Eosinophilic arthritis

Abstract

Objective. To report the clinical picture, laboratory findings and management of 10 patients presenting with acute polyarthritis and hypereosinophilia of unknown causation. Methods. Patients presenting with acute arthritis and elevated eosinophil counts (> 0.7 x 109 cells/l) or percentage (> 11%) were studied during the period 1990-1997. Exhaustive investigations were carried out to exclude allergy, parasitic and infectious diseases, autoimmune disorders and malignancy. They were managed by standard treatment with oral non-steroidal anti-inflammatory drugs (NSAIDs), failing which, some were given oral corticosteroids. Those resistant to corticosteroids were treated empirically with diethylcarbamazine citrate or levamisole. All were closely monitored. Results. Nine females and one male were found to have acute polyarthritis of 1-6 weeks duration. Most affected were the large joints: knees, ankles, elbows and shoulders. Except for localized urticarial rash, none had constitutional symptoms or extra-articular manifestations. Mild to moderate eosinophilia (absolute count 0.7-7.08 x 109 cells or 11-63%) was detected at the disease onset, but other laboratory findings were generally non-contributory. Treatment with oral NSAIDs did not relieve the joint symptoms nor reduce the hypereosinophilia, but oral prednisolone brought rapid recovery to five out of eight patients. Three of the corticosteroid-resistant patients were treated with an oral diethylcarbamazine, an anti-filarial drug. Complete resolution of arthritis and normalization of eosinophil count were observed after 2-3 weeks. Similar success was obtained in one patient after a single dose of levamisole. No side-effects or relapse were encountered. It was also observed that there was a good correlation between joint activity and the eosinophilic count, indicating the joint as the possible target end organ of these cells. Conclusion. Ten patients were found to have an acute polyarthritis without systemic involvement, but with marked hypereosinophilia of unknown aetiology. They had clinical and laboratory findings which differed from other diseases with eosinophilia, especially the idiopathic hypereosinophilic syndrome (HES) and parasitic or infectious conditions. The response to NSAIDs, corticosteroids and, most interestingly, to anthelmintic drugs, like diethylcarbamazine citrate and levamisole, was noteworthy, although the basic mechanism remains unknown. The term eosinophilic arthritis (EA) is used here to describe this group of arthritides which has a benign course and is most likely a reaction to some occult allergen or agent.