Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

10 types of drugs in current use believed to induce cataracts are identified and the evidence of their role is presented. Allopurinol, an antihyperuricemic used to treat gout, may induce cataracts in young subjects after longterm treatment. Experimental results suggest a relationship between the rate of circulating allopurinol, the extent of exposure to ultraviolet light, and perhaps individual susceptibility. Amiodarone hydrochloride is a benzofurane derivative used to combat cardiac arrhythmia since 1960. Cataracts are infrequently observed in users and the complication may be encouraged by association with other medications. Use of anticholinesterasics to treat chronic or acute glaucoma leads to cataracts in 20-50% of cases according to different workers. The rate is about the same for all anticholinesterasics but may be higher in older subjects. The drugs should not be used if the tension can be controlled by parasympathicomimetics and epinephrine or perhaps carbon anhydrase inhibitors. If they are used, the patient should be carefully examined every 6 months for vacuoles. The smallest possible dose should be used. Synthetic antimalarials, the chelator deferoxamine, inorganic mercury, and the phenothiazines have all been associated with cataract formation. The risk of cataracts associated with corticoids increases with the amount of the daily dose and the duration of treatment, with individual susceptibility apparently also playing a role. Sex is not a factor but young children may be at greater risk. Among the cytostatics, the alkylants have been implicated in development of ocular lesions, although the metaphase inhibitor vincristine has been shown in vitro to be responsible for cataracts as well. There is some evidence that diphenyl hydantoine used with phenobarbitol to treat epilepsy may induce cataracts. Some cases of cataracts have been reported in young women using combined oral contraceptives (OCs) for whom no other etiology was found. The implicated OCs had higher hormonal contents than those currently in use. A prospective study by Faust and Tyler did not uncover any evidence of the etiologic role of OCs, but elsewhere a case was reported in which evolving cataracts were stabilized on termination of OC use. Another study found no increase in opacities after 6 months of treatment with OCs. Experimental evidence of a link was found in rabbits but the doses were so high that they cannot be considered to confirm a toxic effect in women using OCs. It appears difficult to establish a relationship except of coincidence between OC use and appearance of cataracts. OCs should not be reported to cause cataracts only because no other etiology has been found.
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PMID:[Cataracts]. 286 44

We have shown that an unusual morphological thinning of the anterior clear zone of the lens is found in patients with gout on long term Allopurinol therapy. The significance of this is discussed.
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PMID:The prevalence and morphology of cataract in patients on allopurinol treatment. 325 96

Although allopurinol is primarily known as an effective medication for gout, it has been shown to enhance tissue survival in a wide range of ischemic conditions. The study reported here investigated the effects of allopurinol on flap survival in a dorsal rat model. In a preliminary study, animals were given varying doses of allopurinol (0 to 400 mg per kilogram). A clinically efficacious dose was established upon conclusion of the test period by laboratory determinations and necropsy data. Other animals were divided into 3 groups: 1 (saline control), N = 11; 2 (50 mg per kilogram of allopurinol daily), N = 10; 3 (100 mg per kilogram of allopurinol qd), N = 11. Flaps were raised and necrosis assessed at 8 days. Flaps treated with allopurinol 100 mg per kilogram had significantly better survival than the controls (p less than 0.001) and 50 mg per kilogram (p less than 0.01). Allopurinol 50 mg per kilogram had no effect on flap survival.
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PMID:Augmentation of skin flap survival with allopurinol. 360 84

Allopurinol (4-hydroxypyrazolo (3,4-d)-pyrimidine) is a potent xanthine oxidase inhibitor which inhibits the oxidation of naturally occurring oxypurines, thus decreasing uric acid formation. The clinical and metabolic effects of this agent were studied in 80 subjects with primary and secondary gout and other disorders of uric acid metabolism. Allopurinol has been universally successful in lowering the serum uric acid concentration and uric acid excretion to normal levels, while not significantly affecting the clearance of urate or other aspects of renal function. Oxypurine excretion increased concomitantly with the fall in urine uric acid. The agent is particularly valuable in the management of problems of gout with azotemia, acute uric acid nephropathy and uric acid urolithiasis. The minor side effects, clinical indications and theoretical complications are discussed.
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PMID:The treatment of gout and disorders of uric acid metabolism with allopurinol. 592 71

It has been recognized that primary disorders of uric acid metabolism result from impaired renal excretion or increased endogenous production of uric acid. It has also been found that these two mechanisms do not comprise two distinct syndromes, but may each constitute a group of syndromes. Contrary to earlier as well as currently published reports we conclude from our clinical and experimental experience that the fraction of so-called over-producers is less than 1% of all patients with primary hyperuricaemia and gout. A procedure for the diagnosis of uric acid overproduction is suggested. The manifestation of hyperuricaemia and gout mainly depends on renal uric acid clearance and is greatly influenced by dietary habits in most of the patients. An impaired renal uric acid excretion results in an increased intestinal excretion; this partly compensates for the defect. Normalization of serum uric acid should be achieved by dietary regimens with or without additional drug treatment, but not by drug treatment alone. With drug treatment xanthine oxidase inhibitors are preferable to uricosurics; no other xanthine oxidase inhibitor besides Allopurinol has been in clinical trial, however. Due to the enhancement of uric acid clearance with uricosurics, there are groups of patients who should not be treated with these drugs. Fixed combinations of Allopurinol and uricosurics should not be used. Drugs which have uricosuric as well as other pharmacologic properties are under investigation. So far they have not reached general clinical application.
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PMID:Gout and uric acid nephropathy: some new aspects in diagnosis and treatment. 668 51

In a metabolic ward study of five patients, azapropazone lowered plasma uric acid but exerted only a modest and variable uricosuric effect without altering urinary xanthine and hypoxanthine levels. An alternative mechanism other than uricosuria or xanthine oxidase inhibition must account for some of the hypouricaemic action of this drug. During the first day of treatment urine volume and pH declined sharply. In a separate investigation, 22 patients were given azapropazone and 18 were given allopurinol combined with colchicine for 3 months. Allopurinol reduced plasma uric acid more quickly but at the end of the study there was little difference in the hypouricaemic results achieved by both drugs. Recurrent gout occurred more frequently with allopurinol but side-effects were confined to those taking azapropazone. A slight rise in blood urea and creatinine and a fall in haemoglobin were also features of long-term azapropazone treatment.
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PMID:Azapropazone--a treatment for hyperuricaemia and gout? 669 72

The potential etiologic relationship between uric acid in its microcrystalline monosodium urate form and psoriasis was examined by 1) substantiating the reported correlation between hyperuricemia and psoriasis using the phosphotungstate method; 2) examining psoriatic tissue samples for the presence of urates under a microscope using polarized light and a compensator; 3) attempting to induce psoriasis-like symptoms in laboratory animals with purine-to-uric acid metabolism by increasing serum uric acid level; and 4) observing psoriasis-hyperuricemic patients following treatment for their hyperuricemia with Allopurinol. As expected, both men and women psoriatics had higher uric acid levels than did their counterparts in a control group. Monosodium urate crystals were found in samples from psoriatic plaques by both methods used. They were clustered particularly around sweat pores and Munro abscesses, but were found only occasionally in epidermal tissue taken from nonpsoriatics. Psoriasis-like symptoms were induced in laboratory animals (the South American boa, Constrictor constrictor) when they were fed doses of uric acid. Patients with psoriasis and hyperuricemia showed marked improvement in psoriasis when treated for their hyperuricemia. Psoriasis, like gout, may be, at least partly, a result of disorder of purine metabolism and monosodium urate crystals may be responsible for the cell proliferation that is characteristic of psoriatic plaques. Monosodium urate crystals were found by the author to be strikingly segmented. This structure may result in ease of fragmentation, thus increasing the difficulty in identifying urates in any tissue.
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PMID:Uric acid in the etiology of psoriasis. 733 93

Six members of kindred with only one surviving male in three generations, a history of an unusual combination of precocious gout in a girl of nine and rapidly progressive renal disease in young women, have been investigated. Sensitive indicators of the familial defect were the early development of hyperuricemia, an inability to concentrate the urine, and a patchy non-specific interstitial nephritis at biopsy. All these features were disproportionately severe for the young age and sex of affected subjects, and the relatively moderate reduction of GFR in some. Identification of these characteristics enabled the recognition of an early stage of the disease in one young family member whose renal function had previously been normal. The histopathology of the renal lesion in this normotensive teenage girl was similar to that frequently attributed to ageing or hypertension in the archetypal middle-aged gouty male, indicating that neither age nor vascular lesions are necessarily implicated in the latter. Allopurinol has halted further progression of the renal lesion in this young girl over two years. It is thus possible that early diagnosis may benefit the subsequent clinical course and may be important since the number of such families in our experience suggests that precocious familial gout with renal failure is more prevalent than currently recognized.
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PMID:Familial gout and renal failure in young women. 742 92

Nonsteroidal anti-inflammatory drugs (NSAIDs) are now commonly used for the treatment of acute gout, but caution is required in view of their adverse effects, especially in the elderly. Colchicine is still an effective acute agent, but care must be taken to monitor toxicity. Intra-articular glucocorticosteroid therapy is useful and very safe; oral steroids and corticotrophin (adrenocorticotrophic hormone) may have a small role in acute therapy and seem safe when used over short time spans. Low dose colchicine may have a cost and toxicity advantage over NSAIDs in the prophylaxis of gout when commencing therapy aimed at reducing elevated plasma urate concentrations. Allopurinol is more frequently used than uricosuric agents such as probenecid, and toxicity may be largely avoided by tailoring dosage schedules according to renal function.
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PMID:Risks and benefits of drugs used in the management and prevention of gout. 784 45

The objectives of this study were to establish if, and to what extent, benzbromarone affects allopurinol/oxypurinol kinetics, and to compare the uric acid lowering capabilities of Allomaron (allopurinol 100 mg plus benzbromarone 20 mg) with the effects of allopurinol alone in patients with confirmed gout. We studied 14 adult men in an open randomized cross-over study. After a 14 day run-in period with Zyloprim (2 x 100 mg allopurinol tablets in the morning), the patients were randomly allocated to morning doses of either Allomaron (2 tablets) or Zyloprim (2 tablets). Seven days later cross-over was effected and the alternative treatment was taken for a further 7 days. On days 7 and 14 the patients came into hospital and venous blood samples were taken over 24 h for allopurinol and oxypurinol assays by HPLC. Serum uric acid was determined on days -14, 1, 7, and 14. Benzbromarone lowered plasma oxypurinol concentrations (Allomaron/Zyloprim mean ratio of AUC0-->24 was 59%; 95% confidence interval 54-64%), but did not affect plasma allopurinol concentrations. Despite this pharmacokinetic interaction of benzbromarone with allopurinol, resulting in lower plasma concentrations of oxypurinol, Allomaron was superior to allopurinol alone in lowering serum uric acid, probably because of the added uricosuric effect of benzbromarone.
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PMID:The effect of benzbromarone on allopurinol/oxypurinol kinetics in patients with gout. 843 58


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