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)

Serum intact parathormone (PTH 1.84) and osteocalcin levels were evaluated as early markers for secondary hyperparathyroidism in a group of pediatric patient treated with chronic hemodialysis. PTH 1.84 levels which were more closely related with alkaline phosphatase levels than PTH 53.84 levels, allowed to identify a group of children without biologic or roentgenographic evidence of hyperparathyroidism and with a normal residual hormone level. PTH 1.84 levels seem to be a reliable indicator of parathormone secretion than conventional assays and may be used as a routine test for monitoring children under chronic hemodialysis. Conversely, the plasma osteocalcin level measured by radioimmunoassay was increased in all studied patients regardless of parathyroid status and seemed to be of little value for monitoring renal osteodystrophia. Lumbar vertebral plate bone density studies disclosed abnormalities of bone mineralization in half the children with renal failure. Dialyzed or non dialyzed. Patients with decreased bone mineralization presented, in most of cases, a history of previous steroid treatment. A group of children with very severe renal failure had increased bone mineralization. The interpretation of this abnormality remains to be determined.
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PMID:[Evaluation of new markers of bone metabolism in renal osteodystrophy in children]. 218 14

From June 1986 to October 1989, ten children suffering from end stage renal disease (ESRD) were treated with continuous ambulatory peritoneal dialysis (CAPD). Their ages ranged from 4 to 16 years; 3 were boys and 7 were girls. IgM mesangial nephropathy (IgMN) (three cases) were the most common causes of renal failure in the patients. All patients were trained in the hospital. After CAPD treatment, serum BUN and creatinine dropped significantly. Serum levels of potassium, phosphorus, and alkaline phosphatase dropped and serum sodium and calcium rose significantly after treatment. Improvement of anemic state and control of hypertension were also noted. Hypercholesterolemia and hypertriglyceridemia developed after CAPD treatment. Despite protein loss through the peritoneal cavity, there was no evidence of protein malnutrition. Total serum protein and albumin increased significantly after treatment. The most common complication was peritonitis. Three of these 10 patients developed an episode of peritonitis, or an incidence of 1 episode per 17.2 patient months. To the present, seven patients are still doing well on CAPD. Three patients have received renal transplantation. The majority of the patients experienced an increased sense of well-being, easier diet and fluid management, freedom for travel and daily activities. Physical development also improved, with body length and body weight gaining steadily. It can be concluded that CAPD is a good modality of long-term therapy for ESRD children.
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PMID:Continuous ambulatory peritoneal dialysis for children with end stage renal disease. 226 Apr 64

Acute zinc toxicosis from the ingestion of pennies was diagnosed in a dog with Heinz body hemolytic anemia (PCV = 14%), leukocytosis (51,000 cells/ml) with a left shift (3,060 band neutrophils; 37,740 segmented neutrophils) and monocytosis (4,080 cells/ml), azotemia (BUN = 60 mg/dl), bilirubinemia (total bilirubin = 5.3 mg/dl), hypokalemia (3.0 mEq/L), high serum alkaline phosphatase activity (691 U/L), high total plasma solids (8.1 g/dl), hemoglobinuria, and proteinuria. Despite aggressive medical treatment, renal failure ensued, and the dog died of cardiac arrest. The clinical signs, clinical course, and laboratory findings in this dog were similar to what has been reported in other cases of acute zinc toxicosis in dogs, with the exception of a history of generalized seizures and the findings of Heinz bodies. Although a causative relationship between plasma zinc values and Heinz body formation cannot be proven, their association suggests that oxidative damage to erythrocyte hemoglobin and cell membrane proteins may be involved in the pathogenesis of zinc-induced hemolysis.
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PMID:Heinz body hemolytic anemia associated with high plasma zinc concentration in a dog. 226 50

We report clinical and bone morphometric findings in 18 osteoporotic patients who experienced stress fractures during fluoride therapy. Patients were treated with either sodium fluoride (n = 15), or sodium monofluorophosphate (n = 3). Oral calcium supplementation was given in 11 patients, and vitamin D in 13. Stress fractures occurred after 17.1 +/- 10.3 months of therapy (range: 5-41 months). Atraumatic sudden pain in a lower limb bone extremity, normal initial roentgenogram, high 99technetium uptake on early bone scan, and a 3 to 4 week delay in linear bone condensation area at the same site were characteristics of stress fracture. The most frequent sites were the tibial metaphysis (n = 13), femoral neck (n = 10), and calcaneus (n = 4). Biochemical data showed increased plasma alkaline phosphatase levels in 11 patients, and mild renal failure in 2. Bone histomorphometry was performed on an iliac crest specimen in 10 patients at the time of the stress fracture. Trabecular bone volume was normal, and formation parameters were increased. Features of osteomalacia were encountered in only 2 patients with decreased renal function. Trabecular resorption was increased, as assessed by the osteoclastic surface (1.01 +/- 1.15% bone surface), and the number of osteoclasts (0.44 +/- 0.49 per mm2 bone section). The clinical course was favorable in all patients who stopped fluoride, although 5 patients who continued the treatment had either completion of femoral neck stress fractures to hip fractures (n = 2), or recurrent stress fractures (n = 2), or both (n = 1). Fluoride appears to be a key factor in the pathogenesis of stress fractures, and may be associated with increased trabecular resorption in some treated patients.
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PMID:Stress fractures of the lower limbs in osteoporotic patients treated with fluoride. 233 28

Elevated values of pancreatic-type amylase activity in serum were found in 59% of patients with liver cirrhosis not complicated with renal failure, in 67% of patients with chronic renal failure not complicated with hepatopathy and in 95% of patients with chronic renal failure complicated with hepatopathy. In all the three groups, a significant positive correlation was found between the pancreatic-type amylase and intestinal isoenzyme of serum alkaline phosphatase which is an asialoglycoprotein. However, in pancreatitis a prevalence of an increase in pancreatic-type amylase with respect to intestinal alkaline phosphatase was found. A multivariate analysis showed that in chronic renal failure not complicated with hepatopathy, and in chronic renal failure complicated with chronic liver disease, the changes in calcium homeostasis and also the liver disorder, respectively, contribute significantly to the above-normal values for pancreatic-type amylase.
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PMID:Role of secondary hyperparathyroidism and liver function in hyperamylasemia in chronic renal failure. 241 93

The heights and symptoms of 52 patients, aged at least 18 years, with X-linked hypophosphataemic rickets were analysed retrospectively; 47 had been seen as children and 5 were adult at their first examination. 2 patients were lost to follow-up. 3 patients had died but their adult heights were known. There was no evidence that any form of treatment (ie, vitamin D in high doses, vitamin D plus phosphate supplements, or calcitriol plus phosphate) had any effect on adult height, symptoms, or alkaline phosphatase levels. There was a negative relation between adult height and the number of osteotomies undergone. The complications of treatment, such as renal failure, which occurred secondary to vitamin D intoxication in 3 patients in their twenties, may outweight any possible benefits. Until a treatment is established as effective in controlled trials, it may be better that these patients remain untreated.
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PMID:Hypophosphataemic rickets: final height and clinical symptoms in adults. 196 43

Parenteral administration of iron nitrilotriacetate (FeNTA) to rats resulted in marked loss in body weight, and increases in liver/and kidney/body weight ratios. Fatalities, due to renal failure, depended on dosage and age of the animals, and were greater (70%) after a single large dose (12 mg iron) than after repeated smaller doses (30%). FeNTA administered subchronically gave rise to an increase in ethane exhalation, and to decreased liver glutathione peroxidase activity, and decreased cytochrome P-450 concentration and benzphetamine N-demethylase activity. It also resulted in severe renal tubular necrosis, with deposition of iron in the tubular cells and loss of brush border alkaline phosphatase activity, resulting in a dose-dependent diuresis, with increased urinary excretion of glucose, iron and lipid peroxidation products, and decreased urine creatinine concentration. NTA alone had none of these effects but slightly decreased the hepatic concentration of iron.
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PMID:Effects of acute and sub-chronic administration of iron nitrilotriacetate in the rat. 257 73

This study represents the first randomized prospective, double-blind, placebo-controlled trial of the efficacy of 1,25(OH)2D3 on bone histology and serum biochemistry in patients with mild to moderate renal failure. Sixteen patients with chronic renal impairment (creatinine clearance 20 to 59 ml per min) received either 1,25(OH)2D3, at a dose of 0.25 to 0.5 microgram daily (eight patients), or placebo. Transiliac crest bone biopsies were performed before entrance into the study and after 12 months of experimental observation. None of the patients were symptomatic or had radiological evidence of bone disease. Of the thirteen patients who completed the study, initial serum 1,25(OH)2D levels were low in seven patients and parathyroid hormone levels were elevated in seven patients. Bone histology was abnormal in all patients. 1,25(OH)2D3 treatment was associated with a significant fall in serum phosphorus and alkaline phosphatase concentrations as well as with histological evidence of an amelioration of hyperparathyroid changes. In contrast to previous reports, no deterioration of renal function attributable to the treatment occurred, perhaps because a modest dose of 1,25(OH)2D3 was employed combined with meticulous monitoring. Further investigation is required to determine whether alternative therapeutic strategies (smaller doses or intermittent therapy) may avoid the potential for suppressing bone turnover to abnormally low levels in the long term.
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PMID:1,25(OH)2D3 administration in moderate renal failure: a prospective double-blind trial. 265 58

Rats were subjected to a two-stage 5/6 nephrectomy and treated with aluminum for 2 and 4 weeks with a cumulative dose of 4.2 and 8.4 mg of aluminum, respectively. Other animals were parathyroidectomized and loaded with 8.4 mg of aluminum for 4 weeks. Histomorphometry and electron microscopy (tibiae), aluminum tissue (bone, kidney, liver) determination, serum (Ca, Mg, Zn, P, urea, creatinine, alkaline phosphatase, 1,25(OH)2D3, PTH) and urine (creatinine, A1) revealed that: (a) a dose of 8.4 mg aluminum was sufficient to induce rickets within 4 weeks of treatment and was associated with decreased serum calcitriol values and high aluminum accumulation within organs (electron-dense material was found in osteoblasts only); (b) previous parathyroidectomy prevented the occurrence of any aluminum-induced alteration of bone. It was associated with higher calcitriol and phosphorus values than in corresponding non-parathyroidectomized rats and significantly reduced aluminum accumulation within organs. The results was influenced neither by a drop in serum calcium values nor by different degrees of renal failure. We suggest that aluminum-induced rickets in growing uremic rats is prevented or delayed when previous parathyroidectomy has been performed.
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PMID:The influence of early parathyroidectomy on aluminum-induced rickets in growing uremic rats. 276 4

Osteocalcin (OC), also called Bone Gla Protein (BGP), is a bone matrix protein of 5800 MW synthesized by osteoblasts. Since OC is mainly metabolized in the kidney, its blood concentration is altered in renal failure. The relationship between OC and the calcium-phosphorus regulating hormones (parathyroid hormone, calcitonin) and the biochemical parameters of bone metabolism (serum calcium, serum phosphorus and serum alkaline phosphatase) was studied in 30 patients on chronic hemodialysis (mean age: 51 years; mean duration of dialysis treatment: 39 months). OC levels were significantly elevated in all patients on chronic hemodialysis (34.7 +/- 31.5 ng/ml) when compared to healthy subjects (6.25 +/- 1.39 ng/ml, p less than 0.001). In 2 patients the OC levels were excessively high (127.54 ng/ml; 148.02 ng/ml), which was associated with severe renal osteodystrophy due to secondary hyperparathyroidism. When divided into 2 groups in the patients with secondary hyperparathyroidism the mean OC value was markedly elevated (50.5 +/- 12.7 ng/ml) compared to the patients without secondary hyperparathyroidism (24.1 +/- 2.8 ng/ml) (p less than 0.05). 70 per cent of the patients on chronic hemodialysis with OC levels greater than 30 ng/ml showed moderate to severe scintigraphic findings of bone disease. In neither of the 2 groups could a correlation between OC and serum alkaline phosphatase be demonstrated. The results indicate, that OC levels could be useful additional parameter in hemodialyzed patients with secondary hyperparathyroidism and OC levels could reflect bone formation in these patients.
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PMID:[Osteocalcin in chronic hemodialysis patients as an additional parameter in the diagnosis of advanced secondary hyperparathyroidism]. 278 25


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