INTRODUCTION: Pulmonary Sarcoidosis in a Human Immunodeficiency Virus-infected Patient.
CASE PRESENTATION: The patient is a 43-year-old white male smoker with a known diagnosis of Human Immunodeficiency Virus (HIV) and chronic obstructive pulmonary disease who presented with a one-week history of increased cough and worsening pulmonary infiltrates. The patient's cough was productive of yellow phlegm and associated with a right-sided pleuritic chest pain and intermittent use of supplemental oxygen. Fourteen months prior to admission his CD4 count was 17 mm3 and his HIV RNA (viral load) was 530,000 copies/mL. He was initiated on atazanavir, ritonavir, emtricitabine/tenofovir disoproxil fumarate. One month prior to admission he developed a ground glass infiltrate and a nodular infiltrate in the right upper lung. On admission the patient's CD4 count was 270 mm3. Past medical history was otherwise significant for history of transfusion in 1982, community acquired pneumonia 4 months previous, depression, post-traumatic stress disorder, and hypothyroidism. Family history was significant for lung cancer and laryngeal cancer in his parents. Medications also included albuterol/atrovent, beclomethasone, anti-hypertensives, vitamins, actonel, fluoxetine, and levothryroxine. Social history was significant for incarceration, tobacco, marijuana, alcohol, and crack cocaine use. A chest x-ray revealed diffuse interstitial and ground glass infiltrates. Bronchoalveolar lavage was performed. Fungal special and regular smears, acid fast, legionella, and Pneumocystis smears were negative. Pneumocystis and influenza A and B PCR were negative. Serum calcium was slightly elevated and lymphocyte count was reduced. Patient's transbronchial biopsies demonstrated non-caseating granuloma. Patient was diagnosed with HAART-associated sarcoidosis secondary to Immune Reconstitution Inflammatory Syndrome (IRIS) and initiated on prednisone 40 mg by mouth daily. On follow-up one month later patient responded well to treatment with resolution of his dyspnea, lung crackles, and cough.
DISCUSSIONS: IRIS is an inflammatory disorder that occurs upon initiation of HAART in patients with HIV. IRIS has varying characteristics depending on what is triggering the immune response. The criteria for IRIS are not standardized. In our patient, the presence of HIV, a pretreatment CD4 count <100 mm3, a dramatic reduction in the HIV viral load, improvement in the CD4 count, and the absence of infection all support the diagnosis. Timing of IRIS can occur from a few days to years after initiation of HAART. IRIS has been reported in association with infections such as hepatitis B and C, leishmaniasis, Pneumocystis, Mycobacteria, cytomegalovirus, Cryptococcus, JC virus, herpes simplex virus, varicella zoster virus, parvovirus B19. In addition IRIS has been rarely reported with Kaposi's sarcoma, autoimmune thyroiditis and sarcoidosis. IRIS-associated sarcoidosis has been reported to be observed or treated with corticosteroids. Patients have been reported with skin, pulmonary, muscle, renal, eye and lymphadenopathy features. Our patient responded well to corticosteroid therapy.
CONCLUSION: IRIS rarely manifests as IRIS-associated sarcoidosis. We report one such case with lung manifestations that responded to steroid therapy.
DISCLOSURE: Cassie Kennedy, None.