Pancreaticoduodenal Artery Aneurysm Rupture Presenting as Duodenal Obstruction Successfully Treated with Early Transcatheter Arterial Embolization: A Case Report of Suspected Segmental Arterial Mediolysis.

Visceral aneurysms are a rare but important form of abdominal vascular disease. Rupture of the aneurysms leads to serious symptoms, such as acute abdomen or abdominal bleeding. However, duodenal obstruction due to arterial rupture of an aneurysm is very rare. We herein report a 50-year-old woman with suspected segmental arterial mediolysis (SAM) who was first diagnosed with acute abdomen and duodenal obstruction. Rupture of a pancreaticoduodenal artery aneurysm was confirmed, and she was treated with transcatheter arterial embolization. In cases of acute abdomen, SAM is a rare but important possibility to consider as a differential diagnosis.

Spontaneous regression of a rectal tonsil presenting as a large submucosal tumor.

Rectal tonsils are localized hyperplastic lymphoid tissues in the rectum, and the initial endoscopic findings are consistent with those for neoplastic lesions. However, rectal tonsils are benign entities, and the diagnosis should be made cautiously. A 70-year-old man presented with pain on defecation with rectal bleeding. Colonoscopy revealed a 3-cm protruding mass in the rectum with mucosal erosion, but no malignant features were observed on forceps biopsy. Endoscopic ultrasonography (EUS) showed that the lesion was a hypoechoic mass without blood flow. Fine needle aspiration under EUS revealed no malignant components, although the size of the lesion had shrunk, and symptoms, such as blood-stained stool, tenesmus, and discomfort during defecation, had resolved. A second forceps biopsy showed intermediate-sized lymphocytes without lymphoepithelial lesions. Based on immunostaining, the lesion was diagnosed as a rectal tonsil. Rectal tonsils occur due to localized proliferation of reactive lymphoid follicles in the submucosa or muscularis mucosa. However, endoscopic diagnosis is difficult since less invasive treatment is performed for neoplastic lesions of the rectum to preserve the function of the anal sphincter. Diagnosis and treatment of small lesions might be possible by endoscopic resection; however, for relatively large lesions, formulating a diagnosis based only on biopsy specimens becomes even more difficult. Therefore, repeated biopsies might be helpful for the diagnosis of rectal tonsils and for excluding other neoplasms.

[A case of systemic amyloidosis with cholangiectasis diagnosed by liver biopsy].

A 60-year-old man presented with fever and fatigue in a medical clinic and was given a diagnosis of cholangitis with mild cholangiectasis. The cholangiectasis remained even after treatment with an appropriate antibiotic agent. When the patient was transferred to our hospital for further examination, he was newly suffering from orthostatic hypotension and peripheral facial nerve palsy. Computed tomography (CT) scan revealed multiple low-density areas in the liver and intrahepatic bile duct dilatation. We performed percutaneous liver biopsy, and histopathological findings showed amyloid deposition around the portal vein. We diagnosed his condition as AL amyloidosis. Oral administration of melphalan and dexamethasone improved his clinical features and CT findings. We consider this case as rare in that the deposition of amyloid protein caused cholangiectasis.

Association of gene expression involving innate immunity and genetic variation in interleukin 28B with antiviral response.

UNLABELLED: Innate immunity plays an important role in host antiviral response to hepatitis C viral (HCV) infection. Recently, single nucleotide polymorphisms (SNPs) of IL28B and host response to peginterferon α (PEG-IFNα) and ribavirin (RBV) were shown to be strongly associated. We aimed to determine the gene expression involving innate immunity in IL28B genotypes and elucidate its relation to response to antiviral treatment. We genotyped IL28B SNPs (rs8099917 and rs12979860) in 88 chronic hepatitis C patients treated with PEG-IFNα-2b/RBV and quantified expressions of viral sensors (RIG-I, MDA5, and LGP2), adaptor molecule (IPS-1), related ubiquitin E3-ligase (RNF125), modulators (ISG15 and USP18), and IL28 (IFNλ). Both IL28B SNPs were 100% identical; 54 patients possessed rs8099917 TT/rs12979860 CC (IL28B major patients) and 34 possessed rs8099917 TG/rs12979860 CT (IL28B minor patients). Hepatic expressions of viral sensors and modulators in IL28B minor patients were significantly up-regulated compared with that in IL28B major patients (≈ 3.3-fold, P < 0.001). However, expression of IPS-1 was significantly lower in IL28B minor patients (1.2-fold, P = 0.028). Expressions of viral sensors and modulators were significantly higher in nonvirological responders (NVR) than that in others despite stratification by IL28B genotype (≈ 2.6-fold, P < 0.001). Multivariate and ROC analyses indicated that higher RIG-I and ISG15 expressions and RIG-I/IPS-1 expression ratio were independent factors for NVR. IPS-1 down-regulation in IL28B minor patients was confirmed by western blotting, and the extent of IPS-1 protein cleavage was associated with the variable treatment response. CONCLUSION: Gene expression involving innate immunity is strongly associated with IL28B genotype and response to PEG-IFNα/RBV. Both IL28B minor allele and higher RIG-I and ISG15 expressions and RIG-I/IPS-1 ratio are independent factors for NVR.

Wernicke's Encephalopathy in a Patient with Peptic Ulcer Disease.

We report a 74-year-old man with Wernicke's encephalopathy (WE) whose only prior illness was peptic ulcer disease. Upper gastrointestinal endoscopy demonstrated gastric ulcer scars accompanied by marked deformity, without pathologic evidence of malignancy. WE due to peptic ulcer disease in previous reports was substantially associated with thiamine deficiency due to recurrent vomiting or surgical procedures. In our case, however, there was no history of vomiting or gastrointestinal surgery. Besides, we thoroughly ruled out other known clinical settings related to WE. There is the possibility that peptic ulcer disease itself provoked thiamine deficiency due to malabsorption.