30 research outputs found
Influence of Membrane CD25 Stability on T Lymphocyte Activity: Implications for Immunoregulation
CD25, a component of the IL-2 receptor, is important in T cell proliferation, activation induced cell death, as well as the actions of both regulatory (Treg) and effector (Teff) T cells. Recent genome wide association studies have implicated the CD25 locus as an important region for genetic susceptibility to a number of autoimmune disorders, with serum levels of soluble CD25 receptor (sCD25) serving as a potential phenotypic marker for this association. However, the functional impact of CD25 cleavage, as well as the influence of sCD25 on immunoregulatory activities, remain largely unknown and form the basis of this effort.The generation of sCD25 by Treg (CD4(+)CD25(+)) and Teff (CD4(+)CD25(-)) cells was examined during in vitro suppression assays, efforts that demonstrated constitutive and stable surface CD25 expression on Treg throughout the period of in vitro assessment. In contrast, Teff cells increased CD25 expression during the process of in vitro suppression, with supernatant sCD25 levels correlating to the amount of cellular proliferation. Interestingly, under serum-free conditions, Tregs partially lost their characteristic anergic and suppressive properties. sCD25 supplementation at physiological concentrations to serum free in vitro suppression assays reduced Teff proliferation without specifically influencing suppression. Indeed, sCD25 production within these cultures correlated with cell death.These results support the notion that sCD25 functions as both a surrogate marker of T cell activation as well as an indicator of subsequent cellular death. In addition, the role of CD25 in immunomodulation is likely dependent on the local inflammatory milieu, with molecules capable of modulating surface CD25 expression playing a key role in defining immune responsiveness
Intractable Fasting Hypoglycemia as a Manifestation of Hepatocellular Carcinoma
Non-islet cell tumor hypoglycemia (NICTH) is a rare and serious paraneoplastic complication of both malignant and benign tumors to consider when evaluating fasting hypoglycemia, especially in the setting of liver diseases. We present a case of NICTH in a 54-year-old male with hepatocellular carcinoma (HCC) who presented with symptomatic intractable hypoglycemia (IH) after bowel preparation and fasting for screening upper endoscopy and colonoscopy
Intractable Fasting Hypoglycemia as a Manifestation of Hepatocellular Carcinoma
Non-islet cell tumor hypoglycemia (NICTH) is a rare and serious paraneoplastic complication of both malignant and benign tumors to consider when evaluating fasting hypoglycemia, especially in the setting of liver diseases. We present a case of NICTH in a 54-year-old male with hepatocellular carcinoma (HCC) who presented with symptomatic intractable hypoglycemia (IH) after bowel preparation and fasting for screening upper endoscopy and colonoscopy
Mo1058 Overall Survival of Patients With Unresectable Hepatocellular Carcinoma Treated With Sorafenib: A Single-US Center Prospective Clinical Experience
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M1879 MELD Score Predicts 3-Month Mortality in Hepatitis C Liver Transplant Patients with Recurrent Graft Cirrhosis
Su2054 Relationship Between Model for End-Stage Liver Disease (MELD) Score at the Time of Initial Diagnosis and Survival After Transarterial Chemoembolization (TACE) for Hepatocellular Carcinoma
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The natural history of hepatitis C cirrhosis after liver transplantation
Hepatitis C after liver transplantation leads to graft cirrhosis in up to 30% of patients within 5 years, but limited data exist regarding the clinical course of cirrhosis after transplantation. The aims of this study were to report the natural history of hepatitis C cirrhosis after liver transplantation and to identify risk factors for decompensation and survival. Hepatitis C patients underwent protocol liver biopsies yearly after liver transplantation. After cirrhosis was identified by biopsy, the outcomes of interest were the development of decompensation, death, or retransplantation for hepatitis C. Kaplan-Meier and Cox regression analysis was used to determine survival and risk factors for decompensation and mortality. Out of 502 liver transplants performed for hepatitis C, 88 patients (18%) had cirrhosis within 3.7 years. Seventy-one patients were compensated at diagnosis. The cumulative probability of decompensation 1 year after cirrhosis was 30%. A Model for End-Stage Liver disease score >or= 16 was predictive of decompensation and poor survival, whereas successful interferon treatment was found to reduce this risk (relative risk = 0.05). Once decompensation occurred, 1-year survival was 46%. In conclusion, the results confirm an accelerated natural history of hepatitis C cirrhosis after liver transplantation and demonstrate poor survival after decompensation. The Model for End-Stage Liver Disease can stratify risk for decompensation and survival, whereas successful antiviral therapy may be protective