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Immune reconstitution complicated by systemic lupus erythematosus: case report A 38-year-old woman developed immune reconstitution complicated by systemic lupus erythematosus (SLE) following treatment with abacavir, emtricitabine, etravirine, raltegravir, and tenofovir disoproxil fumarate. Her treatment with etanercept additionally contributed to the SLE [dosages, routes, duration of treatments to reaction onsets not stated]. The woman with a history of inflammatory arthritis and HIV amongst other conditions, presented with myalgia, headaches, generalised malaise, neck stiffness, fatigue, and photophobia for 3 weeks. She had been diagnosed with HIV in 2006 and had been receiving treatment from the time. She moved to UK in 2008 and had been immune competent since. Her medications included etanercept, etravirine, raltegravir and emtricitabine. In 2012, autoimmune hepatitis was suspected and her antiretroviral therapy (ART) with tenofovir disoproxil fumarate was stopped. In 2013, abacavir was discontinued because of a suspected hypersensitivity reaction and pyrexia. Upon presentation, she was tachycardic, febrile and showed axillary lymphadenopathy with facial swelling due to parotid enlargement. Her blood work was significant for non-haemolytic anaemia, neutropenia and lymphopaenia. She showed 284 log 2.5 copies of Epstein–Barr virus (EBV) , whereas cytomegalovirus was negative. A lumbar puncture revealed lymphocytic pleocytosis. Her cerebrospinal fluid (CSF) EBV copy number was 1128 log 3.1. Tests for tuberculosis, viral and bacterial PCR, and CSF cytology were all negative. A MRI scan of the brain detected a well-circumscribed hyper-intense lesion not amenable to biopsy in the right cerebellar peduncle. Immunological testing revealed positive antibodies to nucleosomes, anti-histone, ribosomal-P, ribonuclear proteins, dsDNA, SSA and ANA positivity. She was found to be hypocomplementaemic (C3 0.28 and C4 0.03). A urine analysis revealed a protein-to-creatinine ratio greated than 1473 mg/mmoL, with >10g protein/24 hours. Antiphospholipid antibodies were negative. A renal biopsy revealed immune complex deposition consistent with class III lupus nephritis along with mild interstitial fibrosis. An electron microscopy showed effacement of the foot processes. Thus, she was diagnosed with SLE, secondary to immune reconstitution. A CT scan of the abdomen, thorax and pelvis showed enlarged inguinal, axillary, pelvic and mediastinal nodes, small pericardial effusion and a mildly enlarged spleen. Excisional biopsy of two axillary nodes was performed, which revealed necrotising lymphadenitis. The woman was treated with prednisolone. In the subsequent days, her SLE symptoms resolved. She additionally received rituximab infusion on day 3 of treatment, which was repeated on day 15. At 2 month follow-up, a repeat MRI scan revealed a complete resolution of her cerebellar lesion. Her urine protein-to-creatinine ratio was found to be normal consistent with a complete renal response. She was treated with hydroxychloroquine and myco