African Journal of Biotechnology Vol. 10(6), pp.

996-998, 7 February, 2011
Available online at http://www.academicjournals.org/AJB
DOI: 10.5897/AJB10.1930
ISSN 1684–5315 © 2011 Academic Journals

Short Communication

Obesity and the risk of hyperuricemia in Gadap Town,
Karachi
Muhammad Akram1, H.M.Asif2, Khan Usmanghani1, Naveed Akhtar2, Qaiser Jabeen2,
Asadullah Madni2, Tariq saeed3, Riazur Rehman2, Khalil Ahmed2 and S.M. Ali Shah2
1

Shifa ul Mulk Memorial Hospital, Hamdard University, Karachi, Pakistan.
Faculty of Pharmacy and Alternative Medicine, Islamia University of Bahawalpur.
3
University College of Pharmacy, Punjab University, Lahore, Pakistan.

2

Accepted 30 December, 2010

Obesity is a known risk factor for hyperuricemia. However, the effect of the interaction between obesity
and hyperuricemia is not well understood. Previous study has shown a relationship between
hyperuricemia and obesity, but the evidence from prospective studies of an association between
obesity and uric acid risk is limited. We prospectively evaluated the association between obesity and
the incidence of uric acid in obese individuals.In a population-based cohort, obesity and weight gain
was found to be strongly associated with hyperuricemia. Additionally, all patients who developed
hyperuricemia were obese at baseline. Obesity is a risk factor for hyperuricemia and may be useful for
prediction of incident gout in individuals.
Keywords: Lipids, cardiology, hypertension.
INTRODUCTION
Hyperuricemia
Uric acid is the end product of purine metabolism. Synthesis of uric acid occurs in liver. Gout is an abnormality
of uric acid metabolism that results in the deposition of
sodium urate crystals in joints, soft tissues and urinary
tract. Gout may be caused by impaired excretion of uric
acid or overproduction of uric acid. An abnormality in
handling uric acid can cause attacks of painful arthritis
(gout attack), kidney stones and blockage of the kidneyfiltering tubules with uric acid crystals, leading to kidney
failure. On the other hand, some people may only
develop elevated blood uric acid levels (hyperuricemia)
without having manifestations of gout, such as arthritis or
kidney problems. The state of elevated levels of uric acid
in the blood without symptoms is referred to as asymptomatic hyperuricemia. Asymptomatic hyperuricemia may
ultimately result to disease conditions like gout and
kidney stone. Gouty arthritis is typically an extremely
painful attack with a rapid onset of joint inflammation. The

joint inflammation is precipitated by deposits of uric acid
crystals in the joint fluid (sensorial fluid) and joint lining
(synovial lining). Intense joint inflammation occurs as the
immune system reacts, causing white blood cells to
engulf the uric acid crystals and chemical messengers of
inflammation to be released, and this leads to pain, heat
and redness of the joint tissues. As gout progresses, the
attacks of gouty arthritis typically occur more frequently
and often in additional joints (Garg et al., 2005).
It is estimated that approximately 15 out of every 1,000
male between 35 and 45 years of age have hyperuricemia. Hyperuricemia afflicts an estimate of 840 out of
100,000 people. Men tend to have higher uric acid levels
than women. International prevalence of hyperuricemia is
0.3%. Hyperuricemia has a 90% male predominance.
Fairly substantial proportion of patients with hyperuricemia (10 to 20%) has a family history of hyperuricemia
(McCarty, 1994).
Causes of hyperuricemia and gout

*Corresponding author. E-mail: makram_0451@hotmail.com.
Tel: 92-021-6440083. Fax: 92-021-6440079.

Gout occurs as a result of excess uric acid (urate) in the

extensor areas of the limbs. Multiple joints are affected in only 10 to 20% of first attacks. it may be seen as radio opaque (Chung et al. renal pelvis or the ureter and results in impaired urine flow. Some of these medications are used as indicated. hands and wrists. increased purine synthesis de novo due to hypoxanthine guanine phosphoribosyl transferase reduction (an x linked inborn error causing the lesh nyhan syndrome) and phosphoribosyl-pyrophosphate synthetase over activity. When urate accumulates in a supersaturated medium. primary hyperparathyroidism. Occasionally. cyclosporine. and over the Achilles tendons. use of diuretics. increased lactic acid production and glucose 6 phosphatase deficiency. Hyperuricemia can also result in uric acid nephrolithiasis and possible nephropathy if uric acid accumulates in the renal interstitium and tubules. others are used off-label. Diagnosis The serum urate level is usually raised but it is important to appreciate that this does not prove the diagnosis because asymptomatic hyperuricemia is very common. decreased alcohol ingestion. diet (organ meat. shoulder. The most frequently affected joints are the foot. After the most severe pain subsides. pressure areas such as the finger pads. drug therapy. it can occur any time after puberty. Impaired excretion of uric acid has primary and secondary causes. Symptomatic hyperuricemia usually requires medication. Later attacks are likely to last longer and affect more joints. Over production of uric acid causes idiopathic (primary) gout. but when it occurs over a calcified nodule. and subside after 5 to 7 days. knees. The pain is likely to be most severe within the first 12 to 24 h after it begins. Most often. 2009). it can be deposited in soft tissues or bones and form a tophus. Uric acid urolithiasis (uric acid kidney stones) accounts for approximately 10% of all urinary calculi (stones) in the US (Pearle et al. In men. Lowering the blood concentration of uric acid may permit any existing crystals of uric acid to be gradually dissolved into the blood. elbow and hand. in the lower legs and feet. by interfering with xanthine oxidase. possible synovial fluid should be aspirated and examined under polarizing light. Useful dietary and lifestyle changes include weight reduction. Several other kinds of medications . Xanthine oxidase inhibitors decrease the production of uric acid. Used alone. decreased consumption of foods with a high purine content and control of hyperlipidemia and hypertension. knee. Although they may show characteristic punched out erosion associated with the soft tissue swelling of urate tophi. if more than one joint is affected. People who are overweight. however.. In general. Symptoms can also occur in other parts.Akram et al. by reducing the reabsorption of uric acid once the kidneys have filtered it out of the blood. tender and red. hypothyroidism. It also affects the elbow. Urate nephropathy is the result of the deposition of monosodium urate crystals in the renal interstitial tissue. The cascade of pathologic events leads to acute inflammation of the joint or soft tissue. ankles. which is the treatment goal for the prevention of acute gout attacks. symptoms first start in one joint. Secondary cause includes chronic renal disease. It occurs due to impaired excretion of uric acid from the kidney. lead toxicity.. the diagnosis will be clinically apparent in such patients and in others the erosions may be indistinguishable from those seen in various forms of inflammatory arthritis (Martinez et al. dehydration. Primary cause is idiopathic. The pain usually occurs in joints of one side of the body and it is usually. whereas in women it is uncommon before the menopause. Maintaining a lower blood concentration of uric acid. wrist. 1997). An untreated attack will typically peak 24 to 48 h after the first appearance of symptoms. In about 10% of such cases. Uric acid nephropathy is caused by the deposition of uric acid crystals in the collecting tubules. Gout is a common joint disease which affects over five times more men than women. ankle. However. wrist and metacarpophalangeal joints. while others persist as long as several weeks (Brule et al. However. 1988). It is rare in children. they are not seen on physical examination but are noted on x-ray films as cystic or mass like lesions. should similarly reduce the formation of new crystals. there is a family history of the disorder. a tophus on radiographic films is radiolucent. 1994). have high blood pressure. Acute attacks can be precipitated by several factors such as increased alcohol consumption (especially beer). Calcium oxalate urolithiasis also occurs in hyperuricemic patients. joint comfort may last from a few days to a few weeks. such as hypouricemic agents (Beutler and Schumacher. Tophi can be present in the 997 helices of the ears. hypertension. Most medications often used to treat hyperuricemia are of two kinds: xanthine oxidase inhibitors and uricosurics. blood and tissues. shellfish) and any drug that can lead to sudden changes (increase or decrease) in urate levels. but it can occur in the feet. occasionally flecked with calcium. The affected joint or joints become swollen.. Treatment of hyperuricemia that leads to gout Serum uric acid concentrations may be reduced with non pharmacologic therapy. eat diets rich in protein and drink large quantities of alcohol have an increased risk of developing gout (Shiraishi and Une. some attacks last only for hours. these measures will probably not reduce serum uric acid levels to normal. 2005). 1992). Joint radiographs are seldom useful in establishing the diagnosis. from where the dissolved uric acid can be excreted. Signs and symptoms of hyperuricemia that leads to gout Gout usually affects the large joint of the big toe.. Uricosurics increase the excretion of uric acid. trauma.

Martinez E. So. 560 participants developed hyperuricemia. Postgrad. It is clearly indicated that body mass index (BMI) is correlated with circulating urate concentrations. 2009. Ohno et al. Garg et al. were thoroughly examined and clinical history was recorded. J. Rheum. Nutr. Imaging of tophaceous gout. Curhan GC (2005). 560 developed hyperuricemia. Coll. and as such. Am. serum uric acid is independently associated with all these conditions.P. Changes in serum and urinary uric acid levels in normal human subjects fed purine-rich foods containing different amounts of adenine and hypoxanthine. J. Roentgenol. e. Babani A. 173: 848-857. MATERIALS AND METHODS The evaluations of parameters like body mass index and serum uric acid were conducted at Shifa-ul-Mulk Memorial Hospital. all were free of hyperuricemia. 1992. 168: 523-527. Additionally. Okabe H. J. (1994). who are also hyperuricemic. Higgens CS (1992). Our results suggest that obesity results in a multiplicative increase in the risk of hyperuricemia. Conclusion These findings suggest a modest positive association between obesity and hyperuricemia. Sarwar G. Biotechnol. Akram. RESULTS Prevalence of hyperuricemia was seen in obese individuals. diabetes mellitus. Concomitant gout and rheumatoid arthritis. 35 to 70 years) living in Gadap Town. 2009). McCarty DJ (1994). Am. Blair A (1993). At baseline. Garg JP. J. uric acid synthesis increased and uric acid excretion from the kidney decreased. Saikawa H. all of the individuals who developed hyperuricemia were obese. The effect of the interaction between obesity and drinking on hyperuricemia in Japanese male office workers. Am. So it can be inferred that obese patients. 19: 12-14. Hosoya T (2009). Jurdi R (1997). Although these conditions are also associated with obesity. Hyperuricemia is one of these conditions. J. Ichida K. Uetake D. During a median 5 year follow-up. Chasan-Taber S. Gout and pseudo gout. 51: 259-261. suffer more commonly from diabetes mellitus. More work needs to be done in this regard in order to establish the mechanism of the association between obesity and serum uric acid level. Chiu MJ. Cush JJ. 15: 1307-1311. Rheum. Arth.05). for Eastern Medicine. Martin RL. Schumacher Jr. Shiraishi H. Obese people show hyperuricemia. and serum uric acid concentrations predict subsequent weight gain. Serum uric acid is also a reliable indicator for the pre-metabolic syndrome in obese patients. Gout without hyperuricemia. Our study showed positive association between obesity and serum uric acid level (p < 0. out of 3000 obese participants. Wainscott MS (1994). Arth. The patients were registered in the general O. it can significantly reduce serum uric acid (Shrestha et al. M. Scott JT. Garg JP. 1994. Pearle MS. 95: 103-106. Shrestha M. Med.g. Beutler A. Urologic Diseases of America Project: Urolithiasis. J.D and hospitalized in the clinical Research ward of the Hospital. Diuretic induced gout: a multifactorial condition.. Hikita M. Blair A (2005). We conducted a community-based prospective cohort study of 3000 participants (age range. DISCUSSION Many diseases and complication are associated with obesity. For people receiving hemodialysis. Of the 3000 individuals with serum urate measurements.. REFERENCES Akram M (2009). Epidemiol.11: 353-358. J. Effects of sevelamer and calciumBased phosphate binders on uric acid concentrations in patients undergoing hemodialysis: a randomized clinical trial. . Recht M. Treatment of acute gouty arthritis with intramuscular ketoralac tromethamine. Prevalence of Hyperuricemia is seen in obese individuals. it is possible that increased levels of serum uric acid may be a cause of weight gain rather than result of it. Ann. Med. 44-89. hypertension and ischemic heart disease. at least in some cases. Mechanism by which serum uric acid is increased in obese patients is not known but it has been observed that uric acid is a significant determinant factor of changes in body mass index. Calhoun EA. Rheum. hypertension and ischemic heart disease when compared with patients who are obese but not hyperuricemic. 560 participants (18%) developed hyperuricemia over five years of followup. 52: 290-295. Increased levels of serum uric acid also increase morbidity and mortality in these patients. 48: 415-420. Serum uric acid is not only associated with obesity but it is also positively and significantly associated with many other clinical conditions. All the patients selected for the study.998 Afr. Med. During a median 5 year follow-up. 52: 372-374. Hamdard University.. Scott and Higgens. Une H (2009). Effects of sevelamer and calcium-based phosphate binders on uric acid concentrations in patients undergoing hemodialysis: a randomized clinical trial. Ohno I. Urol. It is recommended that serum uric acid should be routinely measured in all obese and overweight patients in order to prevent or at least delay complications due to raised serum uric acid. Chung C. 271: 302-304. have potential for use in treating hyperuricemia. Savoie L (1992). Brule D. Rheumatol. JAMA. Dailiana T. Clinical Evalution of Herbal Medicine for Hyperuricemia. Sevelamer decreases serum uric acid concentration through adsorption of uric acid in maintenance hemodialysis patients. Trevino SC. Yamaguchi Y. Guillermo E (1988). 1993. Emerg. Chasan S. which is associated with metabolic syndrome in obesity. Phil Thesis. Int. pp. 12: 454-455. who were found to be free of uric acid and cardiovascular disease during baseline assessment at study entry in 2005.