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GOUT AND ITS COMORBIDITY AMONG NIGERIANS BY DR. S.A. OGUNTONA MBChB, FWACP. CERT. RHEUM. DEPARTMENT OF MEDICINE OLABISI ONABANJO UNIVERSITY/ OLABISI ONABANJO UNIVERSITY TEACHING HOSPITAL. SAGAMU. OGUN STATE. NIGERIA. CORRESPONDENCE TO : DR. S.A. OGUNTONA P.O.BOX 231, SAGAMU. OGUN STATE. NIGERIA. Mobile- 08035534449 E-mail- [email protected], [email protected] 1 GOUT AND ITS COMORBIDITY AMONG NIGERIANS ABSTRACT Background- Gout is a chronic disease associated with excessive high levels of serum urate (hyperuricaemia) with resultant deposition of monosodium urate crystals in the tissue. It presents with both articular and non-articular features. Patients with gout frequently experience a range of co-morbidities which complicates management and affects long-term prognosis. Method Included in the study are patients that met the American College of Rheumatology criteria for the diagnosis of gout. Serum uric acid level was determined in all patients. Other relevant investigations as related to the associated comorbid condition were requested for. Results Hypertension was the leading comorbid condition found (62.5%), followed by obesity, diabetes and chronic renal failure. None of those patients was however found to have ischaemic heart disease. Conclusion Patients with hyperuricaemia and gout should be considered at risk for other comorbid conditions. Therefore, appropriate and aggressive urate-lowering pharmacotheraphy should be instituted in a goal-oriented approach to reach a serum uric level within normal range. Key words- Gout, comorbidity, South West Nigeria 2 Introduction Gout is a multi-systemic disease in which metaboloic, excretory, and excessive purine intake contributes to high level of serum urate (hyperuricaemia) with subsequent deposition of monosodium urate crystals in the tissues1. Patients with hyperuricaemia or gout, or both often experience high rates of comorbidity with attendant management challenges2. In many cases, there is clear evidence that gout may be a consequence of comorbidity. For example, gout occurs frequently in patients with chronic kidney disease. On the other hand, it is important to consider the extent to which hyperuricaemia or gout per se may contribute to the genesis of comorbidity3. In the latter case, both hyperuricaemia and gout are treatable. An appropriate diagnosis and goal oriented treatment should be carried out in order to prevent those comorbidity. Comorbidity with gout can also impair quality of life4. Using a variety of distinct validated measures, patients with gout have been shown to experience a significant overall reduction in quality of life4. 3 Materials and methods This is a prospective study of all gout patients seen over three years (July 2009-June 2012) in a private rheumatology clinic. Both patients with hyperuricaemia and features of gout with elevated serum uric acid level were enlisted in the study. Serum uric acid was determined at first consultation in all patients. Also determined alongside serum uric acid level were body mass index (BMI), fasting lipid profile, urinalysis, electrolyte, urea and creatinine. Electrocardiogram (ECG), echocardiogram were demanded where necessary. Also requested for were fasting blood sugar, HbA1C and plain chest radiographs. Results 28 cases of hyperuricaemia/gout were seen over the study period, representing 8.3% of total cases of rheumatology seen. 22 males (78.6%) and 6 females (21.4%) were seen. Mean age of males at presentation was 42.5years, and mean age of females at presentation was 63.6years. Serum uric acid ranged between 9.6mg/dl to 15.7mg/dl and the mean was 12.5mg/dl. Males generally had higher values than females. Comorbid condition was found in 16 patients (57.1%), 14 males (87.5%) and 2 females (12.5%). Treatment with allopurinol was helpful in all patients, with reduction in the serum uric acid level and symptomatic relieve of arthritic pain. 4 Discussion The aim of this study is to review some of the comorbid conditions that occur in gout patients among the people of south west Nigeria, and to determine if hyperuricaemia/gout may represent modifiable risk factor for the comorbid conditions. The leading comorbid condition in this study was hypertension (62.5%). This result agrees with some other earlier studies in African countries where hypertension was found to be the leading comorbid state with hyperuricaemia/gout. Hypertension accounted for 39% in the study by Mijinyawa in Togo5, 42% in the study by Mody et al in South Africa6. Oyoo reported 61.5% in Kenya7, and Adelowo et al reported 49.3% in Nigeria (in press). Most earlier studies agreed that most patients with hyperuricaemia and gout frequently suffer hypertension and therefore concluded that even in the absence of gout, hyperuricaemia may directly promote hypertension8. Ouppatham and colleagues conducted a study on more than 5500 members of the Thai Armed Forces, and they demonstrated that the presence of hyperuricaemia predicts increased systolic and diastolic blood pressure9. Feig and coworkers assessed whether hyperuricaemia might affect blood pressure in humans, by recruiting a group of adolescents with new onset hypertension and relative hyperuricaemia. As a group, these individuals experienced a reduction of blood pressure towards or into normal range during treatment with 400mg daily of allopurinol. This decrease in blood pressure was reversed on discontinuation of allopurinol10. It is a well-accepted concept that impaired renal function can decrease urate filtration and consequently hyperuricaemia11. The question of whether hyperuricaemia can promote kidney disease has been debated for years. Many clinical studies indeed suggest that hyperuricaemia provides risk for renal disease12. Several recent studies also provide evidence that lowering urate concentration with allopurinol may slow the progression of chronic kidney disease13. It is also well documented that individuals with metabolic syndrome have a higher incidence of gout, so by extrapolation, it can be inferred that individuals with hyperuricaemia may also have an increased incidence of insulin resistance. Yoo and colleagues in one study showed that the incidence of insulin resistance in gout patients may be increased by as much as 35% over individuals without gout 14. Choi and colleagues also concluded in their study that gout conveyed 35% to 65% increase in risk for future incidence of Type 11 diabetes15. 5 Many studies has associated hyperuricaemia with cardiovascular disease 16,17,18. In a review by Johnson and coworkers, everyone of 14 large population studies identified hyperuricaemia as a risk factor for cardiovascular disease and 10 of the 14 studies favoured hyperuricaemia as an independent risk factor19. Similarly, Wheeler and associates performed a meta-analysis of 15 studies and each demonstrated a modest overall increased relative risk for cardiovascular disease for patients with hyperuricaemia20. Baker and colleagues examined 21 population studies on hyperuricaemia and cardiovascular disease and concluded that it is possible that hyperuricaemia is a more important cardiovascular risk factor in patients already at risk for cardiovascular disease21. In an analysis of the MRFIT (Multiple Risk Factor Intervention Trial) investigation, Krisshan and coworkers observed a modest increase for risk of myocardial infarction (MI) in patients with either hyperuricaemia or gout, and patients with gout appeared to have an increased risk of MI relative to patients with hyperuricaemia alone 22. These data was however not analyzed to determine whether the increase in all the gout patients over the hyperuricaemia ones was statistically significant. It can therefore be concluded that hyperuricaemia and gout appear to be independent risk factors for hypertension, renal disease, and cardiovascular disease. Physicians should therefore consider and look for comorbid conditions in patients with gout and treat them appropriately and aggressively. 6 Table 1 -SPECTRUM OF RHEUMATOLOGY CASES SEEN OVER 3 YEARS (JULY 2009- JUNE 2012) Serial No 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. Condition Osteoarthritis Rheumatoid arthritis Cervical spondylosis Lunbar spondylosis Low back pain Gout SLE Shoulder pain syndrome Hypermobility syndrome Fibromyagia Polymyalgia rheumatica Bursitis Trigger finger Sjorgren’s syndrome Reiter’s syndrome Septic arthritis Lateral epicondylitis Medial epicondylitis Scleroderma Psoriatic arthropathy Plantar fasciitis Carpal tunnel syndrome Archilis tendinitis Number 104 12 Male 32 4 Percentage Female 30.8 72 33.3 8 Percentage 69.2 66.7 36 23 63.9 13 36.1 25 21 56 14 44 48 37 77.1 11 22.9 28 6 12 22 1 4 78.6 16.7 33.3 6 5 8 21.4 83.3 66.7 8 0 0 8 100 6 2 0 0 0 0 6 2 100 100 4 16 1 3 6 0 75 37.5 O 1 10 1 25 62.5 100 1 1 100 0 0 2 0 0 2 100 2 2 100 0 0 2 2 100 0 0 2 1 0 1 0 100 2 0 100 0 7 2 28.6 5 71.4 3 1 33.3 2 66.7 8 1 12.5 7 87.5 336 160 176 7 Table 2 COMORBID CONDITIONS ASSOCIATED WITH GOUT (16 patients had comorbid conditions) CLINICAL CONDITION PERCENTAGE Hypertension NUMBER OF PEOPLE WITH COMORBIDITY OUT OF TOTAL OF 16 10 Chronic renal failure 3 18.8 Heart failure 1 6.3 Obesity 6 37.5 Diabetes mellitus (type 11) 4 25 Ischaemic heart disease None 0 Stroke 1 6.3 62.5 Table 3 Comparative characteristics of gout among various African populations (%). Adapted from Adelowo et al. Comorbid condition Togo South Mijinyawa5 Africa Cassim et al South Africa Mody et al6 South Kenya Africa Oyoo7 Tikly et al Nigeria Adelowo et al (in press) Nigeria Oguntona (present study) Hypertension 39.0 - 42 - 61.5 49.3 62.5 Obesity 38 - - - 90.5 12.7 37.5 Diabetes - - 10.5 - 7.7 4.1 25 (type 11 DM) Alcohol 74.0 - - - 100 17.8 - - - - 15.4 10.3 - Osteoarthritis - 8 References 1. Choi HK, Mount DB, Reginato AM. Pathogenesis of Gout. Ann Intern Med 2005; 143: 499-516 2. Riedel AA, Nelson M, Wallace K, et al. Prevalence of comorbid conditions and prescription medication use among patients with gout and hyperuricemia in a managed care setting. J Clin Rheumatol. 2004 Dec;10(6):308-314. 3. Sanchez-Lozada LG, Soto V, Tapia E, et al. Role of Oxidative Stress in the Renal Abnormalities Induced by Experimental Hyperuricemia. Am J Physiol Renal Physiol. 2008 Oct;295(4):F1134-1141; 4. Roddy E, Zhang W, Doherty M. Is gout associated with reduced quality of life? A case-control study. Rheumatology (Oxford) 2007;46:1441–1444 5. Mijinyawa M. Gout in patients attending the rheumatology unit of Lome hospital Br J of Rheum 1995;34:843-846 6. Mody GM, Naidoo PD. Gout in South African Blacks. Ann Rheum Dis 1984;43:394-397 7. Oyoo GO. Gout in patients attending a rheumatology clinic in Nairobi, Kenya Health Line 2004; 8(4) 8. Johnson RJ, Kang DH, Feig D, et al. Is there a pathogenetic role for uric acid in hypertension and cardiovascular and renal disease? Hypertension. 2003 Jun;41(6):1183-1190. 9. Ouppatham S, Bancha S, Choovichian P. The relationship of hyperuricemia and blood pressure in the Thai army population. J Postgrad Med. 2008 OctDec;54(4):259-262. 10. Feig DI, Soletsky B, Johnson RJ. Effect of allopurinol on blood pressure of adolescents with newly diagnosed essential hypertension: a randomized trial. JAMA. 2008 Aug 27;300(8):924-932. 11. Kang DH, Nakagawa T. Uric acid and chronic renal disease: possible implication of hyperuricemia on progression of renal disease. Semin Nephrol 2005;25:43-9. 12. Chang HY, Tung CW, Lee PH, et al. Hyperuricemia as an independent risk factor of chronic kidney disease in middle-aged and elderly population. Am J Med Sci. 2010 Jun;339(6):509-515. 13. Goicoechea M, de Vinuesa SG, Verdalles U, et al. Effect of allopurinol in chronic kidney disease progression and cardiovascular risk. Clin J Am Soc Nephrol. 2010 Aug;5(8):1388-1393. 14. Yoo HG, Lee SI, Chae HJ, Park SJ, Lee YC, Yoo WH. Prevalence of insulin resistance and metabolic syndrome in patients with gouty arthritis. Rheumatol Int. Advance access published December 20, 2009, doi 10.1007/s00296-009-1304x. 15. Choi HK, De Vera MA, Krishnan E. Gout and the risk of type 2 diabetes among men with a high cardiovascular risk profile. Rheumatology (Oxford). 2008 Oct;47(10):1567-70. 16. Choi HK, Curhan G. Independent impact of gout on mortality and risk for coronary heart disease. Circulation. 2007 Aug 21;116 (8):894-900. 9 17. Ioachimescu AG, Brennan DM, Hoar BM, et al. Serum uric acid is an independent predictor of all-cause mortality in patients at high risk of cardiovascular disease: a preventive cardiology information system (PreCIS) database cohort study. Arthritis Rheum. 2008 Feb;58 (2):623-630. 18. Niskanen LK, Laaksonen DE, Nyyssonen K, et al. Uric acid level as a risk factor for cardiovascular and all-cause mortality in middle-aged men: a prospective cohort study. Arch Intern Med. 2004 Jul 26;164 (14):1546-1551. 19. Johnson RJ, Kang DH, Feig D, et al. Is there a pathogenetic role for uric acid in hypertension and cardiovascular and renal disease? Hypertension. 2003 Jun;41 (6):1183-90. 20. Wheeler JG, Juzwishin KD, Eiriksdottir G, et al. Serum uric acid and coronary heart disease in 9,458 incident cases and 155,084 controls: prospective study and meta-analysis. PLoS Med. 2005 Mar;2 (3):e76. 21. Baker JF, Krishnan E, Chen L, Schumacher HR. Serum uric acid and cardiovascular disease: recent developments, and where do they leave us? Am J Med 2005;118: 816–826. 22. Krishnan E, Svendsen K, Neaton JD, et al. Long-term cardiovascular mortality among middle-aged men with gout. Arch Intern Med. 2008 May 26;168 (10):1104-1110. 10