Antisynthetasis syndrome mimicking rheumatoid arthritis

Introduction: Antisynthetase syndrome (SAS) is an idiopathic inflammatory myopathy (IIM) characterized by the presence of autoantibodies against the tRNA synthetase enzyme, primarily anti-Jo1. It exhibits a wide range of symptoms, varying in severity and extent of involvement, including extramuscular manifestations such as interstitial lung disease (ILD) and arthritis, in addition to Raynaud's phenomenon (RF), “mechanic's hands” and fever. This article proposes to describe a clinical case of rheumatoid arthritis (RA) in a patient with SAS. Rheumatoid arthritis is a symmetric peripheral inflammatory polyarthritis of unknown etiology that leads to joint deformities and destruction. Objective: The SAS can mimic other rheumatological disorders with similar clinical features, and its diagnosis often relies on testing for novel autoantibodies. This article aims to present one of the clinical forms of SAS, elucidating the diagnostic process and discussing differential diagnoses. Methods: Data for this case report were collected from the patient's medical records, test results, and photographic documentation of consultations. Result: The patient, a 59-year-old white female, experienced non-specific and non-limiting arthralgia in the hands and feet starting in August 2022, accompanied by dyspnea during physical exertion. By January 2023, the condition worsened, manifesting pain and swelling in the proximal interphalangeal and metacarpophalangeal joints, inflammatory arthralgia in the elbows, ankles, and midfeet, presenting as additive, bilateral, and symmetrical, with morning stiffness (MS) exceeding one hour and an aggravation of dyspnea even with minimal effort. The patient sought consultation with a rheumatologist, who requested laboratory tests revealing C-reactive protein (CRP) 36 mg/liter and erythrocyte sedimentation rate (ESR) 22 mm/h, but negative Rheumatoid Factor (RF). There was also a slight increase in AST and ALT, but normal blood count and urine 1. Treatment commenced for possible "seronegative" Rheumatoid Arthritis using chloroquine diphosphate, prednisone, and symptomatic relief. Subsequently, a Chest Computed Tomography (CT) was performed, showing findings consistent with Non-Specific Interstitial Pneumopathy (NSIP), and the patient was referred for further evaluation. Additional laboratory tests revealed positive anti-Jo1 antibodies, leading to a diagnosis of incomplete SAS (without myositis). Treatment initiated with pulse therapy of methylprednisolone (1 gram for 3 days), followed by prednisone (0.75mg/kg/day) in a weaning scheme, associated with azathioprine (2 mg/kg/day). Conclusion: This case underscores the importance of considering SAS as a differential diagnosis, even in the absence of the classic triad of arthritis, pneumonitis, and myositis in its initial.