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Biomedical subjects

A D Meisel

Publications and source records attributed to A D Meisel.

17 recordsLinked to original sources
PubMed1986

Clinical benefits and comparative safety of piroxicam. Analysis of worldwide clinical trials data.

In response to concerns raised about the safety of piroxicam, Pfizer Inc. has reviewed three sets of data that constitute the largest body of current evidence regarding the efficacy and safety of piroxicam. First, data from all comparative clinical trials of piroxicam worldwide sponsored by Pfizer Inc. are reviewed with regard to safety issues, with particular attention to gastrointestinal side effects and safety among elderly patients. Second, the principal findings of a large Norwegian multicenter trial of piroxicam and naproxen, comprising 2,035 patients, are summarized. Finally, the worldwide database of more than 77,000 patients monitored in postmarketing surveillance studies is examined to assess gastrointestinal side effects and the relation of age and sex to these adverse events. There is no evidence in any of the comparative clinical data or postmarketing surveillance data to indicate that piroxicam has greater risks of gastrointestinal toxicity than do other nonsteroidal anti-inflammatory drugs, irrespective of patient age.

Adult↗
PubMed1985

The efficacy of piroxicam in comparison with sulindac in the treatment of rheumatoid arthritis.

The efficacy of piroxicam 20 mg/qd was compared with that of sulindac 200 mg twice a day in 49 patients with rheumatoid arthritis. Both nonsteroidal anti-inflammatory agents showed statistically significant improvement in efficacy variables including duration of morning stiffness, disease activity as judged by the examiner and by the patient, patient assessment of feeling, total joint pain, total joint swelling, and performance of daily activities. The overall frequency of adverse reactions was similar with both treatment regimens, and required discontinuance in three patients in each treatment group. However, the number of moderate/severe adverse reactions in the sulindac-treated patients was greater than that in the piroxicam-treated patients, and there was a trend toward the differences between the two groups being statistically significant (P = .06). Both drugs were effective in the treatment of rheumatoid arthritis and resulted in comparable improvement in efficacy variables.

Arthritis, Rheumatoid↗
PubMed1979

Effect of frentizole on mitogen-induced blastogenesis in human lymphocytes.

Frentizole is a new immunoregulatory agent developed as an alternative to cytotoxic agents. In human lymphocytes, Frentizole inhibits the response to various phytomitogens without decreasing cell viability. Frentizole (500 ng/ml) inhibited thymidine incorporation into DNA most effectively when added to lymphocyte cultures at the same time as the addition of the mitogen. Frentizole (500 ng/ml) markedly inhibited the response to Con A (% inhibition, corporation was dose dependent with 125 ng/ml of Frentizole sufficient to inhibit significantly the response of all three mitogens. Frentizole (62.5 ng/ml) maximally inhibited uridine incorporation, and inhibition of uridine incorporation was independent of the phytomitogen employed. Increasing concentrations of Frentizole were found to have no effect on thymidine or uridine incorporation into unstimulated normal lymphocytes.

Benzothiazoles↗
PubMed1979

The natural history of urate overproduction in sickle cell anemia.

Serum uric acid and uric acid excretion were studied in 95 patients with sickle cell anemia ranging in age from 17 months to 45 years to ascertain the natural history of urate overproduction. Hyperuricemia was infrequent in children with sickle cell anemia, but was found in 26 of 67 adults (39%). Thirty-six patients studied in a clinical research center had a mean urate clearance of 9.1 +/- 0.8 mL/min. Patients with sickle cell anemia were often normouricemic despite urate overproduction. Normouricemia was maintained by increased urate clearance, which was attributed to increased urate secretion. The hyperuricemic patients had decreased urate clearance with decreased pyrazinamide-suppressible urate clearance. Para-aminohippurate clearance was decreased to 634 mL/min in the hyperuricemic patients with sickle cell anemia compared with 853 mL/min in normouricemic hyperuricosuric subjects with sickle cell anemia. Hyperuricemia occurs only in patients who develop altered renal tubular function with diminished urate clearance secondary to diminished urate secretion.

Adolescent↗
PubMed1977

Effect of pharmacological inhibitors on urate transport during induced uricosuria.

1. The effect on urate excretion of administration of probenecid and pyrazinamide was observed in normal subjects under control conditions and after induction of uricosuria by exogenous urate loading by ribonucleic acid feeding in seven subjects, by volume loading with hypertonic sodium chloride solution infusion in 11 subjects and by partial inhibition of net urate reabsorption with uricosuric drugs in 20 subjects. 2. After ribonucleic acid feeding, the uricosuric response to probenecid was intact and ribonucleic acid feeding did not produce uricosuria after pyrazinamide. 3. After volume loading, the uricosuric response to probenecid was again intact, but infusion of sodium chloride solution still produced uricosuria after pyrazinamide administration. 4. After uricosuric drugs, the uricosuric response to probenecid was diminished. 5. These responses to probenecid and pyrazinamide may reflect different mechanisms of uricosuria. Response to pharmacological inhibitors of urate reabsorption or urate secretion may be useful for classification of induced and clinical uricosuric states.

Adult↗
PubMed1977

Inhibition of probenecid uricosuria by pyrazinamide and para-aminohippurate.

Both para-aminohippurate (PAH) and pyrazinamide inhibited the uricosuric response to probenecid administration. The mechanism of this inhibition of probenecid uricosuria was assessed in 18 male subjects. The decrease in uricosuria was assessed in 18 male subjects. The decrease in uricosuric response to probenecid observed after pyrazinamide administration or PAH infusion occurs by different mechanisms. Administration of PAH and probenecid together resulted in reduced excretion of both drugs. PAH was weakly uricosuric and did not appear to inhibit urate secretion. PAH inhibition of probenecid uricosuria is accounted for by inhibition of probenecid secretion. Probenecid excretion was not affected by pyrazinamide administration. Inhibition of probenecid-induced uricosuria by pyrazinamide is most likely due to inhibition of urate secretion. The urate secretory carrier inhibited by pyrazinamide appears to be independent of that responsible for secretion of probenecid and PAH. Probenecid secretion appears to be required for its uricosuric effect.

Adolescent↗
PubMedDate not supplied

Postsecretory reabsorption of urate in man.

These results are consistent with a model for renal tubular transport of urate in which there is reabsorption of both filtered and secreted urate. Urate secretion greatly exceeds total urate excretion, and most secreted urate is reabsorbed. At least a portion of urate reabsorption occurs at a site distal to or coextensive with the urate secretory site. There appear to be at least two distinct reabsorptive mechanisms for urate. The results of the flow rate and vasopressin studies are consistent with the hypothesis that urate reabsorption occurs in both the distal and the proximal tubule in man. The distal reabsorptive site appears to be quite small. It may be passive since it does not appear to be inhibited by uricosuric drugs. This reabsorptive site may account for less than 15% of total urate reabsorption. Both volume expansion and probenecid may inhibit urate absorption only in the proximal tubule. Thus reabsorption in the proximal tubule coud account for more than 90% of total urate reabsorption. Reabsorption at the postulated collecting duct reabsorptive site appears to be too small in magnitude to account for all reabsorptions of secreted urate. This could be explained if the reabsorptive site in the proximal tubule is coextensive with or distal to the secretory site. Alternatively, there might be two reabsorptive sites in the proximal tubule: a presecretory site accounting for the reabsorption of most filtered urate, and a site either coextensive or distal to the secretory site accounting for a major component of reabsorption of secreted urate. Finally urate reabsorption would also take place in the collecting duct, perhaps at a passive, flow-dependent site.

Aspirin↗
PubMedDate not supplied

Hyperuricosuria in the Fanconi syndrome.

A patient with asymptomatic adult Fanconi syndrome with glycosuria, amino-aciduria, hypophosphatemia, and renal tubular acidosis was found to have hypouricemia (serum uric acid, 1.5-1.8 mg/100 ml) secondary to increased renal clearance of urate (urate clearance/glomerular filtration rate, 32 per cent). Increased urate clearance in this patient with multiple reabsorptive defects probably represents diminished urate reabsorption. Consistent with this, the uricosuric response to probenecid was diminished. Reabsorption of filtered urate appeared to be intact. Inhibition of urate secretion with pyrazinamide completely suppressed the uricosuria in this patient, suggesting that increased urate clearance was due to either enhanced secretion or diminished reabsorption of secreted urate. There was no direct evidence for increased urate secretion. The response of urate excretion to pharmacologic inhibitors of tubular transport of urate differs in various clinical states associated with hyperuricosuria. The responses may reflect different mechanisms of hyperuricosuria.

Fanconi Syndrome↗