br Discussion Cytomegalovirus CMV is a
Discussion Cytomegalovirus (CMV) is a herpes virus that causes primary infection in normal hosts and re-activation infection in compromised hosts with impaired CMI, e.g., organ transplants. Following primary infection, which may be severe, CMV becomes latent in lymphocytes. Reactivation may occur with added or subsequent immunosuppression due to diseases, e.g., HIV or medications, e.g., steroids.5, 6, 7 CMV is an immunosuppressive virus, i.e., CMV infection itself further impairs CMI. The clinical manifestations of acute CMV infection includes encephalitis, retinitis, hepatitis, splenomegaly, splenic infarction, adenopathy, pneumonia, myocarditis, colitis. However, in immunocompetent hosts the commonest manifestation of primary infection is CMV infectious mononucleosis (IM).8, 9, 10, 11, 12 (Table 1). Splenic infarction occurs when the blood supply to the splenic artery or vein is impaired resulting in ischemia and/or necrosis of the spleen (infarcts may be focal or global). Typically, the clinical presentation is that of left upper quadrant pain often with left shoulder pain (Kehr\'s sign).13, 14, 15, 16 Abdominal CT is the preferred test for diagnosis. Etiology of splenic infarcts varies and is often related to hematological disorders, hypercoagulable states, malignancies or infectious causes (embolization from cardiac sources, e.g., myocardial infarction, ventricular mural thrombi, cardiac catheterization) or more commonly atrial fibrillation (Table 2).17, 18, 19, 20 This case was interesting because of the new splenic infarct on abdominal CT scan which explained her LUQ pain. Pathogenesis of splenic infarcts depends on, i.e., etiology. Transient antiphospholipid (APL) Epigallocatechin have been associated with some viral infections, e.g., HIV, CMV, EBV, VZV, parvovirus B19. This was a most challenging case because of seemingly unrelated findings. Firstly, the patient had a past history of sarcoidosis. Her splenomegaly was thought to be due to latent sarcoidosis since it showed no enhancement on gallium uptake. She developed an acute febrile illness characterized by fever, night sweats, profound fatigue, weight loss and anorexia which suggested a lymphoma, i.e., sarcoidosis-lymphoma syndrome. Lymphoma may follow sarcoidosis years after the initial diagnosis and the incidence of lymphoma is sarcoidosis is increased over five fold than in the general population. In a patient with the differential diagnosis of sarcoidosis-lymphoma syndrome, certain findings point to lymphoma. Firstly, sarcoidosis with otherwise unexplained fever should suggest possible lymphoma. With sarcoidosis, a pleural effusion, rare in sarcoidosis, suggests possible lymphoma. A highly elevated ESR and ferritin levels point to possible lymphoma in a sarcoid patient.23, 24, 25, 26 In this case, these tests were not highly elevated, and the clues to the diagnosis were a normal WBC count and ESR with mildly elevated transaminases and atypical lymphocytes.27, 28, 29, 30 The differential diagnosis included acute EBV or CMV infectious mononucleosis. Acute EBV and CMV IgM titers were sent, but results not reported until days later. In hospital, her illness was resolving with only 2% atypical lymphocytes in her WBC count (Fig. 1). An abdominal CT showed hepatomegaly which was not unexpected with acute CMV, but she also had a large splenic infarct. However, after excluding other causes, acute CMV IM was the most likely cause of her splenic infarct (Table 2). This case of CMV infectious mononucleosis involving the lungs and liver with procoagulant manifestations and a splenic infarct is instructive, i.e., all splenic infarcts are not due to endocarditis or cardioembolic events. She had no malignant or hypercoagulable disorders. Importantly, transient hypercoagulability may occur with CMV IM. The association of splenic infarcts and CMV (as well as EBV) has also been ascribed to transient antiphospholipid (APL) antibodies during acute infection. After the acute phase of infection, APL antibodies gradually disappear.