[A case of incomplete torsion of the gallbladder due to partial torsion of the gallbladder neck].

A 57-year-old man was admitted to our hospital because of low-grade fever and pain in the right hypochondrium. Abdominal ultrasonographic (US) examination revealed a hyperechoic mass in the body of the gallbladder. The wall of the gallbladder towards the fundus was markedly thickened, while the wall near the gallbladder neck showed no abnormality. Power Doppler and contrast-enhanced CT of the abdomen revealed absence of blood flow in the fundic wall of the gallbladder, however, a contrast-enhanced image of the entire wall was obtained by contrast US, although the blood flow to the fundus was decreased. Torsion of the gallbladder was diagnosed and laparoscopic cholecystectomy was performed. The gallbladder was found to be a wandering gallbladder, Gross I type, and slight counterclockwise torsion was found at the neck of the gallbladder. We report a case of partial torsion of the gallbladder neck, in which the details of the ischemic hemodynamic changes could be observed by contrast-enhanced US.

Factors regulating tumor pressure in cases of small hepatocellular carcinoma.

BACKGROUND/AIMS: There is scare information regarding tumor pressure in hepatocellular carcinoma. As the tumor diameter increases, histological manifestations become more diverse. Therefore, studies based on relatively small tumors are needed in order to search for those underlying factors that are directly related to tumor pressure in hepatocellular carcinoma. The purpose of this study was to determine which factors regulate tumor pressure in cases of hepatocellular carcinoma where the diameter of the tumor is 3cm or less. METHODOLOGY: The study included 54 patients with small hepatocellular carcinoma in whom tumor pressure had been determined and in whom the tumor had been confirmed histologically. Tumor pressure was determined percutaneously under ultrasonographic guidance. RESULTS: Hepatic tissue pressure (p = 0.01), tumor size (p < 0.01), number of tumors (p = 0.01), degree of tumor differentiation (p < 0.01), ultrasonographic halo (p < 0.01), angiographic tumor staining (p < 0.01) and angiographic tumor vessel (p = 0.03) all showed significant correlation with tumor pressure. Multivariate analysis revealed that angiographic tumor staining (p = 0.001), hepatic tissue pressure (p = 0.013), and tumor size (p = 0.044) were significant factors associated with tumor pressure. CONCLUSIONS: It was suggested that tumor pressure in small hepatocellular carcinoma was mainly regulated through development of the neovasculature.

Usefulness of tumor pressure as a prognostic factor in cases of hepatocellular carcinoma where the diameter of the tumor is 3 cm or less.

BACKGROUND: The current study was designed to determine the usefulness of pretreatment tumor pressure as a new prognostic factor in patients with small hepatocellular carcinoma (HCC; 3 cm or smaller in diameter). METHODS: The study included 39 patients with small HCC in whom tumor pressure was determined. They underwent percutaneous ethanol (with Lipiodol) injection therapy (Lp-PEI) or transcatheter arterial embolization (TAE) of the hepatic artery. Tumor pressure was determined percutaneously under ultrasonographic guidance. The factors analyzed were age, gender, mean blood pressure, the presence/absence of antibody to hepatitis C virus (anti-HCV), alcohol abuse, Child's classification, the presence/absence of esophagogastric varices, serum alpha-fetoprotein (AFP) level, tumor size, number of tumors, degree of tumor differentiation, the presence/absence of tumor capsule, tumor pressure, and the method of treatment. Multivariate analysis using Cox proportional hazards model was conducted on the factors that may have affected prognosis (P < 0.25) according to the univariate analysis using a proportional hazards model. RESULTS: The rates of local and distant recurrence were higher (P < 0.01, P < 0.01, respectively) and the survival rate was lower (P = 0.03) in patients with high tumor pressure than in those with low tumor pressure. Multivariate analysis revealed that tumor pressure (P < 0.01), AFP level (P = 0.01), and age (P = 0.01) were significant predictive factors associated with local recurrence. Tumor pressure (P < 0.01) and AFP level (P < 0.01) were both significantly associated with distant recurrence. The only significant predictive factor associated with survival rate was tumor pressure (P < 0.04). CONCLUSIONS: The current study revealed that tumor pressure was associated significantly with survival rates after Lp-PEI or TAE in patients with small HCC. There were also significant predictive factors associated with local recurrence, these being tumor pressure, AFP level, and age, and with distant recurrence, namely, tumor pressure and AFP level. Tumor pressure measured before the initial treatment of patients with small HCC may be a useful new prognostic factor.

M6P/IGF2R tumor suppressor gene mutated in hepatocellular carcinomas in Japan.

Mannose 6-phosphate/insulin-like growth factor II receptor (M6P/IGF2R) tumor suppressor- gene mutation is an early event in human hepatocellular carcinoma (HCC) formation in the United States, but its role in hepatocarcinogenesis in Japan is unclear. We therefore determined M6P/IGF2R mutation frequency in HCCs from patients who resided in the southern, central, and northern regions of Japan. Ten single nucleotide polymorphisms were used to identify HCCs and dysplastic liver nodules with M6P/IGF2R loss of heterozygosity. The retained allele in these tumors was also assessed for point mutations and deletions in the M6P/IGF2R ligand binding domains by direct sequencing of polymerase chain reaction (PCR) amplified DNA products. Fifty-eight percent (54 of 93) of the patients were heterozygous at the M6P/IGF2R locus, and 67% (43 of 64) of the HCCs and 75% (3 of 4) of the dysplastic nodules had loss of heterozygosity. The remaining allele in 21% of the HCCs contained either M6P/IGF2R missense mutations or deletions, whereas such mutations were not found in the dysplastic lesions. In conclusion, M6P/IGF2R is mutated in HCCs from throughout Japan with a frequency similar to that in the United States. Loss of heterozygosity in dysplastic liver nodules provides additional evidence that M6P/IGF2R haploid insufficiency is an early event in human hepatocarcinogenesis.