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 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

Secondary hyperparathyroidism is found in a large proportion, but not all patients on dialysis. Calcitriol controls moderate hyperparathyroidism in most patients but only in a proportion of those with advanced hyperparathyroidism. Patients with nodular parathyroid hyperplasia respond less frequently, presumably because of monoclonal growth and diminished calcitriol-receptor expression by parathyroid cells. In patients with nodular parathyroid hyperplasia, parathyroidectomy is an important alternative to calcitriol treatment. A priori reasoning indicates that prophylactic administration of calcitriol (to prevent parathyroid hyperplasia) is a reasonable option, but currently no controlled evidence for long-term efficacy of this approach without side effects is available. Intermittent administration of calcitriol by intravenous or oral routes is effective and, at least in experimental studies, superior to continuous calcitriol. However, in clinical comparisons, no superiority of intravenous versus oral or daily versus intermittent calcitriol has been documented. Calcitriol treatment must be closely supervised to prevent hypercalcemia, hyperphosphatemia, and excessive suppression of parathyroid hormone. Because of an altered dose response relationship, parathyroid hormone levels should not be completely normalized so as to prevent low bone turnover (adynamic bone lesion).
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PMID:Vitamin D therapy in patients receiving dialysis. 761 32

Secondary hyperparathyroidism (2'HPT) improves after renal transplantation (RTx) along with recovered function of the renal allograft. However, normal renal function does not last long due to rejection, drug-induced nephrotoxic nepthropathy, or recurrence of post-transplant glomerulonephritis. Therefore, improved calcium and phosphate metabolism, and parathyroid function after RTx fluctuate in accordance with the function of the renal allograft. In cases with severe 2'HPT, parathyroidectomy should be performed before RTx because hypercalcemia due to secondary or tertiary hyperparathyroidism aggravates the renal allograft function. In the follow-up of mild 2'HPT after RTx, hypercalcemia and vascular calcification should be monitored carefully by serum parathyroid hormone, calcium and phosphate concentrations, alkaline phosphatase activity, and bone X-ray film. If serum calcium level exceeds 12 mg/dl, parathyroidectomy (PTx) should be performed to prevent the acceleration of vascular calcification. Total PTx with forearm allograft is a preferred surgical procedure for 2'HPT even after RTx.
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PMID:Renal transplantation and secondary hyperparathyroidism. 908 65

Secondary hyperparathyroidism is a common feature of chronic renal failure and vitamin D deficiency plays an important role in the development of this abnormality. Several therapeutical calcitriol schedules have been used in treating uremic hyperparathyroidism but recently oral boluses have been proposed as more effective. In this study we compare the efficacy of three different oral calcitriol regimens in suppressing iPTH secretion in predialytic chronic renal failure. Sixteen (16) patients (mean age 51 +/- 16 years; creatinine clearance 22.9 +/- 9.8 ml; range 8-32 ml/min) were treated in a cross-over randomized design with oral daily calcitriol 0.5 micrograms/die (Treatment A), three oral boluses of 2 micrograms of calcitriol a week (Treatment B) and a single oral bolus of 2 micrograms of calcitriol a week (Treatment C). All treatment periods lasted three months and were followed by a wash-out period of one month. Serum iPTH (Allegro Nichols), 1-25 vitamin D (IRMA-MAB), total and ionized calcium (Nova 8 Pabish), serum phosphate, alkaline phosphatase and creatinine clearance were measured every two weeks. Serum iPTH was also determined in a control group of fifteen (15) patients (mean age 47 +/- 12 years, creatinine clearances of 21 +/-12 ml/min) observed for three months without calcitriol treatment. Daily oral intake of 0.5 micrograms of calcitriol prevents an increase of iPTH without causing hypercalcemia, but only oral boluses (B and C) decreased iPTH: from 270 +/- 169 pg/ml to 135 +/- 76 pg/ml (p < 0.01; B) and to 165 +/- 121 pg/ml (p < 0.05; C). Serum iPTH increased from 293 +/- 121 to 323 +/- 129 pg/ml (p = n.s.). No significant differences in renal function were observed during the different study periods. Our results confirm the good efficacy of multiple calcitriol oral boluses but also suggest for the first time a single weekly bolus as a reliable approach to the treatment of secondary hyperparathyroidism in pre-dialytic renal failure.
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PMID:Calcitriol oral therapy for the prevention of secondary hyperparathyroidism in patients with predialytic renal failure. 958 56

Secondary hyperparathyroidism contributes to significant morbidity in patients with chronic renal failure. The treatment of this disorder with vitamin D compounds, such as calcitriol, although effective at suppressing parathyroid hormone (PTH) secretion, may promote the development of hypercalcemia and hyperphosphatemia, thus increasing the risk for metastatic calcification. A new vitamin D analogue, 19-nor-1alpha,25-(OH)2D2 (paricalcitol; Zemplar, Abbott Laboratories, Inc, Chicago, IL) has recently been developed for the treatment of secondary hyperparathyroidism, and, in experimental animals, it was found to be less calcemic and phosphatemic than calcitriol. In double-blind clinical trials, paricalcitol effectively decreased the levels of PTH by 60%, yet the mean serum calcium values remained within the normal range. The few episodes of hypercalcemia that occurred in the paricalcitol-treated patients (8 of 400 determinations > or =11.0 mg/dL in 7 patients) were associated with marked decreases in PTH levels (87% +/- 2% less than baseline) and absolute values of PTH less than 100 pg/mL in four of the seven patients. PTH values less than 100 pg/mL, however, occurred in 15 patients, but were not invariably associated with frank hypercalcemia, although serum calcium levels increased to 10.63 +/- 0.3 mg/dL, slightly greater than the upper limits of normal. Additional studies to evaluate the conversion from calcitriol to paricalcitol therapy showed that a dose ratio of 1:4 (calcitriol:paricalcitol) could maintain control of high levels of PTH without significant alterations in serum calcium and phosphorus levels. These studies indicate that effective control of hyperparathyroidism can be achieved with paricalcitol therapy with minimal perturbation of serum calcium and phosphorus levels, and may have a therapeutic advantage over current treatment strategies.
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PMID:Therapy of secondary hyperparathyroidism with 19-nor-1alpha,25-dihydroxyvitamin D2. 980 45

Secondary hyperparathyroidism complicating chronic kidney disease requires therapy to minimize the effects of parathyroid hormone (PTH) on bone and other tissues. Low levels of calcitriol in blood play a major role in the initiation and maintenance of hyperparathyroidism. Accordingly, administration of calcitriol has been demonstrated to be an effective form of therapy. While this therapy is effective in controlling hyperparathyroidism, side effects of calcitriol, including increased intestinal absorption of calcium and phosphate, often complicate therapy by giving rise to hypercalcemia and hyperphosphatemia, which may be important risk factors for extraskeletal calcifications. Over the last several years, interest has turned toward vitamin D analogs, which may be able to affect parathyroid function with lesser effects on calcium and phosphorus in serum, and thereby, minimizing the undesirable toxicities of vitamin D therapy. Two vitamin D analogs are available in this country for the control of hyperparathyroidism in the setting of advanced kidney disease, and include 19-nor-1,25-dihydroxyvitamin D(2) (paricalcitol), and more recently, 1-alpha-hydroxyvitamin D(2) (doxercalciferol). 19-nor-1,25-dihydroxyvitamin D(2) is widely used and was evaluated extensively in animals, revealing that this vitamin D sterol had a selective effect on increasing PTH suppression, with lesser effects on calcium and phosphorus metabolism. These studies lead to clinical trials which showed the efficacy of this therapy in that PTH could be lowered satisfactorily in patients with calcium and phosphorus values within the normal range. The selectivity of 19-nor-1,25-dihydroxyvitamin D(2) seen in animals has also been found in humans, such that therapy with this sterol can achieve control of hyperparathyroidism with a wider therapeutic window than the predecessor, calcitriol. 1-alpha-hydroxyvitamin D(2) has recently been introduced, but in contrast to paracalcitol, there is little reason to believe that there is any selectivity in its actions in terms of suppressing PTH, compared with its ability to raise serum calcium or phosphorus in serum. However, this vitamin D sterol can effectively decrease PTH levels in patients with advanced renal failure. Comparative studies of paricalcitol and doxercalciferol have not been undertaken at the present time. Further studies on the mechanism of actions might explain the differences between these sterols and their effects on the intestinal absorption of calcium and phosphate. At the present, the use of vitamin D analogs can achieve control of hyperparathyroidism with a wider therapeutic window than the native sterol, calcitriol.
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PMID:Vitamin D analogues for the management of secondary hyperparathyroidism. 1168 85

Secondary hyperparathyroidism (2HPT), a common disorder in patients with chronic renal failure, develops in response to phosphate retention and low serum 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3), calcitriol). Replacement therapy with calcitriol or its precursor 1alpha-hydroxyvitamin D(3) (1alphaOHD(3), alfacalcidol) often produces hypercalcaemia, especially when combined with calcium-based phosphate binders. In addition, these vitamin D compounds can aggravate the hyperphosphataemia in these patients. Several vitamin D analogues have been developed that retain the direct suppressive action of 1,25(OH)(2)D(3) on the parathyroid glands but have less calcaemic activity, thereby offering a safer and more effective means of controlling 2HPT. 1,25-Dihydroxy-19-norvitamin D(2) (19-norD(2)) and 1alpha-hydroxyvitamin D(2) (1alphaOHD(2)) are available in the US and 1,25-dihydroxy-22-oxavitamin D(3) (22-oxacalcitriol, OCT) and 1,25-dihydroxy-26,26,26,27,27,27-hexafluorovitamin D(3) (1,25(OH)(2)26,27F6 D(3), falecalcitriol) have been approved for use in Japan. Animal studies have demonstrated that OCT and 19-norD(2) have a wider therapeutic window for suppression of parathyroid hormone (PTH) because of their lower calcaemic and phosphataemic activities. The low calcaemic activity of OCT has been attributed to its rapid clearance, which prevents sustained effects on intestinal calcium absorption and bone resorption, but still allows a prolonged suppression of PTH gene expression and parathyroid cell growth. The calcaemic activity of 19-norD(2) diminishes with the duration of treatment by as yet unknown mechanisms. The lower toxicity of 1alphaOHD(2), compared with 1alphaOHD(3), has also been noted with chronic, but not acute administration, perhaps due to differential metabolism. The unique actions of falecalcitriol may also result from an altered metabolism. A clear understanding of the molecular basis for the selectivity of vitamin D analogues on parathyroid function may allow the design of even more effective analogues.
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PMID:Vitamin D analogues for secondary hyperparathyroidism. 1238 64

Secondary hyperparathyroidism (2HPT) is characterized by an abnormal threshold for suppression of parathyroid hormone (PTH) secretion by serum ionized Ca (ICa). It is therefore critical to examine the threshold of PTH secretion in chronic renal failure patients in relation to the physiopathological conditions and the severity of 2HPT. The effect of 1,25-dihidroxy-22-oxavitamin D(3) (22-oxacalcitriol, OCT) on parathyroid gland function was investigated in six haemodialysis patients with 2HPT. OCT was administered three times a week for 26 consecutive weeks. The maximum serum PTH (PTHmax), the minimum serum PTH (PTHmin), and ICa concentration required to inhibit 50% of PTHmax were estimated based on the model formula of the sigmoid curve describing the relationship between ICa and intact-PTH levels. The sigmoid ICa-PTH curves displayed a downward shift at 12 and 26 weeks of OCT treatment. Parathyroid gland function, as reflected by both PTHmax and PTHmin, decreased over time. A steep slope was found at 12 and 26 weeks, compared with that at the start of OCT treatment. There were no marked changes in the set point of calcium. Hypercalcaemia and elevated creatine phosphokinase, probably due to OCT therapy, were observed during the study period. In view of the findings that the sigmoid ICa-PTH curve displayed a downward shift, that both PTHmax and PTHmin decreased, and that functional mass of the parathyroid gland was reduced, OCT appears to be useful in ameliorating parathyroid gland function, contributing to the management of 2HPT.
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PMID:Effects of 1,25-dihydroxy-22-oxavitamin D(3) on parathyroid gland function in haemodialysis patients with secondary hyperparathyroidism. 1238 65

Secondary hyperparathyroidism is a major complication in uremic patients undergoing dialysis. Various active metabolites of vitamin D are used as oral treatment; however, in some patients, parathyroid hormone (PTH) is not ideally suppressed. Intravenous injection of an active form of vitamin D inhibits PTH more effectively than does oral administration. However, intravenous administration is often restricted by the complication of hypercalcemia. In the calcitriol analog 22-oxacalcitriol (OCT), the 22nd carbon atom is replaced by oxygen. The OCT analog has been reported to have a lesser hypercalcemic effect than does calcitriol. The present study was planned to determine whether intraperitoneal administration of OCT would be a more effective treatment of secondary hyperparathyroidism than intravenous administration is in CAPD patients who manage themselves at home. The results showed that OCT is stable in dialysis solution and that its intraperitoneal administration was effective for suppressing PTH in patients with secondary hyperparathyroidism.
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PMID:The effect of intraperitoneal 22-oxacalcitriol on secondary hyperparathyroidism in continuous ambulatory peritoneal dialysis patients (IPOX study). 1476 68

Although secondary hyperparathyroidism is improved by pharmacological therapy; 10-30% of patients with chronic renal failure undergo parathyroidectomy. The authors report on their experience with 66 cases of secondary hyperparathyroidism surgically treated over the period from January 1991 to December 2002. The surgical indications included: persistent hypercalcaemia, osteodystrophy with bone fractures, joint pain, itching and ectopic calcifications. The median preoperative parathyroid hormone level was 400 pg/ml. The operations performed were: subtotal parathyroidectomy (PTX 7/8) in 43 cases; total parathyroidectomy with autotransplantation (PTXt + At) in 13 cases; total parathyroidectomy (PTXt) alone in 6 cases and incomplete parathyroidectomy (PTXi) in 4 cases. The immediate results were satisfactory in each group. Calcium levels reverted to normal 24-48 hours postoperatively in 37 patients with PTX 7/8, in 11 patients with PTXt + At, in 5 patients with PTXt; 4 patients with PTXi showed a reduction, but no normalization, of calcium levels. Almost all patients, except those undergoing PTXi, showed an acceptable reduction in PTH levels in 25-35 days. Secondary hyperparathyroidism relapsed in 3 cases with PTXt + At and in 2 cases with PTX 7/8, while it proved persistent in 50% of patients with PTXi and in 7% of patients with PTX 7/8. Patients with PTXt mainly showed a substantial reduction of calcium levels. Parathyroidectomy is indispensable for the treatment of secondary hyper-parathyroidism. In our opinion, PTX 7/8 is the surgical treatment of choice because it is the easiest technique to perform and has the lowest relapse rate.
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PMID:[Indications and efficacy of parathyroidectomy in the treatment of secondary hyperparathyroidism in patients with chronic renal failure: our experience]. 1503 47


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