I clearly remember this photo from the medical school lecture on gout. The image a a demon chewing on the toe of the suffering patient was lasting. In my clinic, often times, this picture is unfortunately only too true. Many people come in with this demon chewing away. Often it is not just the one toe, and in some cases, it is lots of joints.
It hurts like the devil, so what causes it? The short answer is urate crystals in excessive amounts (for the long answer look here Ann Intern Med 2005 Oct 4;143(7):499). Urate is common in the body, and as long as there is not too much of it, things go on pretty smoothly. However, when there is too much, then it can start to form crystals and these are very irritating. These crystals tend to form on locations that are a little cooler (such as toes and fingers) and under greater pressure (such as the big toe). An individual may either make to much urate or get rid of it too slowly, either way it leads to excess.
It never happened before, why did it happen now? There are several ‘risk factors‘ associated with the development of gout. Like many other diseases, gout is linked to obesity, weight gain, and over consumption (especially alcohol, sugary soft drinks, seafood, meat) as well as high blood pressure and some of the medications we use to treat high blood pressure (Arch Intern Med 2005 Apr 11;165(7):742 , BMJ 2008 Feb 9;336(7639):309 , N Engl J Med 2004 Mar 11;350(11):1093 and Lancet 2004 Apr 17;363(9417):1277). The blood pressure medications that are the most likely contributors include diuretics (the water pills), beta-blockers (like metoprolol or carvedolol), ACE inhibitors (rampart, lisinopril, fosinopril) and some angiotensin II receptor blockers (except losartan). This is a shame since these are all really good medications for treating high bold pressure, but there it is (BMJ 2012 Jan 12;344:d8190).
Besides hurtin’ is there anything else ‘gout’ can do? By far the most debilitating aspect of gout is the pain. However, when folks with gout are observed over time, it seems to be associated with reduced life expectancy (J Epidemiol 2000 Nov;10(6):403). It is not clear if this is due to the complicating conditions that give rise to increased risks of gout, or gout itself.
Ok, so how do I know if it is gout? Usually, the sudden onset of extreme pain in a single joint without any recent trauma is all the history that is needed to make gout the number one item on your diagnostic list. The pain usually begans and peaks in 24-48 hours and if we don’t do anything else, it will resolve in 3-14 days (Rheumatology (Oxford). 2007 Aug;46(8):1372-4. Cleve Clin J Med. 2008 Jul;75 Suppl 5:S22-5. .and Cleve Clin J Med. 2008 Jul;75 Suppl 5:S5-8.). The pain may be so intense that you cannot tolerate putting anything (even bed linen) on the affect part. It is classically the big toe, but can affect any joint. The gold standard for diagnosis remain examination of some joint fluid under a microscope and finding the little gout crystals (and also rule out infection as the cause). It is also helpful to take a blood sample and see if the urate is elevated.
If it goes on long enough then a build up of urate in the joint may cause it to bulge and potentially leak out (warning images may be a bit graphic fingers with tophi and surgical removal of thophi). As things settle down and we look back on the history, often a precipitating event may be identified (such as new medication, recent infection, change in diet, or such).
So how do we treat it? Treatment falls into two camps, acute and prevention. Treating the acute attack is really important (especially if you are the one with gout), and it consists of reducing the inflammation. So, the steps to reduce inflammation include anti-inflammatory medications such as NSAIDs (like indomethacid) or steroids. The traditional treatment has been colchicine but data indicates that it works slower than NSAIDs (Rheumatology (Oxford) 2007 Aug;46(8):1372). The treatment usual needs to run for about two weeks. The second phase of treatment is prevention. This includes weight loss, improving your diet, and possibly medication to lower the urate levels. All of this should be started about two weeks after the attack has settled down. There is some question as to whether or not the medication really decreases the frequency of the attacks. The medications work by increasing the the amount of urate that is filtered out through the kidney.
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