CONTENTS

1. Introduction
2. Pathophysiology
3. Sign/symptom
4. Risk factor
5. Diagnosis
6. Prevention

7. Literature review
8. Treatment
9. Nutrition and its role
10.Role of Nutrition in Gout treatment
11.Prognosis
12.Conclusion
13.Bibliography

INTRODUCTION

INTRODUCTION
GOUT
Gout is a disease that results from an overload of uric acid in the body. This overload
of uric acid leads to the formation of tiny crystals of urate that deposit in tissues of the
body, especially the joints. When crystals form in the joints, it causes recurring attacks
of joint inflammation (arthritis). Gout is considered a chronic and progressive disease.
Chronic gout can also lead to deposits of hard lumps of uric acid in the tissues,
particularly in and around the joints and may cause joint destruction, decreased
kidney function, and kidney stones (nephrolithiasis).
Gout has the unique distinction of being one of the most frequently recorded medical
illnesses throughout history. It is often related to an inherited abnormality in the
body's ability to process uric acid. Uric acid is a breakdown product of purines that
are part of many foods we eat. An abnormality in handling uric acid can cause attacks
of painful arthritis (gout attack), kidney stones, and blockage of the kidney-filtering
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 is considered a precursor
state to the development of gout. The term gout refers the disease that is caused by an
overload of uric acid in the body, resulting in painful arthritic attacks and deposits of
lumps of uric acid crystals in body tissues.
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 (synovial 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, leading
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.

Who is affected by gout?

Over 8 million people in the United States suffer from gout. (Did you know that none
other than Benjamin Franklin had terribly painful gouty arthritis?) Gout is nine times
more common in men than in women. It predominantly attacks males after puberty,
with a peak age of 75. In women, gout attacks usually occur after menopause.
While an elevated blood level of uric acid may indicate an increased risk of gout, the
relationship between hyperuricemia and gout is unclear. Many patients with
hyperuricemia do not develop gout (asymptomatic hyperuricemia), while some
patients with repeated gout attacks have normal or low blood uric acid levels. In fact,
the blood level of uric acid often lowers during an acute attack of gout. Among the
male population in the United States, approximately 10% have hyperuricemia.
However, only a small portion of those with hyperuricemia will actually develop gout.

Gout and hyperuricemia facts

Painful gouty arthritis is caused by uric-acid-crystal deposits in joint tissue.

Gout is a chronic, progressive disease.

The tendency to develop gout and elevated blood uric acid level
(hyperuricemia) is often inherited.

Gout and hyperuricemia are aggravated by obesity, weight gain, alcohol

intake, high blood pressure, fructose in corn syrup found in soft drinks,
abnormal kidney function, and certain medications.

Gouty arthritis attacks can be precipitated by dehydration, injury, fever, heavy

eating, heavy alcohol consumption, and recent trauma or surgery.

The most reliable diagnostic test for gout is the identification of crystals in
joints, body fluids, and tissues.

The treatment of an attack of gouty arthritis is different than the treatment of

hyperuricemia. There are two key concepts essential to treating gout. First, it
is critical to stop acute inflammation of joints affected by gouty arthritis.
Second, it is important to address the long-term management of the gout
disease in order to prevent future gout arthritis attacks and shrink gouty tophi
crystal deposits.
3

Signs and symptoms

Fig :01 Gout presenting in the metatarsal-phalangeal joint of the big toe: Note the slight
redness of the skin overlying the joint.

Gout can present in a number of ways, although the most usual is a recurrent attack of
acute inflammatory arthritis (a red, tender, hot, swollen joint).[2] The metatarsalphalangeal joint at the base of the big toe is affected most often, accounting for half of
cases.[3] Other joints, such as the heels, knees, wrists and fingers, may also be affected.
[3]

Joint pain usually begins over 24 hours and during the night.[3] The reason for

onset at night is due to the lower body temperature then. [1] Other symptoms may
rarely occur along with the joint pain, including fatigue and a high fever.[1][3]
Long-standing elevated uric acid levels (hyperuricemia) may result in other
symptomatology, including hard, painless deposits of uric acid crystals known as
tophi. Extensive tophi may lead to chronic arthritis due to bone erosion.[4] Elevated
levels of uric acid may also lead to crystals precipitating in the kidneys, resulting in
stone formation and subsequent urate nephropathy.[5]

Cause
Hyperuricemia is the underlying cause of gout. This can occur for a number of
reasons, including diet, genetic predisposition, or underexcretion of urate, the salts of
uric acid.[2] Renal underexcretion of uric acid is the primary cause of hyperuricemia in
about 90% of cases, while overproduction is the cause in less than 10%. [6] About 10%
of people with hyperuricemia develop gout at some point in their lifetimes. [7] The risk,
however, varies depending on the degree of hyperuricemia. When levels are between
415 and 530 mol/l (7 and 8.9 mg/dl), the risk is 0.5% per year, while in those with a
level greater than 535 mol/l (9 mg/dL), the risk is 4.5% per year.[1]

Lifestyle
Dietary causes account for about 12% of gout,[2] and include a strong association with
the consumption of alcohol, fructose-sweetened drinks, meat, and seafood.[4][8] Other
triggers include physical trauma and surgery.[6] Recent studies have found dietary
factors once believed to be associated are, in fact, not, including the intake of purinerich vegetables (e.g., beans, peas, lentils, and spinach) and total protein. [9][10] The
consumption of coffee, vitamin C and dairy products, as well as physical fitness,
appear to decrease the risk.[11][12][13] This is believed to be partly due to their effect in
reducing insulin resistance.[13]

Genetics
The occurrence of gout is partly genetic, contributing to about 60% of variability in
uric acid level.[6] Two genes called SLC2A9 and ABCG2 have been found to
commonly be associated with gout, and variations in them can approximately double
the risk.[14] A few rare genetic disorders, including familial juvenile hyperuricemic
nephropathy,
synthetase

medullary

superactivity,

cystic
and

kidney

disease,

phosphoribosylpyrophosphate

hypoxanthine-guanine

phosphoribosyltransferase

deficiency as seen in Lesch-Nyhan syndrome, are complicated by gout.[6]