Acute cytomegalovirus infection complicated by vascular thrombosis: a case report.

We present a case report of a previously healthy adult with cytomegalovirus infection that was complicated by extensive mesenteric arterial and venous thrombosis. To our knowledge, this is the first reported case of this syndrome in an immunocompetent individual who had no predisposing risk factors for thrombosis, and it demonstrates the propensity for cytomegalovirus to be involved in vascular disease.     

Acute portal and mesenteric thrombosis: unusual presentation of cytomegalovirus infection

Cytomegalovirus infection is a benign disease in immunocompetent patients. In-vitro and in-vivo studies show that cytomegalovirus may cause arterial and venous thrombosis through different mechanisms. We describe two cases of acute cytomegalovirus infection complicated by portal and mesenteric vein thrombosis leading to intestinal ischemia. Both patients carried the heterozygous prothrombin G20210A mutation. The presence of this unusual complication should be searched for in patients with acute cytomegalovirus infection and abdominal symptoms in order to start early anticoagulation. The necessity for full thrombophilic screening is also pointed out.     

Type II cryoglobulinemia and brain hemorrhage.

By virtue of an understanding of hemostasis and coagulopathy using modern techniques, the exact role of individual serum protein in vascular thrombosis or hemorrhage becomes more apparent. Cryoglobulin causes vasculitude and thrombosis in various vascular beds, but its role in brain hemorrhage is unknown. We encountered a cryoglobulinemic patient to have cryoglobulinemia, hypocomplementia, and cerebellar hemorrhage during a reactivation of cytomegalovirus infection. Because cryoglobulin is harmful to vessel and hemostasis, and often increases nonspecifically in response to incitement, its weight in vascular syndrome must seriously be reviewed. Coagulopathy in a reactivation of latent virus such as cytomegalovirus should be cautioned in older patients.     

Mesenteric vein thrombosis associated with primary cytomegalovirus infection: a case report.

In the past few years several studies have supported an interplay between cytomegalovirus infections and a prothrombotic state. We describe a case of primary cytomegalovirus infection in an immunocompetent adult that was complicated with mesenteric vein thrombosis. Transient protein C deficiency, lupus anticoagulant and activated protein C resistance were found, in combination with a heterozygous prothrombin G20210A mutation. We discuss the possible mechanisms of cytomegalovirus-related venous thrombosis.     

Acute partial Budd-Chiari syndrome and portal vein thrombosis in cytomegalovirus primary infection: a case report

Background  

Splanchnic vein thrombosis may complicate inherited thrombotic disorders. Acute cytomegalovirus infection is a rare cause of acquired venous thrombosis in the portal or mesenteric territory, but has never been described extending into a main hepatic vein.     

Cytomegalovirus infection of bile duct epithelial cells, hepatic artery and portal venous endothelium in relation to chronic rejection of liver grafts

BACKGROUND/AIM: Chronic rejection is an important cause of graft loss following liver transplantation. A number of risk factors for chronic rejection have been identified previously, albeit inconsistently. These include cytomegalovirus infection detected by a number of different techniques, including immunohistochemical staining and in situ hybridisation of liver grafts. However, tissue-based techniques for the detection of CMV have not been applied to grafts lost to conditions other than chronic rejection. The purpose of this study was to investigate the relationship between the presence of cytomegalovirus infection detected by in situ hybridisation and immunohistochemistry with respect to graft outcome, the presence of cytomegalovirus infection detected by other techniques and in addition, the type of infected cell. METHODS: The 29 patients studied included 15 patients who lost their primary liver graft to chronic rejection in 8 cases, to hepatic artery thrombosis in 4 cases and to causes other than chronic rejection or hepatic artery thrombosis in 3 further cases. In each case, sections containing septal or large ducts and vessels were selected (usually blocks) since these may be more representative. Needle biopsies from 14 further patients who ultimately achieved satisfactory graft function served as control tissue. Of these, ten had evidence of cytomegalovirus infection at the time of study by serum/urine PCR, DEAFF testing or seroconversion, while 4 patients had no evidence of cytomegalovirus infection according to these techniques. RESULTS: Cytomegalovirus infection was detected in the liver of 12 of the 29 patients. These included 8/15 grafts lost, which comprised 3/8 with chronic rejection, 2/3 with hepatic artery thrombosis and 3/4 with grafts lost to other causes, as well as 4/14 who retained grafts. CMV was detected most commonly in association with symptomatic infection and notably was detected only by in situ hybridisation in two cases. Predominant cell types that contained cytomegalovirus were hepatocytes and mononuclear cells. However, bile duct epithelial cells, hepatic artery endothelial cells and portal venous endothelial cells also contained cytomegalovirus in some cases. CONCLUSIONS: These data support previous studies that cytomegalovirus infection is detectable in patients with chronic rejection and are consistent with the theory that CMV is involved in chronic rejection. However, cytomegalovirus infection was detected in explanted grafts lost to conditions other than chronic rejection, and the association may not be causal but a consequence of graft injury.     

CASE REPORT: Cytomegalovirus infection as a cause of acute portal vein thrombosis

We report on the case of a 31-year-old woman who developed acute portal vein thrombosis during the course of an acute cytomegalovirus (CMV) infection. We suggest a relationship between CMV infection, its endothelial cell-damaging effects and portal vein thrombosis.     

Cytomegalovirus infection and thrombosis: a causative association?

Venous thrombosis is a well-organised complication of hospitalisation and has often been reported in the context of HIV infection. Less frequently cytomegalovirus (CMV) has been implicated in the development of thrombosis, although usually in the context of immunosuppression. We report the case of a young, immunocompetent individual who developed pulmonary emboli as a complication of CMV infection and describe the three proposed mechanisms by which this is thought to occur. The probable mechanism in our patient is discussed.     

Thrombophlébite cérébrale : une complication rare de l’infection aiguë à cytomégalovirus

Introduction

Acute cytomegalovirus (CMV) infection increases the risk of vascular thrombosis but reports of cerebral venous thrombosis are rare.

Case report

We report a 36-year-old woman who presented with a cerebral venous thrombosis and acute CMV infection heralded by a cytolytic hepatitis. Heterozygous factor V Leiden mutation was also identified. The patient was treated with anticoagulation for 1 year with favourable outcome.

Conclusion

Serologic tests for CMV infection should be performed in case of cerebral venous thrombosis with liver cytolysis or flu-like symptoms. CMV infection often triggers thrombosis in combination with other inherited or genetic predisposing risk factors that should always be searched.     

Portal thrombosis complicating an acute cytomegalovirus infection in an immunocompetent patient

INTRODUCTION: The cytomegalovirus (CMV) infection is most often asymptomatic. The grave forms concern the immunocompromised patients. We report a new case pf acute CMV hepatitis complicated with portal thrombosis in an immunocompetent patient. EXEGESIS: A 29 year old man has presented a CMV hepatitis proved by the presence of pp65 protein and the viral DNA in serum. This infection was complicated by a portal thrombosis and the evolution was rapidly favourable under anticoagulant treatment. Eleven cases of major thrombosis complicating acute CMV infection in immunocompetent patients were previously reported in the English and French literature. The absence of local and general cause, the remission without anticoagulation, the elevated risk of thrombosis in both HIV and CMV seropositive patients, and in CMV seropositive renal transplant patients suggest a causal relation. Various pathogenic hypotheses were raised: presence of antiphospholipid antibodies, absent in our case, procoagulant phenotype induction of infected endothelial cells, proliferation induction of smooth cells. CONCLUSION: The acute CMV infection can be considered such as a possible cause of major thrombosis.     

Pulmonary embolism and portal vein thrombosis in an immunocompetent adolescent with acute cytomegalovirus hepatitis

Cytomegalovirus infection is usually asymptomatic or resembles infectious mononucleosis with fever, pharyngitis, arthralgias, lymphadenopathy, and atypical lymphocytosis. Even though primary CMV infection is usually self-limited in healthy individuals, significant complications can develop in immunocompromised patients. Venous or arterial thromboembolic phenomena are uncommon, yet very serious complications of CMV infection. Most published reports describe immunosupressed patients after organ transplantation or in the presence of HIV co-infection. However, thrombotic events in CMV infected immunocompetent individuals may occur. We describe the case of an immunocompetent adolescent with acute cytomegalovirus hepatitis that was complicated with pulmonary embolism and portal vein thrombosis. To our knowledge, this is the first reported case in which these two thrombotic phenomena occurred simultaneously in an adolescent with no obvious predisposing factors for thrombosis in the setting of an acute CMV infection.     

Thrombosis and occlusion of vascular access in hemodialyzed patients

Patients undergoing chronic hemodialysis have a high risk of arterial thrombotic events as well as vascular access thrombosis (VAT). The latter complication has been consistently associated with inherited (i.e., the prothrombin 20210 polymorphism, and polymorphisms in the genes encoding for transforming growth factor-β1, nitric oxide synthase, plasminogen activator inhibitor-1, angiotensin converting enzyme, and methylene tetrahydrofolate reductase), and acquired thrombotic risk factors (i.e., diabetes, obesity, atrial fibrillation, hypertension, hyperhomocysteinemia, hyperlipoproteinemia(a), low serum albumin, antiphospholipid antibodies, autoantibodies against protein C and S, erythropoietin administration, malnutrition, and cytomegalovirus infection). The three main factors involved in the pathogenesis of VAT overlap those of venous thrombosis and therefore include endothelial cell injury, blood stasis, and hypercoagulability. These changes are characteristic of patients affected by end-stage renal disease and might be further aggravated during and after hemodialysis. The aim of this review is to describe the epidemiology and pathogenesis of thrombosis of dialysis vascular access and to discuss the application of therapeutic interventions in prevention and treatment of this clinical problem.     

Hughes syndrome associated with cytomegalovirus infection

We report the case of a patient with an acute cytomegalovirus (CMV) infection who developed Hughes syndrome, manifested by a common iliac vein thrombosis. IgM anticardiolipin antibodies (aCL) appeared with the onset of the infection, followed later by IgG aCL. Five months later, both IgM and IgG aCL levels disappeared from the serum. This is the second case of Hughes syndrome associated with CMV infection to be reported in the literature.     

Cytomegalovirus colitis--an unusual cause for diarrhoea in an elderly woman

BACKGROUND: Clinically apparent cytomegalovirus (CMV) disease is uncommon in the immunocompetent host, despite the high seroprevalence rate of CMV in the general population. CASE REPORT: Here, we report the case of CMV colitis in an immunocompetent elderly woman who developed a large pulmonary embolism during her illness. DISCUSSION: The diagnosis of CMV colitis is made on histological examination of biopsy specimens obtained at sigmoidoscopy or colonoscopy. Extensive CMV disease can be accompanied by vascular thrombosis.     

Cavernous sinus thrombosis caused by zygomycosis after unrelated bone marrow transplantation

Abstract: Invasive zygomycosis is a devastating fungal infection occurring as an opportunistic infection after bone marrow transplantation (BMT). Sinusitis can lead to fungal infection in immunosuppressed patients, and cavernous sinus thrombosis, an uncommon condition in immunocompetent patients, typically follows an infection involving the medial third of the face, nose, or paranasal sinuses. Patients undergoing unrelated-donor BMT (UD-BMT) are prone to develop life-threatening infections because of poor recovery of cellular immunity. Despite adequate clinical evaluation and treatment, the prognosis of patients with invasive fungal infections is dismal, especially when intracerebral structures are affected. We describe a case of a patient who underwent an UD-BMT and developed cavernous sinus thrombosis after sinusitis due to zygomycosis. Moreover, he also had disseminated fungal ( Zygomycetes and Aspergillus ) and viral (cytomegalovirus and adenovirus) infections.     

Viral hepatitis and thrombosis: a narrative review

Venous thromboembolism (VTE) is a multicausal disease. Among minor risk factors, acute infections in general are associated with a transient increased risk of VTE. However, acute hepatitis is usually not reported as a potential risk factor for VTE. Recent studies suggest a possible role of viral hepatitis in the development of VTE and, in particular, of portal vein thrombosis. In this narrative review, we will discuss the possible pathogenetic roles of cytomegalovirus, Epstein-Barr virus, and hepatitis A, B, and C viruses in VTE occurrence, and clinical evidence supporting this hypothesis. The hemostatic state in chronic liver disease and the role of coagulation in liver fibrosis will also be discussed.     

Inherited and acquired predispositions for thrombosis in immunocompetent patients with cytomegalovirus-associated thrombosis

BackgroundThrombosis is a rare complication of cytomegalovirus (CMV) infection in immunocompetent patients. The clinical circumstances of this complication have never been studied, to the best of our knowledge.AimWe reviewed all reports on CMV-associated thrombosis in immunocompetent adults found in the literature, in search for thrombosis risk factors other than CMV.MethodsOur search yielded 32 case reports and case series on CMV-associated thrombosis in immunocompetent adults. Reports on immunocompromised patients, infants and elderly patients were excluded. All reports were reviewed for other, acquired as well as inherited, predispositions for thrombosis.ResultsReports on 39 immunocompetent adults were reviewed, mean age for which was 34.9 ± 10.8 years. Overall, 14 (35.9%) patients had one or more acquired predispositions for thrombosis; 16 (45.7%) of the 35 patients that were investigated for inherited thrombophilias had one or more inherited predispositions for thrombosis. Only 12 (34.3%) patients were found to have no acquired or inherited predispositions for thrombosis other than CMV. The most common (n = 13; 33.3%) acquired predisposition for thrombosis was daily use of oral contraceptives. The most common (n = 6; 17.1%) inherited predisposition for thrombosis was factor V Leiden mutation.ConclusionsMost immunocompetent adults with CMV-associated thrombosis have other acquired or inherited predispositions for thrombosis. Hence, addressing these predispositions in patients with CMV-associated thrombosis may be of great clinical importance.     

Cytomegalovirus ischemic colitis: a near-fatal presentation of HIV infection

Cytomegalovirus infection occurs in immunocompromised patients. We present a 45-year-old male with no prior medical history who presented to the hospital with weight loss and non-bloody diarrhea. During hospitalization, he developed severe hematochezia and hypotension. Colonoscopy revealed dusky, friable mucosa. The patient arrested and was resuscitated. Specimen from emergent colectomy showed ischemic changes secondary to cytomegalovirus infection of endothelium and small-vessel thrombosis. An HIV test was subsequently positive with CD4 count of 2 per microliter. The patient was treated with antiretroviral therapy and ganciclovir. He survived postoperative infections and was eventually discharged. In summary, this case of near-fatal cytomegalovirus colitis represents an unusual presentation of undiagnosed HIV infection. Cytomegalovirus infection should be included in the differential diagnosis of immunocompromised patients with gastrointestinal symptoms. Hematochezia may be from intestinal ulceration or severe ischemic damage. Antiretroviral therapy and ganciclovir or foscarnet should be initiated promptly. Surgery is indicated in life-threatening hemorrhage or obvious bowel necrosis.     

Portal vein thrombosis in children: clinical and laboratory study of 26 cases]

Portal vein thrombosis represents one of the most frequent causes of portal hypertension in childhood. The aim of the present study was to describe the clinical and laboratorial characteristics of portal vein thrombosis in pediatric patient. We studied 26 children with diagnosis of portal vein thrombosis through splenoportography (two patients) and ultrasound scan (24 patients) which ages varied from 2 months to 11 years and 4 months (median-5 years and 3 months). Data of the patient history, physical and laboratories examination were used to a retrospective study which was done through medical record analysis. The main complaint of the examination was hematemesis, which was found in 57.6%. In 26.9% a possible risk factor for portal vein thrombosis was found [catheterization of the umbilical vein (four), sepsis (two), omphalitis (one)]. Splenomegaly was present in all cases and the associated illness to portal vein thrombosis were: hepatoportal sclerosis (three), cytomegalovirus infection (two), blastomycosis (two), virus C (two), virus B (one) and virus A (one). The time between the first bleeding and the examination at University of Campinas Hospital, in Campinas, SP, Brazil, varied from 0.23 months to 54 months with a median of 12 months. Only 11.5% of patients underwent the endoscopy with sclerotherapy before going to University of Campinas Hospital. Aminotransferases' activities were considered normal in 20 patients. We could conclude that: 1. The most frequent initial symptom was hematemesis. 2. The known risk factors for portal vein thrombosis were present in about 1/3 of the cases. 3. Laboratorial exams usually indicated absence of hepatocitic lesions. 4. The efforts towards sending the patient to a reference center were late with a delayed diagnostic and with delayed effective therapeutic conduct. 5. In about 50% of the cases there was PVT associated with other hepatic diseases.