2 Figure 1 admission returned at 169 cells/mm3, with a nondetectable viral load. His blood pressure was 97/62 mm of Hg, temper- ature 99.9◦F, heart rate 131 beats/minute and respiratory rate of 20 breaths/minute, with an oxygen saturation of 96% on room air and 95% after walking. On physical examination the patient was dehydrated. The rest of the examination was unremarkable. The complete blood count, comprehensive metabolic proﬁle, and the chest radiograph were normal. A repeat CT scan of the chest without contrast revealed a peripherally located patchy airspace opaciﬁcation on the right side. Blood cultures showed no growth. Bronchoalveolar lavage was performed and cultures were negative for bacterial, viral, mycobacterial, or fungal growth. A Doppler ultrasound of both lower extremities did not show evidence of DVT. A CT scan of the chest with contrast (Figure 1) was performed to evaluate for pulmonary embolism due to the persistent cough. It revealed ﬁlling defects consistent with pulmonary embolism in the right main pulmonary artery [red arrow] and large arterial branches to the right upper, middle, and lower lobes and smaller emboli in the distal branches of the left lower lobe as well. The peripheral opacity in the right lung ﬁeld was a wedge infarct [blue arrow]. Antibiotics were discontinued and the patient was started on intravenous heparin and coumadin. The patient is doing well 6 months after hospitalization. 3. Discussion The synergistic interplay of multiple risk factors may con- tribute to the increased risk of developing a thrombo- embolic phenomenon in patients with chronic HIV infec- tion. These include coagulation abnormalities, presence of opportunistic infections, malignancies [5], and severity of HIV infection. A number of abnormalities of coagulation have been described in patients with HIV infection. The most com- Case Reports in Medicine mon is the lupus anticoagulant found in up to 60% of the patients and may be associated with major thrombo- embolic phenomena [6]. The increase in procoagulant factors like tissue factor and elevated concentrations of microparticles are important contributing factors. Micropar- ticles are relatively small cellular remnants circulating in plasma originating from platelets and endothelial cells. In HIV patients, microparticles also originate from CD4+ lymphocytes, as a direct consequence of HIV infec- tion and possibly as a reﬂection of CD4+ lymphocyte apoptosis [1]. Other coagulation abnormalities include reduced levels of antithrombin III, activated protein S [1, 7], and activated protein C [8], acquired heparin cofactor II deﬁciency [9] and increased levels of ﬁbrino- gen, d-dimer, Von-Willibrand factor, plasminogen activator inhibitor-1, and tissue-type plasminogen activator antigen [10]. Two epidemiological studies showed higher risk of venous thromboembolism in patients with CD4 cell count less than 200 cells/mm3. This level of CD4 count predisposes to many opportunistic infections further contributing to a procoagulant state through enhancing the active ongoing immune response. Several opportunistic infections, partic- ularly Cytomegalovirus and Herpes simplex virus types 1 and 2, may contribute to the prothrombotic state by converting vascular endothelial cells from a noncoagulative to a proco- agulative phenotype, leading to expression of procoagulant phospholipids [8]. An association between cigarette smoking and spontaneous thrombosis in HIV patients has been men- tioned [11] and was reported to aﬀect 77% of the patients [12]. Pulmonary embolism can masquerade pneumonia. In patients with a new diagnosis of pulmonary embolism but with no previous history of thromboembolic or cardiopul- monary disorders, cough (28%), pleuritic pain (57%), fever (3%), and abnormal lung examination (26%) [13] may be present at initial presentation mimicking a pneumonia or opportunistic pulmonary infection. The use of protease inhibitors has also been implicated in hypercoaguability [1, 8, 14]. Majluf-Cruz et al. [8] found that the incidence of venous thrombotic events increased dramatically from 0.19% before the introduction of protease inhibitors to 1.07% afterwards. An interesting suggestion by Saif et al. [15] was that because aspartyl proteases such as renin, endothelin, and cathepsin D are involved in the regulation of coagulation, and because the HIV protease is an aspartyl protease, inhibition of these native proteases by HIV-protease inhibitors may lead to a prothrombotic state. The relationship between HIV infection and the devel- opment of thrombotic events, either arterial or venous, is dependent on the interplay amongst multiple fac- tors, which include coagulation abnormalities, status of immunity, and ARVs. Because, available evidence support- ing the above relationship is limited, more research is required in this area. Physicians need to be aware of the increased risk of thrombo-embolic disorders in HIV-infected patients so that they can be appropriately recognized and treated.