium for treatment of dogs and cats with hypercalcemia. 1571 44

Whether elderly patients with asymptomatic or minimally symptomatic primary hyperparathyroidism (PHPT) should be treated or not is still under debate. Several literature reports have shown improvements in terms of bone density and physical and mental well-being after surgical resolution of PHPT. Here, we present the case of a 93-year-old hypertensive woman, who had suffered for one year from cognitive impairment, accompanied during the last month by behavioral alterations (and polyuria and polydipsia), which resulted in sopor leading to hospitalization. A CT brain scan evidenced cortical atrophy and cerebrovascular disease, and biochemical analyses were remarkable for hypercalcemia (11.4-12.6 mg/dL, corrected for albumin levels) associated with increased parathormone levels (95.4-100.6 pg/mL). A diagnosis of PHPT was established. Densitometry evaluation of radius showed osteopenia. Withdrawal of psycho-therapy drugs and thiazidic, together with i.v. saline hydration and loop diuretics, significantly improved the patient's mental state and resolved behavioral alterations. As the patient and her relatives refused the surgical option, and the clinical situation improved after medical normalization of calcium levels, PHPT was managed conservatively, and calcium levels were maintained within the normal range through i.v. administration of zoledronate at 8-week intervals. Our case highlights the importance of considering hypercalcemia as the cause of onset of behavioral alterations and worsening of mental condition in elderly patients with cognitive decline. Therapy with bisphosphonates in patients with PHPT who are unfit for or refuse surgery seems advisable, but needs further study.
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PMID:Primary hyperparathyroidism and neuropsychiatric alterations in a nonagenarian woman. 1584 25

A three-year-old Border collie was presented with a two-week history of lethargy, stiff gait, polydipsia and polyuria. Biochemical analysis revealed hypercalcaemia. Serum concentrations of 25-hydroxyvitamin D (25[OH]D) and 1,25-dihydroxyvitamin D (1,25[OH]2D) were markedly elevated and parathyroid hormone was undetectable. Subsequent analysis of the dog's diet revealed that the food contained excessive amounts of vitamin D. The hypercalcaemia resolved following treatment with bisphosphonates and dietary change. Hypervitaminosis D was diagnosed in a second unrelated dog, which had been fed the same brand of dog food as case 1. The dog was also hypercalcaemic and had markedly elevated serum concentrations of 25(OH)D and 1,25(OH)2D. Hypervitaminosis D in dogs has been reported to occur secondarily to ingestion of either rodenticides containing cholecalciferol or antipsoriatic ointments that contain vitamin D analogues. Hypervitaminosis D has also been reported following the treatment of hypoparathyroidism. To the authors' knowledge, this is the first report of hypervitaminosis D in dogs following the accidental over supplementation of a commercial diet with vitamin D. While the benefits of adequate dietary vitamin D are well established in dogs, the potential deleterious effects of over supplementation of vitamin D should also be acknowledged.
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PMID:Hypercalcaemia in two dogs caused by excessive dietary supplementation of vitamin D. 1603 50

We present three cases of primary hyperparathyroidism (PHPT) in pregnancy. The clinical presentation of PHPT is not altered by pregnancy; however, the disease constitutes a serious risk for the foetus and the newborn. Although rare, hypercalcaemia should be suspected in pregnant women presenting with polydipsia, polyuria and fatigue as well as hypertension or preterm labour.
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PMID:[Primary hyperparathyroidism in pregnancy]. 1615 62

We used the mouse nephrin promoter to express a constitutively active Galphaq [Galphaq(Q>L)] transgene in mice. As previously reported, the transgene was expressed in kidney, pancreas, and brain, and the kidney phenotype was characterized by albuminuria and reduced nephron mass. Additional studies revealed a second phenotype characterized by polyuria and polydipsia. The polyuric phenotype was not caused by abnormal glucose metabolism or hypercalcemia but was accompanied by reduced urinary concentrating ability. Additional studies found that 1) water restriction was associated with an appropriate increase in serum vasopressin levels in transgenic (TG) mice; 2) the urinary concentrating defect was not corrected by administration of desamino-d-arginine vasopressin (DDAVP); and 3) papillary length was similar in TG and non-TG mice. To examine the renal response to DDAVP at the molecular level, we monitored aquaporin 2 (AQP2) and vasopressin V2 receptor (V2R) mRNA levels in mouse kidney. Consistent with the known effects of vasopressin, administration of DDAVP caused a decrease in V2R mRNA levels and an increase in AQP2 mRNA levels in both TG and non-TG animals, suggesting an appropriate renal response to DDAVP in the TG mice. To determine whether the urine concentrating abnormality was the result of primary polydipsia, water intake by TG mice was restricted to the amount ingested by non-TG animals. After 5 days, urinary concentrating ability was similar in TG mice and non-TG littermate controls. These data are consistent with the notion that expression of the Galphaq(Q>L) transgene in the brain induced primary polydipsia in the TG mice.
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PMID:Galphaq-dependent signaling cascades stimulate water-seeking behavior. 1660 48

This report describes an uncommon clinical case of cystic parathyroid adenocarcinoma. A 17-year-old male Persian cat was presented for evaluation of a ventral cervical mass. The cat was inappetent and showed weight loss, polydipsia and vomiting. Serum biochemistry and urinalysis revealed moderate hypercalcaemia, a mild increase of creatinine, isosthenuria and proteinuria. Sodium dodecyl sulphate-agarose gel electrophoresis showed a mixed tubular proteinuric pattern, in accordance with histological examination that revealed interstitial nephritis and glomerulonephritis. Diagnosis of parathyroid carcinoma was based on histopathological findings.
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PMID:Parathyroid adenocarcinoma in a nephropathic Persian cat. 1665 Oct 17

Parathyroid carcinoma constitutes less than 1 % of primary hyperparathyroidism. The male to female ratio is approximately equal and the mean age at presentation is 40 years. In about half of the patients there is a palpable cervical mass, and serum calcium level is usually above 14 mg/dl. In a case report we present a 21-year-old man with a non-tender, non-mobile bulging mandibular mass. He suffered from fatigue, recent weight loss, hoarseness, polydipsia, polyuria, hematuria, recurrent renal stones and bouts of constipation and diarrhea. A mandibular biopsy confirmed brown tumor. Serum calcium level was 15.4 mg/dl. Cervical ultrasound revealed a hypoecho area suspicious of parathyroid adenoma. Parathyroid carcinoma was later confirmed and en bloc resection was performed. During a two-year follow up there has been no evidence of recurrence or hypercalcemia. This unique case of parathyroid carcinoma in conjunction with brown tumor is the second reported case worldwide.
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PMID:Parathyroid carcinoma: A rare case with mandibular brown tumor. 1677 84

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

Although the clinical symptoms of patients with benign parathyroid adenoma are usually nonspecific and benign, a malignant presentation of the benign disease may sometimes occur. Here, we report a case of a 58-year-old woman who presented with aggravated sacrum pain, general malaise, and polydipsia. Initial laboratory findings revealed hypercalcemia, normocytic anemia, and impaired renal function. Acute hypercalcemic crisis manifested and primary hyperparathyroidism was diagnosed together with myelofibrosis on account of the result of bone marrow biopsy. Excision of a parathyroid adenoma was performed, and the anemia and bone marker regressed later. These findings suggested that benign parathyroid adenoma may mimic the clinical presentation of parathyroid carcinoma, releasing excess parathyroid hormone and resulting in hyperparathyroid crisis. In addition, primary hyperparathyroidism can be associated with anemia and myelofibrosis.
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PMID:Benign parathyroid adenoma presenting with unusual parathyroid crisis, anemia and myelofibrosis. 1749 90


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