Hindawi Publishing Corporation Case Reports in Medicine Volume 2010, Article ID 394546, 3 pages doi:10.1155/2010/394546 Case Report Pulmonary Embolism Mimicking Pneumonia in a HIV Patient Vivek Nagaraja,1 Joel A. Terriquez,1 Hemanth Gavini,1 Lokesh Jha,1 and Stephen A. Klotz2 1 Department of Internal Medicine, University Physicians Healthcare, Tucson, AZ, USA 2 Section of Infectious Diseases, Department of Medicine, University of Arizona, Tucson, AZ, USA Correspondence should be addressed to Stephen A. Klotz, sklotz@u.arizona.edu Received 11 February 2010; Accepted 6 May 2010 Academic Editor: Charlie Strange Copyright © 2010 Vivek Nagaraja et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Recent studies have shown an increased risk of arterial and venous vascular diseases in HIV patients, pulmonary thromboembolism being one of them. HIV-infected individuals may have procoagulants predisposing them to thromboembolism. Patients with thromboembolism may have a clinical presentation mimicking common opportunistic infections. It is important to consider pulmonary embolism in the diﬀerential of HIV patients with fever, cough, and dyspnea, particularly in those with well-controlled HIV infection. 1. Introduction Infection with the human immunodeﬁciency virus (HIV) is now a chronic disease in the developed world. HIV- infected patients have a better life expectancy with the advent of highly potent antiretroviral therapy (ARV) than in the past. However, chronic HIV infection and ARVs are now associated with long-term complications [1]. In recent literature, the relationship between HIV infection and cardiovascular disease has been addressed. Studies have shown an increased risk of arterial and venous vascular diseases in HIV patients. For example, a cohort study comparing 4993 HIV patients revealed an incidence of myocardial infarction of 0.59 to 3.41/1000 patient-years [2], another with 23,468 HIV-positive patients found an incidence of myocardial infarction of 3.5/1000 patient-years [3]. In a systematic review of literature from 1986 to 2004, Klein et al. reported that the incidence of venous thrombotic events in HIV-infected patients was increased two to ten-fold in comparison with healthy individuals of similar age [1]. In a series of HIV-positive patients with venous or arterial thrombosis, pulmonary emboli accounted for 66% of all thrombotic events [4]. 2. Case Presentation A 41-year-old man with a history of HIV (diagnosed in 1988) on ARVs presented with three days of non- productive cough, intermittent fever, chills, dyspnea on exertion, and generalized fatigue. His past medical history included Cytomegalovirus retinitis with bilateral blindness, Kaposi’s sarcoma, lipodystrophy and lipoatrophy, hypothy- roidism, and hypertension. His medications included aba- cavir/lamivudine, ritonavir, atazanavir, pravastatin, met- formin, levothyroxine, and valsartan. The patient’s last CD4 cell count was 800 cells/mm3, and the viral load was undetectable ﬁve months previously while on his current antiretroviral regimen. The patient was febrile at 100.8◦F, pulse of 118/min, blood pressure 93/65 mm of Hg, respiratory rate 18/min, and oxygen saturation of 93% on room air. The chest was clear with normal heart sounds on auscultation. He was treated with intravenous ceftriaxone and trimetho- prim/sulfamethoxazole for presumed community-acquired pneumonia and possible PCP. The complete blood count and comprehensive metabolic panel were unremarkable. The chest radiograph revealed normal lung ﬁelds. Blood cultures were negative. A high resolution CT scan of the chest was performed and was normal. The patient reported subjective clinical improvement after 48 hours of hospitalization. He was discharged with a diagnosis of a probable viral upper respiratory tract infection. One week later the patient returned to the emergency department with three days of intermittent fever, cough, and dyspnea. The CD4 cell count obtained during the previous