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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of acute lymphoblastic leukemia that appeared as hypercalcemia with radiologic osseous abnormalities and back pain is described. Pathophysiologic mechanisms of hypercalcemia and treatment are reviewed. After initial treatment with phenobarbital and saline solutions, followed by specific treatment for the leukemic process, hypercalcemia descended to normal values.
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PMID:[Hypercalcemia in acute lymphoblastic leukemia (author's transl)]. 106 73

A 67-year-old previously well man was admitted with hypercalcemia after a 7-day history of fever, night sweats, and back pain. The blood showed 5% multilobated lymphoid cells. A multilobated non-Hodgkin lymphoma associated with marked reticulin fibrosis was diagnosed on a bone marrow biopsy. During the next 7 days, in the absence of specific therapy, his symptoms disappeared. Three weeks after admission his biochemical abnormalities had resolved and after 9 weeks his bone marrow examination was normal. He remains in clinical and laboratory remission 16 months after presentation.
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PMID:Spontaneous remission of multilobated non-Hodgkin lymphoma. 160 76

A child with acute lymphoblastic leukemia, spinal osteoporosis with vertebral compression fractures, and hypercalcemia appearing early in the course of the hematologic disease was followed for two and a half years. Bone mineral density (BMD), measured by single photon absorptiometry at the radial shaft, was within normal limits for age and sex. However, x-rays of vertebrae and vertebral BMD, measured by dual photon absorptiometry, showed marked demineralization. Despite leukemic remission, the spinal osteoporosis became worse and the patient required aggressive treatment for eight months. Treatment included 50 units of calcitonin subcutaneously every other day, 1,000 mg/day of oral calcium, and 3,000 IU/day of vitamin D. The back pain disappeared quickly, and laboratory controls showed a significant diminution of bone turnover. No new compression fractures occurred. Eighteen months later, the patient continued in remission and menarche had occurred. Dual photon absorptiometry revealed a significant "catch up" of the lumbar spine BMD. X-ray examination showed a marked remodeling of the vertebral bodies. BMD measurements in this child indicate that bone loss affected the trabecular bone compartment or occurred only at active bone marrow sites. The rapid clinical amelioration and objective biochemical, densitometric, and radiologic evidence of bone improvement warrant further clinical trials on similarly affected patients.
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PMID:Vertebral compression fractures at the onset of acute lymphoblastic leukemia in a child. 183 Feb 97

Self-rated psychiatric symptoms were investigated in 30 patients referred for surgery because of primary hyperparathyroidism (HPT) (serum calcium, 2.87 +/- 0.21 mmol/L) in 38 subjects detected in a health screening, with 15 years of mild hypercalcemia and probable HPT (serum calcium, 2.66 +/- 0.09 mmol/L), and in 38 normocalcemic control subjects. The psychiatric symptomatology was evaluated by use of the Hopkins Symptom Checklist (HSCL-56), a self-rating symptom scale. The patients with verified HPT had the highest mean HSCL score, 89.1 +/- 20.1 before surgery, compared with 76.6 +/- 17.0 (p less than 0.01) in the health survey hypercalcemic patients and 73.8 +/- 16.0 (p less than 0.001) in the controls. The factors for anxiety, depression, and cognitive symptoms were the most pronounced in the HPT patients and were also increased among the mildly hypercalcemic persons of the health survey, compared with the controls. Somatic symptoms such as headache, back pain, chest pain, and weakness were equally common in HPT and in the controls, and measurements of isometric muscle strength of knee extension did not demonstrate reduction of muscle strength in the health survey hypercalcemic patients. Follow-up of the HPT patients 1 year after parathyroid surgery revealed a marked improvement in mental health (HSCL score 73.2 +/- 13.7, p less than 0.001). In the health survey hypercalcemic patients, neither the psychiatric symptomatology nor the muscle strength were influenced by 6 months of oral vitamin D therapy (alphacalcidol). The results demonstrate that psychiatric symptoms are experienced frequently by patients with HPT and minimum to moderate increases in the serum calcium level and that these disturbances are reversed by parathyroid surgery.
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PMID:Self-rated psychiatric symptoms in patients operated on because of primary hyperparathyroidism and in patients with long-standing mild hypercalcemia. 291 6

Rhabdomyosarcoma and other small round-cell neoplasms of infancy and childhood frequently involve the bone marrow. An unusual clinical presentation of diffuse bone marrow involvement as the sole manifestation of the disease represents a difficult diagnostic challenge. We report the case of an 18-year-old boy presenting with lower back pain, sternum tenderness, anemia, thrombocytopenia, leukoerythroblastic blood film, hypercalcemia, and renal failure. No solid tumor was found. A diagnosis of rhabdomyoblastic bone marrow metastatic involvement was initially suggested by the morphological picture, and later confirmed by the ultrastructural findings. Hypercalcemia and renal failure were controlled, initially, with furosemide and calcitonin. The patient was treated with intensive chemotherapy, including vincristine, actinomycin D, cyclophosphamide, and doxorubicin. A remission was achieved, lasting 5 months until relapse.
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PMID:Rhabdomyosarcoma presenting with diffuse bone marrow involvement, hypercalcemia and renal failure. 335 35

A 70-year-old woman presented with back pain due to vertebral crush fractures and was found to have hypercalcaemia. Investigation revealed evidence of both primary hyperparathyroidism and Bence Jones myeloma and this was subsequently confirmed at necropsy. This is the first description of a case in which the simultaneous occurrence of both diseases was reliably established. The case illustrates the difficulty in identifying the cause of hypercalcaemia in some patients, and emphasises the need to consider the diagnosis of myeloma in all cases of hypercalcaemia.
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PMID:Hypercalcaemia due to the coexistence of parathyroid adenoma and myelomatosis. 709 95

The development of renal cell neoplasms ranging from adenoma to metastatic carcinoma is the most serious complication of acquired cystic kidney disease (ACKD). A comprehensive review of the pertinent literature shows that there is up to 50-fold increased risk of renal cell carcinoma in ACKD compared to the general population. The ACKD-associated renal cell carcinoma is seen predominantly in males, occurs approximately 20 years earlier than in the general population, and is frequently bilateral (9%) and multicentric (50%). Acquired cystic kidney disease-associated renal cell carcinoma is frequently asymptomatic (86%), but may be associated with bleeding, abrupt changes in hematocrit, fever, and flank pain or rarely with hypoglycemia, hypercalcemia, or metastases at presentation. Computed tomography seems to provide a better diagnostic yield than sonography or magnetic resonance imaging; nevertheless, large (up to 8 cm) tumors not visualized by any imaging techniques have been reported. It is generally agreed that there is a need for regular screening of symptomatic ACKD patients for early detection of renal cell carcinoma; however, whether screening is needed for asymptomatic patients remains controversial. Nephrectomy is indicated for tumors larger than 3 cm. Management for tumors smaller than 3 cm with persistent symptoms, such as back pain or hematuria, remains controversial, but nephrectomy may be recommended since many of these tumors turn out to be unequivocal renal cell carcinoma. Asymptomatic tumors smaller than 3 cm should be serially screened, and tumor enlargement may be an indication for nephrectomy. Acquired cystic kidney disease-associated renal cell carcinoma accounts for approximately 2% of deaths in renal transplant patients. A median length of survival of approximately 14 months and a 5-year survival rate of 35% are comparable to the same data for renal cell carcinoma in the general population. Successful renal transplant probably decreases the risk of renal cell carcinoma in ACKD patients, but this preliminary observation needs confirmation. The development of ACKD-associated renal carcinoma is a continuous process with evolving phenotypic expression, including damaged renal tubule, simple cyst, cyst with atypical lining, adenoma, and, finally, carcinoma. The pathogenesis of this continuous process is not entirely known, but growth factor-induced compensatory growth of tubular epithelium initiated by the changes of end-stage kidney disease, and probably perpetuated by activation of proto-oncogenes, seems to be the most significant factor.
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PMID:Renal neoplasm in acquired cystic kidney disease. 761 Dec 40

Hypercalcemia in adult T-cell leukemia has been attributed to increased levels of 1,25-dihydroxyvitamin D (1,25(OH)2D), whereas in other types of leukemia, hypercalcemia has been blamed on direct skeletal invasion by malignant cells, ectopic parathyroid hormone (PTH) production or bone-resorbing cytokines. A 51-year-old man was studied who presented with back pain, circulating myeloblasts, and hypercalcemia. The bone marrow revealed acute myeloblastic leukemia. While the ionized calcium concentration was 8.17 mg/dL (normal, 4.73 to 5.21 mg/dL), the levels of PTH, PTH-related peptide, vitamin D, and thyroxine were normal or subnormal. Bone histomorphometry showed a decreased cortical width with intracortical erosion cavities dissecting into the marrow space. In cancellous bone, the osteoid area, osteoblast perimeter, and tetracycline fluorescence were sparse, whereas the osteoclast perimeter was increased. Persistent marrow fat, the general absence of trabecular narrowing, and the prompt response to calcitonin suggest that the osteoclasts caused the hypercalcemia and lytic lesions, rather than pressure atrophy or osteolysis by leukemic infiltration. Osteoclast activation and subsequent hypercalcemia may have been due to a locally produced cytokine, such as interleukin-1 beta or tumor necrosis factor.
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PMID:Case report: hypercalcemia in acute myeloblastic leukemia is caused by osteoclast activation. 812 79

This 20 year old man suffered increasingly from multifocal bone- and back pain over the last 6 months. Painful weakness of the left leg with dysesthesia of the 4th and 5th toe, a weight loss of 15 kg and polydipsia and pollakiuria had developed. The clinical workup disclosed hard tumors in the right mandible and tibia, a waddling gait with bilateral sign of Trendelenburg, reduced muscular force in the left leg with missing achilles tendon reflex and a loss of sensibility in the distal S1 segment, epigastric tenderness on pressure and hypertension with a value of 160/100 mmHg. X-rays revealed multiple cystic bone lesions at all sites. Hypercalcemia and massively elevated parathyroid hormone were measured. Since the parathyroids were enlarged on sonography, primary hyperthyroidism with fibrosing osteitis v. Recklinghausen was diagnosed.
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PMID:[Bone pain, polydipsia, polyuria]. 818 45

In patients with multiple myeloma, despite a major reduction of bone pain achieved with chemotherapy, skeletal disease continues to progress. The effects of clodronate, an inhibitor of osteoclastic bone resorption, are evaluated on the natural history of skeletal disease in patients with newly diagnosed multiple myeloma. Within the framework of the VIth MRC Multiple Myeloma Trial, 536 patients (218 women, 318 men) with recently diagnosed multiple myeloma were randomized to receive either clodronate 1600 mg daily (n=264) or an outwardly identical placebo (n=272) in addition to chemotherapy. Treatment with clodronate was associated with a 50% decrease in the proportion of patients with severe hypercalcaemia (5.1% v 10.1%, P=0.06) and a similar reduction in reported non-vertebral fractures (6.8% v 13.2%, P=0.04). Fewer patients receiving clodronate sustained vertebral fractures after entry to the trial (38% v 55%, P=0.01) and patients also lost less height over 3 years compared to those receiving placebo (2.0 v 3.4 cm, P=0.01). Biochemical indices of bone turnover were significantly lower in patients receiving concomitant clodronate, both at plateau and at disease relapse. The frequencies of back pain and poor performance status were significantly lower at 24 months in clodronate than in placebo-treated patients (10.9% v 19.9%, P=0.05, and 18.3% v 30.5% P=0.03 respectively.) There was no statistically significant difference in survival between the clodronate and placebo treated patients. The study indicates that long-term oral clodronate slows the progression of skeletal disease in multiple myeloma and decreases the associated morbidity. Patients without overt skeletal disease at diagnosis were also found to benefit from clodronate, indicating that this treatment should be initiated as early in the course of the disease as possible.
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PMID:A randomized trial of the effect of clodronate on skeletal morbidity in multiple myeloma. MRC Working Party on Leukaemia in Adults. 948 19


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