Professor and Chair, Department of Internal Medicine, The University of Oklahoma College of Medicine, Tulsa, Oklahoma

Skeletal muscles may be involved with inflammation or metabolic abnormalities.The clinical effects of muscle involvement include weakness, fatigue, and muscle cramping.The diagnosis is made by demonstrating muscle weakness, muscle involvement as indicated by an elevation of the CPK, an abnormality on EMG, and the pathology on muscle biopsy.

The antihyperuricemic properties of amflutizole were investigated in studies designed to determine its efficacy and mechanisms of action in individuals with gout and hyperuricemia. In a randomized double blind, multiple dose, crossover study of 29 patients, amflutizole caused a significant dose dependent reduction in serum urate concentrations. Mean serum urate concentrations decreased significantly from 9.6 +/- 1.5 mg/dl to 7.2 +/- 1.3 mg/dl with the 500 mg dosage (p less than 0.01). Detailed studies in 5 patients demonstrated evidence for modest xanthine oxidase inhibition. However, the majority of the antihyperuricemic effect was derived from an enhanced renal clearance of uric acid. Although the drug has significant antihyperuricemic properties, these were inadequate to achieve adequate control of the serum urate concentration in hyperuricemia and gout at the doses utilized.

International Journal of DermatologyVolume 23, Issue 6 p. 411-413 Nonsteroidal Antiinflammatory Drugs (NSAIDs) Common Chemical and Clinical Characteristics Mary E. Cronin M.D., Corresponding Author Mary E. Cronin M.D. Rheumatology Section, Department of Internal Medicine, Medical College of Wisconsin, Milwaukee (Wood), WisconsinAddress for reprints: Mary E. Cronin, M.D., Rheumatology Section, Department of Internal Medicine, Medical College of Wisconsin, Veterans Administration Medical Center, Milwaukee (Wood), WI 53193.Search for more papers by this authorRobert L. Wortmann M.D., Robert L. Wortmann M.D. Rheumatology Section, Department of Internal Medicine, Medical College of Wisconsin, Milwaukee (Wood), WisconsinSearch for more papers by this author Mary E. Cronin M.D., Corresponding Author Mary E. Cronin M.D. Rheumatology Section, Department of Internal Medicine, Medical College of Wisconsin, Milwaukee (Wood), WisconsinAddress for reprints: Mary E. Cronin, M.D., Rheumatology Section, Department of Internal Medicine, Medical College of Wisconsin, Veterans Administration Medical Center, Milwaukee (Wood), WI 53193.Search for more papers by this authorRobert L. Wortmann M.D., Robert L. Wortmann M.D. Rheumatology Section, Department of Internal Medicine, Medical College of Wisconsin, Milwaukee (Wood), WisconsinSearch for more papers by this author First published: July 1984 https://doi.org/10.1111/j.1365-4362.1984.tb03204.xCitations: 4AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat References 1 Calin A: In common clinical usage nonsteroidal anti-inflammatory drugs infrequently produce adverse effects on the kidney. Am J Kidney Dis 2: 485, 1983 2 Corre K, Rothstein R: Anaphylactic reaction to zomepirac. Ann Allergy 48: 299, 1982 3 Dietz A: Necrotizing vasculitis. Arch Intern Med 142: 416, 1982 4 Goodwin J, Ceuppens J: Effect of nonsteroidal anti-inflammatory drugs on immune function. Semin Arth Rheum 13: 134, 1983 5 Henrich W: Nephrotoxicity of nonsteroidals anti-inflammatory agents. Am J Kidney Dis 2: 478, 1983 6 Hudson C, Lawlor F, Wacks H: Benoxaprofen for nodular acne. Lancet 1: 1415, 1982 7 Lipschitz M: Renal effects of nonsteroidal anti-inflammatory agents. J Lab Clin Med 102: 31, 1983 8 Moore M: A rheumatologist's view of nonsteroidal antiinflammatory drugs. Clin Therapeutics 4: 137, 1981 9 Savage WD, Reader F: Benoxaprofen: Effect on cutaneous lesions in psoriasis. Br Med J 285: 1241, 1982 10 Simon LS, Mills JA: Nonsteroidal anti-inflammatory drugs. N Engl J Med 302: 1179, 1980 11 Weissmann G: Pathways of arachidonate oxidation to prostaglan dins and leukotrienes. Semin Arth Rheum 13: 123, 1983 12 Winthrop GJ: Does meclofenamate help psoriasis and arthritis. N Engl J Med 307: 1528, 1982 Citing Literature Volume23, Issue6July 1984Pages 411-413 ReferencesRelatedInformation

Individuals occupying the position of chief medical resident have the opportunity to influence significantly the quality and tenor of medical education and medical practice. To assess the status of the position, the authors surveyed chief medical residents completing their tenure in 1980. These residents distributed their time among administrative (41 percent), teaching (35 percent), patient care (21 percent), and research (3 percent) activities. They reported that their experience was quite positive. However, overall satisfaction was significantly negatively correlated with percentage of time spent performing administrative tasks. The percentage of time chief medical residents allocate to administration has increased during the past decade, while time spent teaching and delivering patient care has decreased. Based upon this survey, recommendations for improved utilization of the time and talents of these individuals are presented.

An economical, computerized system was developed for producing the annual schedule of monthly assignments for medical house officers. This program can generate schedules that conform to the individual preferences of the house officers while meeting the requirements of the residency program. As a result, more individual requests of the house officers are granted than under the previous manual system. Besides providing these direct benefits, the system ensures that house officers are assigned to each rotation according to their appropriate level of skill.

Sixty-four patients were evaluated prospectively for a reflex sympathetic dystrophy syndrome (RSDS), using quantitative clinical measurements, high-resolution roentgenography and scintigraphy. Five separate groups were identified by their clinical features, allowing us to distinguish patients with definite or incomplete forms of the RSDS as well as 16 patients with other disorders. Scintigraphy was found to be a useful diagnostic study that may also provide a method of predicting therapeutic response. Systemic corticosteroid therapy proved to be a highly effective mode of treatment for up to 90 percent of the patients with the RSDS.

Sixty-four consecutive patients were studied for possible reflex sympathetic dystrophy syndrome (RSDS). They were divided into five groups, based upon specific clinical criteria, and the radiographic and scintigraphic findings in each group were examined. Osteoporosis was the most common radiographic abnormality, present in 69% of subjects with definite, probable, or possible RSDS, as compared with 21% opf those with RSDS. Scintigraphic abnormalities were noted in 60% of RSDS patients but in only 7% of the others. These findings included increased blood flow and enhanced periarticular radionuclide activity in the affected extremity. Of 11 patients with serial scintigraphy, six (55%) demonstrated a return to normal, symmetrical patterns following successful therapy. The scan may reflect an active, potentially reversible disorder of local blood flow in RSDS. Furthermore, the scintigraphic patterns may be useful in the diagnosis and in predicting which pattients are likely to respond to systemic steroid therapy.

The value of the uric acid to creatinine ratio and the uric acid to creatinine clearance ratio in predicting 24-hour urinary uric acid excretion was assessed in 49 patients with normal enzyme activity and 22 patients with purine enzyme deficiencies. A 24-hour urinary uric acid to creatinine ratio greater than 0.75 was found in six of nine patients with a partial deficiency of hypoxanthine-guanine phosphoribosyltransferase and in all patients with Lesch-Nyhan syndrome. A ratio of less than 0.10 suggested xanthinuria or severe purine nucleoside phosphorylase deficiency. Neither ratio calculated from 2-hour timed collections of the 24-hour specimen showed a high correlation with 24-hour urine uric acid excretion in patients with normal enzyme activity, perhaps because of a diurnal variation in urinary uric acid excretion. The spot-urine uric acid to creatinine ratio does not accurately predict the 24-hour urine uric acid excretion in patients with normal enzyme activity.

Deoxyadenosine metabolism was investigated in cultured human cells to elucidate the biochemical basis for the sensitivity of T lymphoblasts and the resistance of B lymphoblasts to deoxyadenosine toxicity. T lymphoblasts have a 20-to 45-fold greater capacity to synthesize deoxyadenosine nucleotides than B lymphoblasts at deoxyadenosine concentrations of 50--300 micron. During the synthesis of dATP, T lymphoblasts accumulate large quantities of dADP, whereas B lymphoblasts do not accumulate dADP. Enzymes affecting deoxyadenosine nucleotide synthesis were assayed in these cells. No substantial differences were evident in activities of deoxyadenosine kinase (ATP: deoxyadenosine 5'-phosphotransferase, EC 2.7.1.76) or deoxyadenylate kinase [ATP:(d)AMP phosphotransferase, EC 2.7.4.11]. The activity of 5'-nucleotidase (5'-ribonucleotide phosphohydrolase, EC 3.1.3.5) was increased 44-fold for AMP and 7-fold for dAMP in B lymphoblasts. A model for the regulation of deoxyadenosine nucleotide synthesis by 5'-nucleotidase activity is proposed on the basis of the observations.

The rate of DNA synthesis in cultured diploid fibroblasts, nonmalignant human cells, is decreased by 50 microM 2'-deoxyadenosine when adenosine deaminase is inhibited and 2'-deoxyadenosine is phosphorylated to dATP. No inhibiton of DNA synthesis occurs with 100 microM adenosine under identical conditions or with 50 microM deoxyadenosine when adenosine deaminase is not blocked. Inhibition of DNA synthesis may be an important link between adenosine deaminase deficiency and severe combined immunodeficiency if the tissue culture model is relevant to lymphocyte function in man.

This chapter contains section titled: Properties of the Normal Enzyme Properties of Mutant Enzymes Acknowledgements References Discussion References