Dr. Rohini Handa, a noted Rheumatologist from Delhi with rich experience in his field, explains in detail about the clinical presentation of gout and the interesting myths, facts, and science surrounding the disease.

Gout is often dubbed as the king of diseases and a disease of the kings. It is crystal arthritis characterized by hyperuricemia and deposition of monosodium urate (MSU) crystals. Aging of the population and lifestyle changes, especially the epidemic of metabolic syndrome in Indians, has made this disease ubiquitous. Despite its commonality, the disease is shrouded in myths. This write up dispels some long-held misconceptions while discussing the current concepts in light of the new knowledge that has become available.

The clinical picture

The clinical picture of a classical attack of gout is so characteristic that investigations are not needed. Contrary to popular perception, the role of serum uric acid (SUA) is more in monitoring therapy than in diagnosis.

The gold standard for diagnosis is the demonstration of MSU crystals in synovial fluid. Though MSU crystals may be picked up on ordinary light microscopy, polarized light microscopy which permits detection of birefringence characteristics is ideal. Crystal identification relies on shape and birefringence. MSU crystals may be intracellular or extracellular, are needle-shaped and exhibit strongly negative birefringence.

‘Strong’ birefringence means that crystal is bright and easily seen whereas ‘weakly’ birefringent crystal is subdued and difficult to see. ‘Positive’ and ‘negative’ birefringence refers to colors in reference to the alignment of the red compensator. MSU crystals are yellow when parallel to the slow axis of the red compensator (negative birefringence).

A high serum uric acid in the context of a typical clinical setting substantiates the diagnosis. However, elevated SUA does not always mean gout. Clinical correlation and pattern recognition are important. Conversely, SUA may be normal during an acute attack because ACTH released in response to stress is uricosuric.

Recommended dietary restrictions

Diet in gout is a matter of endless debate and ceaseless controversy. Most of the aphorisms are rooted in hearsay and not in science.

Purines in the diet should be restricted to <200 mg/day. However, dietary purine restriction has only a modest effect on SUA lowering.

A low purine diet is not the same as a low protein diet.

Myths and Facts associated with Gout

Protein intake needs to be restricted only in those consuming very high amounts of proteins which is not common in Indians.

Items rich in purine which should be avoided include red meat, liver, kidney, sardines, shellfish and some other varieties of seafood. The total amount of purine in the diet is more important than the item consumed. Spinach, pulses (lentils), peas, mushrooms, cauliflower, soya beans etc are rich in purines but cause a much lower rise in SUA than meat.

Moderate intake of purine-rich vegetables is not a problem.

There is no rationale behind totally stopping tomatoes, spinach, pulses, peas, mushrooms etc. in all patients.

Blanket dietary restrictions are difficult to enforce. Moderation rather than total abstinence is key to ensuring adherence. Skimmed milk and curd (yogurt) and low-fat dairy are beneficial.

Patients with gout should be encouraged to abstain from alcohol. Amongst alcoholic drinks, beer is the biggest offender while wine (especially red wine) is the least with whiskey figuring in between wine and beer.


 

Dr. Rohini Handa throws light on the treatment for Gout. Read it here.

This article was originaly published on 19.06.18

Disclaimer- The views and opinions expressed in this article are those of the author's and do not necessarily reflect the official policy or position of M3 India.