Gout and high blood uric acid levels (hyperuricaemia)
What is it?
Gout is an excruciatingly painful acute arthritis seen almost exclusively in men above 40 years of age; children and women in reproductive age do not get gouty arthritis. Similarly, it is very uncommon to see gouty arthritis in men below 40 years of age. Gout is often a familial arthritis with history of similar acute attacks in father, uncles, grandfather. It belongs to a major class of arthritis called ‘crystal-deposition arthritis’. A gouty attack usually starts in the middle of the night after a big party where the patient might have indulged in heavy eating and binge drinking. There is a sudden acute severe painful swelling of any of the joints in the ankle-feet region, but most often in the joint at the base of the big toe. In its acute stage, usually a single joint is affected. The joint swells up with excruciating pain; even touching the joint with a soft cloth elicits sever pain. The overlying skin becomes severely inflamed with dusky reddish-brown discolouration.
If untreated, it may take several days for slow improvement with decreasing pain and swelling associated with scaling and peeling of the overlying skin. Initially, such attacks of acute gouty arthritis are infrequent and if untreated, may take a week or 10 days before subsiding slowly, with no symptoms between these episodes (called intercritical gout). Over a period of next several years, if not treated, the attacks of acute gouty arthritis become more frequent and may affect more than one joint. After several years, slowly a chronic painful arthritis affecting several small and large joints in the extremities develops. As against acute gouty arthritis, this stage of gout is called chronic gouty arthritis. Associated chalky-white deposits of monosodium crystal under the skin, called gouty tophi. Develop at different sites including pinna, over and adjacent to the joints, over elbow (called olecranon bursitis). By this time many of the chronically affected joints get badly damaged and deformed. This stage is often called chronic tophaseous gout.
What are the causes?
The characteristic acute inflammatory arthritis of gout is caused by the deposition of needle-shaped crystals of uric acid (mono-sodium urate) in the joints. Uric acid is a waste product produced in the body that passes through the kidneys into the urine. Some people, due to their genetic makeup, do not excrete adequate amounts of uric acid from their kidneys. Decreased removal of uric acid for kidneys over time leads to a slow but steady increase in the level of uric acid content of their body that may also cause a high blood uric acid level.
Research has shown that in general population there are individuals whose blood uric acid levels are much higher than the range seen in normal persons. While the majority of such individuals may never develop acute gouty arthritis attack, most of them would be candidates for high blood pressure, coronary heart disease, brain ‘stroke’ and kidney damage (discussed below). Such individuals are called hyperuricaemic individuals i.e. those having high blood uric acid levels. While most hyperuricaemic men would never get acute gouty attack, a few of them, especially those with family history of gout would start developing acute gouty arthritis attacks by the age of about 40 years. Interestingly, blood uric acid levels generally falls during acute attack of gout. Therefore, testing blood uric acid for diagnosing an acute joint problem as ‘gouty arthritis’, is not recommended.
Research has also shown that men with gout almost always have several associated diseases – often identified by a term called ‘metabolic syndrome’ that includes obesity, high blood pressure, high cholesterol levels, tendency for developing diabetes and very high risk for getting heart attack and brain ‘stroke’. Research has also shown that high blood uric acid is directly related to poor cardiovascular health causing high blood pressure and damage of blood vessel lining further adding to the cause for early age heart attack and brain ‘stroke’. High blood uric acid is also injurious to kidney tissue. Thus, over a period of time most patients with gout develop slowly progressive kidney damage. It is very important to mention that only a small proportion of persons having high blood uric acid level would ever get actual acute gout attack and gouty arthritis. Most of them will never get gouty attack yet, they are prone to heart attack, brain ‘stroke’ and other features of metabolic syndrome.
In this regard it is important to mention that although high blood uric acid levels are directly toxic to blood vessels and cause high blood pressure. Once that happens, the high blood pressure becomes a permanent feature. Therefore, reducing blood uric acid levels by uric acid lowering drugs do not cause lowering of blood pressure. Such patients would require life-time treatment for high blood pressure with appropriate blood pressure lowering drugs.
How is the diagnosis made?
Acute gouty arthritis attack can be diagnosed by typical clinical symptoms easily recognised by a trained physician. Sudden acute onset of red hot, and very painful swelling at the base of the big toe or any one of the joints in ankle-feet region (described above) where touching even with a soft cloth causes excruciating pain, occurring in a male above 40 years of age, often with family history, and history of similar previous attacks of acute joint problems, should be considered acute gouty arthritis. Such a patient often has some ‘trigger’ (see above) that precipitates the acute attack. He should immediate seek medical attention, preferably from a trained rheumatologist (physicians trained in the evaluation, diagnosis and treatment of joint diseases).
The diagnosis is confirmed by demonstrating uric acid crystals (that look like small needles) in the joint fluid. This procedure is best done by a trained rheumatologist who would also examine the fluid and confirm if uric acid crystals are present in the fluid. It is useful to remember that testing for blood uric acid level does not give the diagnosis of gout. As mentioned above, blood uric acid level is usually normal during acute gouty attack. Therefore, a high blood uric acid level does not necessarily mean that the person has gout, nor does a normal blood uric acid level exclude the possibility of acute gouty arthritis attack. Therefore, the diagnosis of gout should be left to the rheumatologist who would see the clinical picture as well as try to demonstrate uric acid crystals in the joint fluid.
Chronic gouty arthritis affecting several joints in the extremities is even more difficult to diagnose and only well-trained and experienced rheumatologist will be able to diagnose this condition with certainty. Of course chronic tophaseous gout is so striking in appearance that it is easy to diagnose by simply looking at the joints of the patients.
What is the treatment?
Treatment of acute gouty attack requires immediate control of the acute joint symptoms followed by strategies to prevent future possible attacks, and joint and tissue damage due to the deposition of uric acid crystals in the long run. Acute attack is treated with the use of fast acting anti-inflammatory drugs. Commonly used drugs belong to the category of so-called non-steroidal anti-inflammatory drugs (NSAIDs). There are several of them like ibuprofen, diclofenac, naproxen, indomethacin. However, most of them have a major side-effect i.e. severe irritation of the gastrointestinal tract that may even lead to ulcer formation (called peptic ulcer). The newer anti-inflammatory drugs called coxibs (celecoxib, etoricoxib) have much less gastrointestinal toxicity with equal efficacy in controlling acute gouty attack.
A recent report recommends that patients who cannot take NSAIDs (due to allergy or GI disease), one of the best methods for quick relief for acute gouty attack is prescribe prednisolone 35 mg daily for 5 days. It is said to be a highly effective, cheap and safe treatment for acute gouty attack. Injection of depot-preparations of glucocorticoids (e.g. depot-methylprednisolone or triamcinolone acetonide) in the joint itself.After the acute attack subsides, the person must be investigated to find out if he has any underlying renal disease, or he is taking some drugs that cause rise in blood uric acid levels. If the rheumatologist finds a definite cause for high blood uric levels, all efforts must be made to correct it. However, in the majority of such patients no obvious cause is found and such person are labelled as having ‘primary gout’.
Such persons are advised as follows:
- General positive health practices:
- Dietary precautions (see Appendix – I – above)
- Regular fitness workouts especially aerobic exercises, control of cholesterol, high blood pressure. It is important to reduce weight very gradually as sudden weight loss can also precipitate an acute attack of gout.
- Plenty of fluids on a regular basis.
- Avoid all the drugs that can cause acute gouty attack or raise the blood uric acid levels (aspirin is one of them).
If these measures do not prevent further attacks of gout and blood uric acid remains persistently high, then, under careful guidance of the doctor, uric acid lowering drugs can be instituted. These include allopurinol, sulfinpyrazone, and probenecid. It is important to remember that, if given for the first time in a person who has had acute attacks of gouty arthritis in the past; these drugs may precipitate an acute attack of gout. Therefore, it is necessary to take these drugs under the guidance of the doctor who may prescribe some additional drugs to prevent acute attack of gout during the initiation period with these drugs (e.g. colchicines). Therefore, the bottom-line of treatment of gouty arthritis should be to consult a well-trained and experienced rheumatologist and follow the advice given by him/her. The rheumatologist now have several effective drugs to keep uric acid levels below 5 mg/dL to completely prevent any further attacks of gouty arthritis.
What are the dietary and lifestyle advice?
There is clear scientific evidence to implicate imbalanced diet that is low in roughage and fibres and high in refined food items with concentrated high calorie (fatty food, white flour, processed grains, etc. for example - typical Indian Party food) with excess of sugary soft drinks (rich in fructose), sea food and red meat; ingesting beer on a regular basis, eating more than body’s requirement, and not taking large amounts of fruits and salads in daily diet, is the main cause of high blood uric acid.
Of course, genetic (familial) factors, sedentary habits and lack of exercise are the additional factors that cause high blood uric acid.It has also been shown that most of the old beliefs regarding dietary and food restrictions are wrong and must be discarded. Thus in the past, it was believed that vegetables and ‘daals’ that are rich in purines (e.g. asparagus, cauliflower, spinach (palak), beans, peas, mushrooms, tomatoes) could be the cause of high blood uric acid.
However, new research has completely discarded this wrong notion. Now it has been proven that purines from vegetarian diet are NOT harmful in gout and does not cause rise in blood uric acid levels. Therefore, there is no need to avoid ‘daals’, asparagus, cauliflower, spinach (palak), beans, peas, mushrooms, tomatoes any more. Put in simple words, gout and hyperuricaemia are simply problems of over-eating, especially refined food that is grossly short on fruits, salads, and fibre. Excess alcohol (mainly beer), soft sugary drinks high in fructose, sea food, red meat, are especially bad as these food items are known to causes further rise in the levels of blood uric acid. There is now scientific evidence that milk and milk products are good for such patients. But, it must be ensured that cream has been removed so that the caloric value does not increase. Thus, based upon this new knowledge persons with high uric acid or having gouty arthritis are advised a normal, healthy, balanced diet high in fruits, salads and fibres and low on total calories (to keep you within the normal range of body weight / body mass index), completely avoiding the following items: beer, sugary soft drinks high in fructose, red meat, sea food.
The details are as follows:
Diet should be balanced in protein, carbohydrate, fat, vitamins and minerals. It should have adequate calories for maintaining normal weight/body mass index; it should be high in calcium and vitamin D, and high in fibre content (at least 50 gm of both soluble and insoluble type), normal allowance of carbohydrates and proteins, low cholesterol, low salt, with 28% of the total calorie from fats (with the following proportion: monounsaturated [olive oil, ground-nut oil] 10%, polyunsaturated [sunflower, corn, mustard] 10%, saturated [‘ghee’, butter, full-fat milk] 8%); containing at least 5 servings of fresh fruits, green vegetables / salads daily.
A word on so-called ‘Indian Vegetarian Diet’ in the context of high blood uric acid and gout is necessary. Simple balanced Indian vegetarian diet consisting of lots of fruits, green vegetables, including peas and legumes, and rough grains (ordinary daal, rice and whole wheat bread) with milk and milk products, would be ideal for persons with high blood uric acid and gouty arthritis. However, ‘rich Indian vegetarian diet’ that usually consists of ‘parathaas’, ‘poori’, ‘kachoori’, ‘samosaas’, bread made of ‘maidaa’ (refined white flour), deep fried vegetables full of ‘ghee’ and butter, ‘namkeen’ and ‘mithai’, and lots of sugary soft drinks full of fructose – are extremely rich in concentrated calorie and lack roughage and fibre. This kind of diet, although vegetarian, would be extremely harmful for those with hyperuricaemia and gouty arthritis. As most of these persons also have features of metabolic syndrome, such a diet would worsen metabolic syndrome as well causing early-age heart attack and brain stroke.
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