Hyperuricemia & Gout - Rhode Island Medical Society

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REFERENCES 1. Arromdee E, Michet CJ, et al. Epidemiology of gout. J Rheumatol 2002; 29:2403-6. 2. Lally EV, Ho Jr G, Kaplan SR. The clinical spectrum of gouty arthritis in women. Arch Intern Med 1986; 146:2221-5. 3. De Souza AWS, Fernandes V, Ferrari AJL. Female gout. J Rheumatol 2005; 32:2186-8. 4. Harrold LR, Yood RA, et al. Sex differences in gout epidemiology. Ann Rheum Dis 2006; 65:1368-72. 5. Puig JG, Michan AD, et al. Female gout. Arch Intern Med 1991; 151:726-32. 6. Meyers OL, Monteagudo FS. A comparison of gout in men and women. S Afr Med J 1986; 70:721-3. 7. Hak EA, Choi HK. Menopause, postmenopausal hormone use and serum uric acid levels in US women – The third national health and nutrition examination survey. Arthritis Research & Therapy 2008; 10:R116. 8. Pui K, Waddell C, Dalbeth N. Early onset of hyperuricaemia and gout following treatment for female to male gender reassignment. Rheumatol (Oxford) 2008;;47:1840-1. 9. Yu T. Some unusual features of gouty arthritis in females. Semin Arth Rheum 1977; 6:247-55. 10. Hayem G, Delahousse M, et al. Female premenopausal tophaceous gout induced by long term diuretic abuse. J Rheumatol 1996; 23:2166-7. 11. Nakazawa F, Ishihara H, Tanaka K. A case of female premenopausal tophaceous gout requiring surgical management. Mod Rheumatol 2004; 14:383-7. 12. Rott KT, Agudelo CA. Gout. JAMA 2003; 289:2857-60. 13. Choi HK, Ford ES. Haemoglobin A1C, fasting glucose, serum C-peptide and insulin resistance in relation to serum uric acid levels-the third national health and nutrition examination survey. Rheumatol 2008; 47:713-7. 14. Chou P, Lin KC, Tsai ST. Gender differences in the relationships of serum uric acid with fasting serum insulin and plasma glucose in patients without diabetes. J Rheumatol 2001; 28:571-6. Jill McClory, MD, formerly a Fellow in Rheumatology at Rhode Island Hospital, is a rheumatologist with Piedmont Rheumatology, PA, in Hickory, North Carolina. Nuha Said, MD, is a member of the academic rheumatology faculty at Roger Williams Medical Center. Disclosure of Financial Interests The authors have no financial interests to disclose. CORRESPONDENCE Nuha Said, MD Roger Williams Medical Center Division of Rheumatology 825 Chalkstone Ave Providence, RI 02908 e-mail: nuhasaid@yahoo.com 368 MEDICINE & HEALTH/RHODE ISLAND
Treatment Failure Gout Saman Ali, MD, and Edward V. Lally, MD Treatment options for gout are well established and reasonably effective. 1 They include anti-inflammatory agents such as non-steroidal anti-inflammatory drugs (NSAIDS), glucocorticoids and colchicine and urate-lowering therapies such as allopurinol and probenecid. However, despite the availability of effective urate-lowering therapy, there remains a subset of patients with gout who, despite aggressive therapy, have intractable disease, manifest as recurrent gout flares, chronic arthritis and progressive tophaceous deposits. These patients are referred to as having “refractory gout” or “treatment failure gout” (TFG). 1 The term “treatment failure gout” includes five ways by which patients may develop poorly controlled disease. These pertain mainly to the use of urate-lowering therapy and include delayed prescribing, inadequate dosage, intolerance, noncompliance and inadequate response in spite of generally acceptable dosages. 2 (Table 1) The new xanthine oxidase inhibitor febuxostat (Uloric) has not been studied in TFG, but may ultimately prove useful for this indication. Febuxostat is discussed elsewhere in this journal. Regardless of the pathway, all patients with treatment failure gout are unable to reduce and maintain serum urate below the therapeutic target of 6 mg/dl. 2 An estimated 100,000 to 300,000 of the nearly 3 million cases of gout in the US are not adequately managed with current therapies. 3 Additionally, many patients with gout have significant and multiple co-morbidities that preclude the use of those therapies. Allopurinol, the most common treatment used to lower serum urate levels, is generally regarded as safe and effective. 3 It lowers serum urate by inhibiting the purine nucleotide pathway enzyme xanthine oxidase. However, about 20% of patients receiving allopurinol report side effects and about 5% discontinue the medication due to intolerance. 4 Allopurinol may also be contraindicated because of potential adverse drug interaction with azathioprine. 5 Moreover, the presence of kidney disease may preclude adequate dosing because allopurinol-related toxicity is increased in the presence of significant renal impairment. Even though severe toxicity is rare, inadequate dosing of allopurinol to achieve target serum urate level
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Page 7 and 8: Medical Implications of Hyperuricem
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