M K Mam
Gout is a disease known since centuries; however its prevalence has markedly increased over the last two decades or so. It is a metabolic disorder characterized by increase in the level of serum uric acid.
Uric acid is normally produced either as a result of the breakdown of a chemical called purine which occurs naturally in the body and is also found in certain foods . Uric acid is eliminated from the body mainly by kidneys in urine. SUA level increases when there is decreased renal excretion of uric acid or when there is an overproduction of uric acid. A balance is normally maintained between production and excretion, and that determines the level of serum uric acid (SUA). Increased production of uric acid is responsible for only 10% of cases of gout while the remaining 90% are caused by its renal under-excretion. Urate is the ionized form of uric acid present in the body. When SUA level rises above the normal threshold, urate crystals are deposited in synovial membrane, articular cartilage, tendons and bursae (sacs of fluid) around the joint. The urate crystals initiate inflammation in these tissues, which subsequently leads to chronic synovitis, bony erosions and cartilage damage. These deposits may at times increase in size and form small lumps called tophi. These urate crystals can also get deposited in kidneys and result in formation of kidney stones and in severe cases impairment of kidney function can also occur.
Overproduction of uric acid: Overproduction of uric acid can occur due to some genetic or an acquired problem with purine metabolism. It is usually seen when there is excessive destruction of cells in body as happens in malignant tumors, multiple myeloma, leukemia or when a patient is on chemotherapy.
Decreased excretion of uric acid: Decreased excretion of uric acid by kidneys is the primary factor in 90% of cases of gout and this could be due to some genetic disorder. Certain drugs such as anti TB drug – pyrazinamide, diuretic- thiazides, niacine etc. increase urate reabsorption by kidneys, thus increase the SUA level.
Food: Intake of foods rich in purine like beef, pork, lamb , offal such as liver, kidney , heart and seafood like shell fish, shrimps and crab certainly increase SUA. Again, yeast containing foods are also rich in purates. All forms of alcohol promote hyperurecemia and development of gout; however it varies with the types of alcohol consumed. Beer has a high content of readily absorbable purine, thus is the worst in causing hyperurecemia and gout when compared to other liquors. Certain vegetables like green peas, beans, lentils, mushrooms cauliflower, broccoli, and spinach are rich in purine, however various studies have shown that there is no significant association between consumption of purine rich vegetables and gout, and they do not increase the risk of gout and recurring gout attacks.
Gout is of two types i) primary ii) secondary. In most of the cases (95 %), it is primary in nature as there is no obvious cause and there is decreased excretion of urate at the kidneys. Secondary gout may be due to rare hereditary conditions or secondary to some diseases like malignant tumors, multiple myeloma, leukemia, renal failure or when a patient is on chemotherapy or diuretics. Clinical picture: It commonly occurs in men in third and fourth decade. Onset of gout in men prior to adulthood or in women before menopause is rare. Ninety percent of women, who develop gout, have it after menopause. Family history is positive in around 20% of patients. Gout usually affects one joint and Metatarso-phalangeal joint i.e. proximal joint of the big toe is the most often involved. Occasionally other joints like ankle, knee, mid-foot, elbow and wrist can be involved. It can also affect bursa (small sac of fluid) over the point of the elbow and back of heel. It usually presents with a sudden attack of excruciating pain with marked swelling, redness over the joint, increased temperature of the affected joint and the patient may be unable to walk. Attacks usually begin at night. Skin over the joint is reddish, tight and shiny. At times the inflammation is so gross that it may resemble acute infective process like cellulitis or septic arthritis. The mild attacks usually resolve spontaneously within couple of days and severe attacks subside in a week or so, however there is repetition of acute attacks in untreated cases. In a chronic stage patient presents with persistent pain in the joint. It is also a fact that many people have asymptomatic hyperuricemia as there are no symptoms or signs and high SUA level is accidentally discovered when it is measured. Some of these patients develop gout while majority of these hyperuricemic patients never develop gout.
Treatment: The main aim of the treatment in acute gouty arthritis is to give pain relief, reduce the inflammation of the affected joint and prevent acute attacks, and for that an appropriate drugs are given. Rest, elevation of the affected limb and topical ice application helps in reducing pain and swelling. Applying a splint gives rest to the affected part. Anti inflammatory drugs (NSAIDs), certainly are very useful in patients of acute gout. However, we need to be careful as many of these patients have associated medical problems like peptic ulcers, kidney and heart problems etc and as such NSAIDS may be unsuitable for them. We have drugs which help in decreasing formation of uric acid and drugs which help in increasing the excretion of uric acid in the urine and appropriate ones have to be given. Once acute gout has subsided, our aim should be to prevent the disease recurrence. SUA level should remain under 6mg/dL and this has to be a lifelong process. SUA level has to be monitored regularly. The treatment has to be continued for a prolonged period so as to keep SUA levels under control and thus patient remains symptom free and does not have acute gout attacks. Occasionally large gouty tophi may need surgical excision. Once a while there are patients that are refractory to treatment and this certainly is a challenge to the treating doctor. It is also known that gout is often poorly diagnosed and sub optimally managed.
Patient education and adherence to the treatment is very essential for better outcomes. It is all the more important that we explain and educate the patient about the gout and the importance of maintaining SUA levels under control. Appropriate lifestyle advice, weight reduction and dietary advice including reduction of alcohol intake are a must.
(The author is formerly, Vice Principal, Professor and Head. Deptt. of Orthopaedics, Christian Medical College, Ludhiana)
M K Mam