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)

To evaluate the relationship between autonomic neuropathy, and biochemical and X-ray parameters of secondary hyperparathyroidism, we examined 19 predialysis and 24 haemodialysis non-diabetic uraemic patients. Autonomic neuropathy was assessed using four tests: deep breathing, Valsalva manoeuvre, lying to standing, and postural hypotension. Serum Ca, Ca2+, P, Mg, alkaline phosphatase, iPTH, and osteocalcin were assayed. Hand X-ray was obtained to evaluate acro-osteolysis (score A) and subperiosteal resorption (score B). Ten predialysis patients (52%) and 15 haemodialysis patients (62%) showed one or more abnormal autonomic tests. Age, dialysis duration, and biochemical parameters of secondary hyperparathyroidism did not differ significantly in uraemic patients with and without abnormal autonomic tests. Furthermore, there was no significant relation between autonomic tests and iPTH or osteocalcin. Score A and score B was significantly greater in patients with abnormal tests than in patients without (P less than 0.009 and P less than 0.025). When predialysis and haemodialysis patients were considered separately the correlation between score A, score B, and autonomic neuropathy was confirmed only in haemodialysis patients. In conclusion, autonomic neuropathy does not seem to be related to the biochemical parameters of secondary hyperparathyroidism, while it appears significantly associated with the radiological signs of osteodystrophy, suggesting a possible pathogenetic linkage between autonomic neuropathy and secondary hyperparathyroidism.
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PMID:Autonomic neuropathy and secondary hyperparathyroidism in uraemia. 212 43

Renal osteodystrophy is multifactorial. Decreased calcium absorption from the GI tract, secondary to low calcitriol levels; hyperphosphatemia; skeletal resistance to the action of parathormone; and aluminum deposition on the surface of the bones are its main pathogenetic mechanisms. Its biochemical features include abnormalities in serum calcium, phosphate, alkaline phosphatase, parathormone, calcitriol, and aluminum concentration. Radiographic methods are of little use in the characterization of the type of osteodystrophy present, but they may be of help in assessing mineral loss from the skeleton. Clinical manifestations are from bones (pain, deformities, fractures) or from metastatic calcifications. Bone biopsy is the definitive means of diagnosis. The main histologic types of osteodystrophy include osteitis fibrosa, osteomalacia, mixed form (with features of both osteitis fibrosa and osteomalacia), and aluminum osteodystrophy (presenting as either osteomalacia or aplastic lesion). The management of renal osteodystrophy should address all the pathogenetic mechanisms. Correction of the abnormalities in calcium and phosphate metabolism and prevention of aluminum osteodystrophy are the cardinal rules of management. Specific measures (parathyroidectomy, chelation of aluminum) have clear-cut indications and usually require a bone biopsy.
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PMID:Diagnosis and management of bone disorders in chronic renal failure and dialyzed patients. 219 65

To evaluate the relationship between autonomic neuropathy, and biochemical and radiological parameters of secondary hyperparathyroidism, we examined 19 predialysis and 24 hemodialysis non-diabetic uremic patients. Autonomic neuropathy was assessed using four cardiovascular tests. Ten predialysis and 15 hemodialysis patients showed abnormalities in one or more autonomic tests. Ca, Ca2+, P, alkaline phosphatase, immunoreactive parathyroid hormone and osteocalcin did not significantly differ in uremic patients with and without abnormal autonomic test results. Radiological markers of hyperparathyroidism such as acro-osteolysis (score A) and subperiosteal resorption (score B) were more common in patients with abnormalities in autonomic tests than in patients without. When predialysis and hemodialysis patients were considered separately, the correlation between score A, score B and autonomic neuropathy was confirmed only in hemodialysis patients. In conclusion, autonomic neuropathy is not related to biochemical parameters of hyperparathyroidism, while it appears correlated with radiological signs of osteodystrophy, suggesting a possible pathogenetic link between autonomic neuropathy and secondary hyperparathyroidism.
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PMID:Autonomic neuropathy and secondary hyperparathyroidism in uremia. 221 78

X-Ray signs of hyperparathyroid osteodystrophy (HPOT) have been singled out in analysis of roentgenograms of 86 patients. Hypercalcemia has been detected in 76 +/- 5% of patients presenting an x-ray picture of HPOT, hypophosphatemia has been diagnosed in 66 +/- 5%, hypercalciuria in 72 +/- 6%, and increased alkaline phosphatase activity in 67 +/- 7%. Studies of the P-Ca metabolism should be carried out repeatedly over the course of hyperparathyrosis. Combined analysis of laboratory and x-ray findings will help improve the diagnosis and differential diagnosis of HPOT.
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PMID:[A comparative study of laboratory and x-ray data in the diagnosis of hyperparathyroid osteodystrophy]. 247 66

99mTc-HEDP bone scan was carried out on 12 long-time haemodialysed patients, suffering from bone pains. X-ray examinations of the bone and laboratory tests (serum calcium, -phosphor, -alkaline phosphatase, -parathormone, -aluminium, -ferritin) were also performed. The scintigrams were evaluated by two semiquantitative scores. Based on diffuse, increased radiopharmacon uptake of the bones and more than five points in the Fogelman score 5 patients most likely had serious and 3 had moderate hyperparathyroidism. In two patients osteomalacy was presumed based on decreased radiopharmacon uptake of the bones, increased uptake of the soft tissues and zero Fogelman score. Mixed or other bone disease was suggested in two other patients. Good correlation was found between the results of bone scans, the parathormone values and the results of histology obtained after parathyreoidectomy of 4 patients and autopsy of two others. This non-invasive examination (ie. bone scan) is helpful in differential diagnosis of uraemic osteodystrophy and its wide use is proposed in domestic nephrological practice.
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PMID:[Bone scintigraphy in uremic osteodystrophy]. 260 56

The bone metabolism was evaluated in 20 patients after successful transplantation of the kidneys. In case of a functional graft within 22 months after transplantation of the kidneys complete regression of histological signs of secondary hyperparathyroidism was found, i.e. of fibrous osteodystrophy with a decline of the osteoclastic absorption and in 50% of the patients bone histology revealed osteomalacia. On the X-ray of the skeleton in 65% signs of osteoporosis were found, incl. 10% where the results were in discrepancy with the histological finding. The normal plasma calcium level before and after transplantation of the kidney was not affected. Other basic indicators of bone metabolism--phosphates, alkaline phosphatase, the bone isoenzyme of alkaline phosphatase and parathormone attained normal levels within 22 months after transplantation. Bone fluorides remain elevated also after 22 months following successful transplantation of the kidneys, although significantly less than before.
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PMID:[Bone metabolism in patients after kidney transplantation]. 266 Mar 98

Ten patients are reported following parathyroidectomy (PTX). In 9 all identifiable parathyroid tissue in the neck was deliberately removed, and in the tenth (operated 14 years ago) the remnant which had been left probably did not function. Their post-operative course resembled that of patients treated conventionally, and their subsequent course was likewise uneventful with disappearance of all symptoms associated with their osteodystrophy. All patients required oral calcium supplementation but none were given vitamin D compounds after the initial period of repletion following surgery. Mean serum values were (before PTX and current) for calcium 2.63 +/- 0.14 and 2.33 +/- 0.08 mmol/liter, P = NS, for phosphorus 1.96 +/- 0.13 and 1.38 +/- 0.09 mmol/liter, P less than 0.01, and for alkaline phosphatase 713 +/- 191 and 101 +/- 14 IU, P less than 0.05. Evidence for residual parathyroid tissue was present in each case; one patient remained mildly hyperparathyroid and several were mildly hypoparathyroid by the IRMA PTH assay. Bone histomorphometry in five subjects post-PTX showed either normal or low turnover. Radiologically, striking remineralization was seen with disappearance of all erosive changes. We suggest that residual areas of parathyroid tissue are stimulated and continue to secrete hormone even when all the discrete glands have been removed. It is recommended that when indicated, and in the absence of aluminum excess, total PTX without autotransplant should be the preferred form of therapy for long-term dialysis patients.
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PMID:Elective total parathyroidectomy without autotransplant in end-stage renal disease. 277 Jan 17

Three different pathophysiological mechanisms are probably responsible for hereditary pseudohypoparathyroidism: 1) a defect at the prereceptor-level, 2) a defective membrane N-protein accounting for diminished second messenger production, and 3) a defect in the cytosolic response to the hormone. In a cooperative, study 24 patients (mean age, 13 yr; range, 3-23 yr, 8 girls, 16 boys) receiving vitamin D metabolites (5,000-80,000 U/day) were examined and compared to a control group of 36 normal children. Immunoreactive N-terminal PTH (N-PTH), mid-C-regional PTH (mid-C-PTH), intact PTH and bio-PTH, vitamin D metabolites, and serum calcium and phosphate, alkaline phosphatase activity, and the N-protein activity of erythrocyte membranes were measured in each subject. By clinical and biochemical criteria three groups were differentiated. Eight patients had the completely expressed features of Albright's Hereditary Osteodystrophy (AHO+), including brachydactyly and/or sc calcifications, and increased N-PTH, mid-C-PTH, and alkaline phosphatase activity. Bio-PTH, intact PTH, and N-protein were normal. Nine additional patients with complete (AHO+) had elevated levels of bio-PTH, N-PTH, and mid-C PTH, normal hydroxylation of vitamin D, but decreased N-protein activity. Seven patients with pseudohypoparathyroidism had no features of AHO (AHO-), no increase of urinary cAMP excretion after exogenous PTH, normal PTH peptide levels and N-protein activity, but elevated 25-hydroxyvitamin D and decreased 1,25-dihydroxyvitamin D concentrations. In conclusion, we identified three subpopulations of PsHP: group a had a dissociation of N-PTH and bio-PTH suggesting a defective N-PTH causing renal resistance, whereas their bones respond to PTH. Group b had defective N-protein causing generalized PTH resistance. Group c was characterized by high 25-hydroxyvitamin D and relatively low 1,25-dihydroxyvitamin D levels, thus providing evidence for a defect in the cytosolic interaction of the two different second messengers for PTH, cAMP, and calcium.
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PMID:Multiple pre- and postreceptor defects in pseudohypoparathyroidism (a multicenter study with twenty four patients). 300 Nov 27

Sprague-Dawley rats were dosed by gavage daily for 28 days with 5, 15, or 50 mg/kg of N-(all-trans-retinoyl)-DL-leucine (RL), N-(all-trans-retinoyl)glycine (RG), or all-trans-retinoic acid (RA). On the basis of mortality incidence, fracture incidence, body weight, and histopathologic effects, RG was slightly to moderately less toxic than RA, and RL was significantly less toxic than RA or RG. Doses that had no effect on weight loss and produced no bone fractures were approximately 5 and 15 mg/kg/day for RA administered to males or females, respectively; greater than 15 mg/kg/day for RG administered to males or females; and greater than 50 mg/kg/day for RL administered to males or females. At these doses, RA and RG produced effects, detectable at the microscopic level, of lymphoid hyperplasia and hematopoietic cell proliferation in the spleen, lymphoid hyperplasia in lymph nodes, necrosis of the cortex of the thymus, hypertrophy of the zona fasciculata of the adrenal, a periportal pattern of cytoplasmic vacuolization in hepatocytes, hematopoietic cell proliferation in the liver, epithelial hyperplasia and subacute inflammation in the forestomach, and osteodystrophy. Serological alterations consisted of reduced serum albumin levels and elevated levels of triglycerides and alkaline phosphatase. For RL, similar microscopic effects, dependent on dose level and sex, were observed in spleen, thymus, adrenal, and liver. In vitro, RL was as active as RA in potentiating pokeweed mitogen-induced lymphocyte proliferation; RG was inactive. This study indicates that, relative to RA and RG, RL has less toxicity but similar immunological effects. Since RL and RG expressed little or no binding affinity for cellular RA-binding protein, the immunological effects of these retinoids may be expressed by mechanisms not linked to this protein.
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PMID:Toxicologic and immunologic evaluations of N-(all-trans-retinoyl)-DL-leucine and N-(all-trans-retinoyl)glycine. 319 15

Plasma alkaline phosphate activity is a important marker of increased skeletal turnover (both resorption and formation) and bone disease in uraemia, but its value after renal transplantation is uncertain. The rate of fall of alkaline phosphatase was compared in three groups of uraemic patients with osteodystrophy and elevated serum alkaline phosphatase undergoing either renal transplantation, parathyroidectomy or therapy with 1a hydroxylated vitamin D derivates. Alkaline phosphatase fell after transplantation, irrespective of graft function, with a half-time significantly less than the other treatments (p less than 0.001). We suggest that this represents a direct inhibitory effect of steroids on osteoblasts and that alkaline phosphatase is thus an unreliable marker of bone resorption after transplantation.
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PMID:Rapid suppression of plasma alkaline phosphatase activity after renal transplantation in patients with osteodystrophy. 329 29


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