See

discussions, stats, and author profiles for this publication at: https://www.researchgate.net/publication/260228523

Obesity and the risk of Hyperuricemia in Gadap

Town, Karachi
Article in AFRICAN JOURNAL OF BIOTECHNOLOGY February 2011

CITATION

READS

163

10 authors, including:
Muhammad Asif

Qaiser Jabeen

The Islamia University of Bahawalpur

The Islamia University of Bahawalpur

68 PUBLICATIONS 200 CITATIONS

37 PUBLICATIONS 580 CITATIONS

SEE PROFILE

SEE PROFILE

Tariq Saeed

Dr Syed Mohammad Ali Shah

University of the Punjab

Government College University Faisalabad

37 PUBLICATIONS 144 CITATIONS

42 PUBLICATIONS 126 CITATIONS

SEE PROFILE

All in-text references underlined in blue are linked to publications on ResearchGate,

letting you access and read them immediately.

SEE PROFILE

Available from: Akhtar Naveed

Retrieved on: 20 September 2016

African Journal of Biotechnology Vol. 10(6), pp. 996-998, 7 February, 2011

Available online at http://www.academicjournals.org/AJB
ISSN 16845315 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.

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

*Corresponding author. E-mail: makram_0451@hotmail.com.

Tel: 92-021-6440083. Fax: 92-021-6440079.

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

Akram et al.

blood and tissues. It occurs due to impaired excretion of

uric acid from the kidney. Impaired excretion of uric acid
has primary and secondary causes. Primary cause is
idiopathic. Secondary cause includes chronic renal
disease, drug therapy, hypertension, lead toxicity, primary hyperparathyroidism, hypothyroidism, increased
lactic acid production and glucose 6 phosphatase
deficiency. Over production of uric acid causes idiopathic
(primary) gout, 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. Gout is a common joint disease which
affects over five times more men than women. It is rare in
children. In men, it can occur any time after puberty,
whereas in women it is uncommon before the menopause. In about 10% of such cases, there is a family
history of the disorder. People who are overweight, have
high blood pressure, eat diets rich in protein and drink
large quantities of alcohol have an increased risk of
developing gout (Shiraishi and Une, 2009).
Signs and symptoms of hyperuricemia that leads to
gout
Gout usually affects the large joint of the big toe, but it
can occur in the feet, ankles, knees, hands and wrists.
The pain is likely to be most severe within the first 12 to
24 h after it begins. After the most severe pain subsides,
joint comfort may last from a few days to a few weeks.
Later attacks are likely to last longer and affect more
joints. The affected joint or joints become swollen, tender
and red. Most often, symptoms first start in one joint.
Symptoms can also occur in other parts, if more than one
joint is affected. Multiple joints are affected in only 10 to
20% of first attacks. The most frequently affected joints
are the foot, ankle, knee, wrist, elbow and hand. The pain
usually occurs in joints of one side of the body and it is
usually, in the lower legs and feet. An untreated attack
will typically peak 24 to 48 h after the first appearance of
symptoms, and subside after 5 to 7 days. However, some
attacks last only for hours, while others persist as long as
several weeks (Brule et al., 1992). It also affects the
elbow, shoulder, wrist and metacarpophalangeal joints.
The cascade of pathologic events leads to acute inflammation of the joint or soft tissue. Hyperuricemia can also
result in uric acid nephrolithiasis and possible nephropathy if uric acid accumulates in the renal interstitium and
tubules. Acute attacks can be precipitated by several
factors such as increased alcohol consumption (especially beer), trauma, use of diuretics, dehydration, cyclosporine, diet (organ meat, shellfish) and any drug that
can lead to sudden changes (increase or decrease) in
urate levels, such as hypouricemic agents (Beutler and
Schumacher, 1994). When urate accumulates in a supersaturated medium, it can be deposited in soft tissues or
bones and form a tophus. Tophi can be present in the

997

helices of the ears, extensor areas of the limbs, pressure

areas such as the finger pads, and over the Achilles
tendons. Occasionally, they are not seen on physical
examination but are noted on x-ray films as cystic or
mass like lesions. In general, a tophus on radiographic
films is radiolucent, but when it occurs over a calcified
nodule, it may be seen as radio opaque (Chung et al.,
1997). Urate nephropathy is the result of the deposition of
monosodium urate crystals in the renal interstitial tissue.
Uric acid nephropathy is caused by the deposition of uric
acid crystals in the collecting tubules, renal pelvis or the
ureter and results in impaired urine flow. Calcium oxalate
urolithiasis also occurs in hyperuricemic patients. Uric
acid urolithiasis (uric acid kidney stones) accounts for
approximately 10% of all urinary calculi (stones) in the
US (Pearle et al., 2005).
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.
However, possible synovial fluid should be aspirated and
examined under polarizing light. Joint radiographs are
seldom useful in establishing the diagnosis. Although
they may show characteristic punched out erosion associated with the soft tissue swelling of urate tophi,
occasionally flecked with calcium, 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., 1988).
Treatment of hyperuricemia that leads to gout
Serum uric acid concentrations may be reduced with non
pharmacologic therapy. Useful dietary and lifestyle
changes include weight reduction, decreased alcohol
ingestion, decreased consumption of foods with a high
purine content and control of hyperlipidemia and hypertension. Used alone, however, these measures will
probably not reduce serum uric acid levels to normal,
which is the treatment goal for the prevention of acute
gout attacks. Symptomatic hyperuricemia usually requires medication. Lowering the blood concentration of
uric acid may permit any existing crystals of uric acid to
be gradually dissolved into the blood, from where the
dissolved uric acid can be excreted. Maintaining a lower
blood concentration of uric acid, should similarly reduce
the formation of new crystals. Most medications often
used to treat hyperuricemia are of two kinds: xanthine
oxidase inhibitors and uricosurics. Xanthine oxidase
inhibitors decrease the production of uric acid, by
interfering with xanthine oxidase. Uricosurics increase the
excretion of uric acid, by reducing the reabsorption of uric
acid once the kidneys have filtered it out of the blood.
Some of these medications are used as indicated; others
are used off-label. Several other kinds of medications

998

Afr. J. Biotechnol.

have potential for use in treating hyperuricemia. For

people receiving hemodialysis, it can significantly reduce
serum uric acid (Shrestha et al., 1994; Garg et al., 1993;
Ohno et al., 2009; Scott and Higgens, 1992; Akram, 2009).
MATERIALS AND METHODS
The evaluations of parameters like body mass index and serum uric
acid were conducted at Shifa-ul-Mulk Memorial Hospital, for
Eastern Medicine, Hamdard University. The patients were registered
in the general O.P.D and hospitalized in the clinical Research ward of
the Hospital. All the patients selected for the study, were thoroughly
examined and clinical history was recorded.
We conducted a community-based prospective cohort study of
3000 participants (age range, 35 to 70 years) living in Gadap Town,
who were found to be free of uric acid and cardiovascular disease
during baseline assessment at study entry in 2005. During a
median 5 year follow-up, 560 participants developed hyperuricemia.

RESULTS
Prevalence of hyperuricemia was seen in obese
individuals. During a median 5 year follow-up, out of 3000
obese participants, 560 developed hyperuricemia. Prevalence of Hyperuricemia is seen in obese individuals. Of
the 3000 individuals with serum urate measurements, all
were free of hyperuricemia. Additionally, 560 participants
(18%) developed hyperuricemia over five years of followup. At baseline, all of the individuals who developed
hyperuricemia were obese.
DISCUSSION
Many diseases and complication are associated with
obesity. Hyperuricemia is one of these conditions. Our
study showed positive association between obesity and
serum uric acid level (p < 0.05). Serum uric acid is not
only associated with obesity but it is also positively and
significantly associated with many other clinical conditions, e.g. diabetes mellitus, hypertension and ischemic
heart disease. Although these conditions are also
associated with obesity, serum uric acid is independently
associated with all these conditions. So it can be inferred
that obese patients, who are also hyperuricemic, suffer
more commonly from diabetes mellitus, hypertension and
ischemic heart disease when compared with patients who
are obese but not hyperuricemic. Increased levels of
serum uric acid also increase morbidity and mortality in
these patients. 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. Serum uric acid is
also a reliable indicator for the pre-metabolic syndrome in
obese patients. 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, and serum uric acid
concentrations predict subsequent weight gain. So, it is
possible that increased levels of serum uric acid may be
a cause of weight gain rather than result of it, at least in
some cases. 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.
Conclusion
These findings suggest a modest positive association
between obesity and hyperuricemia. Our results suggest
that obesity results in a multiplicative increase in the risk
of hyperuricemia. It is clearly indicated that body mass
index (BMI) is correlated with circulating urate concentrations. Obese people show hyperuricemia, which is
associated with metabolic syndrome in obesity, and as
such, uric acid synthesis increased and uric acid
excretion from the kidney decreased.
REFERENCES
Akram M (2009). Clinical Evalution of Herbal Medicine for
Hyperuricemia. M. Phil Thesis. pp. 44-89.
Beutler A, Schumacher Jr. (1994). Gout and pseudo gout. Postgrad.
Med. 95: 103-106.
Brule D, Sarwar G, Savoie L (1992). Changes in serum and urinary uric
acid levels in normal human subjects fed purine-rich foods containing
different amounts of adenine and hypoxanthine. J. Am. Coll. Nutr.11:
353-358.
Chung C, Recht M, Dailiana T, Jurdi R (1997). Imaging of tophaceous
gout. Am. J. Roentgenol. 168: 523-527.
Garg JP, Chasan-Taber S, Blair A (1993). Effects of sevelamer and
calcium-based phosphate binders on uric acid concentrations in
patients undergoing hemodialysis: a randomized clinical trial. Arth.
Rheum. 52: 372-374.
Garg JP, Chasan S, Blair A (2005). Effects of sevelamer and calciumBased phosphate binders on uric acid concentrations in patients
undergoing hemodialysis: a randomized clinical trial. Arth. Rheum.
52: 290-295.
Martinez E, Babani A, Trevino SC, Guillermo E (1988). Concomitant
gout and rheumatoid arthritis. J. Rheumatol. 15: 1307-1311.
McCarty DJ (1994). Gout without hyperuricemia. JAMA. 271: 302-304.
Ohno I, Yamaguchi Y, Saikawa H, Uetake D, Hikita M, Okabe H, Ichida
K, Hosoya T (2009). Sevelamer decreases serum uric acid
concentration through adsorption of uric acid in maintenance
hemodialysis patients. Int. Med. 48: 415-420.
Pearle MS, Calhoun EA, Curhan GC (2005). Urologic Diseases of
America Project: Urolithiasis. J. Urol. 173: 848-857.
Shiraishi H, Une H (2009). The effect of the interaction between obesity
and drinking on hyperuricemia in Japanese male office workers. J.
Epidemiol. 19: 12-14.
Shrestha M, Chiu MJ, Martin RL, Cush JJ, Wainscott MS (1994).
Treatment of acute gouty arthritis with intramuscular ketoralac
tromethamine. Am. J. Emerg. Med. 12: 454-455.
Scott JT, Higgens CS (1992). Diuretic induced gout: a multifactorial
condition. Ann. Rheum. 51: 259-261.