Pathology of gout

2021-01-26 12:00 AM

Since the blood uric acid increase to the first gout attack usually takes 20-30 years and it is found that 10-40% of gout patients have kidney cramps even before arthritis.


The disease is common among people with high living standards, the rate in some European countries is about 0.5% of the population, men 10 times that of women. In Vietnam, the disease has not been seen much, but in recent decades, the disease has increased clearly.

Gout is a metabolic disease, characterized by acute attacks of arthritis and the deposition of sodium urate in the organs, caused by increased uric acid in the blood.

Metabolism of uric acid

Uric acid is a degradation product of purines based on nucleotides. There are 3 sources of uric acid:

Due to the degradation of nucleic acids from food intake.

Due to the degradation of nucleic acids from dead cells

Due to endogenous synthesis and metabolism of purines in the body thanks to specific enzymes. Uric acid is excreted in urine 450-500 mg/day and in faeces 200 mg/day. When passing through the kidneys, the urate is completely filtered by the glomerulus, and then reabsorbed almost completely in the proximal tubule, which is excreted by the distal tubule. In the faeces, uric acid is broken down by bacteria.

The concentration of uric acid in the blood according to the Vietnamese constant is 45 ± 10mg / l (208-327 μmol / l). When the concentration is> 70mg / l (> 416.5 μmol / l), it is called hyperuricemia.

The causes of hyperuricemia:

Increased production of uric acid: Use more foods containing many purines, increase the degradation of cell nucleoproteins, increase endogenous purine synthesis.

Reducing uric acid urinary excretion: reducing glomerular filtration, reducing renal tubular secretion.

Occasionally decreased uric acid degradation by bacteria in faeces.

Classification of hyperuricemia and gout

Idiopathic hyperuricemia syndrome and primary gout

This form most commonly accounts for up to 85% of the cases, family and genetic due to disorders of metabolism of purines.

Hyperuricemia syndrome and yeast gout disorder

In general, this form is rare.

Secondary hyperuricemia syndrome

Can occur due to kidney failure, in some blood diseases, endocrine diseases ...

Mechanism of pathogenesis

When uric acid in the blood increases, the fluid is saturated with sodium urate and there will be deposition of urate in some organizations, especially synovial membrane, bone cartilage, tendons, subcutaneous organs, parenchyma. Kidney and pyelonephritis ...

In the joints, long-term hyperuricemia leads to the formation of micronutrients in the cells covering the synovial membrane, deposition of sodium urate in cartilage. Uric acid microcrystals can appear in the synovial fluid and when a certain amount is reached, arthritis and is a manifestation of an acute gout attack. In gout, a series of reactions will occur in joints: the white blood cells focus on phagocytes to release lysozymes, which cause inflammation; The microcrystals also activate the Hageman factor leading to the formation of kallikrein and kinin, which are responsible for arthritis; activating complement and plasminogen, leading to the formation of end products, also plays a role in arthritis.

Since the blood uric acid increase to the first gout attack usually takes 20-30 years and it is found that 10-40% of gout patients have kidney cramps even before arthritis.


First acute gout attacks usually appear between the ages of 35-55, rarely before the age of 25 or after age 65. In women less often before menopause, in younger men, the worse the disease.

Favorable conditions: sometimes unknown, but can occur after a meaty meal, after strong emotions, after trauma including micro-trauma (wearing tight shoes), after infection, using diuretics such as thiazide, liver essence, Steroid, Vitamine B12 ...

Acute gout attack

Appears suddenly at night, the patient wakes up from pain in the joints, usually the big toe joint (60-70%): the joint is swollen, red, edematous, shiny, severe and increasing pain, and Light touch is also very painful; Other joints may suffer: ankles, pillows, hands, wrists, elbows. Rarely found in hip, shoulder, and spine joints. At first only one posterior joint may have many joints.

The attack lasts for many days, usually 5-7 days and then the inflammatory signs subside. Completely restored joints completely normal. During the attack may have a moderate or mild fever, the rate of blood sedimentation increased, synovial fluid saw leukocytes about 5000 / mm3, mostly multinuclear, under the microscope, saw many crystals of sodium urate. The attack easily recurs when conditions are favorable.

In addition to the typical form, it may also be acute: the inflamed joint is intensely inflamed, the pain is much, and the mild, discreet formless painful is less easily ignored.

Deposition of urate

Formation of particles under the skin and urate joint disease

Tophi: Usually appears slowly, decades after the first gout attack. Once present, it is easy to increase in number and volume and can cause ulcers. Tophi is found in elbow cartilage, big toe, heel, instep, Achille tendon. Size from a few millimeters to many centimeters, slightly firm or soft, not moving due to sticking to the bone below.

Joint disease caused by urate: stiff joints, pain when moving and limited movement, joints are swollen moderately, not asymmetric, may also be attached. On radiographs, fissure stenosis, defect, cavity-shaped bones are seen.

Expressed in the kidneys

Urat is scattered in the interstitial organization, renal pelvis, ureter.

Kidney stones: 10 - 20% of gout cases, the favorable conditions are that the urine pH is too acidic, the concentration of uric acid is high. Urea stones are usually small and not obstructive.

Kidney damage: At first only proteinuria, red blood cells, microscopic leukocytes may be present, then gradually progress to kidney failure. Renal failure is common in the form of metphi, progressing slowly and is the cause of death.

Diagnostic standards

Rome Standard 1963

Acid uric in blood > 70mg/l (416,5 μmol/l).

Has Tophi gout.

There are sodium urate crystals in synovial fluid or urate deposition in organizations during microscopy or chemical examination.

The history of osteoarthritis is clear, at least at the onset of arthritis, arthritis appears suddenly, severe pain and completely resolves after 1-2 weeks.

Only two criteria are needed for a solid diagnosis.

New York Standard 1966

At least 2 episodes of acute inflammation of a joint in the limb, with sudden onset of illness and recovery after 1-2 weeks.

There is one such episode above but involving the big toe joint.

There is a bet.

Using colchicine significantly reduced inflammation in 48 hours. Just having 2 criteria is enough.



Reduce substances high in purines such as animal viscera, meat, fish, shrimp, crab ... do not overeat. Reduce calories if fat.

Don't drink alcohol.

Drink plenty of water 2 - 4l / day, especially water with bicarbonate.


Treatment goals:

Treatment of arthritis during acute gout attacks.

Prevention of recurrence of gout attacks, prevention of urate deposition in organizations, and complications through treatment of hyperuricemia syndrome.

Treatment of arthritis during an acute gout attack:

Taking nonsteroid anti-inflammatory drugs:

Colchicine: The phagocytic effect of leukocytes on urate microcrystals, is the best drug to date.

Usage: 1mg x 3 times in the first day; 1mg x 2 times on day 2 and 1mg from day 3 on. Maintenance dose to avoid relapse is 0.5 -2mg / day (1mg) orally for 3 months.

Side effects: Increased gastrointestinal motility, easy to lose; sometimes causes bone marrow suppression, hair loss, gas damage, respiratory depression.

Many nonsteroid anti-inflammatory drugs have been studied and used, the results are also good but not as good as colchicine: Phenylbutazon, Indomethacin, Naproxen, Ibuprofen, Piroxicam, Diclofenac.

Corticosteroids reduce inflammation quickly, but after the drug ends, arthritis returns. On the other hand, it increases blood uric acid so it is not used.

Treatment of hyperuricemia syndrome:

Assign after having cut gout attacks. Long-term medication can make the bowl smaller or disappear, the joints stiffen or return to normal, limit the deterioration of kidney failure, reduce the attacks of arthritis.

The drug increases uric acid excretion:

The effect of reducing the reabsorption of the renal tubules can easily cause kidney stones, so it is necessary to use a small dose and then increase gradually, and at the same time give more bicarbonate water 2 - 4l / day.

Benziodoron (Amplivix 100mg): dose 100 - 300mg / day. Few side effects sometimes have digestive disorders.

Drugs that reduce uric acid biosynthesis:

Allopurinol (zyloric 100mg): xanthin-oxidase inhibitor, which degrades hypoxanthine to xanthin and xanthin to uric acid and reduces purine biosynthesis. The drug can be used when there is kidney failure.

Dose: 200 - 300mg / day orally once. Fewer side effects, sometimes digestive disorders, skin rash, headache, dizziness, drowsiness.

Drugs that destroy uric acid in the blood :

Uricozym: is an enzyme urate-oxidase that degrades uric acid to allantoin, this substance is 10 times more soluble than uric acid and easily excreted by the kidneys. Uricozym very strongly reduces uric acid.

Inject TM or TB 1000-2000 units / day.

In the course of taking drugs that reduce uric acid in the blood, it is necessary to monitor the concentration of uric acid in the blood and the amount of uric acid in the urine to adjust the maintenance dose, to keep the concentration in the blood <60 mg / l.