Hepatitis C Cirrhosis, Hepatitis B Superimposed Infection, and the Emergence of an Acute Portal Vein Thrombosis: A Case Report

Acute portal vein thrombosis (PVT) is a complication of liver cirrhosis. The presence of viral infections such as hepatitis B (HBV) and hepatitis C (HCV) can further increase cirrhotic patients\u27 risk of developing PVT, especially in the rare case when there is superinfection with both HBV and HCV. We present a patient with HCV cirrhosis whose clinical condition was decompensated secondary to the development of superimposed HBV infection, who developed acute PVT during hospitalization. This case offers a unique presentation of acute PVT that developed within several days of hospitalization for decompensated liver disease, as proven by the interval absence of portal venous flow on repeat imaging. Despite the workup on the initial presentation being negative for PVT, reconsideration of differentials after the change in our patient\u27s clinical status led to the diagnosis. Active HBV infection was likely the initial trigger for the patient\u27s cirrhosis decompensation and presentation; the subsequent coagulopathy and alteration in the portal blood flow triggered the development of an acute PVT. The risk for both prothrombotic and antithrombotic complications remains high in patients with cirrhosis, a risk that is vastly increased by the presence of superimposedinfections. The diagnosis of thrombotic complications such as PVT can be challenging, thus stressing the importance of repeat imaging in instances where clinical suspicion remains high despite negative imaging. Anticoagulation should be considered for cirrhotic patients with PVT on an individual basis for both prevention and treatment. Prompt diagnosis, early intervention, and close monitoring of patients with PVT are crucial for improving clinical outcomes. The goal of this report is to illustrate diagnostic challenges that accompany the diagnosis of acute PVT in cirrhosis, as well as discuss therapeutic options for optimal management of this condition

Circulating Mucosal Associated Invariant T Cells Are Activated in Vibrio cholerae O1 Infection and Associated with Lipopolysaccharide Antibody Responses

Background: Mucosal Associated Invariant T (MAIT) cells are innate-like T cells found in abundance in the intestinal mucosa, and are thought to play a role in bridging the innate-adaptive interface. Methods: We measured MAIT cell frequencies and antibody responses in blood from patients presenting with culture-confirmed severe cholera to a hospital in Dhaka, Bangladesh at days 2, 7, 30, and 90 of illness. Results: We found that MAIT (CD3+CD4−CD161hiVα7.2+) cells were maximally activated at day 7 after onset of cholera. In adult patients, MAIT frequencies did not change over time, whereas in child patients, MAITs were significantly decreased at day 7, and this decrease persisted to day 90. Fold changes in MAIT frequency correlated with increases in LPS IgA and IgG, but not LPS IgM nor antibody responses to cholera toxin B subunit. Conclusions: In the acute phase of cholera, MAIT cells are activated, depleted from the periphery, and as part of the innate response against V. cholerae infection, are possibly involved in mechanisms underlying class switching of antibody responses to T cell-independent antigens

THE COMPLICATION-RIDDEN DESTINY OF THE SYSTEMIC RIGHT VENTRICLE IN L-TRANSPOSITION OF THE GREAT ARTERIES: MANAGEMENT DILEMMAS

Background: Congenitally corrected levo-transposition of the great arteries (L-TGA) is a congenital heart disease in which the ventricles and great arteries are transposed from their typical anatomy. In L-TGA, the double discordance, atrioventricular and ventriculoarterial, create an acyanotic milieu which allows patients to survive their early decades, however, progressive systemic right ventricle (sRV) dysfunction creates complications later on. Case: A 40-year-old male with L-TGA presented with symptoms of acute decompensated heart failure (ADHF). In childhood, he had surgical repair of a ventricular septal defect. In adulthood, he developed sRV dysfunction, systemic tricuspid valve (sTV) regurgitation, and left-bundle branch block for which he underwent cardiac resynchronization therapy. Transthoracic echocardiogram obtained during the admission showed a sRV ejection fraction of 40%, severe sTV regurgitation, and a newly identified sRV apical thrombus; the thrombus was confirmed by ultrasound-enhancing agents and transesophageal echocardiography. Decision-making: Our patient was optimized with guideline-directed medical therapy and diuresis. The presence of a sRV thrombus posed a dilemma given the limited literature. Guidelines for intracardiac thrombus in patients with structurally typical hearts recommend anticoagulation with a vitamin K antagonist (VKA) followed by echocardiography to assess for resolution. However, multiple case reports and small-scale studies support the use of direct oral anticoagulants. It is unknown whether these principles can be extrapolated to patients with congenital heart disease. Review of literature identified no cases of sRV thrombus making this one of the first reports. Our patient was anticoagulated with a VKA and later referred for evaluation by advanced heart failure and heart transplant services. Conclusion: We describe one of the first reported cases of sRV thrombus in L-TGA presenting with ADHF. This case illustrates the natural history of L-TGA and highlights the importance of surveillance and monitoring in these patients with dedicated cardiac imaging including advanced imaging modalities to identify complications

CD38⁺CD161^loVα7.2⁺ cells are inversely associated with age and changes in MAIT cells.

<p>A) Spearman correlation of day 2 to day 7 fold changes in %MAIT cells with fold changes across the same days in i) CD161^loVα7.2⁺, and ii) CD38⁺CD161^loVα7.2⁺ cells. B) Spearman correlation of CD38⁺CD161^loVα7.2⁺ cells with age for i) healthy controls and ii) cholera patients on day 7 after presentation.</p

Class-switched antibody responses against LPS are correlated with MAIT cell responses.

<p>Antibody responses against A) LPS, and B) CtxB, of cholera patients at days 2, 7, and 30 after hospitalization, displayed as mean with standard errors. Compared with day 2, * P<0.05; ** P<0.01; *** P<0.001. Correlation of fold changes in %MAIT cells and fold changes in antibody response against C) LPS, and D) CtxB, of cholera patients.</p