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PubMed1996

The management of gout.

We now have sufficient knowledge to be able to identify the factors contributing to hyperuricemia in most patients with gout. Some of these factors, such as obesity, a high-purine diet, regular alcohol consumption, and diuretic therapy, may be correctable. In patients with persistent hyperuricemia, regular medication should lower the serum urate concentration to an optimal level. The continuing challenge is to educate patients about correctable factors and the importance of regular medication and ensure their compliance so that attacks of gout do not recur.

Acute Disease↗
PubMed2005

Suboptimal physician adherence to quality indicators for the management of gout and asymptomatic hyperuricaemia: results from the UK General Practice Research Database (GPRD).

OBJECTIVES: : To examine adherence to validated quality indicators assessing the quality of allopurinol use in the treatment of gout and asymptomatic hyperuricaemia. METHODS: We determined physician adherence in the UK General Practice Research Database (GPRD) to three validated quality indicators developed to assess the quality of allopurinol prescribing practices. These indicators were developed to assess: (i) dosing in renal impairment; (ii) concomitant use with azathioprine or 6-mercaptopurine; and (iii) use in the treatment of asymptomatic hyperuricaemia. We also examined the association of patient-level factors (sociodemographics, comorbidity, follow-up duration and concomitant medicine use) with the treatment of asymptomatic hyperuricaemia using multivariable logistic regression. RESULTS: Of the 63 105 gout patients, 185 (0.3%) were eligible for Quality Indicator 1 and 52 (0.1%) were eligible for Quality Indicator 2. There were an additional 471 patients with asymptomatic hyperuricaemia eligible for Quality Indicator 3. Rates of practice deviation for the three individual quality indicators ranged from 25 to 57%. Male sex, older age, a history of chronic renal failure, and a greater number of concomitant medications were significantly associated with increased odds of inappropriate treatment for asymptomatic hyperuricaemia. Hypertension and diuretic use were associated with lower odds of this practice. CONCLUSIONS: One-quarter to one-half of all patients eligible for at least one of the validated quality of care indicators were subject to possible allopurinol prescribing error, suggesting that inappropriate prescribing practices are widespread with this agent. Future interventions aimed at reducing inappropriate allopurinol use are needed and should be targeted towards high-risk groups, including older men and those receiving multiple concomitant medications.

Adult↗
PubMed2000

Gout update: from lab to the clinic and back.

Reviews and opinion articles stressing the need for better reproducibility of crystal identification in synovial fluid continue to be published. The possibility of definitive diagnosis of gout by crystal identification during intercritical periods appears now established. The problems associated with the use of allopurinol have also received some attention, as well as the strategies of dealing with allopurinol hypersensitivity. Gout in transplanted patients is reviewed, with special attention to the difficulties related to its treatment; various therapeutic options for this group are reviewed. The use of benzbromarone to reduce uricemia appears to be especially appropriate for this group of patients, in whom allopurinol is problematic. Finally, the pathogenetic mechanisms of the disease, and the relation between urate crystals and inflammation are reviewed.

Crystallization↗
PubMed2006

The inflammatory process of gout and its treatment.

Gouty arthritis is a characteristically intense acute inflammatory reaction that erupts in response to articular deposits of monosodium urate (MSU) crystals. Important recent molecular biologic advances in this field have given us a clear picture of the mechanistic basis of gouty inflammation. The innate immune inflammatory response is critically involved in the pathology of gout. Specifically, MSU crystals promote inflammation directly by stimulating cells via Toll-like receptor signaling and by providing a surface for cleavage of C5 and formation of complement membrane attack complex (C5b-9), culminating in secretion of cytokines, chemokines, and other inflammatory mediators with a dramatic influx of neutrophils into the joint. Despite the detailed mechanistic picture for gouty inflammation, there are no placebo-controlled, randomized clinical studies for any of the therapies commonly used, although comparative studies have demonstrated that many nonsteroidal anti-inflammatory drugs are equivalent to indomethacin with respect to controlling acute gouty attacks. In general, the first line of anti-inflammatory therapy for acute gout is nonsteroidal anti-inflammatory drugs, and the selective cyclo-oxygenase-2 inhibitor celecoxib can be used where appropriate. The second line of treatment is glucocorticosteroids, given systemically (oral, intravenous, or intramuscular) or intra-articularly. Alternatively, synthetic adrenocorticotropic hormone is effective, partly via induction of adrenal glucocorticosteroids and partly via rapid peripheral suppression of leukocyte activation by melatonin receptor 3 signaling. The third line of treatment is oral colchicine, which is highly effective when given early in an acute gouty attack, but it is poorly tolerated because of predictable gastrointestinal side effects.

Adrenal Cortex Hormones↗
PubMed1994

Risks and benefits of drugs used in the management and prevention of gout.

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.

Adrenocorticotropic Hormone↗
PubMed1998

Stopping progression to tophaceous gout. When and how to use urate-lowering therapy.

Although the prevalence of tophaceous gout has decreased in the past few years, the disease still exists, and without accurate diagnosis and therapy, it can still result in destructive arthritis. However, use of urate-lowering drugs may reduce plasma urate concentrations enough to allow resorption of tophi and prevent painful tophaceous gout. Some patients may have mechanical problems from tophi, despite adequate control of acute arthritis; in such situations, joint replacement or surgical excision of tophi may be necessary.

Adrenal Cortex Hormones↗
PubMed2001

Gout, bradycardia, and hypercholesterolemia after renal transplantation.

Approximately 17,000 solid organ transplantations are done annually in the United States. Increasingly, care of these patients will be provided by primary care physicians. In this report, we illustrate the complexity of common medical problems in a patient who had cellulitis and who had had a cadaveric renal transplantation 10 years earlier. Immunosuppressive therapy was cyclosporine (100 mg twice a day) and prednisone (10 mg once a day). The patient's hospital course was complicated by acute gout and symptomatic bradycardia. In both instances, usual treatment--full-dose indomethacin for gout and withholding verapamil for bradycardia--could have had significant interaction with the cyclosporine. At the time of discharge, a therapeutic plan for long-term management of hypercholesterolemia included possible drug interactions with cyclosporine. The potential for drug toxicity in the transplant patient necessitates careful monitoring of immunosuppressive drug levels. Ongoing communication with the transplant center is also needed.

Bradycardia↗
PubMed2005

Clinical, humanistic, and economic outcomes of gout.

Gout is a low prevalence disease not often considered by managed care organizations with regard to cost management. Understanding the development of the disease and its potential long-term, high-cost consequences can lead to appropriate treatment strategies and cost-management opportunities that can improve patient outcomes and potentially lower the overall cost of treatment of patients with gout in a managed care organization. The acute and chronic nature of the disease is best managed up front to avoid negative long-term effects. Adherence to medications can also impact the manifestation of the disease.

Adult↗
PubMed2006

Dose adjustment of allopurinol according to creatinine clearance does not provide adequate control of hyperuricemia in patients with gout.

OBJECTIVE: Published guidelines state that allopurinol doses should be adjusted according to creatinine clearance. We investigated whether such dosing provides adequate control of hyperuricemia. METHODS: We studied 250 patients with gout attending rheumatology clinics in South Auckland from 2001 to 2004. Allopurinol dose, creatinine clearance, and serum uric acid (SUA) level were recorded. We analyzed the relationship between recommended allopurinol dose and SUA lowering to <or= 0.36 mmol/l. RESULTS: For patients taking allopurinol, 70.9% were taking recommended doses, based on published allopurinol dosing guidelines. There were 4 (1.6%) patients with cutaneous hypersensitivity reactions to allopurinol, but none of these patients were taking higher than recommended allopurinol doses. The proportion of patients achieving SUA <or= 0.36 mmol/l was lower in those taking recommended doses, compared with those taking higher than recommended doses (19% vs 38.1%; p < 0.01). CONCLUSION: Adherence to published allopurinol dosing guidelines led to suboptimal control of hyperuricemia in this population of patients with gout. Further work is required to clarify the safety and efficacy of allopurinol dose escalation, particularly in patients with renal impairment.

Adult↗
PubMed2006

Gout in 2006: the perfect storm.

Mechanistic and therapeutic advances in gout have been moving swiftly in the past decade. Clinically, the disease is changing in character. This review discusses several of the pertinent recent developments in understanding gout and in novel therapeutics for the disease. Subjects addressed include the role of URAT1-mediated renal proximal tubule epithelial cell urate anion reabsorption in hyperuricemia. We discuss the therapeutic limitations of allopurinol and uricosurics and the potential applications of novel xanthine oxidase inhibitors and of recombinant uricase preparations. Last, we summarize understanding of the central role of the early induced innate immune response in gouty inflammation, which has suggested the potential value of new strategies for treating gouty inflammation by targeting caspase-1 or IL-1beta.

Global Health↗
PubMed1987

[Rehabilitation of patients with gout during outpatient follow-up].

The authors presented the results of a 5-year follow-up of 50 gout patients who had been regularly (no less than 3-4 times a year) examined in outpatient clinics. Dispensary examinations of the patients resulted in a decrease in the level of uric acid and in the number of exacerbations of gouty arthritis, the reduction of the sizes of tophi or their disappearance. Regular examination and ultrasonic investigation made it possible to prevent in some cases attacks of urolithiasis, and to reduce 4-fold a disability time-period and to preserve working capacity in 96% of the patients. The study showed that in most of the patients with essential hypertension and coronary heart disease arterial pressure got stable and the number of angina attacks was on a decrease. The data obtained indicated a high efficacy and appropriateness of combined rehabilitation activities in gout patients.

Adult↗
PubMed1985

Antihyperuricemic properties of amflutizole in gout.

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.

Adult↗
PubMed1994

Gout.

In theory gout is easy to diagnose and treat. In reality gout is difficult to treat because of; the important drug and disease interactions of NSAIDs, the frequency of toxicity with colchicine and the requirement for high degrees of compliance when using hypouricaemic agents.

Acute Disease↗
PubMed1998

Diagnosis and management of complicated gout.

Although a diagnosis of gout can be confirmed by the presence of monosodium urate crystals in synovial fluid, arriving at the suspected diagnosis and managing the disease can be a challenge for primary care physicians and specialists alike. Symptoms of gout can mimic other forms of inflammatory arthritis such as rheumatoid arthritis, pseudogout, or septic arthritis. Treatment can be complicated by the patient's need for drugs that contribute to hyperuricemia. Once other diagnoses are ruled out and urate crystals are detected under polarized light microscopy, treatment to end the acute attack and follow-up treatment designed to lower serum urate levels can be undertaken.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1998

Chronic tophaceous gout in a patient with a history of allopurinol toxicity.

We present an unusual complication of chronic tophaceous gout in a 63-year-old man with a 27-year history of gout, who could not be treated with allopurinol due to previous allopurinol-induced neutropenia. The patient presented with a progressively enlarging, painful mass on the bottom of his right foot, which caused difficulty wearing shoes and walking. Extirpation of the tophus and first metatarsophalangeal joint arthroplasty were successfully employed for management of this condition.

Allopurinol↗
PubMed2003

Association of emphysema, gout, and inflammatory markers with long-term incidence of age-related maculopathy.

OBJECTIVE: To examine the relationship of 2 diseases associated with systemic inflammatory response, emphysema and gout, and selected markers of systemic inflammation with the 10-year incidence of age-related maculopathy. DESIGN: Population-based cohort study. PARTICIPANTS: We included persons aged 43 to 86 years at baseline examination from 1988 to 1990 living in Beaver Dam, Wis, of whom 3684 subjects participated in a 5-year follow-up examination and 2764 participated in a 10-year follow-up. METHODS: Standardized protocols for physical examination, blood collection, administration of a questionnaire, and stereoscopic color fundus photography to determine the presence of age-related maculopathy. Standard univariate and multivariate analyses were performed. MAIN OUTCOME MEASURES: Incidence and progression of age-related maculopathy. RESULTS: While controlling for age, sex, and other factors (history of heavy drinking or smoking, systolic blood pressure, and vitamin use), a higher white blood cell count at baseline was associated with the 10-year incidence of drusen 125 microm or greater in diameter (risk ratio [RR] per 10(6)/ microL = 1.10; 95% confidence interval [CI], 1.03-1.17), retinal pigment epithelial depigmentation (RR = 2.08; 95% CI, 1.01-1.16), and progression of age-related maculopathy (RR = 1.09; 95% CI, 1.03-1.15). A lower serum albumin level was associated with the incidence of exudative macular degeneration (RR per grams per deciliter = 0.31; 95% CI, 0.13-0.76). A history of emphysema at baseline was associated with the incidence of retinal pigment epithelial depigmentation (RR = 2.84; 95% CI, 1.40-5.78), increased retinal pigment (RR = 2.20; 95% CI, 1.11-4.35), and exudative macular degeneration (RR = 5.12; 95% CI, 1.63-16.06); a history of gout was associated with the incidence of pure geographic atrophy (RR = 3.48; 95% CI, 1.27-9.53). CONCLUSIONS: These findings indicate modest relationships between both increased white blood cell count and emphysema and the increased 10-year incidence of lesions defining early and late age-related maculopathy. Further investigation of these relationships in other studies is needed.

Adult↗
PubMed1998

Medullary cystic kidney disease with hyperuricemia and gout in a large Cypriot family: no allelism with nephronophthisis type 1.

We describe a large Cypriot family with an interstitial type of nephropathy, inherited as an autosomal dominant trait that led to end stage renal failure between 51 to 78 years of age (mean 62.2 years). Twenty-three people are known to be affected, but several younger relatives with normal renal function may remain undiagnosed because of the absence of precise clinical and laboratory diagnostic criteria. This nephropathy is associated with medullary renal cysts, hypertension, hyperuricemia, and gout. Several relatives have typical medullary cystic disease (MCD), while in the others the findings are compatible with this diagnosis. Due to the similarity of clinical and pathologic findings, earlier reports had suggested that MCD may be allelic to autosomal recessive familial juvenile nephronophthisis, which was mapped recently to chromosome band 2q13. Linkage analysis of the present family with a closely linked marker excluded linkage to the above locus. Linkage was also excluded to the PKD1 locus of adult polycystic kidney disease type 1, and up to 5 cM on either side, on chromosome 16. We suggest that because of the element of hyperuricemia and gout found in this family, although with reduced penetrance, it may represent a variant of autosomal dominant MCD of the adult type. This variability may be the result of allelic or locus heterogeneity. Molecular genetic approaches including linkage analysis on appropriate families will certainly assist in classifying such related genetically heterogeneous disorders.

Adult↗