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We read with great interest the article by Feletar et al.1 We were surprised by their findings of only a modest response to infliximab treatment in patients with treatment refractory psoriatic arthritis (PsA), as this seems to be in contrast with our observations.
Since 2001 nine patients with refractory PsA according to American College of Rheumatology criteria have been treated with infliximab at our division. All patients had active joint disease with a tender joint count (TJC) and a swollen joint count (SJC) of at least 6, with the exception of one patient (patient 3), whose cervical spine was affected. Quantitative assessment of skin involvement was not available. Table 1 shows further demographic data.
Seven patients received infliximab for more than 52 weeks, and five of those for more than 78 weeks. Clinical assessment, including TJC and SJC, performed by experienced rheumatologists, and laboratory tests (haematology, biochemistry, antinuclear antibodies (ANA), including subsets) was made routinely at each visit (fig 1). During the treatment period toxicity occurred on three occasions, including one labial herpes infection (patient 4), one leucopenia of 2.6×109/l (patient 3), which led to the discontinuation of methotrexate, and one allergic reaction (patient 9). Patient 9 had to stop infliximab treatment permanently despite an excellent clinical response, whereas the other two patients received infliximab again after the adverse events resolved. Six of the nine patients became positive for ANA—titre >1/80 on at least two successive visits. No serum conversion of ANA subsets occurred and no lupus-like symptoms were seen.
Eight of the nine patients showed rapid improvement and a clinical response. Only 1 patient (patient 8) was unresponsive to the treatment regimen, which was stopped. At 52 weeks five patients met the PsA response criteria,2 four patients were in complete remission (patients 1, 3, 5, 6) of joint tenderness and swelling, one patient (patient 2) had an incomplete response. Patient 4 stopped infliximab treatment in week 49 for 10 weeks because of a labial herpes infection that was treated with acyclovir. Thereafter tumour necrosis factor blocking therapy was successfully restarted.
At 78 weeks 4/5 patients (patients 1, 3, 4, 5) were in complete remission. One patient (patient 2) who had an incomplete response with a 6 weeks’ treatment interval showed complete remission after the interval was shortened to 4 weeks. Patient 1 who received his first infliximab dose at our division 160 weeks ago had been responding so well to the treatment that we stopped giving infliximab after his 16th infusion at the end of week 120. Because of disease exacerbation, treatment had to be restarted 26 weeks later and within a few days (data not shown) the patient regained complete remission.
These data, although only retrospectively obtained, suggest that infliximab is a valuable therapeutic tool for treating refractory PsA. So far, permanent discontinuation of treatment owing to toxicity or inefficiency has only been necessary for one of the nine patients.
One possible reason for the different outcome in the effect of infliximab on PsA in our patients and those of Feletar et al might be the severity of the joint disease in Feletar’s patients. Fifteen out of 16 of their patients had mutilating arthritis, whereas this form of joint destruction was not present in our group. To clarify this possibility, further studies with larger groups and well defined joint disease are necessary.
Yazdani-Biuki et al were surprised that our data on 16 patients with arthritis treated with infliximab demonstrated only a modest response.1 They contrast our data with data from nine patients with psoriatic arthritis (PsA) treated with infliximab in their centre. Although they mention nine patients, only seven were treated for more than 52 weeks. They claim that eight of the nine patients demonstrated rapid clinical response, but provide information on only five patients who demonstrated a PsA American College of Rheumatology response, four of whom are said to be in complete remission. It is not clear whether the other patients discontinued the drug, in which case their withdrawal rate would be 22%.
This is in contrast with the results of our study, which demonstrated a high toxicity rate, and high level of discontinuation (6/16 or 38%). We had previously suggested that the difference between our study and others might reflect the severity of our patient group. The group treated by Yazdani-Biuki et al was demographically somewhat different from our group. There were more men in our study (12/16 v 4/5), they were older (48 v 41), and had longer disease duration (14 v 10.5). However, the same average number of disease modifying antirheumatic drugs had been used in the two groups. Yazdani-Biuki et al did not provide information on damage in their patients. Our group included five patients with arthritis mutilans; however, all these patients had evidence of inflammatory arthritis. The other five patients may have had evidence of damage but did not demonstrate arthritis mutilans. Because we have previously shown that the presence of damage predisposes not only to progression of damage but also to early mortality in this patient group, we felt it was important to give these patients the best available treatment.2,3
We agree with Yazdani-Biuki et al that the difference between the results of our two studies may be related to the difference in disease severity between the two groups. However, the number of patients is too small to draw valid conclusions. It is important to gain more experience with anti-tumour necrosis factor agents both in randomised clinical trials and clinical observational studies, including a wide range of patients with PsA, so that the true level of response and toxicity can be identified.