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)

Elevated serum transaminases, particularly SGOT, as a result of acetylsalicylic acid (ASA) therapy have been reported in patients with juvenile rheumatoid arthritis (JRA). In order to evaluate the possibilities that these elevated transaminases may result from JRA itself or from concomitant muscle injury, we correlated liver function tests and a specific test for muscle damage, creatine phosphokinase (CPK), with ASA therapy in 37 patients. These JRA patients were evaluated serially; 20 took ASA continuously, 6 took it intermittently, and 11 were on no therapy. Thirty-five healthy children were also studied to establish normal control values for the serum enzyme tests. Mean SGOT and SGPT in the 11 untreated subjects were significantly (P less than.001) higher than normal controls while CPK and alkaline phosphatase (AP) were not elevated. Mean SGOT and SGPT were also significantly (P less than .001) elevated in 20 children receiving ASA continuously; CPK was normal and AP less (P less than .05) than normal. CPK was elevated in 13 patients. Elevation of enzymes was sporadic and there was no correlation with serum salicylate, sex, age, disease duration, type, or activity. We conclude that mild abnormalities of SGOT and SGPT in JRA patients are common, but that they occur sporadically and elevated values appear to be unrelated to ASA therapy.
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PMID:Serum enzyme abnormalities in juvenile rheumatoid arthritis. 98 Jun 5

Recent reports of and our own experience with biochemical alterations of liver function secondary to salicylate therapy stimulated this prospective study. Thirty-four children with juvenile rheumatoid arthritis, 6 children with acute cartilagenous necrosis of the hipfollowing slipped capital femoral epiphysis, and 2 children with ulcerative colitis and hip disease who were on salicylates were followed over a period of 1-27 months with serial determinations of serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), lactic dehydrogenase (LDH), alkaline phosphatase (AP), bilirubin, and serum salicylate. Prothrombin time was measured in 14 children. Twenty-two of 34 children with rheumatoid arthritis and none of the 8 controls demonstrated abnormalities of various liver functions at serum salicylate levels between 7.0 and mg%. Three children demonstrated severe abnormalities characterized by marked elevation of SGOT, SGPT, LDH, and AP, prolongation of prothrombin time, and epistaxis. This type of reaction occurred within 5-14 days of initiation of aspirin therapy and occurred at serum salicylate levels between 18 and 43 mg%. Moderate changes in various liver function tests were observed in 19 other children. None of those children who were tested showed prolongation of prothrombin time. The serum salicylate level in this group varied between 7.0 and 38.2 mg%. The abnormal liver function tests returned to normal in 6 children upon withdrawal of aspirin and in 12 others even when salicylates were continued. Therefore, despite the occurrence of biochemical abnormalities following chronic salicylate therapy, it does not appear to be necessary to discontinue their use except in those children who develop bleeding.
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PMID:Aspirin-induced hepatotoxicity in juvenile rheumatoid arthritis. A prospective study. 115 54

We studied a case of Fahr's disease type idiopathic intracerebral calcification (Fahr's disease) associated with juvenile rheumatoid arthritis. The patient was a 15-year-old male with a chief complaint of gait disturbance. His family members had no similar signs and symptoms. His parents had no consanguinity. He was born with the normal perinatal course at 1967. He had repeated episodes of convulsive attacks during fever elevation from 2 years and 8 months to 9 years of age. Morning stiffness of bilateral hands, and pernio in the auricles, fingers, planta, and toes had occurred in every winter, since 6 years old. Swelling and pain of the bilateral knee and foot joints appeared, making ambulation difficult in 1983 (15 years old), and the patient was admitted to our hospital in July, the same year. On admission, congenital anomalies such as epicanthus and high-arched palate were noted, and swelling, deformation and contracture of limb joints, and Raynaud phenomenon were shown. His ocular fundus showed no arteriosclerotic change. He didn't have Albright's sign. Mild mental retardation and bilateral pyramidal tract signs were noted, but extrapyramidal tract and cerebellar signs, and sensory disturbance were absent. Laboratory findings exhibited markedly elevated ESR, positive CRP, RA, and antinuclear antibody. The levels of serum Ca, P, alkaline phosphatase and parathyroid hormone were normal. Peripheral blood study showed microcytic and hypochromic anemia. Anti-DNA antibody was negative. Ellsworth-Howard test was positive. Elevated antibody titer to toxoplasma, rubella virus, herpes simplex virus and cytomegalovirus were not proven. He had no chromosomal change.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of Fahr's disease associated with juvenile rheumatoid arthritis]. 179

Deflazacort was substituted for Prednisone (based on the equivalence 1 mg Prednisone equals 1.2 mg Deflazacort), during maintenance glucocorticoid therapy in 9 children, 5 with renal diseases and 4 with connective tissue or immunoproliferative disorders. Six patients received 0.26-0.35 mg/kg body weight (B.W.)/day and 3 0.48-1.2 mg/kg B.W. on alternate days, for 10-16 months. Except for a child with chronic juvenile arthritis, who was also unresponsive to Prednisone, the therapeutic effects of Deflazacort were excellent. Steroid side effects present in 8 patients decreased or disappeared. Plasma Ca, P, Mg, creatinine, alkaline phosphatase, iPTH(1-34), urinary excretion of Ca, cAMP, and TRP remained normal. Plasma iPTH(1-84) remained normal in 5 children; in the other 4 patients it increased from normal to slightly elevated values. On Deflazacort, plasma calcidiol concentrations were within the normal range in 6/8 patients prescribed daily doses of vitamin D2 (1,600-2,400 IU) or calcidiol (20 micrograms). Plasma 1,25(OH)2D levels monitored in 5 children were also normal. The osteoporosis, evaluated on the tibial cortico-diaphyseal ratio and the trabecular aspect of bone radiograms, present in 5 patients, persisted in 1 and improved in the others. On Deflazacort, statural growth proceeded normally in all subjects, with a modest acceleration of growth velocity in 3 children. These results seem encouraging for extending clinical trials with Deflazacort to the active phase of pediatric diseases requiring glucocorticoid.
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PMID:Effects of long-term maintenance therapy with a new glucocorticoid, deflazacort, on mineral metabolism and statural growth. 311 67

A patient who developed chronic salicylism associated with salicylate therapy for treatment of juvenile rheumatoid arthritis is described, and the clinical presentation and treatment of chronic salicylism are reviewed. A 5 1/2-year-old boy was receiving aspirin 150/mg/kg/day for treatment of juvenile rheumatoid arthritis. While on salicylate therapy, the patient developed tachypnea and became increasingly hyperthermic, lethargic, and disoriented. The patient developed a maculopapular rash, weakness, and a decreased level of consciousness during the 11 days before admission to the hospital. Physical examination and laboratory determinations revealed that the patient had hypoprothrombinemia, hypoglycemia, and severe hepatic encephalopathy secondary to long-term salicylate toxicity. The patient was treated for hypoglycemia, electrolyte imbalances, thrombocytopenia, and anemia and was discharged after 24 days. Diagnosing chronic salicylism with hepatic dysfunction was difficult because the symptoms are similar to those of stage I to stage II Reye's syndrome. Liver enzymes, including aspartate aminotransferase (also called SGOT), alanine aminotransferase (also called SGPT), alkaline phosphatase, and lactate dehydrogenase, may be elevated in juvenile arthritis patients with hepatic dysfunction. Liver dysfunction usually improves when salicylate therapy is discontinued. Supportive therapy should always be used in symptomatic patients. Children on long-term, high-dose salicylate therapy should be monitored closely, and baseline liver function tests should be performed. The clinical effectiveness of administering sodium bicarbonate in attempts to alkalinize urine and increase salicylate elimination is controversial. In patients with juvenile rheumatoid arthritis who develop chronic salicylism, careful analysis of the patient's medication history, laboratory values, and clinical presentation are necessary to rule out Reye's syndrome.
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PMID:Chronic salicylism in a patient with juvenile rheumatoid arthritis. 370 82

Juvenile Rheumatoid Arthritis (JRA) is frequently associated with osteoporosis. In order to determine if JRA osteoporosis is related to reduced formation or to increased bone resorption or both, serum levels of calcium (Ca), phosphorus (PO4), magnesium (Mg), alkaline phosphatase (ALP), parathormone (PTHi), 25-hydroxyvitamin D3 (25-OHD) and 1,25-dihydroxyvitamin D3 (1,25-(OH)2D), osteocalcin (OT), carboxyterminal propeptide (P-coll-1-c), and carboxyterminal telopeptide of type I collagen (ICTP) were evaluated in 47 JRA children, 33 with active disease and 14 in remission. The therapy consisted of nonsteroidal antiinflammatory (NSAIDs) drugs in pauciarticular subset, NSAIDs and Methotrexate (MTX) in polyarticular, NSAIDs and steroids in systemic onset. OT reflects bone formation, P-coll-1-c reflects collagen production and bone formation, ICTP, marker of collagen degradation in bone, indicates bone destruction. Serum levels of Ca, PO4, Mg, ALP, PTHi 25-OHD and 1,25-(OH)2D were comparable in JRA children and in controls. OT (8.7 +/- 3.7 ng/ml vs 9.6 +/- 5.1), P-coll-1-c (301.2 +/- 118.4 ng/ml vs 264.1 +/- 100.1) and ICTP (15.7 +/- 5.7 ng/ml vs 16.1 +/- 6.1) did not differ statistically in the whole group of JRA children vs controls. OT (8.0 +/- 3.5 vs 10.4 +/- 3.8) and ICTP (14.4 +/- 5.4 vs 18.8 +/- 5.4) were significantly lower in active than inactive group. In polyarticular and systemic onset OT and ICTP were significantly lower than in pauciarticular. No difference was found in active patients treated with steroids vs active patients treated with NSAIDS and NSAIDs plus MTX. The lower serum levels of OT and ICTP in active disease support the hypothesis that both bone formation and resorption are reduced in JRA bone turnover.
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PMID:Bone turnover is reduced in children with juvenile rheumatoid arthritis. 963 20

The enzyme-linked immunospot (ELISPOT) assay is an efficient technique for the enumeration of single cells secreting antibodies and cytokines. For simultaneous differentiation of individual cells producing interleukin-2 (IL-2) and interleukin-4 (IL-4) at a single cell level in human peripheral blood mononuclear cells (PBMCs), a human dual-color ELISPOT assay has been optimized. In the present system, the red spots corresponding to IL-2-secreting cells (T helper type 1, Th1, cells) were developed with horseradish peroxidase and the amino ethyl carbazole (AEC)/H2O2. The blue spots corresponding to IL-4-secreting cells (T helper type 2, Th2, cells) were developed with an alkaline phosphatase and the Vector blue. The usefulness of the assay method was tested. With this system, we could detect the IL-2- and IL-4-secreting cells simultaneously in human PBMCs of a juvenile rheumatoid arthritis (JRA) patient. This procedure provides useful information on clinical immune disorders.
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PMID:A human dual-color enzyme-linked immunospot assay for simultaneous detection of interleukin 2- and interleukin 4-secreting cells. 1497 69

Benign transient hyperphosphatasemia of infancy and early childhood is a self-limiting condition characterized by transiently increased serum alkaline phosphatase in the absence of liver, kidney or metabolic bone diseases. It is often accidentally found in children under five years old and it might be associated with a variety of underlying clinical disorders. Its pathophysiology remains unclear. Herein, we report a case of a 4-year-old girl with a 1-year history of persistent oligoarticular Juvenile Idiopathic Arthritis, who was found to have transient hyperphosphatasemia during a periodic check-up. This clinical case underlines the importance of promptly recognizing this benign condition, which avoids unnecessary extensive investigations.
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PMID:Benign transient hyperphosphatasemia in Juvenile Idiopathic Arthritis: a case report. 3228 64