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 six-month-old, female German shepherd dog was presented because of depression, anorexia, vomiting, polyuria, and polydipsia of approximately 10 days' duration. The puppy was depressed, and pain could be elicited on palpation of both shoulders and hips. The most significant results of serum chemistries and hematology were hypercalcemia; increased blood urea nitrogen, creatinine, and alkaline phosphatase; and leukocytosis with neutrophilia. Thoracic radiographs revealed a large thymic mass, diagnosed on histological examination as a thymic lymphoma. Radiographs of the shoulders revealed destructive bone lesions involving the proximal metaphyses of the humeri, causing slipped epiphyses. Bone lesions were found at necropsy on the proximal and distal aspects of both humeri and femurs. Bone resorption was due to local neoplastic infiltration and presumed humoral factors secreted locally and systemically by neoplastic thymic lymphocytes.
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PMID:Multiple metaphyseal involvement of a thymic lymphoma associated with hypercalcemia in a puppy. 782 Jul 70

109 patients with multiple myeloma were studied. In 35 (32%) of them calcium level was elevated above 2.65 mmol/l and increased significantly with the clinical stage of the disease. A various degree of nitrogen retention, which was not statistically significantly dependent on the clinical stage, was found in 65 (56%) patients. There was a moderate positive correlation (r = +0.46) between the renal failure and Bence Jones proteinuria. In 27 patients, 77% of the hypercalcaemic and 44% of the azotaemic patients, both the calcium level and azotaemia were increased. In the patients with reversible and partially reversible azotaemia the occurrence of hypercalcaemia as well as the absolute values of serum calcium and creatinine showed parallel dynamics after treatment. The progression of calcaemia with the increase of nitrogen retention is a characteristic feature of renal failure in multiple myeloma. Hypercalcaemia and azotaemia are mutually interacting pathogenetic factors and the correction of increased calcium level is a must in modern therapeutic strategies.
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PMID:Hypercalcaemia and azotaemia in multiple myeloma--clinical and biochemical parallels. 786 92

We have attempted to examine the effects of long-term treatment with 1 alpha-hydroxyvitamin D3 (1 alpha-OHD3; 0.5-1.0 microgram/day) on bone and chemical parameters in osteoporosis, retrospectively. Twenty-six pairs of age-, period of observation- and initial bone mineral density-matched patients with or without treatment were selected from 86 patients with osteoporosis. An 11% decrease (-2.2%/year) and a 6% increase in radial mineral density at the peripheral cortical bone site was observed in the control and the treated group after 5 years, respectively (P < 0.05-0.01). There were no patients who showed hypercalcemia nor an abnormally high blood urea nitrogen (BUN) level in both groups. These results indicate that 1 alpha-OHD3 treatment in osteoporosis is effective and has no serious adverse effects. Although the facts were obtained from observations only at the peripheral cortical bone site, 1 alpha-OHD3 treatment may be considered as a potential mode of therapy for osteoporosis.
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PMID:The ultra long-term treatment of senile osteoporosis with 1 alpha-hydroxyvitamin D3. 849 Mar 26

Among plasma cell disorders, solitary plasmacytoma (solitary plasmacytoma of bone, SPB and extramedullary plasmacytoma, EMP) is rare as compared with multiple myeloma (MM). Furthermore, the relationship between solitary plasmacytoma and MM remains unclear. Between 1960 and 1994, 24 patients with SPB and 20 with EMP were treated. The criteria for diagnosis were: (1) no evidence of other lesions based on clinical and radiologic examinations; (2) biopsy evidence of a plasma cell neoplasm; (3) bone marrow biopsy specimen with negative findings (less than 10% plasma cells); (4) no anemia, hypercalcemia or renal involvement. The average follow-up period was 112 months (from 6 to 360 months). Fifty-four percent of patients with SBP and 40% of patients with EMP developed MM, however, there was no significant statistical difference between SPB and EMP (P > 0.05). We suggested that solitary plasmacytomas be classified as two types, latent and aggressive. The former was histologically well-differentiated plasmacytoma. The latter was poorly differentiated tumors which easily progress to MM. The treatment of choice is wide excision or thorough curettage, by cryogenic necrosis with liquid nitrogen or cautery of the bony wall with phenol and the cavity filled with bone grafts or cementation. All patients with apparently isolated plasmacytoma should receive local radiotherapy after operation. Adjuvant chemotherapy should be given if the tumour turns out to be poorly differentiated, in order to delay their progression to MM.
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PMID:[Solitary plasmacytomas of bone and extramedullary plasmacytomas]. 873 11

Nitrogen retention of various intensity was found in 61 patients with multiple myeloma. In seven (11%) of them the disturbances of the depurative renal function manifested as acute renal failure (ARF). The syndrome was characterised in etiologic, pathogenetic, clinical, therapeutic and prognostic aspects. ARF in the study developed on the background of a light chain proteinuria in patients with hypercalcemia, dehydration, radiocontrast studies, blood loss, surgical interventions, and severe infections. Following conservative treatment, the renal function normalized in one patient, a gradual transition to chronic renal failure was observed in five patients, and lethal outcome in one patient. The average survival rate after ARF was 8 months (1-13 months).
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PMID:Acute renal failure in patients with multiple myeloma. 900 62

The alteration in calcium metabolism in rats ingested with saline was investigated. Rats were freely given saline as drinking water for 2 and 7 days. Calcium concentration in the serum was significantly elevated by saline ingestion for 2 and 7 days, while serum inorganic phosphorus concentration was not altered. Serum urea nitrogen concentration was significantly increased by saline ingestion for 7 days. Calcium content in the femoral-diaphyseal and metaphyseal tissues was not altered by saline ingestion for 7 days. Calcium content in the kidney cortex was significantly elevated by saline ingestion for 7 days. Ca2+-ATPase activity in the basolsateral membranes of kidney cortex was clearly increased by saline ingestion for 2 and 7 days. The enzyme activity was not altered by the addition of sodium chloride (10(-3) and 10(-2) M), parathyroid hormone (10(-7) and 10(-6) M), and calcitonin (3 x 10(-8) and 3 x 10(-7) M) in the enzyme reaction mixture. A calcium-binding protein regucalcin mRNA expression in the kidney cortex was markedly suppressed by saline ingestion for 7 days, although such a suppression was not seen for 2 days. These results suggest that saline ingestion causes the disturbance of calcium transport system in the kidney cortex of rats, and that the renal disorder may induce hypercalcemia.
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PMID:Alterations in Ca2+-ATPase activity and calcium-binding protein regucalcin mRNA expression in the kidney cortex of rats with saline ingestion. 914 14

Evaluation of growth hormone therapy in burns is limited and none is reported from developing countries where burns still carry high mortality. We analysed serial observations on the clinical and biochemical profiles in 13 patients with second and third degree burns who received recombinant human growth hormone (rhGH) (0.5 IU/kg body wt) for 2 weeks in addition to standard conservative treatment and in 9 patients who were managed with standard conservative treatment only. The two groups of patients had burns, comparable in extent and severity. Additional rhGH treatment resulted in improved wound healing (p < 0.001), delayed separation of eschars (p < 0.01), increase in haemoglobin (p < 0.05), serum albumin (p < 0.01), calcium (p < 0.05), phosphorus (p < 0.001), glomerular filtration rate (p < 0.05) and 7 fold elevation in IGF-1. Also, a reduction in weight loss (p < 0.01), nitrogen production rate (p < 0.05), catabolic index (p < 0.01), duration of sepsis (p < 0.01) and hospital stay by 40% (p < 0.01) was noted with rhGH therapy. Transient hypercalcemia (3 patients), albuminuria (2 patients) and elevated blood glucose (one patient) were noted in the rhGH treated group not necessitating any specific therapy. Mortality in rhGH treatment group was 8.3% compared to 44.5% in the "no rhGH" treatment group. These observations suggest significant benefits of short term rhGH treatment in burn patients on conservative management.
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PMID:Effect of growth hormone therapy in burn patients on conservative treatment. 991 74

We have shown previously that chronic hyperchloremic metabolic acidosis (CMA) induces severe negative nitrogen balance and renal phosphate depletion and decreases serum insulin-like growth factor-1 (IGF-1) in association with growth hormone (GH) insensitivity in humans. The present study investigated whether acidosis-induced renal nitrogen wasting and renal phosphate depletion are mediated by GH insensitivity/low IGF-1 and thereby responsive to GH treatment. The effects of GH on acidosis-induced changes in divalent cation metabolism and acidosis-induced hypothyroidism were also investigated. CMA (delta[HCO3], -10.5 mmol/L) was induced in six healthy male subjects ingesting 4.2 mmol NH4Cl/kg body weight [BW]/d for 7 days. Recombinant human GH (0.1 U/kg BW/12 h subcutaneously) was administered for 7 days while acid feeding was continued. GH increased serum IGF-1 from 22.1 +/- 1.4 to 87 +/- 8.4 nmol/L (control level, 36.4 +/- 2.2). GH decreased urinary nitrogen excretion, resulting in a cumulative nitrogen retention of 2,404 mmol, thereby correcting the acidosis-induced cumulative increase in nitrogen excretion (2,506 mmol) despite continued acid feeding. GH attenuated the acidosis-induced hyperphosphaturia (cumulative phosphate retention, 91 mmol) and corrected the hypophosphatemia. GH did not affect acidosis-induced ionized hypercalcemia, but further exacerbated acidosis-induced hypercalciuria (cumulative loss, 27.3 mmol). GH significantly further increased serum 1,25-dihydroxyvitamin D (1,25(OH)2D) and further decreased intact PTH (from 10 +/- 1 to 6 +/- 1 pg/mL). Acidosis also induced hypomagnesemia and hypermagnesuria (cumulative loss, 9.4 mmol, ie, renal magnesium wasting), a novel finding, which was significantly attenuated by GH (cumulative retention, 5.0 mmol). In conclusion, GH corrected acidosis-induced renal nitrogen wasting, which may be caused, at least in part, by decreased IGF-1 levels. GH further increased serum 1,25(OH)2D and the systemic calcium load, which account for the suppression of parathyroid hormone (PTH) despite renal PO4 retention and correction of hypophosphatemia. GH attenuated acidosis-induced renal magnesium wasting.
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PMID:Growth hormone corrects acidosis-induced renal nitrogen wasting and renal phosphate depletion and attenuates renal magnesium wasting in humans. 1038 Nov 52

The bisphosphonates are the treatment of choice in hypercalcaemia of malignancy. However, plicamycin (mithramycin) an calcitonin treatment may still be of value should bisphophonate treatment fail, and gallium nitrate has recently been introduced as an alternative therapy. We analysed the tolerability of different treatments based on articles identified in a Medline search covering the period 1979 through September 1998. Articles were included if they met two criteria: (i) quantitative assessment of adverse effects; (ii) inclusion of > or = 10 patients. Although bisphosphonates are generally well tolerated, elevation of serum creatinine level, nausea/vomiting and fever have been reported following their application. Patients receiving etidronate (n = 268) or clodronate (n = 127) more frequently experienced creatinine elevation (8 and 5%, respectively) than did patients receiving pamidronate (n = 424; 2%), aledronate (n = 79; 0%), or ibandronate (n = 203; <1%). The difference in the frequency of reported creatinine level elevations reached statistical significance only for etidronate (z-test: p < 0.001 versus pamidronate; p < 0.02 versus alendronate; p < 0.001 versus ibandronate). With regard to the frequency of creatinine level elevations, clodronate treatment did not differ significantly from treatment with pamidronate, alendronate and ibandronate. An exception among the bisphosphonates is tiludronate, which has been reported on s a treatment of hypercalcaemia in only 1 study (n = 19) resulting in 1 case of lethal and 1 case of manageable acute renal failure. Nausea and vomiting are rare adverse effects of bisphosphonate treatment but seem to be more frequent with first generation drugs: etidronate (8%) and clodronate (7%) versus pamidronate (2%) [p < 0.001 and 0.009, respectively] and versus ibandronate (<1%) [p< 0.002 and 0.02, respectively]. Bisphosphonates containing a nitrogen atom were associated with an acute phase reaction leading to reported fever in 16% of pamidronate, 20% of aledronate, and 11% of ibandronate-treated patients. The most frequently reported adverse effects of treatment with the cytostatic drug plicamycin were hepatotoxicity (26%), nausea/vomiting (23%), and serum creatinine level elevation (5%). Furthermore. plicamycin application was associated with bone marrow suppression and a bleeding tendency due to abnormalities in multiple clotting factors and platelet dysfunction. The use of calcitonin is limited more by the short duration of its therapeutic effect than by toxicities (most frequent: nausea/vomiting in 16% of treated cases). The few publications on gallium nitrate in the treatment of hypercalcaemia of malignancy characterise it as an efficient drug, which is, however, associated with a higher frequency of renal toxicity (10%) and of nausea and vomiting (14%) than are the bisphosphonates.
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PMID:Comparative tolerability of drug therapies for hypercalcaemia of malignancy. 1055 53

A retrospective study was conducted to characterize the diseases, clinical findings, and clinicopathologic and ultrasonographic findings associated with hypercalcemia (serum calcium concentration >11 mg/dL) in 71 cats presented to North Carolina State University Veterinary Teaching Hospital. The 3 most common diagnoses were neoplasia (n = 21), renal failure (n = 18), and urolithiasis (n = 11). Primary hyperparathyroidism was diagnosed in 4 cats. Lymphoma and squamous cell carcinoma were the most frequently diagnosed tumors. Calcium oxalate uroliths were diagnosed in 8 of 11 cats with urolithiasis. Cats with neoplasia had a higher serum calcium concentration (13.5 +/- 2.5 mg/dL) than cats with renal failure or urolithiasis and renal failure (11.5 +/- 0.4 mg/dL; P < .03). Serum phosphorus concentration was higher in cats with renal failure than in cats with neoplasia (P < .004). Despite the fact that the majority of cats with uroliths were azotemic, their serum urea nitrogen and creatinine concentrations and urine specific gravity differed from that of cats with renal failure. Additional studies are warranted to determine the underlying disease mechanism in the cats we identified with hypercalcemia and urolithiasis. We also identified a small number of cats with diseases that are not commonly reported with hypercalcemia. Further studies are needed to determine whether an association exists between these diseases and hypercalcemia, as well as to characterize the underlying pathophysiologic mechanism for each disease process.
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PMID:Hypercalcemia in cats: a retrospective study of 71 cases (1991-1997). 1077 91


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