It’s important to avoid tunnel vision and consider alternatives when faced with suboptimal treatment responses to psoriasis and joint pain.
Welcome to the latest edition of Rheumatology Reasoning, where we explore a common case, the thought process behind each test, key diagnostic questions, and an effective management approach. This practical approach is based on experience and evidence, aiming to be useful in your day-to-day practice.
I received a referral for a 39-year-old male with psoriasis who reported increasing joint pain.
He has struggled with psoriasis for 20 years, and previous treatments include methotrexate, cyclosporine, neotigasone, light therapy and a decade of biologic use. Among the biologics tried, adalimumab, etanercept and ustekinumab had suboptimal response, but secukinumab finally yielded positive results. The Psoriasis Area Severity Index (PASI) reduced from 30 (very severe disease) to 8 (moderately well-controlled) with secukinumab. Methotrexate 10mg weekly further reduced the PASI to 5, although nausea and fatigue from oral methotrexate limited the dose.
The patient’s rheumatological presentation involved grumbling ankle, midfoot and knee pain, hindering daily activity and exercise. He experienced intermittent flares lasting 4 to 5 days, which he managed with NSAIDs. During these episodes, he reported low-grade joint swelling and morning stiffness, and his C-reactive protein (CRP) levels were marginally raised at around 10-20mg/L, but normal at other times.
I suspected active psoriatic arthritis and decided to increase the methotrexate dose by switching to subcutaneous injections for improved tolerability. Subcutaneous methotrexate has shown greater efficacy and better tolerability compared to the equivalent oral dose, and has been easier to use in recent years due to the availability pre-filled syringes on the PBS. This switch proved successful, as he tolerated 20mg SCI weekly without adverse effects, enabling better exercise and less pain.
After a year of treatment with higher-dose methotrexate, the patient’s lower limb symptoms worsened, and flares became more frequent. I considered switching biologics, but due to his history of PBS-recorded biologic fails and the positive response to secukinumab and SCI methotrexate (reducing PASI to 2), I opted to add a small dose of leflunomide 10mg daily to treat the inflammatory arthritis component. Monitoring for potential transaminase increases (>20% of patients) is crucial with this combination.
Despite the added treatment, the patient continued to have painful flares, hindering his efforts to improve his fitness. However, during one of his flares, a white chalky deposit was noticed on his left pinna, suggesting a tophus, a tell-tale sign of gout. Further examination revealed thickening of both olecranon bursae. The revelation struck me – I had been treating psoriatic arthritis when gout was the likely cause of his flares.
Ideally, gout diagnosis is confirmed by visualising urate crystals under birefringent microscopy or with a dual energy CT scan of an affected area. Although high serum uric acid in a blood test may indicate gout, it is not definitive. Considering the recurrent episodes of foot pain but current absence of joint swelling to obtain an aspirate, I chose a dual energy CT scan of both feet, which confirmed multiple uric acid deposits throughout the ankle, midfoot and MTP joints. An alternative diagnostic option would be to lance the small chalky deposit on the ear and send the material for microscopy to confirm urate crystals. Interestingly, he had never had a blood test for uric acid. His gout attacks were atypical, more indolent, and he treated them early with NSAIDs, likely dampening the maximal pain and swelling. His serum uric acid level was 0.55mmol/L, above the threshold of 0.40mmol/L where gout is possible.
Considering the recurrent attacks over the last 18 months, chronic low-grade gout attacks seemed more likely than psoriatic arthritis. Therefore, urate-lowering therapy was warranted, targeting a serum uric acid below 0.30mmol/L. I typically initiate allopurinol 100mg daily and titrate it up by 100mg every two weeks until reaching the target serum uric acid level. He required 400mg daily to achieve this, and I prescribed colchicine 0.5mg BD for prophylaxis against recurrent gout flares whilst titrating the dose.
The patient responded well to this treatment. The tophi diminished rapidly, flares ceased, and he resumed regular exercise. We discontinued leflunomide and the methotrexate dose was slightly lowered to 15mg weekly, without any worsening of his joint pain.
This case highlights the importance of avoiding tunnel vision and considering alternatives when faced with suboptimal treatment responses. Reassessing patients who respond poorly to treatment is essential. Psoriasis and psoriatic arthritis are associated with a range of comorbidities, such as gout, metabolic syndrome, obesity and depression. It is important to consider these comorbidities in managing anyone with psoriasis or psoriatic arthritis. Gout can manifest in various ways, including an indolent form, and may not always present with the classic acute onset lower limb monoarthritis, especially when patients self-treat with medication that alter the clinical course.
Dr Andrew Jordan is a rheumatologist based in Parramatta, Sydney, with a special interest in inflammatory arthritis, gout and PRP injections.