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)

In a randomized study, 63 postmenopausal patients with advanced breast cancer were treated with ethinyl estradiol (EE2) or the antiestrogen tamoxifen to compare the efficacy and side effects of both drugs. EE2 was always given in combination with chlorothiazide to prevent fluid retention. Pretreatment characteristics of the patients of both groups did not differ significantly. Objective remissions were achieved in 31% of the EE2-treated patients and in 33% of the tamoxifen-treated patients. The median duration of remission was 12 months (range, 5-32) for the EE2 group and 11 months (range, 5-26) for the tamoxifen group (P greater than 0.1), and the estimated median survival times from the start of treatment were 31 and 25 months, respectively (P greater than 0.1). The best treatment results in both groups were obtained in patients with estradiol receptor-positive tumors and less advanced disease. After therapy was stopped, objective withdrawal responses were observed in EE2- but not in tamoxifen-treated patients. Two patients receiving EE2 had to discontinue treatment because of drug-related liver function impairment. Both patients had cholelithiasis. Two patients in the tamoxifen-treated group discontinued therapy because of nausea. Deep venous thrombosis occurred in one patient receiving EE2, whereas two patients receiving tamoxifen developed superficial thrombophlebitis. Other side effects in both groups of patients, including initial hypercalcemia, were mild. It is concluded that both treatment regimens, EE2 or tamoxifen, are equally effective with respect to induction and duration of remission in postmenopausal patients with advanced breast cancer. Side effects of EE2 therapy appeared to be more serious than those of tamoxifen treatment.
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PMID:Tamoxifen versus ethinyl estradiol in the treatment of postmenopausal women with advanced breast cancer. 723 48

A 36-year-old with end-stage renal disease secondary to hypertensive nephrosclerosis had a two-day history of epigastric pain and nausea. Soon after admission, multiple grand mal seizures uncontrolled by intravenous phenytoin sodium and diazepam developed. His calcium level was 14 mg/dL and his amylase level was 2,230 mg/dL; lumbar puncture was normal. Hemodialysis lowered his calcium level to 10.7 mg/dL but failed to control his seizures. Secondary hyperparathyroidism was thought to be the cause of his malignant hypercalcemia, and an emergency subtotal parathyroidectomy was performed. Postoperatively, his grand mal seizures resolved. Confusion and aphasia also developed, but they resolved over the ensuing three weeks. Microscopic examination of the parathyroid glands revealed diffuse chief cell hyperplasia. Preoperative parathormone level was 2,196 pg/dL (normal, less than 450 pg/dL). A review of the literature has failed to reveal a similar case.
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PMID:Secondary hyperparathyroidism manifesting as acute pancreatitis and status epilepticus. 728 72

Hyperparathyroid crisis is a rare disease but should be suspected in acutely ill patients complaining of weakness, lethargy, nausea, vomiting, confusion and abdominal pain. Despite the variety of clinical manifestations, the syndrome forms a distinctive pattern which, in the presence of a serum calcium level greater than 16 mg/100 ml, should be recognized. The most difficult problem in diagnosis is the differentiation of hyperparathyroid crisis from ectopic parathyroid hormone-producing tumors. The disease is an endocrine emergency which requires prompt surgery after rapid correction of dehydration and hypercalcemia. The best results are achieved by removing offending parathyroid tissue within 72 hours after the onset of symptoms.
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PMID:Primary hyperparathyroidism: hyperparathyroid crisis. 730 6

To determine the frequency of gastrointestinal symptoms in primary hyperparathyroidism, we retrospectively analyzed 100 consecutive patients seen at Emory University Hospital from Jan 1, 1977 through March 1, 1979. At the time of diagnosis, 28 patients complained of nausea, 19 of vomiting, 29 of abdominal pain, and 33 of constipation. One patient presented with acute pancreatitis and 14 had ulcer disease (two gastric and 12 duodenal ulcers). Hypercalcemia increases gastric acid secretion and may account for associated ulcer disease and the ulcer-like pain in primary hyperparathyroidism. The mechanisms causing the other gastrointestinal symptoms in hypercalcemia remain to be elucidated. These symptoms abate on correction of hyperparathyroidism.
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PMID:Primary hyperparathyroidism and the gastrointestinal tract. 746 39

A 60-year-old woman was admitted to our hospital complaining of nausea, thirst, and dyspnea on exertion. She had skin eruptions on her back and right knee. Her serum calcium level was 12.6 mg/dl. The chest roentgenogram showed diffuse nodular shadows in both lung fields. The level of angiotensin-converting enzyme in serum was markedly high, and epithelioid cell granulomas were found in the specimens obtained by skin biopsy and by transbronchial lung biopsy. Sarcoidosis was diagnosed. After administration of prednisolone, the serum calcium level decreased to within the normal range and the shadows on the chest roentgenogram resolved. Hypercalcemia complicated with sarcoidosis is caused by overproduction of 1 alpha,25-dihydroxyvitamin D in granulomas. The content of 1 alpha, 25-dihydroxyvitamin D in the transbronchial lung biopsy specimen from this patient was higher than that from a sarcoidosis patient whose serum calcium level was normal. A few case reports of sarcoidosis with hypercalcemia have been published in Japan. The association with HLA type and the possibility of overintake of dietary vitamin D are discussed in reference to hypercalcemia in this patient.
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PMID:[Sarcoidosis with hypercalcemia and increased 1 alpha, 25-dihydroxyvitamin D in lung tissue]. 747 74

Bisphosphonates are analogues of inorganic pyrophosphate, a naturally occurring chemical in bone. In vitro and animal experiments demonstrated that these agents were effective inhibitors of bone resorption. Subsequently they were applied to a variety of clinical problems in which increased bone resorption was an underlying feature of the pathology. In 1971 etidronate became the first bisphosphonate shown to inhibit bone resorption in humans when it was given to patients with Paget's disease. Subsequently this agent was also found to be useful in treating the hypercalcemia of malignancy. At the present time cyclic etidronate therapy is also used for the prevention of bone loss in patients with osteoporosis and for the prevention of heterotopic ossification in spinal cord-injured patients and in patients after hip replacement. Newer bisphosphonates are generally more potent than etidronate and do not produce a severe mineralization defect as do higher doses of etidronate. Pamidronate and clodronate are highly effective in the management of Paget's disease, hypercalcemia due to malignancy and immobilization, metastatic bone disease, and hematologic malignancies affecting bone. They are also promising agents for the prevention of osteoporosis. Alendronate, risedronate, and CGP 42446 are highly potent bisphosphonates that look very promising for the treatment of all disorders of bone resorption. It is fortunate that adverse reactions are not a prominent feature of bisphosphonate use. The main side effects are nausea and abdominal discomfort, mainly with oral use, a transient increase in bone pain in patients with Paget's disease, and an acute-phase reaction (fever, myalgia, mild leukopenia) in patients receiving aminobisphosphonates. The evolution of bisphosphonate therapy should be considered one of the major therapeutic events of the past 25 years. Future research should define the optimum use of these agents.
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PMID:Bisphosphonates in the treatment of disorders of mineral metabolism. 767 Oct 99

Primary hyperparathyroidism is a not uncommon disease in the elderly. A prevalence of 3% for women and 1% for men is reported in subjects aged 65 years and over. Routine serum calcium determination and parathyroid hormone radioimmuno-assay allow to make an early diagnosis in still asymptomatic subjects. In the elderly the clinical features of the disease are often aspecific presenting with psychiatric and/or neuromuscular and/or cardiovascular disorders. This report refers to a 75 year-old woman admitted to our Department with a suspicion of senile dementia. She was affected by loss of memory, hallucinations, nausea, loss of appetite, mild polydipsia and polyuria. The patient was dependent in one activity of daily living (Index of Independence in Activities of Daily Living, ADL) and partially dependent in instrumental activities of daily living (Instrumental Activities of Daily Living Scale, IADL). The Short Portable Mental Status Questionnaire (SPMSQ) and the Geriatric Depression Scale (GDS) showed mild mental impairment and mild depression. Routine biochemical screening revealed a significant hypercalcemia. Parathormon assay and parathyroid scintigram were performed to confirm the diagnosis of primary hyperparathyroidism. After treatment of dehydratation and hypercalcemia, parathyroidectomy was performed: a single parathyroid adenoma was found and removed. On discharge the patient was lucid and able to carry out all ADLs and IADLs.
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PMID:[Neuropsychologic symptoms of primary hyperparathyroidism in the elderly. Report of a clinical case]. 773 70

Five young patients with primary hyperparathyroidism were treated in our hospital. Male to female ratio was 3 to 2 and the mean age was 12.2 years old. Hypercalcemia due to a single adenoma of the parathyroid gland was found in all cases. They showed various clinical symptoms, such as abdominal pain, nausea, convulsions and disturbance of walking. Parathyroid tumors usually could be easily identified with ultrasonography or CT scan or thyroid subtraction scintigraphy. But in two cases parathyroid tumor was not found during operation. Angiography and/or venous sampling were performed and they showed the right localization.
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PMID:[Primary hyperparathyroidism in young patients]. 775 82

The Southwest Oncology Group (SWOG) studied the response rate and toxicity of merbarone (1,000 mg/m2 IV continuous infusion days 1-5, q 21 days) in patients with advanced metastatic renal cell carcinoma. Among 36 eligible patients, there was one partial response for a response rate of 3% (95% C.I. 0.1-15%). There were no mixed responses. There were no treatment related deaths or adverse drug reactions. Significant anemia, diarrhea, and hypercalcemia were observed. Mild to moderate degrees of malaise/fatigue/lethargy, dizziness/vertigo, hyperglycemia, creatinine increase, nausea, vomiting, weight loss, pedal edema, dyspnea, and granulocytopenia were noted. Merbarone does not have significant activity as a single agent in advanced renal cell carcinoma.
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PMID:Phase II evaluation of merbarone in renal cell carcinoma. 786 Feb 33

Malignant tumors are often complicated by hypercalcemia (malignancy associated hypercalcemia: MAHC) which causes various clinical symptoms. Hypercalcemia may occasionally lead to death. Unfortunately, many physicians caring for patients with malignant diseases are not aware of this danger. Hypercalcemia is seen in about 15% of patients with solid tumors. This condition is more frequent in some malignant proliferative hematological diseases. In patients with multiple myeloma, the incidence of hypercalcemia is about 20%. The rate of complication by hypercalcemia is as high as 80% in patients with adult T cell leukemia. The symptoms of hypercalcemia include anorexia, easy fatigability, nausea, and vomiting. These symptoms are often mistaken for adverse effects of anticancer drugs or as signs of aggravation of malignant disease. If abnormal thirst and polydipsia are noted in patients with malignant disease, a diagnosis of MAHC should always be considered because these two symptoms are highly characteristic of hypercalcemia. Caution should be exercised when CNS symptoms such as unstable emotions or somnolence are noted. These symptoms in patients with MAHC may lead to death, if untreated. The corrected serum calcium level should always be monitored in patients with malignant disease, so that a possible diagnosis of MAHC may not be overlooked when these symptoms appear. MAHC is caused by the bone resorption stimulating factor (BRSF), which is produced and secreted by the tumor cells. BRSF may act systemically to cause increased bone resorption, resulting in hypercalcemia. MAHC occurring in this manner is called the 'humoral hypercalcemia of malignancy (HHM)'. BRSF produced by multiple myeloma or bone metastasis enhances bone resorption through local osteolysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hypercalcemia in malignancy]. 796 19


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