Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent expansion of the use of recombinant growth hormone (GH) to non-GH-deficient patients demands close attention to possible complications in these patients, including the effects on bone. Recent studies on the use of GH in children with chronic renal failure (CRF) provide some early data. In several studies of GH in CRF no significant differences in radiographic osteodystrophy scores, serum calcium, phosphorus or parathyroid hormone (PTH) levels between treated and untreated groups have been found. Alkaline phosphatase increases transiently. The effect of ROD on growth response has not yet been reported. Children with CRF treated with GH should be serially monitored for ROD with serial radiographs and for serum calcium, phosphorus, alkaline phosphatase and PTH levels.
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PMID:Does renal osteodystrophy develop and/or progress during the course of rhGH treatment? 899 35

We conducted this study on 15 chronic haemodialysis patients to evaluate the efficacy of i.v. calcitriol over a 1-year period in the treatment of severe secondary hyperparathyroidism (HPT), in particular its effect on bone mineral density (BMD) and parathyroid gland mass. Mean age was 39 +/- 11.9 (20-65) years and dialysis duration was 58 +/- 3 (19-130) months. i.v. calcitriol was given at a dose of 1 microg post-dialysis 3 times/week for 3 weeks; the dose was then adjusted to maintain the total serum calcium at less than 2.88 mmol/l. The maximum dose was 3 microg 3 times/week. Serum calcium (Ca) and phosphorus (P) were determined prior to treatment, then weekly for 6 weeks and every 2 weeks thereafter. Skeletal survey, dual photon densitometry and parathyroid ultrasound (US) were done prior to treatment and after 1 year. Bone biopsy was done in 10 patients at the beginning of treatment. There was a significant reduction (p < 0.01) in pre-treatment mid-region serum parathyroid hormone (PTH) from 1,476 +/- 895 to 489 +/- 485 P mol/l, as well as alkaline phosphatase (p < 0.04) from 236.5 +/- 221 to 116.3 +/- 49 U/l. This was without a significant increase in serum Ca (2.15 +/- 0.25 to 2.44 +/- 0.26 mmol/l, p = 0.08). Three patients had recurrent hypercalcaemia which responded to reduction of Ca in dialysate. There was a significant increase in BMD over the spine from 1.071 +/- 0.25 to 1.159 +/- 0.22 g/cm2 (p < 0.003) with a percent increase of 9.3 +/- 8.9% as well as over the femoral neck from 0.834 +/- 0.002 to 0.89 +/- 0.09 g/cm2 (p < 0.001) with a percent increase of 7.45 +/- 6.81%. Five patients had enlarged parathyroid glands by US and in 3 of these, there was a significant reduction to normal with treatment. Bone biopsy was done in 10 patients. Six patients had predominant hyperparathyroid bone disease and 4 had mixed uraemic osteodystrophy. In conclusion, long-term i.v. treatment with calcitriol is effective in the treatment of severe secondary HPT. PTH decreased without a significant increase in serum Ca. BMD also increases during this therapy.
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PMID:Long-term effect of intravenous calcitriol on the treatment of severe hyperparathyroidism, parathyroid gland mass and bone mineral density in haemodialysis patients. 909 41

Hepatic osteodystrophy occurs in up to 50% of patients with chronic liver disease (CLD). The aim of this study was to determine the relative contribution of increased resorption and decreased formation to hepatic osteodystrophy by measuring biochemical markers. Twenty-seven patients with advanced CLD (14 female, 13 male) were enrolled. Bone mineral density (BMD), measured at the lumbar spine, and femoral neck, were measured by dual energy X-ray absorptiometry (DXA); bone turnover was assessed using biochemical markers of bone formation and resorption. Based on WHO criteria, osteoporosis and osteopenia were present in 41% and 18% of patients, respectively. All three markers of bone resorption (free deoxypyridinoline, pyridinoline, and hydroxyproline) were increased significantly in patients with CLD. There was a less marked change in the markers of bone formation (osteocalcin, procollagen type 1 peptide, and bone alkaline phosphatase), resulting in a negative uncoupling index in 23/27 (85%) of the patients. Only two (7%) patients had biochemical changes consistent with osteomalacia. The results suggest that increased bone resorption is the predominant cause of hepatic osteodystrophy and therapeutic strategies should be designed to suppress bone resorption, especially in preparation for liver transplantation. Bone biomarkers may be useful alternatives to bone biopsy in evaluating hepatic osteodystrophy.
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PMID:Bone density, vitamin D status, and disordered bone remodeling in end-stage chronic liver disease. 1008 21

Six weimaraner puppies, five of which were genetically related, showed systemic signs associated with hypertrophic osteodystrophy, including fever and involvement of the gastrointestinal, respiratory or nervous systems, in addition to the metaphyseal lesions. In five of the dogs the clinical signs developed less than 10 days after they had been vaccinated with a modified live virus vaccine. Radiographic findings suggested that both the hindlimbs and forelimbs were equally involved in the disease process. Abnormal haematological findings included leucocytosis with neutrophilia and monocytosis, and there was a consistent increase in the activity of alkaline phosphatase. Serum protein electrophoretic studies of three of the dogs revealed hypogammaglobulinaemia and abetaglobulinaemia in two of them. Conservative treatment with rest and non-steroidal anti-inflammatory drugs had little effect, and treatment with corticosteroids appeared to give the best results.
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PMID:Hypertrophic osteodystrophy in six weimaraner puppies associated with systemic signs. 1199 85

TYPE IB PSEUDOHYPOPARATHYROIDISM: Parathormone resistance is the only manifestation of type Ib pseudohyoparathyroidism, the Albright osteodystrophy and multiple hormone resistance described in type Ia are not observed. In type Ib there is a certain preservation of bone sensitivity to parathormone although the main target organ, the kidney, is resistant. Consequently, excessive bone remodeling can be evidenced by X-ray (subperiosteal resorption, fibrocystic osteitis), chemistry (high serum alkaline phosphatase and osteocalcin, and increased urine hydroxyproline), densitometry (lower bone density), and pathology (reduction in trabecular bone volume). The dissociation of the bone and kidney response corresponds to the pseudohypohyperthyroidism described by certain authors. The genetic substratum leading to type Ib pseudohypoparathyroidism remains to be identified. The pathogenic mechanism generally hypothesized concerns a qualitative or quantitative anomaly of the parathormone receptor but seems to be disproved by recent studies. TYPE II PSEUDOHYPOPARATHYROIDISM: Here there is a characteristic lack of a rise in urine phosphorus, signaling parathormone resistance, and stimulated urinary excretion of cyclic AMP, an expression of the integrity of the transmembrane transduction of the parathormone mediated signal and thus protein G and adenylate cyclase. The anomaly could thus involve a transductional effector situated downstream from adenylate cyclase which would explain the symptoms of type II pseudo-hypoparathyroidsm, with both parathormone resistance and Albright osteodystrophy.
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PMID:[Pseudohypoparathyroidism and the concept of hormonal resistance. Types Ib and II]. 1051 73

Controversy exists among various studies in regard to the efficacy of oral (p.o.) versus parenteral calcitriol. Some studies suggest that intravenous (i.v.) calcitriol is superior to p.o. calcitriol for treating renal osteodystrophy in hemodialysis patients; others suggest that these routes of administration are equivalent. To our knowledge, no large, prospective, randomized study compares intraperitoneal (i.p.) to p.o. calcitriol in adult peritoneal dialysis patients. We conducted a prospective randomized study in 76 patients (38 on i.p. calcitriol and 38 on p.o. calcitriol), whom we followed for 48 months. Of the 76 patients, 34 (18 in the i.p. group and 16 in the p.o. group) completed the 48-month study period. Calcitriol dosing was similar in both groups (3-6 micrograms per week in three divided doses). Dose adjustments were made depending on levels of parathyroid hormone (PTH), serum calcium, phosphorus, and calcitriol. No significant difference was seen between the groups in regard to age, sex, race, body mass index, dialysis duration, or cause of ESRD. Neither was any difference in the incidence of peritonitis seen between the groups. In the first 3-6 months, PTH decreased equivalently in both groups. The PTH level remained suppressed in the i.p. group throughout the remainder of the study, but, in the p.o. group, PTH returned to its pretreatment level after 3-6 months. Mean serum calcium was not different in the two groups. In the p.o. group, a considerably higher mean follow-up phosphorus level (6.8 +/- 2.3 mg/dL versus 4.7 +/- 1.4 mg/dL, p = 0.008), PTH level (384 +/- 146 pg/mL versus 162 +/- 64 pg/mL; p = 0.005), and alkaline phosphatase level (178 +/- 37 IU/L versus 72 +/- 21 IU/L, p = 0.02) were seen as compared to the i.p. group. In the i.p. group, resolution of osteodystrophy occurred in all patients at the end of the study; in the p.o. group, 5 patients maintained or developed osteodystrophy by the end of the study (p = 0.016). We conclude that i.p. calcitriol is more effective than pulse p.o. calcitriol in lowering PTH and alkaline phosphatase levels and in resolving renal osteodystrophy, and that i.p. calcitriol is associated with a lower incidence of hyperphosphatemia and elevated Ca x PO4 byproduct.
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PMID:Pulse oral versus pulse intraperitoneal calcitriol: a comparison of efficacy in the treatment of hyperparathyroidism and renal osteodystrophy in peritoneal dialysis patients. 1104 16

The aim of a study was to estimate the renal osteodystrophy status using bone densitometry in relation to selected biochemical parameters of calcium-phosphate metabolism. The study population consisted of 123 patients with end-stage renal disease, including 24 patients treated with continuous ambulatory peritoneal dialysis (CAPD), aged between 22 and 73 years (mean 49.9 years), on dialysis program for mean period of 14.9 months and 99 patients on maintenance hemodialysis for mean period of 58.8 months, aged between 19 and 72 years (mean 46.6 years). Densitometric measurements using DEXA technique were performed in three different skeletal points: distal ends of both radial bones, lumbar spinal region and femoral neck. Concomitantly, serum concentrations of total and ionized calcium, phosphates and parathormone as well as alkaline phosphatase serum activity were measured. Among male patients treated with CAPD significantly higher BMD values in right forearm were found as compared to women treated with this method (0.769 vs. 0.616; p < 0.001). Higher values of BMD were also found in both forearms in whole CAPD population as compared to those on hemodialysis. However, there was no difference in densitometry results between CAPD and HD patients as well as between men and women within these groups, when measured in femoral neck and lumbar spinal region. Among hemodialysis patients higher levels of phosphates and PTH were found as compared to CAPD, doses of drugs used for treatment of osteodystrophy--calcium carbonate, aluminum hydroxide and active vitamin D were also higher in individuals on HD. In addition, in CAPD patients statistically significant, positive correlations were found between BMD value in lumbar spinal area as well as in femoral neck and amount of ingested calcium carbonate, between BMD in lumbar spinal area and aluminum hydroxide dose taken by patients and between BMD in both forearms and dose of active vitamin D. We failed to demonstrate any relationship between obtained densitometric results as well as biochemical markers of calcium-phosphate metabolism and quantitative parameters of dialysis adequacy in both treatment modes. Obtained results let us to conclude that renal osteodystrophy is less advanced in patients treated with peritoneal dialysis, however this may be related only to markedly shorter renal replacement therapy period in this group. Lack of significant abnormalities in densitometry measurements taken in lumbar spinal area and femoral neck, while they are present in forearms, may suggest that the latter point of skeleton may be most useful for identification of bone mass deficiency in dialyzed patients.
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PMID:[Renal osteodystrophy in dialysis patients as estimated by three-point bone densitometry]. 1110 68

The factors contributing to renal osteodystrophy are still incompletely characterized. A variety of cytokines and growth factors appear to have ill-defined roles in this disease. Our aim is to compare osteoblastic cell growth and different osteoblastic markers in vitro with histomorphometric bone parameters and some serum bone-turnover markers in vivo in dialysis patients with either high- (HTBD) or low-turnover (LTBD) bone disease. Six patients were diagnosed to have LTBD, and another five patients, HTBD. Intact parathyroid hormone (PTH) and osteocalcin (OC) levels in serum were greater in patients with HTBD than in those with LTBD. Osteoblastic cells isolated from iliac crest biopsy specimens were grown in culture medium for different times up to 13 days. Osteoblastic cell growth (cell number and area under the cell growth curve) was greater in patients with HTBD than in those with LTBD. Static and dynamic bone formation parameters correlated with serum PTH levels. No correlation was found between PTH and osteoblastic cell proliferation. OC, C-terminal type I procollagen, and alkaline phosphatase osteoblastic secretion in vitro were similar in the HTBD and LTBD groups. However, interleukin-6 (IL-6) secretion was greater in cells isolated from patients with LTBD. Our results indicate that osteoblastic cell growth and osteoblastic IL-6 secretion are related to bone turnover in patients with osteodystrophy. Our findings support the hypothesis that factors other than PTH level might have an important role in affecting osteoblastic function in renal osteodystrophy.
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PMID:Cultures of human osteoblastic cells from dialysis patients: influence of bone turnover rate on in vitro selection of interleukin-6 and osteoblastic cell makers. 1113 64

Despite improvements in medical management parathyroidectomy has an important role in treatment of refractory renal hyperparathyroidism (HPT). The medical records of all patients who underwent parathyroidectomy from 1991 through 2000 were reviewed to determine the clinical and laboratory features and outcomes of treatment in patients with renal versus primary HPT. Twenty-one of 92 patients who underwent parathyroidectomy had renal HPT with a mean age of 47+/-3 years compared with 56+/-2 years for patients with primary HPT (P < 0.05). Clinical manifestations included osteodystrophy (19), pruritus (six), extraosseous calcification (three), and calciphylaxis (one). Parathyroid hormone, phosphorus, and alkaline phosphatase levels and weights of excised glands were higher in renal versus primary HPT (P < 0.05). Supernumerary glands were found in three patients (14%) with renal HPT and none of nine patients with primary parathyroid hyperplasia. After surgical therapy persistent or recurrent HPT occurred in three (14%) patients with renal and one (1.4%) patient with primary HPT (P < 0.05). Postoperative hypocalcemia occurred in 20 (95%) patients with renal HPT all of whom required intravenous calcium, compared with 25 (35%) patients with primary HPT (P < 0.05) of whom only three (4%) required intravenous calcium (P < 0.05). In contrast to those with primary HPT patients with renal HPT are younger and more likely to have severe osteodystrophy, postoperative hypocalcemia, and persistent or recurrent HPT.
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PMID:Refractory renal hyperparathyroidism: clinical features and outcome of surgical therapy. 1130 95

Congenital contractural arachnodactyly (CCA) is caused by mutations in the gene for fibrillin 2 glycoprotein, a component of connective tissue. The causes of osteodystrophy or osteodysplasia in CCA are unknown. We report bone metabolism in a 28 month-old girl with CCA. Serum alkaline phosphatase and osteocalcin levels were 650 IU/l and 22 ng/ml at 1.5 months old (control: 530+/-65, 16.5+/-4.3), and 580 IU/l and 21 ng/ml at 28 months old (control: 465+/-58, 15.0+/-3.5), i.e. in upper-normal levels. The urinary pyridinoline and deoxypyridinoline levels were 1176 and 194 micromol/mol creatinine at 1.5 months old (control: 329+/-76, 63+/-12), and 407 and 111 micromol/mol cr at 28 months old (control: 231+/-49, 50+/-11), apparently higher than the control values. These findings may indicate that abnormal fibrillin may impair bone metabolism and cause the osteodystrophy or osteodysplasia in CCA.
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PMID:Increased urinary excretion of pyridinoline and deoxypyridinoline in a girl with congenital contractural arachnodactyly. 1151 66


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