¹Ghadeer Alabbadi, ¹Mousa Alabbas, ¹Khalid Aldraan, ²Zakia Almudhry

¹King Fahad Specialist Hospital, ²Dammam Medical complex

Background(s):
Mild and transient eosinophilia can be seen occasionally in patients with early rheumatoid arthritis. And it may be associated with greater disease activity. But still, the most common etiology behind this includes allergy, helminth infection, drug side effects, and hematological-malignancy.

Method(s): We reported a case of a 19-year-old female who was referred to our hospital for evaluation of symmetrical inflammatory polyarthritis, which lasted for a few months. The diagnosis of rheumatoid arthritis was made on the basis of the typical clinical picture associated with positive rheumatoid factor, anti-cylic citrullinated peptide antibodies (anti-CCP antibodies), and elevated CRP. The laboratory findings at the initial visit showed significant hyper-eosinophilia with an absolute count of 13000/mm3.

After extensive unremarkable workup regarding the cause of  hyper-eosinophilia, we concluded with our impression of new-onset rheumatoid arthritis and associated hyper-eosinophilic syndrome.

The patient was started on high-dose Prednisolone 60 mg orally once daily with tapering to manage the hyper-eosinophilia. Methotrexate (15 mg orally once a week) was initiated as a treatment for newly diagnosed rheumatoid arthritis. The patient had complete clinical remission of rheumatoid arthritis along with normalization of eosinophilic count, even after complete tapering down of prednisolone.

However, because of significant hair loss and gastrointestinal upset, the patient was started on anti-TNF, which worsened her hyper-eosinophilia. After trying multiple lines of therapy, including Abatacept and JAK-inhibitors, which failed to control both conditions at the same time.

Result(s): Given the severity of hyper-eosinophilia (51000/mm3) and high risk for end organ damage along with the major concern of steroid side effects, the patient was started on mepolizumab. She was successfully well managed by combination of mepolizumab and leflunamide at the end.

This case highlights the rare adverse events of drug-associated hyper-eosinophilia that get exacerbated in our case by the new initiation of anti-TNF therapy. The role of JAK inhibitors in controlling eosinophilia was mentioned in the literature. The underlaying proposed mechanism was eosinophil apoptosis inhibition by GM-CSF and activated JAK2. And it did work in our patient for the hyper-eosinophilia but not for rheumatoid arthritis.

Conclusion(s): This case report could have important implications for managing patients with similar associated clinical conditions as rheumatoid arthritis and hyper-eosinophilic conditions, which may challenge the plan of treatment for both.