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)

The present study reports of three kinds of experiments of unaffected primary rejection of xenogenous kidney transplanats in the close-related fox-dog species system. The issue is whether there is a relation between the amount of grafted parenchyma and the immune induced potency, that is whether the course of rejection of transplanted single kidneys (group I a) differs from the course after en-bloc transplantation of both kidneys (group I b). In group II alterations of blood chemism and behavior of humoral antibodies are followed in dogs to which a fox kidney was transplanted, while keeping their own functioning kidneys. This experiment is to give information whether the uremic syndrome influences the development of humoral immunity, and what changes of blood chemism may primarily be related to destruction of the graft, under the condition of absent uremia. Untreated graft recipients survived for 5,4 +/- 0,49 days (n = 5) when single kidneys were transplanted (group I a), and 5,2 +/- 0,75 days (n = 5) when both kidneys were grafted en-bloc (group I b). As to the rejecting reactions, both groups are almost equal: the increasing functional failure causes a fast increase of creatinine and urea nitrogen; alkaline phosphatase and LDH show distinct alterations, related to the progress of the graft's destruction. Decrease of albumin level and loss of cholinesterase activity indicate an impaired hepatic function as reaction to uremic intoxication. Gamma-globulins and leucocytes show alterations that can be related to non-specific inflammatory reactions. The immunologically specific initial lymphopenia suggests that after revascularization these cells migrate to the graft, and later react with antigenic structures of vascular endothelium and still later with those of the organ cells. Cytotoxic antibodies appear on the 4th postoperative day in increasing amount. Post mortem histologic examination shows round cell infiltrates in the vastly necrotic renal parenchyma. When the recipient's kidneys are kept in situ and a fox kidney is transplanted (group II) uremia is avoided and the animals survive. During the 30-days period of observation, that is longer than the term of rejection, the titer of cytotoxic antibodies remains stable or tends to increase. LDH and alkaline phosphatase show characteristic changes that are considered sequels from destructed transplantate. The experiments show, aside from certain reservations, that the donor-host combination fox-dog is suitable to serve as preclinic model for human transplantation using xenogenous donors of organs, i. e. anthropoid primates.
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PMID:[The unaffected primary rejection of xenogeneic kidney transplants in the closely related fox-dog species system]. 3 59

The index of the leukocyte alkaline phosphatase activity (LAP-I) was evaluated in 15 patients suffering from chronic uremia immediately before and after hemodialysis, as well as 16 or 18 and 40 or 42 hours thereafter. Immediately following hemodialysis the LAP-I was significantly reduced in comparison with to predialysis values. 16 and 18 hours after hemodialysis the LAP-I had again increased and at 40 and 42 hours exceeded the starting predialysis values. These results are discussed in relation to the dialysis-induced decrease of plasma cortisol and to the consequent ACTH and cortisol overproduction.
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PMID:[The index of leukocyte alkaline phosphatase in patients with hemodialysis (author's transl)]. 19 May 25

The effects of phosphate restriction and of 1 alpha OH D3 administration were investigated in patients with advanced chronic renal failure. Few modifications of the various biochemical parameters in the patients were achieved with the restriction of dietary phosphate while better results were obtained with 1 alpha OH D3 administration. In dialyzed patients the treatment with this drug resulted in a normalization in serum calcium and alkaline phosphatase levels and in a remarkable significant decline in plasma parathyroid hormone and a reduction in the bone disease associated with uremia. This treatment in dialyzed uremic patients could avoid the employment of higher dialysate calcium concentration potentially dangerous for postdialysis hypercalcemia with the risk of metastatic calcifications.
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PMID:Effects of 1-alpha OH D3 therapy in uremic patients in conservative or dialytic treatment. 47 81

The pharmacokinetics of gentamicin, tobramycin, and amikacin in the inner ear fluids and serum of the guinea pig were studied. The concentrations of these antibiotics were determined by a microbiological method and could be confirmed by the use of 14C-labeled gentamicin. Retention was clearly demonstrated in perilymph and endolymph, whereas there was no retention in the cerebrospinal fluid and the compartments of the eye. A linear relation between concentrations in the perilymph and dosage of gentamicin was ascertained. There was no difference between the concentration of drug in endolymph and that in perilymph. The concentrations of these antibiotics in the perilymph were symmetrical and many times higher than those in the brain. Long-term treatment did not influence the pharmacokinetics of the three antibiotics in the inner ear. However, increased levels of drug in the inner ears in animals with uremia and in some animals with otitis media explained the increased ototoxicity that was observed in histological investigations of these two conditions. Cisternal puncture and diuretics did not change the concentrations of aminoglycoside antibiotics in the inner ear. In large experimental series the hair cell degeneration pattern of the new aminoglycoside antibiotics was determined by the surface preparation technique as well as the influence of the different factors upon this pattern. A prophylactic effect on the ototoxicity of the aminoglycoside antibiotics could not be found in the 2,3-dimercaptopropanol, but by dividing the daily dosage administered. Young guinea pigs were generally not very sensitive to gentamicin, in some cases however much more. Late ototoxicity could not be found after administration of gentamicin. The pharmacokinetical and especially the histological investigations allowed an evaluation of the ototoxicity of the new aminoglycoside antibiotics. By histochemical investigations no influence of the new aminoglycoside antibiotics upon the amount of unspecific esterases and alkaline phosphatase in the inner ear could be detected, but an increase of the amount of acid phosphatase in slightly damaged outer hair cells.
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PMID:[Pharmacokinetical, histological, and histochemical investigation on the ototoxicity of gentamicin, tobramycin, and amikacin (author's transl)]. 57 30

Although anemia has not been widely appreciated as a complication of primary hyperparathyroidism, 5.1% of the individuals with this disorder seen at the Massachusetts General Hospital since 1962 had a normochromic, normocytic anemia that could not be related to blood loss,a deficiency state, or uremia. The anemic group had more advanced bone disease and higher levels of serum calcium, alkaline phosphatase, and parathyroid hormone than the nonanemic group. Results of bone marrow biopsies performed in five patients showed variable degrees of myelofibrosis. However, none of the patients had hepatosplenomegaly, a myelophthisic peripheral blood smear, leukopenia, or thrombocytopenia. Removal of the abnormal parathyroid glands led to improvement or correction of the anemia.
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PMID:Anemia in primary hyperparathyroidism. 85 57

A report is given on advances in our knowledge of the ototoxicity of aminoglycoside antibiotics. The pharmacokinetics of gentamicin, tobramycin, sisomicin and amikacin in the inner ear, cerebrospinal fluid, compartments of the eye and serum were determined by means of pharmacokinetical investigations. The influence of long-term treatment, and the effects of otitis media and uremia were also studied. Furthermore, the influence of therapeutic methods on ototoxic damage was investigated, and the ototoxicity of these antibiotics was compared. The experiments were performed in guinea pigs, concentrations of the antibiotics being measured by a microbiological method and confirmed by investigations with C14 labeled gentamicin. The hair cell degeneration pattern after administration of the new aminoglycosides was determined using surface preparations. The prophylactic effect upon ototoxicity of the administration of dimercaptopropanol or of dividing up the daily dosage was examined. Studies were made of ototoxicity in children, and in patients with otitis media or renal impairment, and the effect of simultaneous ethacrynic acid or noise was assessed. The problem of delayed and progressive ototoxicity, and the reversibility of ototoxic damage caused by these antibiotics was examined histologically, and the ototoxicity of gentamacin, tobramycin, sisomicin and amikacin was compared. The influence of the new aminoglycoside antibiotics upon the amount of acidic and alkaline phosphatase and unspecific esterases in the inner ear was studied. The clinical importance of the latest experimental findings is emphasised. The clinical picture of ototoxic damage after administration of the new aminoglycoside antibiotics shows no special characteristics. The ototoxicity of these antibiotics after topical use is mentioned. Attention is drawn to guidelines for the prevention of ototoxic damage by aminoglycosides.
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PMID:[Ototoxicity of the aminoglycoside antibiotics (author's transl)]. 101 84

The use of intestinal segments in the urinary tract can cause metabolic changes that depend on the intestinal segment utilized. The severity of these changes basically depends on the area of the intestinal mucosa in contact with urine, the duration of exposure to urine and renal function. The length of time the intestinal mucosa is in contact with urine largely depends on the surgical technique employed. It is longer for the reservoirs, intestinal neobladders and ureterosigmoidostomies than for the intestinal conduits with cutaneous urinary diversion and therefore carry a higher incidence of metabolic changes. Jejunal urinary diversion causes metabolic acidosis with hypochloremia, hyponatremia, hyperpotassemia, azotemia and dehydration in at least 50% of the cases. Ileal and colonic urinary diversion can cause metabolic acidosis, although the incidence is significantly less. Acidosis presents with hyperchloremia, hyperammonemia, hypersulfatemia, increased osmolality and uremia with normal creatininemia and a tendency to develop hypocalcemia, hypophosphoremia and hypomagnesemia. Recent studies performed in our service show that acidosis is basically due to the secretion of sodium bicarbonate by the intestinal segment used in the urinary tract, which causes water-salt depletion that is compensated by secondary hyperaldosteronism. Mild chronic acidosis is neutralized via the respiratory system and by the bone buffers, which leads to bone remodelling manifested by the significant increase of serum alkaline phosphatase levels and increased calciuria. These calcium phosphate changes, although statistically significant, do not appear to be important since they were not accompanied by changes of serum PTH levels, 25 and 1-25-cholecalciferol. Nicotinic acid as inhibitor of cyclic AMP synthesis failed to correct metabolic acidosis in the patients with transileal diversion.
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PMID:[Physiopathology and treatment of metabolic changes in transintestinal urinary diversions]. 133 44

We have developed an animal model to study the pathogenesis of secondary hyperparathyroidism by inducing stable uremia in Sprague-Dawley rats by selective microligation of terminal branches of the left renal artery, followed by right nephrectomy. After 4 weeks the animals were killed, the parathyroid glands were removed and weighed, and blood samples were obtained. Of 30 rats, uremia developed in 22 (73%; uremic group) and eight (27%) died or did not become uremic. A sham-operated group of 15 rats served as control (control group). Creatinine levels were 1.8 +/- 0.5 mg/dl in the uremic group versus 0.5 +/- 0.1 mg/dl in the control group (p less than 0.0001). Parathyroid glands were hyperplastic in all rats with uremia and were heavier than parathyroid glands of control animals (70.3 +/- 26 vs 19.1 +/- 8 micrograms; p less than 0.0001). In the group with uremia, parathyroid hormone levels were increased over those of the control group (112.6 +/- 13 vs 28.9 +/- 6.2 pg/ml; p less than 0.0001), whereas osteocalcin levels were similar (36.6 +/- 11 vs 37.5 +/- 1 ng/ml). Serum calcium, phosphate, and alkaline phosphatase levels were similar in both groups. Our model can be used to test hypotheses concerning the treatment of secondary hyperparathyroidism and the relative pathogenetic relevance of vitamin D deficiency and phosphate retention.
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PMID:A new experimental model for secondary hyperparathyroidism. 258 5

Osteitis fibrosa, a frequent complication of chronic renal failure, is characterized by increased rates of bone formation and bone resorption due to increased secretion of parathyroid hormone (PTH). Effective treatment with oral calcitriol is often impossible in patients with osteitis fibrosa, because low doses may cause hypercalcemia. Because short-term infusions of intravenous calcitriol are capable of suppressing the secretion of parathyroid hormone in patients with uremia without causing hypercalcemia, we evaluated the effectiveness of long-term intermittent calcitriol infusions (1.0 to 2.5 micrograms three times weekly, during dialysis) in treating severe osteitis fibrosa in 12 consecutive patients on hemodialysis whose disease was refractory to conventional therapy. After a mean (+/- SE) treatment period of 11.5 +/- 1.4 months, the mean bone-formation rate declined from 1642 +/- 277 to 676 +/- 106 microns 2 per square millimeter per day (P less than 0.01) in the 11 patients who successfully completed the study. Similar reductions occurred in the osteoblastic osteoid (18 +/- 3 to 9 +/- 2 percent; P less than 0.01) and the degree of marrow fibrosis (6.2 +/- 1.7 to 3.5 +/- 1.3 percent; P = 0.01). Concomitant serum biochemical changes included increased calcium levels (2.55 +/- 0.03 to 2.67 +/- 0.05 mmol per liter; P less than 0.01), decreased alkaline phosphatase levels (489 +/- 77 to 184 +/- 32 U per liter; P less than 0.001), and decreased levels of PTH (amino-terminal, 172 +/- 34 to 69 +/- 16 ng per liter in five patients, P less than 0.03; and carboxy-terminal, 1468 +/- 467 to 1083 +/- 402 ml-eq per liter in six patients, P not significant). Although the majority of the patients had transient episodes of asymptomatic hypercalcemia, this complication could be quickly reversed by temporarily halting treatment or decreasing the dose of calcitriol. We conclude that long-term intermittent infusions of intravenous calcitriol are effective in ameliorating osteitis fibrosa in patients on dialysis. Patients whose osteitis fibrosa is refractory to oral calcitriol and who are candidates for parathyroidectomy should be considered first for intravenous calcitriol therapy.
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PMID:Intravenous calcitriol in the treatment of refractory osteitis fibrosa of chronic renal failure. 274 71

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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