Newly Diagnosed Hiv? A Case of Severe Lupus in Disguise

Abstract

INTRODUCTION: Systemic lupus erythematosus (SLE) and human immunodeficiency virus (HIV) infection are both systemic disorders presenting with nonspecific constitutional symptoms including fever, fatigue, weight loss, myalgia and arthralgias. Patients with SLE and HIV infection may both develop severe multiorgan dysfunction requiring intensive care unit (ICU) admission. We report a case of misdiagnosed HIV infection in a new-onset SLE patient due to falsely positive HIV antigen/ antibody (Ag/Ab) test resulting in ICU admission.CASE PRESENTATION: A 37-year-old female presented for fatigue, diffuse muscle aches, joint swelling, and oral thrush with dysphagia. She was found to be leukopenic and lymphopenic, with a positive preliminary HIV Ag/Ab Combo test, and absolute CD4 count of 247 cells/mcl. Additional findings included positive cytomegalovirus IgM and nephrotic-range proteinuria. Chest imaging revealed bilateral pleural effusions. She was started on fluconazole for the oral thrush and highly active antiretroviral therapy (HAART) for HIV. However, she further deteriorated clinically with recurrent fevers, declining mental status requiring intubation and ICU admission. The lack of response to therapy prompted alternative diagnosis. Surprisingly, her HIV confirmatory tests was negative, but rheumatologic serology was positive, including high ANA 1:1280 speckled, low complements C3 and C4, positive for anti-Smith antibodies, ds-DNA antibodies, RNP, SSA and SSB, RF, direct coombs, and anticardiolipin antibodies. HAART was discontinued and pulse intravenous (IV) steroid therapy was initiated, which resulted in marked improvement; she was subsequently extubated. Renal biopsy confirmed the diagnosis of lupus nephritis. HIV viral load real-time PCR and genotype analysis were both negative, confirming the false-positive initial test. The patient was optimized and discharged with outpatient follow-up.DISCUSSION: SLE and HIV infection have significant overlapping clinical features. Initial screening HIV tests may be falsely positive due to SLE and antiphospholipid autoantibodies, making it difficult to differentiate the two diseases. A lack of response to initial treatment in our patient prompted the consideration of an alternative diagnosis. Acutely critically-ill SLE patients with major organ involvement are treated with high dose IV methylprednisolone to decrease systemic inflammation. Other immunosuppressive agents such as cyclophosphamide and mycophenolate may also be used. In cases of severe antiphospholipid syndrome with systemic thrombosis and end-organ damage, plasma exchange and IVIG are indicated. CONCLUSIONS:Rarely patients with SLE may present with false-positive HIV screening test, and thus masking and delaying treatment for critical systemic SLE. Clinicians should understand the limitations of initial screening tests and have high suspicion and consideration of diagnoses of both diseases.