Dr Andrew Jordan seeks to demystify for GPs how a rheumatologist thinks and approaches common rheumatic presentations
My aim is to present a common case and work through the reasoning and thought process of how I diagnose and manage a rheumatological presentation. The approach is practical and based upon experience and evidence, where it exists. I hope you will find it useful in your daily practice.
A 53-year-old male presents with recurrent episodes of swelling to both feet, ankles and knees. Each episode is sudden onset and very painful to the point of not being able to mobilise or go to work for a few days. There are about four attacks per year with the interval period being relatively pain free. Only one area is usually affected at a time. There does not appear to be a trigger for the attacks. The episodes appear to be more severe and debilitating. He is centrally obese. At the time of consultation the joints examine normally but there are firm lumps on the olecranon bursa.
The main parts that stand out in the history is that the attacks are sudden onset and involve the lower limbs. This is typical of a crystal arthritis, with gout being the most likely. Calcium pyrophosphate disease (pseudogout) is the other common crystal arthritis, however this usually presents as isolated attacks in an elderly person, commonly involving the knee or wrist. In fact, calcium pyrophosphate disease is the most common cause of a swollen wrist (acute monoarthritis) in an elderly person.
My other main differential would include palindromic rheumatism, which is a condition where one joint becomes suddenly painful and swollen but spontaneously resolves in two to five days. This has a relatively high rate of progression to rheumatoid arthritis.
On further questioning, the patient has a history of gout with the first attack occurring at age 28 years old. He has taken allopurinol 300mg daily for over 10 years. He takes the allopurinol five out of seven days (on average) per week. To treat an attack, he will take colchicine, two tablets initially and then one tablet every two hours until diarrhoea (NB: Taking colchicine this way is not recommended).
If he is taking allopurinol, why is he still getting attacks?
Firstly, I consider if the diagnosis of gout is correct. The history sounds typical and the lumps on the olecranon are typical sites of tophi. To prove the diagnosis, a joint aspirate of an affected joint could be performed to look for urate crystals. Alternatively, a dual energy CT scan (of previously affected areas, or of the tophi) can show the presence of urate crystals or para-articular erosions.
Secondly, I find out what his uric acid level on treatment is. Urate crystals cannot form if the uric acid level is below 0.40mmol/L. This is why rheumatologists talk about “treating to target”. The target uric acid level for all patients is below 0.36mmol/L and below 0.30mmol/L for those with tophi or severe gout.
Large cohorts of patients treated for gout in Australia show that more than 50% of patients treated with allopurinol do not achieve this target and this is the most common reason for recurrent attacks. There are two main reasons for not achieving the target: inadequate dosing and poor adherence to therapy.
Around half of patients on allopurinol will need more than the “standard” 300mg dose.
A review of uric acid levels over the past 18 months show the readings are 0.56, 0.44 and 0.71mmol/L.
The first step is education. I explain that if the uric acid is reduced to target levels, gout will rarely be an issue. It is one of the few inflammatory arthritides where it is possible to “cure”, albeit requiring maintenance medication. The maximum dose of allopurinol is 900mg daily.
The key to treating gout is to slowly increase the allopurinol dose and covering the dose escalation period with prophylaxis, as gout can flare during this period. Allopurinol is generally very well tolerated, however, be on the lookout for a hypersensitivity reaction, which usually involves a rash or fevers in the first two months of treatment.
Allopurinol can be used at all levels of renal function, but the general rule is to start low and increase slowly, especially if there is renal impairment.
I increase allopurinol to 450mg daily for two weeks and then to 600mg daily ongoing. Colchicine is taken as 0.5mg twice a day for prophylaxis. Repeat uric acid level is 0.28mmol/L, indicating that allopurinol 600mg daily is the correct dose. The lumps on the olecranon region are tophi. With adequate persistent reduction of the uric acid level, it is likely the tophi will reduce in size over months to years. There were no further attacks of gout. It is vital at this point to emphasise that allopurinol should be taken indefinitely.
If uric acid is not decreasing despite the patient taking allopurinol, adherence can be monitored by checking oxypurinol (a metabolite of allopurinol). If the patient is adherent to allopurinol and uric acid levels are not decreasing, I would consider the use of febuxostat.
How do I use colchicine to treat gout?
Studies have shown that colchicine is equally effective if taken 0.5mg twice a day as opposed to the old advice of taking a tablet every two hours until diarrhoea.
To treat an acute attack it should be taken very early during an attack before there is significant inflammation.
If using low-dose colchicine for prophylaxis, the first sign of toxicity from colchicine is diarrhoea, so the regular dose of colchicine should be reduced if diarrhoea occurs. I find colchicine most effective if used as prophylaxis while slowly increasing the dose of allopurinol.
If renal function is normal, then 0.5mg twice a day is my usual dose.
If the patient is elderly or has mild renal impairment, reduce the dose to 0.5mg daily and in moderate or advanced kidney disease, colchicine should be used with caution and probably only with specialist advice.
I continue colchicine prophylaxis for three months after the uric acid level has reached target and after there has been no gout attacks for three months.
Dr Andrew Jordan is a Rheumatologist and General Physician based in Paramatta, Sydney. with a special interest in inflammatory arthritis, gout and osteoporosis
