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)

Twenty diabetics with end-stage renal disease who had never previously received dialysis treatment were treated with continuous ambulatory peritoneal dialysis for periods of two to 36 months (average, 14.5). Intraperitoneal administration of insulin achieved good control of blood sugar. Even though creatinine clearance decreased significantly (P = 0.001), control of blood urea nitrogen and serum creatinine was adequate. Hemoglobin and serum albumin levels increased significantly (P = 0.005 and 0.04, respectively). Similarly, there was a significant increase in serum triglycerides and alkaline phosphatase (P = 0.02 and 0.05). Blood pressure became normal without medications in all but one of the patients. Retinopathy, neuropathy, and osteodystrophy remained unchanged. Peritonitis developed once in every 20.6 patient-months--a rate similar to that observed in nondiabetics. The calculated survival rate was 93 per cent at one year; the calculated rate of continuation on ambulatory peritoneal dialysis was 87 per cent. We conclude that continuous ambulatory dialysis with intraperitoneal administration of insulin is a good alternative treatment for diabetics with end-stage renal disease.
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PMID:Continuous ambulatory peritoneal dialysis in diabetics with end-stage renal disease. 703 45

Osteosclerosis, an increased volume of trabecular bone, is a common but often misinterpreted feature of uremic osteodystrophy. Despite the apparent radiographic density of osteosclerotic bone, pain and fracture may be associated. If accumulated osteoid and woven bone exceed the volume of lamellar bone removed in chronic renal insufficiency, bone density may be reduced despite increased trabecular volume. Concomitant histomorphometric and photon absorption determinations of transileal bone biopsies were done to investigate the relationship between quantity and quality of bone in uremic and non-uremic osteopenic patients. In osteopenic patients with uremia, bone core density had no significant relationship to trabecular bone volume or mineralized bone volume whereas in non-uremic osteopenic patients, these parameters were directly related (r = 0.867 and r = 0.921, respectively, p less than 0.001). The bone core density in the uremic patients was negatively correlated with the total osteoid volume (r = -0.764, p less than 0.05) and positively related to the serum phosphorus concentration (r = 0.739, p less than 0.05). Serum levels of immunoreactive parathyroid hormone (iPTH) and alkaline phosphatase activity were higher in the patients with radiographic osteosclerosis than in the other uremic patients. The lack of correlation between bone volume and density indicates a qualitative defect in uremic bone. It appears that in uremia, elevated iPTH and serum phosphorus levels may augment bone formation, albeit poorly mineralized with woven architecture. While radiographic density paradoxically increases, the amount of normally mineralized bone may be reduced.
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PMID:Qualitative bone defect in uremic osteosclerosis. 709 50

Calcium (Ca) metabolism was compared in 2 groups of patients with chronic interstitial nephritis: in 21 patients (AAN-group) nephropathy was due to exposure for 5 to 50 years (mean 21.1) to phenacetin containing analgesics, whereas in 21 other patients (controls) it was due to exposure for 1 to 80 years (mean 21.4) (NS) to other causes. Patients were followed for 2.5 +/- 0.6 and 1.6 +/- 0.6 years respectively (mean +/- SEM) (NS). Blood Ca, P, protein, creatinine, alkaline phosphatase, parathyroid hormone (PTH), 25-hydroxyvitamin D (25-OH-D), together with arterial acid-base status and urinary excretion rate of Ca, P and creatinine were measured serially. For each patient the results were averaged for 2 degrees of renal failure, i.e. for creatinine levels below and above 400 mumol/l (logarithmic mean). Results were included only when P was maintained between 0.7 and 1.9 mmol/l. The range of creatinine levels studied was 95 to 1600 mumol/l. No differences were found between the 2 groups with respect to creatinine clearance, blood, P, protein, arterial pH and urinary excretion rates of Ca and P. There was a trend for blood HCO3 to be lower in the AAN group. Mean plasma Ca was significantly lower, and PTH was significantly higher, in the AAN than in the control group at both degrees of renal failure; mean plasma alkaline phosphatase activity was also significantly higher in the AAN group, but at severe degrees of renal failure only. Significant correlations were observed between individual values of both Ca and PTH (r = -0.747) and PTH and alkaline phosphatase (r = 0.603). The degree of hypocalcemia and of hyperparathyroidism was not related to the plasma level of 25-OH-D. It is concluded that at comparable degrees and duration of renal failure patients with AAN, when compared with patients with interstitial nephritis of other origins, have lower blood Ca and consequently higher PTH levels and alkaline phosphatase activities, suggesting more severe osteodystrophy.
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PMID:[Particularly severe calcium metabolic disorder in nephropathy from analgesic abuse]. 717 76

Renal osteodystrophy, a frequent complication of chronic renal failure, is usually assessed by periodic X-rays of bone which are both poorly reproducible and expensive. Seeking a better screening test for osteodystrophy, we evaluated the usefulness of serum alkaline phosphatase as a predictor of bone disease and of hyperparathyroidism. Alkaline phosphatase, despite nonspecificity, correlates with the severity of osteodystrophy and with the increase in serum parathyroid hormone concentration. Serial measurements of alkaline phosphatase can predict changes in these parameters.
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PMID:Prediction of radiographic severity of renal osteodystrophy by serum values. 723 40

Congenital erythropoietic porphyria (CEP) is a rare disorder of heme biosynthesis. Skeletal abnormalities have been described in patients with this disease. We report a 25-year-old woman with osteodystrophy from CEP. On examination, mild hepatosplenomegaly, multiple hyperpigmented scars, hypertrichosis, erythrodontia and red coloration of urine were found. Biochemical studies showed increased serum levels of alkaline phosphatase, fasting and total 24-h urinary calcium excretion. Serum 250H vitamin-D concentration was low due to avoidance of sun exposure. Skeletal radiographs disclosed marked vertical and horizontal trabecular pattern and biconcavity of most of the dorsal and lumbar vertebral bodies. Several round sclerotic lesions (1-3 cm in diameter) were seen in the skull, pelvis and one lumbar vertebrae. The sclerotic lesions were augmented in size and number compared to X-rays obtained 8 years before. Bone mineral density (evaluated by DEXA) was markedly reduced at the spine and moderately diminished at the proximal femur and total skeleton. Treatment for 11 months with pamidronate (and the addition of hydrochlorotiazide for the last 6 months) reduced to normal values the serum levels of alkaline phosphatase and fasting urinary calcium. The 24-h urinary excretion of calcium and hydroxyproline were also decreased. The BMD increased in all the skeletal areas with presumably hyperactive bone marrow: spine, head, ribs and pelvis (and total skeleton), but did not change at the extremities and diminished at the femoral neck. Patients with CEP may present osteodystrophy characterized by sclerotic lesions and osteopenia, most likely due to accelerated bone turnover in areas of active bone marrow.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Congenital erythropoietic porphyria: skeletal manifestations and effect of pamidronate treatment. 802 43

This is a retrospective, clinical study evaluating the long-term outcome of subtotal parathyroidectomy (PTX) in 60 patients with chronic renal failure and severe secondary hyperparathyroidism. Patients were 41 +/- 2 years old (mean +/- SE) at the time of PTX, and followed for 69 +/- 6 months since the procedure. At the time of PTX, three patients had chronic renal failure, 53 had been on chronic hemodialysis, and four had received successful kidney transplants. In more than 80 per cent of patients, symptoms of hyperparathyroidism (bone pain and muscle weakness) resolved within weeks, and biochemical signs (hypercalcemia, and high plasma alkaline phosphatase and parathyroid hormone concentrations) returned to normal ranges within a year. Subperiosteal resorption, bone fractures, and soft tissue calcification frequently improved. Osteosclerosis (rugger-jersey spine), cystic bone changes, osteopenia, and vascular calcifications were, however, often unchanged or progressive. Five patients (8%) who had either persistent or recurrent hyperparathyroidism required additional surgical procedures, and two had subsequent improvement. Twelve patients who had aluminum associated bone disease diagnosed later continued to progress with a high incidence of bone fractures and severe osteopenia. Cystic bone changes, especially of the carpal bones, in association with carpal tunnel syndrome, probably representing amyloid bone disease, also did not respond to PTX. In conclusion, PTX is an effective surgical procedure to reverse complications of hyperparathyroidism in patients with end-stage renal disease, provided that other causes of osteodystrophy, such as aluminum or amyloid-associated bone diseases, are adequately excluded. We feel that subtotal PTX, leaving a small remnant in place, is the procedure of choice.
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PMID:Long term results of subtotal parathyroidectomy in patients with end-stage renal disease. 806 33

In 1981 cyclosporin A (CyA) became available and replaced azathioprine (Aza) as the immunosuppressive agent in kidney transplantation at the University Hospitals in Basel, Switzerland. Patients on CyA and prednisone (CyA/p) therapy frequently demonstrated an isolated rise in bone-derived serum alkaline phosphatase (aP) concentration, but patients on Aza and prednisone (Aza/p) therapy did not. On the basis of long-term aP concentration and using noninvasive means, the present retrospective study was designed to investigate biochemical markers and radiographic signs of bone disease after successful kidney transplantation in patients on Cya/p treatment. Similar investigations were performed in patients on Aza/p and the results were compared. Follow-up examinations included clinical examination, radiography of the hand, and biochemical analysis of serum and urine. In 139 renal transplant patients on CyA/p, aP increased transiently after successful grafting (at transplantation 84 +/- 43 U/l; on day 90, 112 +/- 82 U/l). In 50 patients aP levels were higher at the time of transplantation (120 +/- 80 U/l) and aP peaked after 8 +/- 6 months, at a mean concentration of 242 +/- 103 U/l. In these patients aP concentrations exceeded the normal range for 16 +/- 10 months. None of the patients on CyA/p showed symptoms of bone disease when aP was increased. Radiological surveys revealed more pronounced osteodystrophy in patients at the time of transplantation, which increased aP to above the normal range after transplantation. Despite this rise in aP, over the long term bone lesions improved radiographically while bone mass remained stable.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cyclosporin A-induced transient rise in plasma alkaline phosphatase in kidney transplant patients. 844 31

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 effects on bone, recent studies on the use of GH in children with chronic renal failure (CRF) provide some early data. Animal models demonstrate that GH stimulates chondrocyte proliferation. Experimental data further suggest that GH can weaken the epiphyseal plate. Slipped capital femoral epiphysis (SCFE) has been reported in GH-deficient patients, having been detected before, during and after GH therapy. In CRF patients treated with GH SCFE has also been reported. As renal osteodystrophy (ROD) and hypocalcemia are risk factors for this condition, the relationship to GH therapy is unclear in this type of patient. Avascular necrosis (AVN) of the femoral head has been reported in children with congenial structural renal abnormalities and GH deficient patients treated with GH. In recent studies in over 200 children with CRF, 15 cases of AVN have been identified in treated patients. Eight were present prior to treatment; the other 7 patients were not examined radiographically prior to their treatment, and thus the relationship to GH is unknown. 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 AVN, SCFE and ROD with serial radiographs and serum calcium, phosphorus, alkaline phosphatase and PTH levels.
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PMID:Bone disease in patients receiving growth hormone. 877 Oct 6

Recent extension of the use of recombinant growth hormone (rhGH) to non-growth hormone-deficient patients necessitates close attention to possible complications in these patients, including effects on bone. Recent studies on the use of rhGH in children with chronic renal failure (CRF) provide some early data. No significant differences in radiographic osteodystrophy scores, serum calcium, phosphorus, or parathyroid hormone (PTH) levels were found between treated and untreated groups. Alkaline phosphatase increased transiently. The effect of renal osteodystrophy on growth response has not yet been reported. Animal models demonstrate that GH stimulates chondrocyte proliferation. Experimental data further suggest that GH can weaken the epiphyseal plate. Slipped capital femoral epiphysis has been reported in GH-deficient patients, before, during, and after GH therapy. In CRF patients treated with GH, slipped capital femoral epiphysis has also been reported. As renal osteodystrophy and hypocalcemia are risk factors for this condition, the relationship to GH therapy is unclear in these patients. Avascular necrosis, known to be associated with slipped capital femoral epiphysis and CRF, has also been reported in patients receiving GH, although the relationship to the therapy is unknown. Children with CRF treated with rhGH should be serially monitored for renal osteodystrophy, slipped capital femoral epiphysis, and avascular necrosis with serial radiographs and serum calcium, phosphorus, alkaline phosphatase, and PTH levels.
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PMID:Is severe renal osteodystrophy a contraindication for recombinant human growth hormone treatment? 879 4

The frequency of metabolic bone disease related to secondary hyperparathyroidism was studied in 47 haemodialysis patients, using biochemical, radiological parameters and bone biopsy (30 males, 17 females; mean age 48 years). The duration on dialysis ranged from 1-5 years. Hypocalcemia was found in 47% while 62% had raised phosphorus levels and 49% raised alkaline phosphatase. Serum parathyroid hormone was elevated in 86%, while in 13% it was markedly raised. On radiological examination there was generalized osteopenia in 49% and decreased bone density in 21%. In 30% no radiological abnormality was detected. In 40% bone biopsy revealed osteomalacia, mixed osteodystrophy 21%, osteoporosis 8.5% and in 25% no histological abnormality was observed.
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PMID:Frequency of metabolic bone disease in haemodialysis patients. 899 60


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