Chih-Wen Lin

Primary hepatic carcinoid tumor: a case report and review of the literature

BackgroundPrimary hepatic carcinoid tumor (PHCT) is very rare and difficult to diagnose before biopsy or operation. We report a patient with a small PHCT and review cases in the literature.Case presentationA 48-year-old Chinese female with underlying hepatitis B virus (HBV) infection was found to have a low echoic hepatic nodule by abdominal ultrasound. Tumor markers were negative. Dynamic liver computed tomography scans showed enhancement of the nodule in the arterial phase and early washout in the portal phase. Hepatocellular carcinoma (HCC) was considered based on the image findings and underlying HBV infection. However, the tumor biopsy revealed a malignant neoplasm that originating from neuroendocrine cells. Pre-operative and intra-operative investigations for the possible other origin of carcinoid tumor were negative, so PHCT was confirmed.ConclusionA small and asymptomatic PHCT is extremely rare. PHCT should be one of the differential diagnoses in patients with small hepatic tumor, even in regions with high prevalence of HBV infection and HCC. Pre-operative biopsy is necessary to avoid misdiagnosis even when HCC is highly suspected clinically.

Clinicopathological differences between hepatitis B viral genotype B‐ and C‐related resectable hepatocellular carcinoma

Summary.  Clinical and pathogenic differences exist between hepatitis B viral (HBV) genotypes B and C, and genotype C has a higher risk of hepatocellular carcinoma (HCC) development than genotype B. The aim of this study was to investigate whether HBV genotypes B and C influence the clinicopathological features of patients with resectable HCC. Stored serum samples from 193 patients with resectable HBV‐related HCC were tested for HBV genotypes by a molecular method. Of 193 patients undergoing resection of HCC, 107 (55%) and 86 (45%) were infected with genotypes B and C, respectively. Compared with genotype C patients, genotype B patients were less likely to be associated with liver cirrhosis (33%vs 51%, P = 0.01). Pathologically, genotype B patients had a higher rate of solitary tumour (94%vs 86%, P = 0.048) and more satellite nodules (22%vs 12%, P = 0.05) than genotype C patients. Our results indicate that genotype B‐related HCC is less associated with liver cirrhosis and has a higher frequency of solitary tumour as well as more satellite nodules than genotype C‐related HCC. These characteristics may contribute to the recurrence patterns and prognosis of HBV‐related HCC in patients with genotype B or C infection.

Complete activation of autophagic process attenuates liver injury and improves survival in septic mice.

ABSTRACT The accumulation of autophagosomes in the terminal step of the autophagic process has recently emerged as a potentially maladaptive process in the septic heart and lung. However, the role of autophagy in the septic liver has not been ascertained. This study was investigated by first examining the entire sequence of the autophagic process in the liver of septic mice. Second, a novel pharmacotherapeutic approach was utilized to treat sepsis with autophagy enhancer/inhibitor. Sepsis was induced by cecal ligation and puncture (CLP). C57BL/6 mice received autophagy enhancer carbamazepine (CBZ), autophagy inhibitor 3-methyladenine (inhibition of autophagosomal formation), or chloroquine (impairment of autophagosomal clearance). We found that the whole autophagic process was activated at 4 h after CLP; however, it did not proceed to completion during the 4- to 24-h time period, as indicated by accumulated autophagosomes and decreased autophagic flux. Carbamazepine, which induced complete activation of the autophagic process, improved CLP survival. This protective effect was also associated with decreased cell death, inflammatory responses, and hepatic injury. However, disruption of autophagosomal clearance with chloroquine abolished the above protective effects in CBZ-treated CLP mice. 3-Methyladenine, which resulted in inhibition of the autophagosomal formation, did not show any above beneficial effects in CLP mice. Impaired autophagosome-lysome fusion resulting in incomplete activation of autophagy may contribute to sepsis-induced liver injury. Treatment with CBZ may serve a protective role in the septic liver, possibly through the effect of complete activation of autophagic process.

Entecavir versus lamivudine in the treatment of chronic hepatitis B patients with hepatic decompensation.

BACKGROUND Lamivudine has been widely used in chronic hepatitis B patients with hepatic decompensation, but its use is limited by drug resistance. This outcome research aimed to investigate the comparative efficacy and safety of entecavir versus lamivudine in decompensated patients. METHODS Between November 2004 and February 2010, 126 consecutive treatment-naive patients received either entecavir (n=53) or lamivudine (n=73) for decompensated chronic hepatitis B. All patients presented with both hyperbilirubinaemia and coagulopathy. Primary outcome was mortality within 1 year; secondary outcomes included liver-related mortality, biochemical and virological response, and improvement of hepatic dysfunction. RESULTS Both treatment groups were comparable in baseline characteristics. A total of 19 (35.8%) entecavir and 33 (45.2%) lamivudine receivers expired within 1 year, respectively (P=0.29, log rank test). Age (hazard ratio [HR] 1.04 per year, 95% CI 1.01, 1.06), cirrhosis (HR 2.07, 95% CI 1.02, 4.23), and international normalized ratio for prothrombin time (HR 1.44, 95% CI 1.20, 1.74) were independent baseline predictors for all-cause mortality. Antiviral therapy was also unrelated to liver-specific death. However, more patients taking entecavir tended to attain aminotransferase normalization (76.5% versus 52.5%; P=0.05) and viral DNA undetectability (100% versus 58.3%; P=0.06). Moreover, entecavir was associated with significantly greater reduction of the model for end-stage liver disease scores (median 10.0 versus 4.3; P=0.02). Overall, 3 (7.5%) lamivudine but no entecavir users acquired drug resistance in 1 year (P=0.25). CONCLUSIONS Entecavir as compared with lamivudine is similar in the effect on short-term mortality but is associated with greater clinical improvement among chronic hepatitis survivors who recovered from hepatic decompensation.

Incidence trends and predictors for cost and average lengths of stay in colorectal cancer surgery

AIM To evaluate the changing trends and outcomes of colorectal cancer (CRC) surgery performed at a large single institution in Taiwan. METHODS This study retrospectively analyzed 778 patients who received colorectal cancer surgery at E-Da Hospital in Taiwan from 2004 to 2009. These patients were from health examination, inpatient or emergency settings. The following attributes were analyzed in patients who had undergone CRC surgical procedures: gender, age, source, surgical type, tumor number, tumor size, number of lymph node metastasis, pathologic differentiation, chemotherapy, distant metastases, tumor site, tumor stage, average hospitalization cost and average lengths of stay (ALOS). The odds ratio and 95% confidence intervals were calculated to assess the relative rate of change. Regression models were employed to predict average hospitalization cost and ALOS. RESULTS The study sample included 458 (58.87%) males and 320 (41.13%) females with a mean age of 64.53 years (standard deviation, 12.33 years; range, 28-86 years). The principal patient source came from inpatient and emergency room (96.02%). The principal tumor sites were noted at the sigmoid colon (35.73%) and rectum (30.46%). Most patients exhibited a tumor stage of 2 (37.28%) or 3 (34.19%). The number of new CRC surgeries performed per 100000 persons was 12.21 in 2004 and gradually increased to 17.89 in 2009, representing a change of 46.52%. During the same period, the average hospitalization cost and ALOS decreased from

Expression of aquaporins in rat liver regeneration.

5303 to

Hepatoid adenocarcinoma of the stomach with liver metastasis mimicking hepatocellular carcinoma: a case report

4062 and from 19.7 to 14.4 d, respectively. The following factors were associated with considerably decreased hospital resource utilization: age, source, surgical type, tumor size, tumor site, and tumor stage. CONCLUSION These results can be generalized to patient populations elsewhere in Taiwan and to other countries with similar patient profiles.

Serum viral load at the virological relapse predicts subsequent clinical flares in chronic hepatitis B patients off entecavir therapy.

Abstract Objective. The remarkable ability of liver to regenerate after insults has been harnessed by surgeons when designing techniques for liver resection or transplantation. However, the underlying mechanisms of liver regeneration are not fully clarified. On the other hand, aquaporins (AQPs) are small transmembrane proteins with unexpected physiological roles in addition to water transport. For example, they play pivotal roles in cell migration, angiogenesis, and cell proliferation, events that are also occurred during liver regeneration. We thus examined the possible involvement of AQPs in this regenerative process. Material and methods. A two-thirds partial hepatectomy (PH) rat model was employed. The temporal expression of various AQPs in the liver following PH was determined by semiquantitative reverse transcription polymerase chain reaction (RT-PCR) and Western blotting. The localization of AQPs was evaluated by immunohistochemistry. Results. As anticipated, AQP0, 8, 9, and 11 were detected mainly in hepatocytes; unexpectedly, Kupffer cells were observed to express AQP8 during a specific period of time in the regenerative process. AQP9 protein was shown to be expressed in a progressively enhanced pattern at early time points after PH. A transient expression of AQP11 in the nucleus of hepatocytes was observed. Conclusion. These findings suggest the possibility that AQP might be involved in the PH-induced liver regeneration.

Change in insulin resistance according to virological response during antiviral treatment for hepatitis C virus infection

IntroductionHepatoid adenocarcinoma is a special type of extrahepatic alpha-fetoprotein-producing adenocarcinoma, which has a morphologic similarity to hepatocellular carcinoma. We report a patient with underlying hepatitis B virus infection and hepatoid adenocarcinoma with liver metastasis mimicking hepatocellular carcinoma.Case presentationWe present the case of a 56-year-old Chinese female with underlying hepatitis B virus infection, who was found to have multiple hepatic tumors by abdominal ultrasound and an elevated level of serum alpha-fetoprotein. Hepatocellular carcinoma was considered based on the image findings, the elevated level of serum alpha-fetoprotein. and underlying hepatitis B virus infection. Moreover, the subsequent endoscopy revealed gastric tumor. However, the tumor histology of the stomach and liver revealed glandular adenocarcinoma with hepatoid foci. The final diagnosis is hepatoid adenocarcinoma of the stomach with liver metastasis.ConclusionHepatoid adenocarcinoma is an aggressive tumor with liver metastasis being the first clinical manifestation of the neoplasm. Hepatoid adenocarcinoma of the stomach with liver metastasis should be considered in older patients with elevated serum alpha-fetoprotein and multiple hepatic tumors with underlying chronic liver disease. An upper gastrointestinal endoscopy should be performed to exclude the possibility of hepatoid adenocarcinoma originating from the stomach to avoid potential misdiagnosis and inappropriate therapy.

Prospective Survey for the Etiology and Outcome of Peptic Ulcer Bleeding: A Community Based Study in Southern Taiwan

Therapeutic duration of nucleos(t)ide analogues for chronic hepatitis B (CHB) is not indefinite in many parts of the world. Viral reactivation is common off therapy, but the risk of subsequent clinical outcome remains unclear and unpredictable. We aimed to quantify the incidence of and explore the predictors for clinical flare following virological relapse in CHB patients who discontinue entecavir therapy.