Gout

Definition: Gout is a hereditary and metabolic disease resulting from defective uric acid metabolism.

Cause: Gout is caused by having higher-than-normal levels of uric acid in the blood. This overload of
uric acid leads to the formation of tiny crystals of monosodium urate monohydrate (MSUM) that deposit
in the cartilage and articular cartilage of the joints. These crystals cause the joint to swell up and become
inflamed (arthritis).

Classification of gout:

 Primary gout: Due to abnormality of uric acid production and metabolism.

 Secondary gout: Excess uric acid production due to excessive breakdown of nuclei secondary
to some disease (leukaemia, pernicious anaemia, hemolytic anemia and polycythemia)

Uric acid metabolism: In a normal subject uric is metabolized by two ways -

 Endogenous uric acid: Uric acid is derived from purine (Purine is derived from the
breakdown or synthesis of nucleoproteins). If the diet is free from purine about 300-600ml uric
acid is derived from the endogenous source and this amount of uric acid is excreted through the
urine of a normal adult person.

 Exogenous uric acid: Diet with high purine and nucleic acid content such as meat, fish and
all other animal tissues. The level of serum uric acid in normal subject is about 3-6mg / dl.

Uric acid level in blood: The level of serum uric acid is generally high in patients suffering from
gout about 6.0-10.0mg / dl, whereas the normal serum uric acid level is 2.0-7.0mg / dl (for male) and 2.0-
6.0mg / dl (for female).

Mechanism for the high serum levels of uric acid: The possible mechanisms for the high
serum levels of uric acid in gout are -

 Increased production of uric acid: There is evidence that in gout there is increased
synthesis of purines in the body, leading to increased production of uric acid (polycythemia,
leukaemia, psoriasis, idiopathic).
  Diminished renal excretion of uric acid: There is also evidence that uric acid excretion by
the kidney is diminished in gout. These abnormalities in the kidneys are seemed to be
hereditary. Other causes include renal failure, drugs, lead poisoning, lactic alcoholism, severe
vomiting.

Metabolic defect in patient with gout: The metabolic defects in the gout are as follow -
 Defective excretion of urate by the kidney (primary renal gout where there is defect in renal
tubule)

 Reduction in the enzyme hypoxyxanthine-guanine phosphoribosyltranferase (catalyses

formation of nucleotides from free purines)

 Reduced urate binding capacity of plasma

Clinical presentation of gout:

 Acute gout:
 Onset is insidious or explosively sudden.
 Pain in the Joint: The metatarsophalangeal joint of a great toe is the site for acute gouty
arthritis in 70% of the patients; the ankle, the knee, the small joints of the feet and
hands, the wrist and elbow follow in decreasing order. The affected joint is hot, red and
swollen.

 Other symptoms: May have fever, anorexia, nausea, change in the mood.

Some patients have only a single attack and some have recurrent attacks.

 Chronic gout:

 Recurrent acute attacks

 Progressive cartilage and bone erosion in association with deposition of urate crystal and
secondary degenerative changes.

 Severe functional impairment and gross joint deformities may occur in chronic gout.
Risk factors: The exact cause of gout is unknown. But the following risk factors are suspected for
developing gout include -

 More common in men

 Women after menopause
 Family history of gout
 Obesity
 Moderate, regular, or heavy consumption of alcohol, especially beer
 A diet rich in meat and seafood, which can be high in purines
 Use of medicines that remove salt and water from the body (diuretics)
 Regular use of aspirin or niacin
 Frequent episodes of dehydration
 Lead exposure (may occur through work, diet, or hobbies)
 Injury to a joint

Certain other conditions and diseases appear more often in people who have gout than in people who
don't, though studies have not shown a clear relationship. It is thought that gout shares risk factors
(such as obesity, hypertension, and high levels of triglycerides) with certain diseases, including -

 Diabetes
 Kidney (renal) disease
 Heart disease
 High blood pressure
 Hypothyroidism

Diagnosis of gout: Diagnosis can be made by examining -

 Serum uric acid level

 Uric acid level in urine
 Synovial fluid of the joint
 X-ray of the joint.

Treatment of gout: Medicines should be taken as soon as possible if there is a sudden gout attack.
 Nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, naproxen, or indomethacin
are given as soon as the symptoms begin. Among them Indomethacin (50mg 6-hourly orally) or
naproxen (500mg 8-hourly) are given until the acute attack subsides. Treatment is then
continued with lower doses for 7-10 days.
  If NSAID contraindicated (i.e. peptic ulcer), then treatment is continued by giving Colchicine
(1mg at once followed by 0.5mg 2-hourly orally). Colchicine is highly effective but causes
vomiting and diarrhoea.

Foodstuffs classified according to the content of purine:

High Moderate Fair Low or absent

300-1000mg / 100gm 150-300mg / 50-150mg / 100gm below 50mg / 100gm
100gm
Fish Meats Whole cereals Milk
.......... .......... Pulses Milk product
Sardines Chicken Vegetables Eggs
Herrings small fish .......... ..........
Liver .......... .......... ..........
Kidney .......... .......... ..........
Heart .......... .......... ..........
Meat extracts .......... .......... Sugar

Diet for adult male suffering from gout (gm / capita / day):

Quantity
Food item
Veg. Non-veg.

Cereals (milled) 400 400

Legumes (pulses) 30 30
Green leafy vegetables 100 100
Other vegetables 100 100
Fruits 100 100
Milk 800 800
Cheese 30 .....
Meat and fish ..... 20
Eggs ..... 30
Fat and oils 40 40
Sugar 50 50
Some key message about diet for goutary patient: (Dietary Management of Gout
patient)

 Calories: The calorie intake should be restricted to that required for person who does
sedentary work.

 Proteins and Purines: The proteins intake should be between 50-60g for an adult. The
proteins should be derived from cereals, milk and eggs. Meat, fish and other animal tissues
should be avoided as they are rich in purines and nucleic acids. Consumption of excess of
proteins may lead to excessive synthesis of purines in the body.

 Fats: Fat consumption should be restricted, as high fat intake tends to decrease uric acid
excretion in the urine.

 Carbohydrates: During the attack of gout, the main source of calories should come from
carbohydrate.

 Fluids: Large volumes of fluid intake are encouraged to take as it increases the volume of
urinary excretion.

 Beverages: Tea, coffee and cocoa contain methyl purines. They are not converted into uric
acid in the body. So 2 to 3 cups of tea / coffee / cocoa per day may be consumed.
 Gradual weight loss in case of obese patient