Social history was not significant, as the patient did not smoke cigarettes, use other tobacco products, or use illicit drugs. a hypercoagulable state caused by CMV hepatitis with CMV-induced PVT. Heparin was transitioned to warfarin at the time of discharge. Interventions: Given the patient’s immunocompetent state and resolution of fevers, antiviral therapy for CMV contamination was not initiated. Outcomes: The patient continued to improve with a normalization of the serum ferritin level and anticoagulation therapy was stopped after 6 months. Lessons: There is mounting Nodinitib-1 support for infectious causes of venous thromboembolism (VTE) based on existing molecular biology and clinical research. Meta-analysis of existing data showed that between 1.9% and 9.1% of patients hospitalized with VTE had concurrent acute CMV infection. Theoretical mechanisms for this association include transient formation of antiphospholipid antibodies, Nodinitib-1 transient formation of antibodies targeting CMV capsule phospholipids with procoagulant properties, and direct infection of the endothelial cells. We hope this case will serve as a reminder to consider CMV as a transient cause of PVT and VTE, particularly in light of 2016 guidelines for unprovoked VTE recommending lifelong anticoagulation. We also plan to prospectively study the association of Itgbl1 unprovoked VTE and acute CMV infection in our own hospital system. strong class=”kwd-title” Keywords: CMV, coagulopathy, cytomegalovirus, portal vein thrombosis, PVT, venous thromboembolism, VTE 1.?Introduction Unprovoked venous thromboembolism (VTE) is a common diagnosis, resulting in thousands of patients being placed on anticoagulation without a clear understanding of the underlying cause of coagulopathy. In such cases, cytomegalovirus (CMV) is usually rarely considered as a possible provoking agent; however, there is emerging data supporting its role as a cause of a transient hypercoagulable state. Herein, we present a case of CMV-induced portal vein thrombosis (PVT) along with a literature review of comparable cases. 2.?Case history A 46-year-old male airline pilot presented as a regional transfer to our facility with progressive abdominal pain for the prior 2 weeks. This was further characterized as a stabbing periumbilical pain associated with nausea, vomiting, watery diarrhea, and recurrent daily fevers over the same period of time. Further history revealed that the patient had been out of work for 3 months due to progressive, debilitating fatigue. Watery diarrhea was occurring approximately twice daily without any associated weight loss. Earlier in the week, the patient had been treated empirically by his primary care physician with a course of azithromycin without any improvement. Social history was not significant, as the patient did not smoke cigarettes, use other tobacco products, or use illicit drugs. In addition, he had avoided alcohol for most of his life due to his profession Nodinitib-1 as a pilot. The patient was unmarried and had not been sexually active in several years. Past medical history was similarly noncontributory, as the patient denied having any known chronic conditions or prolonged hospitalizations and denied taking any medications or supplements. His family history was only significant for Hashimoto disease in his mother, sister, and maternal aunt. Physical examination was notable for a fever of 38.6?C, tachycardia averaging 105 beats per minute, and abdominal tenderness to deep palpation of the periumbilical area and the right upper quadrant. The liver span was 13?cm at the midclavicular Nodinitib-1 line by percussion, suggestive of mild hepatomegaly. He did not have any notable rash, lymphadenopathy, palpable splenomegaly, or any other stigmata of liver disease. There were also no warm, swollen, tender, or immobile joints upon musculoskeletal examination. Initial laboratory findings were consistent with moderate hepatitis with elevated transaminases, moderate hyperbilirubinemia, and moderate hypoalbuminemia without coagulopathy or hyperammonemia (Table ?(Table1).1). The patient also had moderate hyponatremia, elevated C-reactive protein, and elevated lactate dehydrogenase levels. The initial blood counts showed moderate neutrophilia, atypical lymphocytes, and rare smudge cells. Prior to transfer, computed tomography of the abdomen with contrast revealed PVT (Fig. ?(Fig.1A,1A, B). This was confirmed by abdominal ultrasound with portal vein duplex showing retrograde flow and a visible thrombus with normal echogenicity of Nodinitib-1 the liver. With persistent fevers and concern for septic thromboembolism, continuous heparin infusion and intravenous cefepime antibiotic therapy (2?g every 8?hours) were initiated on arrival. Further evaluation for liver disease revealed a ferritin level of 6248?ng/mL (Table ?(Table2),2), which was not accompanied by any other clinical or laboratory evidence of hemochromatosis. Additional workup for liver disease revealed.
