Mac-2-binding protein glycan isomer predicts all malignancies after sustained virological response in chronic hepatitis C.

Despite reports of hepatocellular carcinoma (HCC) in patients with chronic hepatitis C virus (HCV) infection after achieving sustained virological response (SVR), only few studies have demonstrated the incidence of other (non-HCC) malignancies. This study aimed to clarify the incidence, survival probability, and factors associated with malignancy, especially non-HCC malignancies, in patients with chronic HCV infection after achieving SVR. In this retrospective study, records of 3580 patients with chronic HCV infection who achieved SVR following direct-acting antiviral (DAA) treatment were analyzed. The cumulative post-SVR incidence of non-HCC malignancies was 0.9%, 3.1%, and 6.8% at 1, 3, and 5 years, respectively. The survival probability for patients with non-HCC malignancies was 99.1%, 78.8%, and 60.2% at 1, 3, and 5 years, respectively, and the rate was significantly lower than that for patients with HCC. The Cox proportional hazards regression model identified Mac-2-binding protein glycan isomer (M2BPGi) cutoff index (COI) ≥ 1.90 at baseline and ≥ 1.50 at 12 weeks following DAA treatment as significant and independent factors associated with the post-SVR incidence of non-HCC malignancies. Furthermore, patients with either M2BPGi COI ≥ 1.90 at baseline or M2BPGi COI ≥ 1.50 at SVR12 had a significantly higher risk of post-SVR incidence of non-HCC malignancies than of HCC. Conclusion: M2BPGi measurements at baseline and SVR12 may help predict the post-SVR incidence of non-HCC malignancies in patients with chronic HCV infection who achieved SVR following DAA treatment. Early identification of these patients is critical to prolong patient survival.

[Sarcoidosis diagnosed by a tiny esophageal lesion:a case report].

A woman in her 60s was referred to the Department of Gastroenterology with anemia. She had a recurrent transient loss of consciousness 11 years ago, and she was examinated at the cardiology and neurology departments, but the cause was not identified. Epileptic seizures were suspected. Sodium valproate medication was started, and the patient's condition progressed with no recurrence. Esophagogastroduodenoscopy showed a tiny submucosal tumor-like lesion with mild depression in a 21cm thoracic esophagus. Biopsy revealed epithelioid granulomas with multinucleated giant cells in the subepithelial stroma. Computed tomography (CT), positron emission tomography-computed tomography (PET-CT), and magnetic resonance imaging (MRI) showed multiple lesions in the hilar lymph nodes, spleen, and heart that are typical of sarcoidosis. These findings led to the diagnosis of esophageal lesion associated with sarcoidosis. The patient had no subjective symptoms;however, treatment with prednisolone 30mg was started because cardiac sarcoidosis is a risk of death. Gastrointestinal tract involvement in sarcoidosis is rare;esophageal sarcoidosis is particularly rare, and there are few reports on superficial lesions. Here, we report a case of sarcoidosis that was diagnosed from a tiny esophageal lesion.

Risk factors for cholecystitis after stent placement in patients with distal malignant biliary obstruction.

BACKGROUND /PURPOSE: Limited data are available for acute cholecystitis after Self-Expandable Metallic Stent (SEMS) placement in patients with malignant distal biliary obstruction. We aimed to identify risk factors for cholecystitis. METHODS: This was a retrospective, single-center study of 280 patients (336 stents) who received endoscopic SEMS placement between May 2005 and April 2016. Clinical records were used to perform risk factor analyses. RESULTS: Of 336 SEMS placement procedures, 25 (7.4%) led to development of cholecystitis. Logistic regression analysis revealed three independent risk factors: covered SEMS (P = .014), tumor involvement to the cystic duct (P = .017), and presence of gallstones (P = .022). Median time to cholecystitis onset was shorter with covered SEMS than with uncovered SEMS (P = .034), and in patients with pancreatic cancer compared to those with other cancers (P = .001). Severe cholecystitis developed within 30 days after covered SEMS placement in three patients with pancreatic cancer without tumor involvement to the cystic duct. CONCLUSIONS: Use of covered SEMS might be a risk factor for cholecystitis onset within 30 days after placement. Clinicians should be aware of the risk for severe cholecystitis after covered SEMS placement, even if the tumor does not invade the cystic duct.

Long-term pegylated interferon monotherapy following 72 weeks of pegylated interferon and ribavirin in hepatitis C virus genotype-1-infected slow responders.

OBJECTIVE: Slow responders to pegylated interferon (Peg-IFN) and ribavirin (RBV) among patients infected with hepatitis C virus (HCV) genotype 1 may benefit from an extended treatment course. The aim of this study was to determine the efficacy of persistent negative serum HCV RNA over 96 weeks during long-term Peg-IFN monotherapy following 72 weeks of combination therapy. METHODS: A total of 46 HCV genotype 1-infected slow responders were treated for 72 weeks with Peg-IFN and RBV combination therapy alone (n=25) or additional long-term biweekly treatment with 90 µg of Peg-IFN-α2a (n=21). The criterion for the completion of long-term Peg-IFN monotherapy was defined as the attainment of constantly negative HCV RNA in the serum over 96 weeks during IFN treatment. RESULTS: The patients with sustained negative serum HCV RNA during 96 weeks of IFN treatment had a higher rate of sustained virological response (SVR) than those without (81 vs. 40%, p=0.012). A multivariate analysis identified sustained negativity of serum HCV RNA over 96 weeks of IFN treatment to be a predictive factor for SVR. CONCLUSION: In the present study, sustained negative serum HCV RNA over 96 weeks during long-term Peg-IFN monotherapy following 72 weeks of combination therapy of Peg-IFN and RBV resulted in beneficial virological outcomes among HCV genotype 1-infected slow responders.

Hepatocellular carcinoma with mesothelioma-like dissemination.

Reported herein is a case of hepatocellular carcinoma (HCC) with unusual peritoneal dissemination masquerading as peritoneal mesothelioma. A 61-year-old man was clinically found to have multiple tumors in his abdominal cavity; peritonitis carcinomatosa was suspected. An autopsy revealed numerous tumors of various sizes in the abdominal serosa, omentum, and diaphragm. No signs of tumor, fibrosis, or cirrhosis were found in the liver, except for a small nodule in the hepatic triangular ligament. Histologically, the tumor cells proliferated in thick trabeculae or in sheets and formed a few canaliculi and tubules with homogenously brown contents in their lumina, which stained positively with Hall stain. Immunohistochemically, these tumors were positive for hepatocyte, alpha-fetoprotein (AFP) and low-molecular-weight cytokeratin; were focally positive for pan-cytokeratin and epithelial membrane antigen (EMA); and were negative for high-molecular-weight cytokeratin, vimentin, and calretinin. Carcinoembryonic antigen (CEA) produced a bile canalicular immunohistochemical staining pattern. Thus, the tumor was diagnosed as an HCC (Edmondson II type) of the triangular ligament with massive peritoneal dissemination. The origin of this tumor and its differential diagnosis (malignant mesothelioma, hepatoid adenocarcinoma, and hepatoid yolk sac tumor) are discussed.

Primary sclerosing cholangitis associated with limy bile and acute pancreatitis.

Primary sclerosing cholangitis (PSC) as the cause of acute pancreatitis (AP) is a rare phenomenon. Here, we report the first case of PSC associated with limy bile (LB) as well as AP. In this case, spontaneous outflow of the LB occurred, and the AP resolved on its own with conservative management. In addition to the administration of ursodeoxycholic acid, endoscopic intervention was undertaken and the patient remains symptom free to date. This report describes a unique case in which PSC, LB, and AP occurred in the same patient. The association of these rare conditions is also discussed.

Low Grade MALToma and Early Cancer of the Stomach in a Patient with Helicobacter pylori Infection: A Case Report.

A causal relationship has been suggested between Helicobacter pylori infection and gastric malignancy, including both gastric cancer and low grade lymphoma of mucosa-associated lymphoid tissue (MALToma). We describe a rare case of simultaneous occurrence of low grade MALToma and early cancer of the stomach in a 72-year-old woman. In this patient, low grade MALToma not only had preceded gastric cancer by 5 years, but had also disappeared, and subsequently reappeared coexisting with early cancer of the stomach and Helicobacter pylori infection. Eradication therapy for Helicobacter pylori was performed immediately prior to subtotal gastrectomy for early gastric cancer of the pyloric area. Thereafter, regression of MALToma was observed. These results, taken together with a previously reported case of low grade MALToma, suggest that low grade MALToma of the stomach may fluctuate, at least in the initial stages, even in the presence of constant Helicobacter pylori infection.