Subject(s)
Adenocarcinoma, Scirrhous/diagnosis , Carcinoma, Signet Ring Cell/diagnosis , Endoscopy, Digestive System , Gastroscopes , Stomach Neoplasms/diagnosis , Adenocarcinoma, Scirrhous/drug therapy , Aged , Biopsy , Carcinoma, Signet Ring Cell/drug therapy , Diagnosis, Differential , Female , Humans , Stomach Neoplasms/drug therapyABSTRACT
BACKGROUND: Although reactive lymphoid hyperplasia (RLH) can be found in various organs, including the gastrointestinal tract, orbit, lung, and skin, its occurrence in the liver is rare. CASE REPORT: We report the case of a 47-year-old RLH woman who was identified with RLH of the liver during clinical follow- up of primary biliary cirrhosis. The mass, found incidentally during a medical examination, appeared on ultrasonogram as a hypoechoic mass in the 7th segment of the liver. Further analyses using composed tomography, magnetic resonance imaging, and angiography suggested malignancy, and we performed lateral segmentectomy of the liver. Histologically, the tumor was composed of lymphoid follicles with germinal centers that expressed kappa and lambda light-chain B-cell markers at equal frequency, and no IgH gene rearrangements were detected in Southern blots. Based on these results, we identified the lesion as RLH. CONCLUSIONS: We suggest that this diagnosis be taken into consideration in other cases involving a space-occupying liver mass associated with autoimmune disease.
Subject(s)
Liver Cirrhosis, Biliary/complications , Liver/pathology , Pseudolymphoma/complications , Adult , Aged , Aged, 80 and over , Female , Gene Rearrangement, B-Lymphocyte, Heavy Chain/genetics , Humans , Liver/diagnostic imaging , Liver/surgery , Liver Cirrhosis, Biliary/diagnostic imaging , Liver Cirrhosis, Biliary/pathology , Liver Cirrhosis, Biliary/surgery , Male , Middle Aged , Pseudolymphoma/diagnostic imaging , Pseudolymphoma/pathology , Pseudolymphoma/surgery , Tomography, X-Ray ComputedABSTRACT
BACKGROUND: Autophagy has been reported to play a pivotal role on the replication of various RNA viruses. In this study, we investigated the role of autophagy on hepatitis C virus (HCV) RNA replication and demonstrated anti-HCV effects of an autophagic proteolysis inhibitor, chloroquine. METHODS: Induction of autophagy was evaluated following the transfection of HCV replicon to Huh-7 cells. Next, we investigated the replication of HCV subgenomic replicon in response to treatment with lysosomal protease inhibitors or pharmacological autophagy inhibitor. The effect on HCV replication was analyzed after transfection with siRNA of ATG5, ATG7 and light-chain (LC)-3 to replicon cells. The antiviral effect of chloroquine and/or interferon-alpha (IFNalpha) was evaluated. RESULTS: The transfection of HCV replicon increased the number of autophagosomes to about twofold over untransfected cells. Pharmacological inhibition of autophagic proteolysis significantly suppressed expression level of HCV replicon. Silencing of autophagy-related genes by siRNA transfection significantly blunted the replication of HCV replicon. Treatment of replicon cells with chloroquine suppressed the replication of the HCV replicon in a dose-dependent manner. Furthermore, combination treatment of chloroquine to IFNalpha enhanced the antiviral effect of IFNalpha and prevented re-propagation of HCV replicon. Protein kinase R was activated in cells treated with IFNalpha but not with chloroquine. Incubation with chloroquine decreased degradation of long-lived protein leucine. CONCLUSION: The results of this study suggest that the replication of HCV replicon utilizes machinery involving cellular autophagic proteolysis. The therapy targeted to autophagic proteolysis by using chloroquine may provide a new therapeutic option against chronic hepatitis C.
