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)

53 patients were followed up for an average of 3 years after renal transplantation for evaluation of disturbances in calcium-phosphorus metabolism and skeletal diseases. Postoperative hypercalcemia and hypophosphatemia can be related to persistence of hyperparathyroidism when kidney function is restored. Hypercalcemia was observed in 43% of the patients and lasted less than one year in 80% of cases. Transient hypophosphatemia was present in 15%. These abnormalities did not cause clinical symptoms or deterioration of renal function. However, the skeletal diseases are more impressive and in the first place osteopenia. Bone densitometry revealed decreased bone mineral content in two thirds of the females and one fifth of the males. In females the bone density decreased 3.3% during an average observation period of 7 months, but remained constant in males. Renal osteodystrophy is the main cause of the initial osteopenia. The absence of remineralization or the progression of bone losses is related to the initial persistence of hyperparathyroidism and to corticosteroid treatment. According, 12.5% of the patients presented pathological fractures (spine, hip). In 3 patients (5.7%) with reduced transplant function, osteomalacia without hypophosphatemia was observed. 4 patients (7.5%) had osteonecrosis of the femoral head. There was little progression and surgery was not necessary.
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PMID:[Disturbances of the calcium-phosphorus metabolism and skeletal diseases following kidney transplantation]. 701 May 80

Growth arrest and renal osteodystrophy are major problems in renal insufficiency of children. The present report describes our experiences in managing renal osteodystrophy in 14 dialyzed children using 1,25-DHCC for 12 months. Values in plasma of Ca, P, Mg, alkaline phosphatase, iPTH, 25-OH-D, and 1,25-DHCC were determined regulary. Skeletal X-rays and analysis of iliac crest biopsies were obtained in each child. In treatment with 1,25-DHCC episodes of severe but reversible hypercalcemia occurred. Alkaline phosphatase and iPTH normalized completely. Radiographic examinations revealed marked improvement. Histological signs of fibro-osteoclasia and resorptive defects disappeared but there was no recovery of osteomalacia. A reduction of osteoblast population and of bone transformation was obvious. 1,25-DHCC failed to normalize growth in uremic children. In short, neither vitamin D nor 1,25-DHCC can guarantee complete recovery of renal osteodystrophy and growth arrest in uremic children.
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PMID:[Renal osteodystrophy in children. Therapy with 1,25-dihydroxy-cholechalciferol (author's transl)]. 739 29

It has been widely believed that phosphate deficiency causes osteomalacia. Based on this belief, the rickets of familial hypophosphatemia has been attributed to phosphate deficiency associated with the hypophosphatemia. The present studies on rats have, however, demonstrated significant differences between the effects of phosphate deficiency on bone metabolism and the characteristic features of rickets. Weanling rats, maintained on a mildly phosphate deficient diet, had hypercalcemia and hypophosphatemia, and impairment of body growth, bone growth, and bone mineralization. The maximum effect was observed at 5 wk; between 5 and 20 wk the rats improved despite persistent hypophosphatemia. Histologically, at 5 wk the bone showed thick unmineralized osteoid seams covering most bone surfaces, but the epiphyseal cartilage was normal. In addition, the excess osteoid readily incorporated tetracycline indicating normal mineralization and, based on a new sequential pulse labeling technique, the linear bone apposition rate (LBA) was significantly (p < 0.001) increased above control values. This increase was observed within the initial 4 days of phosphate (P) deficiency and persisted up to 15 wk. This effect of P deficiency on LBA was dependent on vitamin D activity. At 4 wk, the mean LBA was 0.106 +/- 0.003 (1 SE) in control rats, 0.149 +/- 0.008 microns/hr in P deficient rats, 0.083 +/- 0.004 microns/hr in vitamin D deficient rats and 0.086 +/- 0.006 microns/hr in rats deficient in both P and vitamin D. We have reported a similar increase in LBA with parathyroid hormone activity. With vitamin D deficiency, phosphate deficient rats showed all the characteristic features of rickets; disorganization of epiphyseal cartilage, excessive unmineralized osteoid, and reduced mineralization based on the incorporation of tetracycline. We conclude that the effects of phosphate deficiency on bone metabolism more closely resembles the effects of PTH activity than the characteristic effects of osteomalacia and rickets.
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PMID:Differences between the effects of phosphate deficiency and vitamin D deficiency on bone metabolism. 745 66

Secondary (renal) hyperparathyroidism appears in chronic renal failure, sometimes in patients on chronic dialysis. Other causes includes rickets and osteomalacia. These diseases are associated with poor calcium and vitamin D absorbtion from the small bowel. Two patients with chronic renal failure maintained on chronic haemodialysis from two and three years, respectively underwent subtotal parathyroidectomy: removal of three glands and preserving a half of a gland in situ. The diagnosis and surgical indication was made upon clinical (bone pain and severe itching), radiological (demineralisation, ectopic calcifications) and biochemical (hypercalcemia, hyperphosphoremia, increased values of alkaline phosphatases) arguments. Postoperatively the improvement is defined by a return to normal in the clinical, laboratory and radiological parametres. The most appropriate operation for secondary hyperparathyroidism is still unresolved one of two techniques is performed according to the preference of the surgeon: subtotal parathyroidectomy or total parathyroidectomy with autotransplantation of parathyroid fragments into forearm muscle.
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PMID:[Secondary hyperparathyroidism]. 749 11

Controlled studies in 1990-1992 with Danish, Sardinian, and Hongkong-Chinese patients consistently revealed a prevalence of goiter of about 50% in lithium treated patients. This is far beyond the frequency generally assumed for Germany, the whole country still known to be an endemic goiter area. Hypothyroidism as a side effect of lithium occurs in a clearly different group of patients and is much less frequent, the overall incidence being not substantially different from the incidence in the general population. But the risk of becoming hypothyroid as well as hyperparathyroid during lithium prophylaxis is markedly higher in women over 45 years of age, who in the general population are also prone to both endocrine dysfunctions. Lithium is considered to have a provoking role. Lithium is known to be accumulated in the bone and an impact on bone metabolism was shown in animal studies. The data reviewed prohibit the use of lithium during lactation and enforce strict indication in children. In adults the effect of lithium on bone should be considered only in osteomalacia and severe osteoporosis. This review is illustrated by the case of a 60-year-old woman, who after 4 years of successful treatment with lithiumcarbonate because of schizoaffective psychosis, developed a syndrome of hypercalcemia. Exstirpation of a parathyroid adenoma rendered her normocalcemic. Moreover, a pre-existing diffuse goiter had grown to a large nodular goiter within the course of her 5-year treatment. As she finally became paraparetic, she was admitted to our rehabilitation center for the diseases of the spinal cord. Her paraparesis may have been caused not only by the lithium-induced primary HPT, but in part by lithium itself. There are a few reports on lithium causing peripheral neuropathy at toxic levels. A transient deterioration of a pre-existing neuropathy, as in our case study, may have happened at lithium serum levels not far beyond the upper limit of 0.8 mmol/l.
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PMID:[Lithium and its effects on the endocrine system, bones and peripheral nerves--a current review]. 775 53

To investigate whether conventional criteria suffice to differentiate between hyperparathyroid and aluminum (Al)-related bone disease, we obtained bone biopsies from 7 patients with chronic renal failure (CRF) at the time of PTX and 3.5-36 months later. All had hypercalcemia and elevated mid-region parathyroid hormone levels and 3 had bone pain at PTX. Bone histomorphometry revealed that 5 patients had hyperparathyroid bone disease at PTX, while 2 had osteomalacia and skeletal Al deposits. Retrospective determination of intact PTH showed normal levels at PTX in the latter two. PTX effectively reduced all indices of parathyroid hyperactivity, but the two patients with Al-related bone lesions did not improve clinically nor histologically after PTX. Intact PTH and/or bone biopsy prior to PTX could have deterred surgery in those with Al-related bone disease.
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PMID:Chronic renal failure: diagnostic measures before parathyroidectomy. 781 73

Drugs can cause accelerated bone loss as well as disturbances in serum calcium levels. This article focuses on chemically induced bone diseases that commonly affect the elderly and result in either osteoporosis, osteomalacia, hypercalcemia or hypocalcemia. Also discussed are drugs that increase the risk of falls, putting those patients with osteoporosis at a greater risk for future.
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PMID:Drug-induced bone disease. 785 Jun 93

A 65-year-old female patient was admitted with complaining chiefly of lower back pains and arthralgia in the bilateral knee joints of 10-years duration. The serum calcium concentration was normal or only slightly increased, whereas the serum intact PTH and 1,25-dihydroxyvitamin D concentrations were substantially increased. Serum phosphate and 25-hydroxyvitamin D concentrations were decreased. Renal function was normal. Serum alkaline phosphatase activity, the osteocalcin concentration and urinary hydroxyproline excretion were markedly increased. Bone X-ray examination showed severe osteopenia and bone biopsy revealed hyperosteoidosis without tetracycline deposition, consistent with osteomalacia. A parathyroid adenoma was demonstrated by echography and CT-scan. Surgical exploration of the neck revealed a chief cell adenoma behind the right upper pole of the thyroid gland. After parathyroidectomy, all the abnormal biochemical data gradually normalized and the patient has been doing well without any symptoms for the last 13 months. These clinical data suggest that osteomalacia of the patient was probably induced by hypophosphatemia of prolonged duration. When hypercalcemia is not evident in a patient with primary hyperparathyroidism, in whom serum alkaline phosphatase and intact PTH levels are inappropriately increased, osteomalacia should be taken into consideration.
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PMID:A patient with primary hyperparathyroidism associated with osteomalacia: markedly increased serum levels of intact PTH and 1,25-dihydroxyvitamin D with normo- and hypercalcemia. 795 85

This article reports the diagnostic experiences of 134 cases of primary hyperparathyroidism (PHPT) confirmed by operation and pathologic examination. The clinical presentations were divided into 4 types: (1) 75 cases (56.0%) with bone resorption; (2) 47 cases (35.0%) with bone lesions plus urinary calculus; (3) 8 cases (6.0%) with urinary calculus only and; (4) 4 cases (3.0%) with hypercalcemia only. Bone lesions included bone resorption, osteomalacia and osteoporosis. Stones at multiple sites in the urinary tract or nephrocalcinosis were found in 41 cases. The measurement of ionized calcium was much more sensitive and accurate than the total calcium assay with the positive rate of 95.3% and 73.4% respectively. The concentration of plasma iPTH was high in the whole group (n = 84), the mean value was 21.4 +/- 17.9 times higher than that of the normal control group. For the localization of the affected parathyroid gland, instiat examination was by neck ultrasonography which gone a positive predictive value of 81.5% (43/53), 99mTc-MIBI scan showed positive rate 94.1% (16/17). The CT scan of the chest was used when ectopic location in mediastinum was highly suspected. If the first operative exploration failed to find the affected parathyroid gland, we performed the determinations of iPTH with samples taken from internal jugular vein through selective venous catheterization; the coincidence rate was found to be 85.2% (23/27).
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PMID:[The diagnosis of primary hyperparathyroidism--analysis of 134 cases]. 795 61

Vitamin D and its metabolites are well-established regulators of bone mineral homeostasis. Their clearest role is in the prevention and treatment of rickets and osteomalacia, bone diseases characterized by inadequate bone formation, and mineralization. Much of the effectiveness of vitamin D and its active metabolite 1,25(OH)2D in treating such disorders rests with their ability to increase serum levels of calcium and phosphate principally by stimulating intestinal calcium and phosphate absorption. Osteoporosis is not a disease resulting from obvious deficiencies in vitamin D, calcium, and phosphate. More subtle deficiencies, however, may be found, especially among the elderly with decreased intake of dairy products, reduced sunlight exposure, and less efficient intestinal absorption of bone minerals. Such subtle deficiencies may account for the ability of vitamin D and calcium supplementation to have a beneficial effect on bone mineral density in this population. Estrogen administration to postmenopausal females raises 1,25(OH)2D levels, presumably through increased renal production, and this increase is associated with increased intestinal calcium transport. Serum measurements of the vitamin D metabolites in general, however, and 1,25(OH)2D in particular do not consistently show evidence of a decrease at the time of menopause. Although most studies show a fall in intestinal calcium transport with age, which can be reversed with 1,25(OH)2D or estrogen, even these observations have not been found consistently. Thus, some investigators have addressed the issue of tissue resistance to 1,25(OH)2D and have noted decreased VDR in the intestine and reduced 1,25(OH)2D accumulation by bone with age. Despite no obvious deficiency of vitamin D in most patients with osteoporosis, clinical trials with vitamin D or 1,25(OH)2D show promise. Vitamin D treatment will probably prove most efficacious in populations with marginal vitamin D intake and/or limited sunlight exposure; high doses would not be required, and the treatment would be safe. This would be a physiologic and not a pharmacologic use of vitamin D. The use of 1,25(OH)2D for treatment of osteoporosis in individuals with adequate nutrition and sunlight exposure may require somewhat higher than physiologic doses to be effective. Perhaps such doses are necessary to stimulate osteoblast activity and/or differentiation; by raising the serum calcium level, such doses of 1,25(OH)2D might block its otherwise stimulatory effect on osteoclast number and activity. Such doses run the risk of hypercalcemia and hypercalciuria, leading to nephrolithiasis and/or nephrocalcinosis. These undesirable side effects appear to be less common with the use of 1 alpha OHD compared with 1,25(OH)2D, but this may be because of the lower levels of calcium consumption in Japan where 1 alpha OHD is widely prescribed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of vitamin D, its metabolites, and analogs in the management of osteoporosis. 798 88


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