Nutrition for Gout

by Juhairina
 What is Gout?

• Gout is a metabolic disease most often affecting middle-aged to

elderly men and postmenopausal women
– A form of arthritis hallmarked by elevated levels of uric acid in the
bloodstream.
– It is the body’s reaction to irritating crystalline deposits in the space
between the bones in a joint.
– The common end point of a group of disorders that produce hyperuricemia
• Due to overproduction or underexcretion of uric acid—sometimes both.
• Crystals of monosodium urate (MSU) or uric acid are deposited on
the articular cartilage of joints, tendons, and surrounding tissues.
• It is marked by transient painful attacks of acute arthritis
– Initiated by crystallization of urates within and about the joints
– Eventually leads to chronic gouty arthritis and the deposition of masses of
urates in joints and other sites, sometimes creating tophi.
• 90% of the sufferers of gout
are middle-aged men
– about half of them have
hereditary predisposition to
the ailment.
– The disease is especially
common in Pacific islanders,
eg, Filipinos and Samoans.
• Men who are overweight or
are suffering from high
blood pressure are
particulary prone to gout.
Global epidemiology of gout
Uric Acid
• Uric acid is produced by
xanthine oxidase from
xanthine and hypoxanthine,
which in turn are produced
from purine.

• Increase production of uric

acid may result from:
– Enzyme defects
– Metabolic defects
– Chronic anemia
– Kidney disease
– Other complex condition
Purine Metabolism
Major risk factors for gout

Hyperuricaemia Genetics

Dietary factors Medications

Comorbidities
Origin of Hyperuricemia
Classification of Gout
Pathogenesis
 Factors Contributing to the Progression from
Asymptomatic Hyperuricemia to Primary Gout
• Age of the individual and duration of the hyperuricemia
– Gout rarely appears before 20 to 30 years of hyperuricemia
• Genetic predisposition
– In addition to the well-defined X-linked abnormalities of HGPRT,
primary gout follows multifactorial inheritance and runs in families.
• Heavy alcohol consumption
– predisposes to attacks of gouty arthritis.
• Obesity
– increases the risk of asymptomatic gout.
• Certain drugs (e.g., thiazides)
– predispose to the development of gout.
• Lead toxicity
– increases the tendency to develop saturnine gout
 Factors that can Precipitate an attack
• Dietary excess
• Trauma
• Surgery
• Excessive ethanol ingestion
• hypouricemic therapy
• Serious medical illnesses
– myocardial infarction and stroke
 Clinical Manifestations
The natural history of gout has four stages:
1. Asymptomatic hyperuricemia
2. Acute gouty arthritis
– sudden onset of excruciating joint pain associated with localized hyperemia,
warmth, and exquisite tenderness.
• Constitutional symptoms are uncommon, except possibly mild fever.
• The majority of first attacks are monarticular; 50% occur in the first metatarsophalangeal
joint.
• About 90% of patients experience acute attacks in the following locations (in descending
order of frequency): insteps, ankles, heels, knees, wrists, fingers, and elbows.
3. Intercritical gout
– Gradually there is complete resolution and the patient enters an
asymptomatic intercritical period.
• In the absence of appropriate therapy, the attacks recur at shorter intervals and
frequently become polyarticular.
4. Chronic tophaceous gout
– Eventually, over the span of years, symptoms fail to resolve completely with
the development of disabling chronic tophaceous gout.
 Causes of Gout
• Over abundance of uric acid
– Gout is caused by an overabundance of uric acid crystallizing in the
joints, allowing the jagged edges to produce inflammation and pain.
High uric acid levels in the blood signal the first stages of gout.

• Hereditary
– Gout does run in families and is carried on through the genes.

• Fungi
– Fungi contaminate rich, fatty foods and alcohol. They are able to
manufacture uric acid in the bodies of people susceptible to fungal
infections.

• Metabolic illnesses
 Causes of Gout
• Diet
– The consumption of proteins, especially meat, rich fatty foods and
alcohol promote uric acid production. Uric acid is a by-product of
protein metabolism in the liver. Gout results from the excess
production of uric acid.

• Age and Sex

– Men over thirty tend to be much more prone than women

• Stress
– Gout attacks are triggered by stress

• Weight
– Excess weight, high blood fat levels and diabetes increase the
incidence of gout
 Symptoms of Gout
• Joint inflammation with acute pain, swelling,
redness and heat.
• An attack of gout can be severely painful and
occurs without warning.
• Main joints affected are the large toe most
often with inflammation.
• Pain in the knee, thumb, and elbow joints.
• May be accompanied by fever and fatigue.
• Alternating chills and fever.
 Lab Findings
• The serum uric acid is elevated (> 7.5 mg/dL)
– However, a single uric acid determination is normal in
up to 25% of cases, so it does not exclude gout,
• ESR and white cell count are frequently elevated.
• Identification of sodium urate crystals in joint
fluid or material aspirated from a tophus
establishes the diagnosis.
– The crystals, which may be extracellular or found
within neutrophils, are needle-like and negatively
birefringent when examined by polarized light
microscopy.
Treatment
 Treatment of Acute attacks
• The mainstay of treatment: Nonsteroidal anti-inflammatory
drugs (NSAIDs), colchicine, or glucocorticoids.
– In attacks involving one or two joints, intraarticular
glucocorticoid injections may be preferable and effective.

• NSAIDs given in full anti-inflammatory doses are effective in

~90% of patients
– resolution of signs and symptoms usually occurs in 5–8 days.
– The most effective drugs are any of those with a short half-life
• Indomethacin, 25–50 mg tid
• Ibuprofen, 800 mg tid
• Diclofenac, 50 mg tid.
 Treatment Between Attacks
• Colchicine
– an alkaloid isolated from the autumn crocus, Colchicum autumnale
– produces its anti-inflammatory effects by binding to the intracellular
protein tubulin inhibiting leukocyte migration and phagocytosis
– used to prevent future attacks
– used when uricosuric drugs or allopurinol are started, to suppress
attacks precipitated by abrupt changes in the serum uric acid level.
• Reduction of serum uric acid
– Uricosuric drugs
• Block the tubular reabsorption of filtered urate thereby reducing the
metabolic urate pool
– Probenecid
– Sulfinpyrazone
– Allopurinol
• The xanthine oxidase inhibitor allopurinol promptly lowers plasma urate and
urinary uric acid concentrations and facilitates tophus mobilization
• Mainstay in prevention of gout.
 Non-pharmacological Treatment
• Controlled weight loss in obese individuals.
• Avoid precipitating factors, such as heavy
alcohol consumption or a diet rich in purines
• Ice pack
• Bed rest
• Heat therapy
 Nutritional Therapy
• Low purine content
– Avoid foods rich in nucleic acids i.e. fish, meat,
and organ meat
• Moderate fats
• Liberal amounts of fluid
 Carbohydrates and Calories
• Calorie restriction for obese individuals
• Maintain weight at normal to reduce joint
damage
• Gradual and controlled weight loss
• During acute attacks the majority of calories
should be from carbohydrates
 Proteins
• Intake should be between 50-60 grams/day.
– From cereal, milk, eggs, and vegetables

• AVOID high purine foods

 Fats
• Moderation!

• High fat intake can decrease urate excretion

 Fluid Intake
• Liberal intake of fluid at least 2-3 liters/day to
increase the volume of urine excreted.
• 2-3 cups of tea or coffee or cocoa a day
– methyl purine content of this beverage is not
converted to uric acid.
• Alcoholic drinks… not a good idea.
 Low and Fair Purine Foods
Below 50 mg purine/100 gms of 50-500 mg purine/100 gms of
edible portion edible portion
• Milk and milk products • Pulses 1 cup/day but
• Eggs
• Cereals
exclude during an acute
• Vegetables attack
• Ice cream • Vegetables like peas, beans,
• tapoica spinach, apple, mushroom,
• Fruits
• Sugar and sweets
cauliflower
• Fats and oil (1-2 tbsps/day) • oatmeal
• Nuts
• Asparagus, legumes, lentils
• Gelatin
• White bread and white rice • Soy, tripe
 High Purine Foods
500-1000 mg purine/100 gms of edible portion
• Fish • Meat
• Sweet bread
• Sardines • Liver
• Mackerel • Kidney
• Pancreas
• Anchovies
• Brain
• Herring • Heart
• Scallops • Gravy
• Broth
• Shrimp • Meat extracts
• Crabs • Bouillon
• Mussels • Dried legumes
• Yeast
 New Developments
• A 2004 study, by Choi HK, et al:
– Suggests that animal flesh sources of purine greatly increase the
risk of developing gout.
– However, high-purine vegetable sources (such as asparagus,
cauliflower, spinach, and green peas) did not.
– Dairy products such as milk and cheese significantly reduced the
chances of gout.
– The study followed over 40,000 men over a period of 12 years,
in which 1,300 cases of gout were reported
• A study published in the March 9, 2009, issue of Archives of
Internal Medicine:
– Found that Vitamin C prevented outbreaks of gout
– Showed that men who had the highest vitamin C intake—1,500
milligrams or higher per day—had a 45% lower risk of gout than
those with the lowest daily intake—less than 250 milligrams per
day
Studies show that drinking low-fat milk and
eating low-fat dairy can reduce your uric
acid levels and risk of a gout attack. The
proteins found in milk promote excretion of
uric acid in the urine.
In one systematic review, 11 studies were investigated for their results
on coffee intake and serum uric acid levels. The researchers found that
while there was evidence to suggest coffee intake reduces gout risk,
the results were not statistically significant enough to matter.
In addition, one study, showed a much different relationship between
coffee intake and serum uric acid levels. In that study, researchers
discovered that uric acid levels increased during coffee consumption
periods and decreased during periods of no coffee intake.

Drinking more than six servings of caffeinated beverages in the

previous day was associated with a 3.3-fold higher risk of a flare-up,
the study of 663 gout patients suggests.
URIC ACID: THE OXIDANT–ANTIOXIDANT PARADOX

Uric acid, despite being a major antioxidant in the human

plasma, both correlates and predicts development of obesity,
hypertension, and cardiovascular disease, conditions
associated with oxidative stress. While one explanation for
this paradox could be that a rise in uric acid represents an
attempted protective response by the host, we review the
evidence that uric acid may function either as an antioxidant
(primarily in plasma) or pro-oxidant (primarily within the cell).
We suggest that it is the pro-oxidative effects of uric acid that
occur in cardiovascular disease and may have a contributory
role in the pathogenesis of these conditions
Uric acid is involved in a complex reaction with several oxidants and
may have some protective effects under certain conditions. On the
other hand, uric acid cannot scavenge all radicals, with superoxide as
an example. Uric acid is an antioxidant only in the hydrophilic
environment, which is probably a major limitation of the antioxidant
function of uric acid. Reactions of uric acid with oxidants may also
produce other radicals that might propagate radical chain reaction and
oxidative damage to cells. In addition, uric acid itself and/or
downstream radicals can engage, as a biologically active
proinflammatory factor, intracellular oxidant production via the
ubiquitous NADPH oxidase-dependent pathway resulting in redox-
dependent intracellular signaling and, in some conditions, oxidative
stress. In our opinion, these considerations taken together may
explain the oxidant-antioxidant paradox.
Case
• A moderate obese 64 y/o male with a wt. of 190
lbs. and a height of 5’5” appeared at the
emergency department complaining of severe
pain of 12-h duration in his left big toe. He stated
that he regularly had at least 2-3 drinks of scotch
whisky every evening after work. He had no
other significant medical history.
• On examination, his left big toe was found to be
red and markedly swollen around the
metacarpophalengeal joint, and exquisitley
sensitive. There was no evidence of arthritis
elsewhere.
• The serum uric acid level was 0.61 mmol/L (N=
0.18-0.41 mmol/L in males); WBC was
increased and x-ray findings were non-
specific, no indication of chronic arthritis was
evident.
• Under local anesthesia, arthrocentesis was
performed on the affected joint, and a small
amount of synovial fluid was analyzed which
revealed typical needle-shaped crystals of
MSU showing negative birefringence.
Desirable body weight
– Ht: 5’5’’ = 67 inches
– =67 x 2.54 cm = 170cm
– = 170-100 –(170 x10%)
– =63 kg

BMR
– 1x24x 63 = 1512 kcal
• Physical Activity: Light
– = 50% x 1512
– =756 kcal

• SDA
– =10% x(1512 +756)
– = 227kcal

• TER
– 1512+ 756+227
– =2495 kcal
• Percentage Distribution:
– 70% CHO
– 10% CHON
– 20% FAT
• CHO =2495x 70% = kcal /4 = 1747 g ~ 437 g
• CHON =2495x 10% = kcal /4 = 250 g ~63 g
• FAT = 2495x 20% = kcal / 9 = 499 g ~55 g
 Diet Prescription
TER= 2495kcal, CHO= 437g, CHON= 63g,
FAT= 55g
Food Number of CHO CHON FAT ENERGY
exchanges

Vegetable A 1
Vegetable B 3 9 3 48
Fruit 6 60 240
Milk 2 24 16 20 40
Sugar 2 10 40
Rice 14 322 28 1400
Meat 2 16 4 100
Fat 6 30 270
Total 425 63 54 2098
 Dividing a Day’s Exchange
Between Meals and Snacks
Food Breakfast Lunch PM Snack Dinner Midnight
Snack

Vegetable A 1

Vegetable B 1 1

Fruit 2 2 1

Milk 1 1

Sugar 1 1

Rice 4 4 4 2

Meat 2 2 2

Fat 2 2
 Translating A Day’s Exchange into
A Day’s Meal
Meal time Food

Breakfast 2 cups of rice

karot
¾ pc. tocino
2 tbsp. of sandwich spread
2 cups of strawberries
½ glass of Cow’s milk
Lunch 2 cups of rice
1 small chicken leg
Talong
Kalabasa
2 tbsp. margarine
2 med. Slice mango
 Translating A Day’s Exchange into
A Day’s Meal
PM Snack 4 pcs. Pandesal
2 tbsp. cream cheese
1 slice pineapple
1 tbsp. Condense milk

Dinner 1 cup of rice

2 strips of bacon
7 tbsp. orange juice
Malunggay
Bedtime ½ glass of Cow’s milk
1 pc. marshmallow
THANKYOU