Age: 46.0
Sex: F
Vaccine: FLUX
Symptoms: Alanine aminotransferase increased, Aldolase abnormal, Antinuclear antibody negative, Antinuclear antibody positive, Antisynthetase syndrome
Clinical narrative: Antisynthetase syndrome; This literature case was received on 07-Feb-2022 and concerned a 46-year-old, female patient.   The patient had no significant relevant medical history. She was healthy and had no any risk factors or family predisposition to autoimmune diseases. The patient's concomitant medications were not reported.  On an unspecified day in Nov-2017, the patient was vaccinated with influenza virus vaccine polyvalent (brand not specified; dose, route of administration and anatomical location: not reported) as routine influenza vaccine. The batch number was not reported.   On an unspecified day in 2017, within the next two days after receiving influenza virus vaccine polyvalent, the patient started to experience facial and periorbital swelling, which was associated with mild shortness of breath and bilateral hip pain. The patient was prescribed naproxen and had a mild improvement in hip pain.  In the following three weeks, the patient's symptoms progressed with worsening facial swelling and severe dyspnoea both on exertion and at rest. She also reported bilateral edema of the hands and diffuse hyperpigmentation. In addition, she complained of severe muscle weakness with inability to lift hip and shoulder musculature progressing to difficulty using the gas pedal when driving.  On an unspecified date, the patient visited the emergency department. On initial triage, the patient was noted to be normotensive, afebrile and saturating well on room air. A physical examination revealed periorbital swelling and edema of her face and musculoskeletal and integumentary examination revealed hyperpigmentation of her hands with mild synovitis of the metacarpal phalangeal joints bilaterally. Also, she was noted to have significant tenderness to palpation over the thighs bilaterally with associated weakness primarily in proximal musculature. Respiratory examination was notable for bilateral crackles on auscultation. Laboratory values revealed as total creatine kinase level of 24.285 U/L with aspartate aminotransferase of 719 U/L and alanine aminotransferase of 537 U/L (reference ranges not provided). Chest x-ray revealed an interstitial disease pattern. At this time, the patient was treated with prednisone at a dose of 60 mg, daily, orally and with an unspecified aggressive intravenous hydration. A myositis panel revealed a positive result for anti-Jo-1, determined by line blot testing with a reference value of positive >1, with a titer of >8.0 and a negative antinuclear antibody result as detected by indirect immunofluorescence test on HEp-2 cells.  On an unspecified date, the patient was admitted to the hospital. During her hospital stay, the patient's respiratory symptoms markedly improved. However, the weakness and pain of her thighs persisted. A magnetic resonance imaging scan of the thighs revealed symmetric muscle inflammation. At this point, an anterior thigh biopsy was performed. The thigh tissue was remarkable for extensive myofiber necrosis and regeneration. The pathology appeared to be primarily necrotizing myopathy with limited inflammation. This prompted human leukocyte antigen class I immunohistochemistry staining, which was positive and consistent with an immune-mediated myopathic disorder.  On an unspecified date, the patient's symptoms improved, and she was discharged from hospital on prednisone at a dose of 60 mg, daily with the plan to follow up in the outpatient rheumatology office. She was referred for pulmonary function testing, which was normal.  On an unspecified date, within four weeks, the patient's muscle pain and weakness slowly improved and within eight weeks, her inflammatory markers, including creatinine kinase and aldolase, normalized.   Over the course of the next six months, the patient was prescribed an unspecified slow steroid taper at a dose of 60 mg and her symptoms did not recur. As reported, she did not require any additional immunosuppressive agents.   On an unspecified date, the patient recovered from the event of antisynthetase syndrome as her symptoms eventually resolved.  The authors assessed the event as related to influenza virus vaccine polyvalent. After extensive investigation, the only inciting factor that could explain her symptoms was the administration of the influenza vaccination less than one week prior to her onset of symptoms. The patient was advised to avoid the influenza vaccination in the future.  The event was assessed as serious due to hospitalization.  In conclusion, acuity from the administration of the vaccine, clinical picture of myositis, and positive biopsy findings with appearance of autoantibodies fulfilled both major and minor criteria in the diagnosis of ASIA syndrome. The interstitial pattern on chest x-ray, clinical picture of myositis with hyperpigmentation, myofiber necrosis on biopsy, and the high-titer anti-Jo-1 antibodies suggested antisynthetase syndrome, which had not been implicated in ASIA prior.    Company comment: A 46-year-old patient experienced antisynthetase syndrome within two days after receiving the suspect product influenza virus vaccine polyvalent. Based on plausible temporal relationship, causality is assessed as possibly related.; Reporter's Comments: After extensive investigation, the only inciting factor that could explain her symptoms was the administration of the influenza vaccination less than one week prior to her onset of symptoms. The patient was advised to avoid the influenza vaccination in the future.; Sender's Comments: A 46-year-old patient experienced antisynthetase syndrome within two days after receiving the suspect product influenza virus vaccine polyvalent. Based on plausible temporal relationship, causality is assessed as possibly related.