Most patients need medications to treat the inflammation that occurs during an acute attack. These include anti-inflammatories, corticosteroid and colchicine.
There are many anti-inflammatories on the market; some are over the counter (such as Nurofen, Brufen, and Voltaren) and the others require prescription. You must let your doctor know if you are already taking an over the counter formulation, otherwise you might be taking two anti-inflammatories at the same time and end up having nasty complications.
Corticosteroid is a compound that is made from our adrenal glands. We need corticosteroid to survive. When our body goes through stress, such as infection or injury, our adrenal glands pump out a large amount of corticosteroid to increase metabolism and to modulate the inflammatory reaction so that it does not get out of control and result in damage to our body tissue. You can think of it as an anti-inflammatory that works via a different pathway, with a very different side effect profile. Corticosteroid can be given as tablets, or even as an injection into the inflamed joint.
Colchicine is a medication derived from a plant, which is also used to treat an attack of gout. In fact, an acute attack may be aborted with the very early use of this medication. Early clinical studies used high doses to treat an acute attack (two tablets every two hours) but that approach was associated with significant side effect including nausea, vomiting, diarrhea, and in some patients, dehydration and multi-organ failure. Subsequent studies showed that smaller doses are equally effective (two to three tablets a day) and have a much lower chance of adverse events (2). Some formulations of colchicine have confusing names such as Lengout or Colgout, which can be easily confused with Progout, a formulation of allopurinol to lower serum uric acid and is used in a different manner.
All the above medications do not lower the uric acid level in blood. They are used to treat an acute attack of gout. They can also be used during the initiation of uric acid lowering therapy to prevent an acute flare up.
The definitive treatment for gout is to reduce the uric acid level in the blood.
Dietary modification can be extremely helpful. Patients with early disease may avoid lifelong pharmacotherapy if dietary change is implemented in combination with regular exercises to lose weight (3). Those with more established disease may require a lower dose of medication if they change their diet and lose some weight. An experienced dietitian can analyse your food diary and provide you advice with regards to which foods to reduce/avoid as well as providing practical alternatives. In addition, they will help you with a weight loss program, and work with you to optimise your long-term adherence to these lifestyle changes.
In contrast to popular belief, a diet that severely restricts purine intake is not essential. Many people find such a diet unpalatable and of its own is not sufficiently effective enough to lower the uric acid below the target range. Instead, emphasis should be on caloric restriction, an increase intake of the right type of protein, and replacement of refined carbohydrates with complex carbohydrates (4).
The most commonly used medication to lower uric acid is allopurinol (Progout, Zyloprim, Allosig, Allohexal). It drops the blood uric acid level very rapidly and this creates a gradient for the uric acid in our joints to move back into the circulation and thereafter be removed by our kidneys. It is believed that this movement of uric acid can precipitate a flare of gout, which is a phenomenon we commonly see when allopurinol treatment is started without treatment to prevent inflammation from occurring.
It is therefore very important that allopurinol is commenced at a small dose, together with preventative treatment, such as an anti-inflammatory, colchicine, or even a low dose of corticosteroid. This approach aims to prevent a flare up of gout whilst allopurinol is being initiated and then increased to reduce the uric acid level to below a specific target.
The dose of allopurinol is slowly increased every few weeks until the target level of uric acid, being <0.36mmol/L, is achieved. The whole process may take up to many months to complete. The most important thing to remember during this period is not to stop the allopurinol if you develop an acute attack, but to immediately notify your rheumatologist to give you extra treatment to settle the inflammation of the acute attack.
Once the target level is achieved, the preventative medications are then slowly withdrawn. Most patients require lifelong allopurinol treatment.
One size does not fit all. Clinical studies have shown that a significant number of patients do not achieve adequate control with the ‘standard dose’ of allopurinol, considered to be 300mg a day. If your uric acid level is persistently elevated despite taking the allopurinol, you should see your rheumatologist, who will supervise further escalation of the allopurinol dose or otherwise add another tablet to lower the uric acid
Lastly, we must not forget that gout is part of a ‘metabolic syndrome’. Hyperuricaemia is an independent risk factor for cardiovascular events such as stroke or heart attack. Your rheumatologist will work with your general practitioner to address the other medical problems that associate with this syndrome, such as hypercholesterolaemia (high cholesterol), diabetes and hypertension (high blood pressure).
- Dual Energy CT in gout: a prospective validation study. Choi et al. Ann Rheum Dis 2012 Sep;71(9):1466-71
- High versus low dosing of oral colchicine for early acute gout flare: Twenty four hour outcome of the first multicenter, randomized, double-blind, placebo controlled, parallel group, dose comparison colchicine study. Terkeltaub et al Arthritis Rheum 2010;62(4): 1060
- Obesity, weight change, hypertension, diuretic use and risk fo gout in men: the health professionals follow-up study. Choi et al. Arch Intern Med. 2005; 165 (7); 742
- Beneficial effect of weight loss associated with moderate calorie / carbohydrate restriction, and increased proportional intake of protein and unstaturated fat on serum urate and lipoprotein levels in gout: a pilot study. Dessein et al. Ann Rheum Dis. 2000; 59(7): 539