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)

Three patients receiving maintenance hemodialysis therapy for end-stage renal failure presented with spontaneous rupture of the quadriceps tendon(s). Biochemical data and the skeletal roentgenograms were compatible with secondary hyperparathyroidism. Histological examination of the excised quadriceps tendon specimens suggested that repeated minor avulsion fractures of the bone cortex at the tendon insertion site had preceded the final total tendon rupture and that osteitis fibrosa was responsible for these minor fractures. Serum alkaline phosphatase level had been increasing continuously for approximately five years prior to the tendon rupture in all three patients, indicating that uncontrolled osteitis fibrosa due to secondary hyperparathyroidism over these years preceded the tendon rupture.
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PMID:Spontaneous rupture of the quadriceps tendon in patients on maintenance hemodialysis--report of three cases with clinicopathological observations. 279 66

We studied the significance of urinary enzyme measurements in diagnosing proximal tubular damage in cirrhosis of the liver. Urinary excretion (u-enzyme) and fractional urinary excretion (FEenzyme) of gamma-glutamyltranspeptidase (GGT), leucine aminopeptidase (LAP), alkaline phosphatase (AP) and beta-glucuronidase (B-GLU) were quantified in 14 control subjects (group I), 12 cirrhotics with functional renal failure (group II), 13 cirrhotics with renal tubular damage (group III) and 7 non-liver patients with renal tubular damage (group IV). Urinary enzyme excretion and fractional enzyme excretion were significantly higher in the cirrhotics of group III than in the controls or group II. In group III, these tests usually reached values within the range of group IV. The sensitivity of urinary enzyme excretion was 0.92 and specificity ranged from 0.75 (u-LAP) to 1 (u-GGT; u-B-GLU). The sensitivity of fractional enzyme excretion was between 0.61 (FEB-GLU) and 0.84 (FEGGT; FELAP), while specificity was from 0.91 (FELAP; FEAP) to 1 (FEGGT; FEB-GLU). The results indicate that measurement of urinary enzymes may be very useful in diagnosing renal tubular damage in cirrhotic patients with impaired renal function.
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PMID:Urinary excretion of enzymes in cirrhotics with renal failure. 287 95

An in vivo model of liver hyperplastic noduligenesis was induced in rats by long-term administration of thioacetamide (TAM) (50 mg/kg/day i.p.). Three doses of 50 mg/kg of an antitumoral Rh(III) complex were administered at 14, 9 and 5 days before the end of TAM treatment. Plasma and urine were obtained from either TAM or Rh(III) complex or TAM plus Rh(III) complex treated rats to determine the interactions of both substances with the biochemical parameters related to liver function. The rise in alkaline phosphatase (ALP), leucine aminopeptidase (LAP), gamma-glutamyl transferase (GGT) and the unchanged activities in the aspartate and alanine aminotransferases (AST, ALT) in plasma of TAM-treated rats indicated that the disease induced by this substance can be considered as a chronic obstructive biliary disease with indices of cell proliferation and tumors. The increased concentration of bilirubin both in the plasma and urine of TAM-treated rats suggested liver cholestasis and hepatobiliary obstruction. The very low values of creatinine clearance indicated that there was some degree of kidney failure due to the effect of TAM. The increased concentration of ammonia both in plasma and urine were probably a consequence of the decreased flux in the urea cycle in the liver. The Rh(III) complex alone did not produce significant changes in the plasma enzyme activities. The only significant changes were found in the concentrations of uric acid and ammonia in the urine. When the Rh(III) complex was administered to TAM-treated rats, significant restoration of the following parameters were observed: plasma enzymatic activities, blood bilirubin and ammonia, uric acid and creatinine in the urine and the creatinine clearance. These results suggest that the altered liver function induced by TAM can be restored by Rh(III) complex. The mechanisms by which this complex acts to counteract the TAM-induced changes are not yet established.
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PMID:Effect of a rhodium complex on alterations of hepatic function in thioacetamide-induced hyperplastic noduligenesis in rats. 288 38

We have re-evaluated the isolation and characteristics of human urinary alkaline phosphatases (ALPs). From the results of physicochemical properties and immunological identification, the urinary ALPs from healthy subjects and patients with hepatoma were found to be similar in nature to liver and/or bone-like ALP. In patients with chronic or acute nephritis, the ALPs contained a major band of kidney-like ALP with a minor band of bone and intestinal ALPs. However, the ALPs in pregnant women had not only liver and bone ALPs but also placental-like ALP. It is interesting that only bone-like ALP was detected in psychiatric patients administered chlorpromazine. In the conditions we investigated, the molecular sizes of the urinary ALPs were similar as those of original ALPs, except for the enzyme from renal failure. Moreover, the total activity of urinary ALP was closely related to the level of serum ALP, being in a ratio of 1/40. In general, urinary ALP may be derived from serum ALP by minor modification, suggesting that the identification of excreted ALP in urine is a good marker for disturbed organs in respective diseases.
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PMID:Organ specific properties for human urinary alkaline phosphatases. 328 Jan 68

Bone disease related to aluminum toxicity (aluminum-related bone disease) presents with variable clinical and biochemical findings in patients with renal failure. Bone pain and muscle weakness are common, although afflicted patients can be asymptomatic. Bone pain can be generalized or localized to the hips, back, feet, or ankles; proximal muscle weakness is common. Most cases in the United States arise from the ingestion of aluminum-containing gels by patients on long-term dialysis treatment. Patients at increased risk for developing aluminum-related bone disease include those with earlier parathyroidectomy, failed renal transplant, previous bilateral nephrectomy, and diabetes mellitus. Biochemical features that are common with aluminum-related bone disease include plasma aluminum levels greater than 100 to 150 micrograms/L, serum parathyroid hormone (PTH) levels equal to or lower than those in dialysis patients without bone disease, and normal or slightly elevated serum calcium levels. Plasma alkaline phosphatase levels are often elevated. In our experience, microcytic anemia has been uncommon. An increase in plasma aluminum levels greater than 200 micrograms/L 24 to 48 hours after the infusion of the chelating agent deferoxamine (DFO) correlates with an increased bone aluminum content, and an increment greater than 400 micrograms/L suggests marked aluminum accumulation. Radiographs are usually nonspecific. When results from indirect diagnostic procedures are equivocal, a bone biopsy is necessary. After a diagnosis of aluminum-related bone disease is established, therapy with DFO may be useful. DFO increases both the total plasma aluminum level and its ultrafilterable fraction. After an infusion of DFO, the removal of aluminum increases from 50 to 300 micrograms to 4 to 8 mg per dialysis session. Aluminum removal is similar during continuous ambulatory peritoneal dialysis after either intravenous (IV) or intraperitoneal (IP) administration of DFO. Usually, 2 to 4 g of DFO is administered once weekly, but the optimal dose and duration of therapy have not been determined. Symptoms usually improve after 4 to 12 weeks, and bone biopsies show improvement after treatment for 6 to 12 months. Further experience with DFO is needed, both to identify the optimal dosage and to clarify the risks of long-term therapy in patients with renal failure.
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PMID:Diagnosis of aluminum-related bone disease and treatment of aluminum toxicity with deferoxamine. 329 88

Because of the suggestion that intestinal alkaline phosphatase was elevated in the serum of patients with chronic renal failure, we studied the serum of 42 patients undergoing hemodialysis with elevated enzyme activity. Using a sensitive and specific electroimmunoassay for the intestinal isoenzyme, 26 of 42 serum samples were positive, compared with 3 of 25 samples obtained from hospitalized patients with elevated phosphatase activity. The fractional amount of this isoenzyme was also higher, ranging from 1.5% to 41% of the total serum phosphatase, compared with 0.1%-1.2% in control sera. Kidneys removed during transplantation or postmortem contained a membranous phosphatase with immunologic activity identical to the intestinal isoenzyme in 5 of 6 patients. This enzyme accounted for 8%-21% of the total kidney phosphatase activity. By morphology the immunoreaction was localized to the apical membranes of the collecting tubules. Thus, the kidney is the likely source of the observed increase in serum intestinal-type phosphatase activity noted in patients with chronic renal failure. An elevation in the intestinal isoenzyme rather than the presence of early metabolic bone disease or hepatic disease should be considered in renal failure patients with mildly elevated (up to 50% over normal) total serum alkaline phosphatase.
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PMID:Intestinal alkaline phosphatase in patients with chronic renal failure. 333 99

Biochemical indices of bone formation (serum osteocalcin and bone alkaline phosphatase isoenzyme) and osteoclastic function (plasma tartrate resistant acid phosphatase) were measured in 43 patients undergoing chronic hemodialysis and in 27 patients with primary hyperparathyroidism. The mean values for bone alkaline phosphatase isoenzyme and plasma tartrate resistant acid phosphatase but not for osteocalcin were significantly higher in primary hyperparathyroidism as compared with dialyzed patients. A significant positive correlation was found between the biochemical indices of osteoblasts and osteoclasts both in primary hyperparathyroidism and in dialyzed patients, indicating biological coupling between bone resorption and formation under these conditions. The regressions of osteocalcin vs bone alkaline phosphatase isoenzyme and/or plasma tartrate resistant acid phosphatase in dialyzed patients paralleled those in primary hyperparathyroidism but their distance differed significantly. It is concluded that in patients with renal failure, an increase in circulating osteocalcin by a relatively constant portion reflects decreased renal clearance. Any additional increase in osteocalcin serum level indicates an increased skeletal production of osteocalcin. The clinical value of bone alkaline phosphatase isoenzyme and plasma tartrate resistant acid phosphatase appears to be comparable with that of serum osteocalcin in primary hyperparathyroidism, and more exact than osteocalcin in renal failure.
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PMID:Serum osteocalcin, bone alkaline phosphatase isoenzyme and plasma tartrate resistant acid phosphatase in patients on chronic maintenance hemodialysis. 350 96

In a group of 58 dogs with proven pyometra, 10 bitches developed renal failure, combined with increased (p less than 0.01) urinary excretion of protein, glucose, gamma-glutamyltransferase (GGT), alkaline phosphatase (AP), amylase, lipase and casts. Thirty-two bitches without renal failure showed nevertheless signs of renal dysfunction as indicated by increased (p less than 0.01) urinary levels of protein, glucose, GGT, AP and amylase. Six bitches without significant proteinuria showed increased (p less than 0.02) urinary levels of GGT, AP as well as amylase. Thus renal injury was detected in 72 per cent of the bitches. Sixteen bitches showed normal urinary levels of protein, glucose, GGT, AP, amylase and lipase, indicating absence of renal disease.
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PMID:Renal injury in dogs with pyometra. 357 95

We examined the effects of the immunosuppressive drug cyclosporine A on male reproduction in sexually mature rats. The drug was administered subcutaneously in 3 doses (10, 20 and 40 mg. per kg. daily) for 14 days. Cyclosporine A administration resulted in a dose-dependent decline in body and reproductive organ weights, histology of the testis showed definite degenerative changes, and sperm counts and motility decreased. Spermatozoa from treated rats retained the cytoplasmic droplet and they were decapitated. Consequently, sterility occurred in rats treated with high doses of cyclosporine A. A reduction in circulating testosterone and an increase in gonadotropins were noted. The possibility existed that the cyclosporine A-induced alterations in the male reproductive system were secondary to the hepatic or nephrotoxic effects of the drug. Therefore, we assessed liver and kidney function by assay of the serum levels of bilirubin, alkaline phosphatase, serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase and creatinine. Except for an increase in bilirubin, none of the other liver function studies was altered, thereby eliminating hepatocellular damage as the etiology of impaired reproductive function in cyclosporine A-treated rats. We observed an increase in creatinine levels in animals treated with higher doses of cyclosporine A, consistent with mild renal failure. However, the fact that a decline in reproductive function was seen even in the group treated with 10 mg. per kg. cyclosporine A daily, which had normal serum creatinine levels, suggests that the alterations in male reproduction seen with this therapy are not entirely the result of nephrotoxicity.
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PMID:Effect of cyclosporine A on male reproduction in rats. 365 81

Common bile duct ligation (CBDL) in rats was used to induce liver disease and secondary kidney damage. The biochemical changes in the liver, kidney and plasma were studied at 3, 6, 10 and 21 days post CBDL. The observed alterations climaxed at the 6th day following ligation. Renal, activities of aldolase (ALD), lactic dehydrogenase (LDH), isocitric dehydrogenase (ICDH), sorbitol dehydrogenase (SDH), and alkaline phosphatase (ALP), were lowered in CBDL rats. Further, microsomal Na,K-ATPase and Mg-ATPase and mitochondrial oxidative-phosphorylation were inhibited. In the liver from CBDL rats the activities of aspartate aminotransferase (AST), Mg-ATPase and ALP were elevated, while SDH, ALD, malic dehydrogenase (MDH), LDH, malic enzyme (ME) and Na,K-ATPase were lowered. Plasma enzymes, AST, ALP, MDH, LDH, ALD, acid phosphatase (ACP) and ICDH and the metabolites bile acids, bilirubin, creatinine and urea were elevated. Addition of bile acids or bilirubin at concentrations comparable to those found in the plasma of CBDL rats, to the reaction mixture of the various enzymes strongly inhibited most, particularly mitochondrial oxidative phosphorylation. High concentrations of these substances in the blood may explain the development of renal failure during liver disease and its reversibility when liver function returns to normal.
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PMID:Biochemical changes in liver, kidney and blood associated with common bile duct ligation. 378 11


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