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)

Predicting the course of parathormone (PTH)-elicited bone turnover in both humans and experimental rat models with moderate chronic uremia, using only standard clinical chemistry analyses, is often difficult. Consequently, rat bone from 1 + 2/3 nephrectomized animals, after 230 days of progressive renal failure, was examined for PTH-stimulated adenylate cyclase (AC) and phospholipase C (PL-C) activities. Correlations to biological parameters related to the function of bone and kidney were made. Reduced renal function was demonstrated by increased serum creatinine; circulating 1,25 dihydroxyvitamin D3 below detection level; diminished renal PTH-elicited AC activity; and decreased urinary cAMP excretion. PTH-activated renal PL-C was also reduced. However, no significant differences were seen in urine creatinine, calcium, phosphate, and hydroxyproline, nor in serum PTH, alkaline phosphatase, calcium, and phosphate. Notwithstanding, renal osteodystrophy developed as estimated by increased plasticity of the long bones, as well as reduction of the diaphyseal (Dd) and inner femoral mid-shaft (Di) diameters. Femoral cancellous bone exhibited a substantial elevation of both eroded surface (ES) and osteoid surface (OS) as well as a marked reduction in trabecular bone volume (TBV). Calvarial PTH-activated AC was enhanced, whereas corresponding PL-C was markedly reduced. PTH-enhanced AC correlated positively with ES and negatively with Di, respectively. PTH-enhanced PL-C, however, correlated positively with bone calcium content and negatively with ES. Our results indicate that bone modeling and remodeling are to a large extent related to PTH-elicited signaling systems, and cannot easily be predicted by standard clinical chemistry analyses.
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PMID:Surgically induced uremia in rats. II: Osseous PTH-susceptible signaling systems as predictors of bone resorption. 782 Jul 79

Cisplatin, a nephrotoxic chemotherapeutic agent, was injected into Sprague Dawley rats, alone or together with cysteine, vitamin E and clonidine. The effects on erythrocyte fragility, serum composition, and kidney and liver enzymes were studied. Cisplatin was administered as two i.p. injections (6 mg/kg body weight) at an interval of 120 hours. The animals were sacrificed 24 hours after the second injection. Erythrocytes were prepared from blood collection with anticoagulant. Serum was prepared from clotted blood, collected without anticoagulant. Kidneys and liver were removed and homogenized, and a supernatant prepared by high speed centrifugation. In cisplatin-treated rats, the serum activities of aspartate aminotransferase, alanine aminotransferase, lactic dehydrogenase and alkaline phosphatase were significantly decreased, whereas the activities of isocitric dehydrogenase and glutathione reductase were increased. Also, concentrations of blood urea nitrogen, creatinine, total lipids and magnesium increased while albumin and glucose decreased. Mean osmotic fragility of erythrocytes from cisplatin-treated rats was decreased, while the haematocrit was increased. In the liver, the only change seen was an increased activity of isocitric dehydrogenase. Much greater changes were found in the kidneys, with increased activity of glucose-6-phosphate dehydrogenase and decreased activities of aspartate and alanine aminotransferases, alkaline phosphatase, malic dehydrogenase, sorbitol dehydrogenase and gamma-glutamyltransferase, as well as a decreased phosphorylation to oxidation ratio in the mitochondria, indicating reduced adenosine triphosphate production. Administration of cysteine and vitamin E together with cisplatin partially reversed the uraemia and many of the biochemical changes induced by cisplatin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in serum, liver and kidneys of cisplatin-treated rats; effects of antioxidants. 788 81

Iliac crest biopsies of normals, uremic patients and subjects with primary hyperparathyroidism (pHPT) were investigated. It appeared that serum 1,25- and 24,25-(OH)2-D3 correlated inversely with basal adenylate cyclase (AC) activity and relative PTH-stimulated AC, respectively. Net PTH-elicited AC (dPTH-AC) activation hence reflected individual vitamin D status. The combination variable serum PTH (s-PTH) x dPTH-AC x [H+] correlated well with resorption surface (RS) in both normals, patients with pHPT or subjects with uremia, while s-PTH, dPTH-AC activity or pH as single variables were only marginally related to RS. For all subjects analyzed, osteoid volume (OV) correlated positively with serum alkaline phosphatase but negatively with serum 1,25-(OH)2-D3. OV showed no correlation with dPTH-AC, while the relationship between OV and s-PTH was strong, suggesting that PTH stimulates osteoid deposition via some signalling pathway other than cAMP. In normals, OV was inversely proportional to s-PTH, due to homologous desensitization of this signalling system. Furthermore, s-PTH was negatively correlated with urine cAMP due to homologous desensitization of the effect of PTH on the kidney 25-(OH)-D3 1 alpha-hydroxylase. This phenomenon was absent in uremic patients. Evaluation of variables by artificial intelligence showed that the prototype uremic patient exhibited serum creatinine > 900 microM, RS > 0.12, pH between 7.15 and 7.34 and s-PTH x dPTH-AC x [H+] between 0.5 and 3.7 units with the distinguishability index 'very good' (< 5% overlap) towards normals. Average similarity of uremic patients with the prototype for normal subjects was only 22%. Cluster analysis of all the variables was conducted for comparison and yielded less clinically relevant information. Hence, emulation done by the expert system was superior and clearly indicates that present treatment modalities restore normal bone turnover only to a minor degree or not at all.
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PMID:PTH-stimulated adenylate cyclase activity and bone histomorphometry in iliac crest biopsies in the evaluation of uremic patients: a pilot study with the use of artificial intelligence. 816 16

The aim of this study was to evaluate the clinical usefulness of the calcitonin test in predicting the hyperparathyroid bone disease severity in uremia. 200 IU of synthetic salmon calcitonin was given intranasally to 77 hemodialysed patients with end-stage renal failure. Before the test, serum calcium, PTH and serum alkaline phosphatase had been sampled; serum calcium was determined also in 2 to 4 hours after. The subjects were divided into 3 groups according to their serum PTH levels. Group I consisted of 24 patients with at least 10-fold serum PTH elevation, group II of 34 patients with intermediate values, and group III of 19 patients with serum PTH within normal range. In the group I the mean serum calcium fall was 0.32 +/- 0.16 mmol/l (1.28 +/- 0.64 mg/dl) (p < 0.001) and 0.27 +/- 0.15 mmol/l (1.08 +/- 0.60 mg/dl) (p < 0.001), after 2 to 4 hours respectively. In the group II serum calcium decreased by 0.16 +/- 0.12 mmol/l (0.64 +/- 0.48 mg/dl) after 2 hours and by 0.14 +/- 0.09 mmol/l (0.56 +/- 0.36 mg/dl) after 4 hours; the differences were statistically insignificant. In the group III no reduction in serum calcium was observed. In the whole 77 patients population significant linear correlations between the hypocalcemic response and iPTH as well as serum alkaline phosphatase were found. Our results confirm that the calcitonin-induced hypocalcemia a test can be, in addition to serum alkaline phosphatase and PTH evaluation, a simple and useful index of advanced hyperparathyroid bone disease in hemodialysed patients with chronic renal failure.
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PMID:[Test with calcitonin as an index of parathyroid function in chronic renal failure]. 850 92

It is still unclear whether dialysis modality, i.e., continuous ambulatory peritoneal dialysis (CAPD) versus hemodialysis (HD) specifically affects bone mineral density (BMD). To answer this question, 34 patients on HD and 25 on CAPD were matched for age, sex, height, and body weight with 125 normal subjects. BMD was measured using dual-energy X-ray absorptiometry (DXA; Hologic QDR 1000/W) at the lumbar spine (trabecular bone), the femoral neck (mixed cortical and trabecular bone), the distal tibial diaphysis (cortical bone), and the epiphysis (trabecular bone) in all subjects. No significant difference for blood hemoglobin, albumin, total and ionized calcium, intact parathyroid hormone (PTH) or phosphorus concentrations, as well as for alkaline phosphatase activity, failed renal allograft, prior steroid therapy, prior parathyroidectomy, duration of uremia, or of dialysis was found between patients on HD and those on CAPD. However, the residual daily urine volume and renal function at the time of the absorptiometry were higher in CAPD than in HD patients (p < 0.05) as well as the mean dialysate calcium concentration during dialysis, the blood bicarbonate concentration, and the residual renal function at the initiation of dialysis (p < 0.01, p < 0.05, and p < 0.005, respectively). In contrast, the total dose of calcium carbonate was lower in CAPD than in HD patients (p < 0.01). Results of BMD were expressed as Z scores (the number of standard deviations from the appropriate mean of BMD of 623 healthy subjects adjusted for age and sex). At the lumbar spine, no significant difference with respect to BMD was observed between the three groups. At the femoral neck and tibial epiphysis, HD patients had lower BMD (p < 0.001) than normal controls, whereas no difference was observed between HD and CAPD patients. At tibial diaphysis, patients on HD had lower BMD (p < 0.001) than patients on CAPD and than normal controls, with the values being similar in patients on CAPD and in normal controls. The results remained identical after exact matching of HD (n = 25) and CAPD (n = 25) patients for dialysis duration (1.9 +/- 0.3 and 1.7 +/- 0.3 years, respectively). Multiple regression analysis revealed significant negative correlations between Z scores at the lumbar spine (p < 0.05), femoral neck (p < 0.02), tibial diaphysis (p < 0.005), and tibial epiphysis (p < 0.05) on the one hand and plasma alkaline phosphatase activity on the other. The Z score at tibial diaphysis was also correlated with residual renal function at the initiation of dialysis (p < 0.05). In conclusion, this study provides evidence for the preservation of cortical bone with CAPD as opposed to HD. The higher residual renal function observed in the former treatment modality might account, at least in part, for this finding.
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PMID:Evidence for preservation of cortical bone mineral density in patients on continuous ambulatory peritoneal dialysis. 877 Jul 2

The activity of gamma-glutamyl transferase (GGT), alkaline phosphatase (AP), lactate dehydrogenase (LDG), N-acetyl-beta-D-glucosaminidase (NAG) was assessed in 53 patients with psoriasis (PS), 24 PS patients with affected kidneys, 50 patients with type 1 diabetes mellitus(DM). Enhanced activity of the enzymes occurred not only in nephropathy patients but also in those without proteinuria. AP and NAG were more active in PS, while LDG and NAG in DM. Both in PS and DM, NAG activity rose 3-4-fold compared to control. A direct correlation was found between enzymuria and uremia, glycemia (in hyperglycemia only) and cholesterolemia. An inverse relationship existed between enzymuria and uricosuria. The above changes in enzymic activity are attributed to impairment of tubules of the kidney induced by PS and DM. Diagnostic significance of enzymuria as a marker of early tubular involvement is confirmed by investigations of renal biopsies.
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PMID:[Urinary enzymes in the assessment of the early stage of kidney involvement in psoriasis and diabetes mellitus]. 877 18

We have previously established a rat model of chronic uremia, which is suitable to investigate the effect of various treatment modalities on renal osteodystrophy [1]. After four months subsequent to 5/6 nephrectomy, some animals were treated by gavage for 9 weeks with tap water (controls), or with aluminium (Al-citrate) 3 x 25 mg/week/kg b.wt +/- subsequent deferoxamine (DFO) 3 x 50 mg/week/kg b.wt. for 4 weeks. At termination of the study, serum clinical chemistry, femoral chemical composition and mechanical properties, calvarial parathyroid hormone (PTH)-elicited adenylate cyclase (AC) and phospholipase C (PLC) activities, cross-sectional femoral area, as well as bone histomorphometry, were analyzed. Animals given Al displayed moderately enhanced serum Al and bone Al accumulation, however, DFO-treatment did not fully alleviate bone Al retainment. A small increase in serum PTH was seen in all animals rendered uremic. Furthermore, a marked fall in serum alkaline phosphatase (ALP) below normal controls was observed in Al +/- DFO-treated animals compared with uremic controls. The uremic condition led to reduced femoral ratios of hydroxyproline (HYP) over Ca(2+) and phosphate (P(i)), while Al-intoxication alone enhanced femoral Hyp contents above values seen for normal controls. The protracted ureamia caused a deterioration of long bone resilience and brittleness, however, Al +/- DFO-treatment seemed to normalize the latter. Contrastingly, Al +/- DFO-gavage enhanced time to fracture. Uremic rats intoxicated with Al showed a complete loss of calvarial PTH-sensitive AC and PLC activities. DFO-treatment normalized PTH-elicited PLC, while PTH-susceptible AC remained super-normal. Al apparently exerts a long term down-regulation of both PTH-sensitive signaling systems as evidenced by studies of rat UMR 106 osteosarcoma cells in culture. The uremic condition enhanced endosteal bone resorption as shown by femoral shaft dimension analysis, while Al +/- DFO-treatment insignificantly reversed the condition. Finally, histomorphometrical analyses showed that DFO-administration tended to normalize aberrant trabecular bone volume, while rectifying both bone resorption and degree of mineralization. In conclusion, we assert that Al-intoxication hampers both processes (i.e. formation and resorption) of bone turnover, and that DFO-treatment to a certain extent prevents the uremia- and Al-induced bone disease in rats.
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PMID:Aluminium-induced bone disease in uremic rats: effect of deferoxamine. 886 40

As with most liver diseases, the symptoms of hepatitis in dogs are nearly always aspecific: the dogs eat less, are apathetic, sometimes have polyuria/polydipsia, and sometimes have diarrhoea. Hepatoencephalopathy and ascites only occur with these symptoms in very advanced stages of chronic hepatitis. Only a part of the dogs have jaundice. Because of these aspecific symptoms, the diagnosis hepatitis is often not taken into consideration, even though the presence of a liver disease can be easily detected by measuring plasma concentrations of alkaline phosphatase and bile acids, one or both of which are elevated. The diagnosis is confirmed by histological examination of a liver biopsy sample. The most common forms of hepatitis are non-specific reactive hepatitis, acute hepatitis, and chronic hepatitis. Non-specific reactive hepatitis is a reaction against endotoxin as a result of sepsis or an increased gastrointestinal absorption. Treatment is directed to the primary process. Leptospirosis also causes non-specific reactive hepatitis, but then renal insufficiency is the most prominent feature. The diagnosis is made not on the basis of a liver biopsy but on the basis of increased IgM titres against Leptospira. Immediate treatment with antibiotics and infusions at the first signs (jaundice and uraemia) can save the animal's life. Acute hepatitis can develop as a result of infection, toxins, or liver hypoxia. There is no specific treatment, but adequate recovery often occurs with supportive treatment. Corticosteroids are contraindicated. Chronic hepatitis, which can lead to cirrhosis, is the most common form of hepatitis. It is an autoimmune inflammatory reaction that is usually caused by a virus infection but sometimes by poisoning (intoxication). Long treatment with prednisolone or azathioprine is usually successful, but early recognition of the disease increases the likelihood of success. Nowadays, chronic hepatitis due to hepatic copper accumulation in Beddlington terriers can be detected by DNA tests. Such tests make it possible to distinguish between carriers and non-carriers. Affected animals can be kept symptom-free by life-long treatment with zinc gluconate or penicillamine.
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PMID:[Hepatitis in dogs; a review]. 958 48

In 25-30% of premenopausal dialysis women low serum estrogen concentrations are observed. This "premature menopause" can significantly contribute to accelerated bone loss. The aim of the study was to evaluate the effect of estrogen-gestagen replacement therapy on bone mineral density (BMD) in hemodialysis women with secondary to uremia estrogen deficiency. Among 20 hemodialysis women, aged 18-45 years, with serum 17 beta-estradiol < 30 pg/ml, ten (group I) received transdermal estradiol with cyclic addition of noretisterone acetate (Estracomb TTS 50/0.25), and another ten formed the control group (group II). BMD was evaluated by dual photon x-ray absorptiometry (DEXA, Lunar) in: lumbar spine (L2-L4), 1/3 distal radius and femoral neck, before and after the study. Serum 17 beta-estradiol concentrations were measured before, and after 1, 3, 6 and 12 months of the study. After one year, in group I, in which serum 17 beta-estradiol normalized already during the first month (p < 0.001), an increase of in BMD was noted, although significant only in L2-L4 (p < 0.05). In group II, no change in serum 17 beta-estradiol and mild but insignificant decrease in BMD were observed. However, a comparison of BMD values after 12 months in both groups revealed the marked differences in all studied sites (p < 0.01, p < 0.02, p < 0.05 in L4-L2, distal radius and femoral neck, respectively). The mean serum calcium, phosphate, PTH and alkaline phosphatase activity were similar in both groups and did not change during the study. In premenopausal hemodialysis women with estrogen deficiency, hormonal replacement therapy inhibits bone demineralization and can be useful in prevention of early osteoporosis.
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PMID:[The prevention of bone mineral loss with hormonal replacement therapy in premenopausal women on dialysis with estrogen deficiency]. 1094 98

The treatment of secondary hyperparathyroidism (HPT) in patients with chronic renal disease has improved markedly in recent years. The skeletal pain, disabling fractures, tendon ruptures, and myriad other symptoms associated with HPT can now be avoided, and the quality of life of patients with end-stage renal disease is improved. Control of hyperphosphatemia, maintenance of normocalcemia, and appropriate dosing of vitamin D analogues can prevent HPT in many cases. Palatable, nutritious diets should be followed; serum calcium, phosphorus, alkaline phosphatase, and parathyroid hormone should be monitored; and treatment regimens should be adjusted accordingly. If prevention fails, and even if severe HPT develops, many of these patients can still be controlled medically with correction of hyperphosphatemia and high doses of intravenous calcitriol. In our experience, only a few patients require surgical parathyroidectomy (usually noncompliant patients or patients whose HPT has been poorly managed from early uremia). The essence to medical management is to correct the two most important pathogenetic factors of HPT, hyperphosphatemia, and calcitriol deficiency. We present the current approach to the management of HPT, with highlights of recent advances.
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PMID:Current medical management of secondary hyperparathyroidism. 1098 84


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