Paphos People February Newsletter

Over and Gout by PARAMED from Houston Medical

Gout is a 20th century success story. Attacks can be treated and prevented and damage to joints and kidneys can be prevented. However, we can never be complacent, as the following case histories illustrate.

Case No 1. John McG. was a heavily built Scotsman, with gout for 15 years. Beer with whisky chasers was his tipple. I told him about his weight, his gout and the poor state of his liver and he promised to stop drinking. We started him on allopurinol (Xyloric) with the usual precautions. Over the next few months his attacks diminished, but not much; his uric acid reduced only a little and his weight remained unchanged. When I asked him about his alcohol, he said: "Of course doc, I've done exactly what you said, I've given up the drink". Me: "Your gout should have improved more than this. So you've given up all your drinking, your beer and your whisky?" To which he replied "Oh! doctor, I didn't think you meant the beer as well, I don't really count that as drinking!"

Case No 2. David R. was a bachelor, who limped into the consulting room on a stick in slippers. He could not wear his normal size 91/2 shoes because of the painful swelling due to his gout. He was taking 900mg of allopurinol per day. The usual dose is 300mg per day, rarely 600! And his gout was still not controlled. Like Mr McG, he drank too much, but he also ate liver, bacon, sausage or kidneys at least four days a week, or steak when out in a restaurant. Similarly on his trips abroad his diet would have made a vegetarian weep.

Once his diet was explained to him, he transformed his life. He stopped eating offal. Three months later he came in to see me without his stick and soon he was down to size 10 shoes. His uric acid fell to normal on 600mg of allopurinol a day.

Historical Background
The picture of gout has changed in the past 100 years or so. During the 17th to 19th centuries the links with rich living caused much humour, although nobody who has gout will find it in the least bit funny! The frequency of gout in those times has been attributed to the high intake, by the rich, of meat, including offal. The poor were not at much risk of gout, illustrating the influence of culture on disease.

What is Gout?
The term gout derives from Gutta which means a "drop", perhaps because it was like a fiery liquid dropping on the foot. Gout can actually affect many other joints, and there is an unrelated form of acute arthritis known as "pseudo-gout."

People get gout because uric acid (which we all have in our blood) can build up and form crystals in the joints and cause them to feel acutely painful. The main symptoms are severe inflammation in joints and soft tissues; however there are pitfalls in trying to apply classical descriptions to all cases.

There are a number of misconceptions about gout, which can be summarised as follows: pain in the foot or toe is not necessarily gout; gout does not necessarily occur only in the foot or toe; it is associated with a raised level of uric acid in the blood; raised level of uric acid in the blood does not necessarily mean a patient has gout; normal level of uric acid in the blood does not necessarily mean that a patient does not have gout; just because uric acid crystals cause gout, that does not mean to say that any other form of acid in the diet has anything to do with gout. The body copes with acids in food very much better than many dietary faddists appreciate.

Diagnosis
The clinical history is the most likely clue to the diagnosis. There is a relatively rapid onset of pain in the relevant part, such as the big toe joint, often at night. The part becomes hot, red and very tender, so that even bedclothes may be too heavy. The only unequivocal way of confirming the diagnosis is by putting a needle into the affected joint, taking off some of the inflammatory fluid and looking under a microscope for crystals of uric acid. Confirmation of gout tends therefore to be by exclusion of other causes of arthritis and by response to treatment.

Treatment
The treatment of an acute attack is different from treatment to prevent attacks. An acute attack is treated with non-steroidal anti-inflammatory drugs or colchicine, which back in the 19th century was the first effective treatment to be developed. It is very important that the acute attacks settle down completely before an attempt is made to reduce the blood uric acid level with one of these long-term treatments.

An untreated attack will last up to two or three weeks. Of course nowadays it is very rarely left to itself. Anti-inflammatory drugs are very effective at treating the acute attack, provided the dose is adequate. The newer COX-2s or coxibs are presumably just as effective, but we have really not had the opportunity to evaluate them.

There are two main drugs for long-term treatment. The 'uricosuric' drugs (principally Probenecid) are less often used nowadays, and allopurinol (Xyloric). This inhibits an enzyme, xanthine oxidase, which activates the production of uric acid. Allopurinol is relatively safe, but potentially all drugs have side effects. Occasionally patients are hypersensitive to allopurinol and develop a nasty rash. This tends to happen in patients who have kidney failure.

If the uric acid is reduced too quickly, acute gout is likely to re-occur, so an anti-inflammatory or colchicine must also be given for the first 3-6 months of treatment with allopurinol or probenecid. Very rarely do we come across patients who have gout that cannot be treated with a combination of allopurinol, plus attention to dietary control. In fact, most patients do not even have to bother much with diet!

Seeing patients with gout provides an opportunity to take a look at their general health: reducing weight, blood pressure and alcohol intake are all part of good management of patients with gout.

Diet
Gout arises from the breakdown of DNA to nucleic acids, then to purines, then to uric acid crystals. Blood uric acid arises from natural breakdown of one's own cells and from food. The more cells there are in a food, the greater the quantity of DNA. A good rule of thumb is that anything you eat that has worked hard for its living is more likely to lead to a high uric acid, for example, the liver and kidneys. White chicken breast meat is lower in purines than chicken legs on which the bird runs about. Active fish, such as sardines or salmon, contain more purines than fish such as plaice.

For alcohol, the picture is more complex. Most alcoholic drinks do not contain much purine, but its metabolism causes the blood uric acid to rise. There is recent evidence that a relative increase in dietary unsaturated fat, from nuts, oils and fish, may be helpful, even with a relatively high intake of protein.

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