Drugs online research references
J Pediatr Gastroenterol Nutr. 1982;1(3):349-54.
Studies on the cause of hyperuricosuria in cystic fibrosis patients.
Niessen KH, Wolf A.
Qualitative and quantitative analyses of the purine contents of 24 pancreatic enzyme preparations currently available in the Federal Republic of Germany were carried out; guanine, adenine, and hypoxanthine were demonstrated in all drugs examined. The contamination level per dosage unit ranged from 2 to 10 mg urate equivalents, which, after purine absorption and metabolism, must be excreted by the kidneys. Although the additional daily urate intake through the ingestion of pancreatic enzyme preparations was less than 70 mg in 16 of 18 cystic fibrosis patients, uric acid excretion was astoundingly high. Compared to the amount of urate excreted in the urine over a 24-h period, urate intake through pancreatic enzyme preparations was so low that these drugs do not represent an important contributing factor for hyperuricosuria. A clear-cut relationship could be demonstrated between the urinary urate concentration and the severity of the disease. The increased catabolism of these patients therefore is more likely the real cause of the hyperuricosuria demonstrable in most cases. Increased fluid intake and administration of allopurinol proved to be an extremely effective means of controlling hyperuricosuria; no side effects were observed.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6926538&dopt=Abstract
J Appl Physiol. 1995 Mar;78(3):1015-22.
Ozone-induced airway hyperresponsiveness: role of superoxide anions, NEP, and BK receptors.
Tsukagoshi H, Haddad EB, Sun J, Barnes PJ, Chung KF.
Department of Thoracic Medicine, National Heart and Lung Institute, Royal Brompton Hospital, London, United Kingdom.
We investigated the role of reactive oxygen species in ozone-induced airway hyperresponsiveness (AHR) in Brown Norway rats. Airway responsiveness to inhaled acetylcholine (ACh) and bradykinin (BK) and inflammatory cell recruitment in bronchoalveolar lavage fluid (BALF) were measured in vivo. Neutral endopeptidase (NEP) activity assay and measurement of BK-receptor binding sites in Brown Norway rat lungs were carried out in vitro. Apocynin (5 mg/kg), an inhibitor of superoxide anion-generating NADPH oxidase, was administered perorally 30 min before a 3- or 6-h exposure to 3 ppm of ozone, and the animals were studied 18-24 h postexposure. Ozone induced increases in airway responsiveness to ACh and BK and in neutrophil counts in BALF. Apocynin inhibited the increase in airway responsiveness to BK but not to ACh without affecting the neutrophil counts in BALF. The antioxidants allopurinol and deferoxamine prevented ozone-induced AHR to both ACh and BK but did not reduce neutrophil counts. To further examine the mechanisms of ozone-induced AHR to BK, we measured NEP activity and the density of BK receptors in vitro after ozone exposure. Ozone exposure had no significant effect either on NEP activity or on the affinity and the number of BK receptors in lungs from rats treated with or without apocynin. We conclude that superoxide anions released from inflammatory cells in the airway may be involved in ozone-induced AHR. Inactivation of NEP or upregulation of BK receptors do not appear to be involved, but the possibility of localized changes cannot be excluded.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7775293&dopt=Abstract
Arthritis Rheum. 1986 Jan;29(1):82-7.
The allopurinol hypersensitivity syndrome. Unnecessary morbidity and mortality.
Singer JZ, Wallace SL.
Patients receiving allopurinol are at risk of developing the allopurinol hypersensitivity syndrome, an immunologic reaction to the drug, characterized by multiple abnormalities such as fever, rash, decreased renal function, hepatocellular injury, leukocytosis, and eosinophilia. The records of 8 patients with the allopurinol hypersensitivity syndrome evaluated at the Downstate Medical Center hospitals and an additional 72 patients described in the literature were reviewed. All were seriously ill. Three of the 8 patients at the Downstate Medical Center hospitals died as a result of allopurinol hypersensitivity; 19 of the 72 previously described patients also died from consequences of taking the drug. Only 1 of our 8 patients with allopurinol hypersensitivity was given allopurinol for an appropriate reason. Eight of the 59 previously described patients on whom there was adequate information had legitimate indications for allopurinol therapy. Severe, often fatal iatrogenic disease occurred unnecessarily in the others.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3947418&dopt=Abstract
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