Search

Background. Patients with chronic kidney disease (CKD) with or without hemodialysis were considered to have bleeding tendency and higher risk for gastrointestinal (GI) bleeding. Previous studies had documented that hemodialysis may increase the gastroduodenal ulcer bleeding. Few studies evaluated the relationship between CKD and lower GI bleeding. Materials and Methods. An observational cohort study design was conducted. The end-stage renal disease (ESRD) patients receiving regular hemodialysis (dialysis CKD), CKD patients without dialysis (dialysis-free CKD), and controls were selected from 1 million randomly sampled subjects in the National Health Insurance Research Database of Taiwan. These three group subjects were matched by age, sex, comorbidity, and enrollment time in a 1 : 2 : 2 ratio. The Cox proportional hazard regression models were used to identify the potential risk factors for lower gastrointestinal bleeding. Results. Dialysis CKD patients (n=574) had a higher incidence of lower GI bleeding than dialysis-free CKD patients (n=1148) and control subjects (n=1148) (12.9% vs. 3.6% and 2.8%; both P<0.001). Multivariate analysis showed that extreme old age (age≥85), male gender, dialysis-free CKD, and dialysis CKD were independent factors of lower GI bleeding. Additionally, dialysis CKD patients also had a higher incidence of angiodysplasia bleeding compared to dialysis-free CKD patients and control subjects (1.1% vs. 0.1% and 0.1%, respectively; both P=0.003). Conclusion. Hemodialysis may have higher risk of lower GI bleeding and angiodysplasia bleeding.

UNLABELLED:It has been observed that enlargement of perihepatic lymph nodes may be seen in patients with chronic hepatitis B, particularly during acute flares of CHB. We hypothesized that there may be a correlation between the nodal change patterns in CHB patients with acute flare and HBeAg status. Perihepatic lymph node sizes of 87 patients with acute flares of CHB were documented, with a median follow up of 43 months. Patients were separated into 3 groups, HBeAg-positive with HBe seroconversion (group 1), HBeAg-positive without HBe seroconversion (group 2), and HBeAg-negative (group 3). Group 1 has the highest incidence of enlarged lymph nodes (92.3%) compared with group 2 (75.8%) and group 3 (46.8%) (p = 0.003). And if nodal width at acute flare was > 8mm and interval change of nodal width was >3mm, the incidence of HBeAg seroconversion will be 75% (p

BACKGROUND AND AIMS In chronic hepatitis C, the change of perihepatic lymph nodal size after antiviral therapy could be a marker of virologic response. Whether the on-treatment nodal manifestations predict virologic responses is unknown. METHODS Patients (n=88) with biopsy-proven chronic hepatitis C received standard doses of bi-therapy for 24 weeks; sequential changes of the perihepatic lymph nodes were evaluated prospectively by ultrasound. Pretreatment and on-treatment factors were analyzed and correlated with sustained virologic response, focusing on early on-treatment nodal changes (12 weeks). RESULTS Perihepatic lymph nodes were prevalent in 75% of the patients; 72 patients (81.8%) achieved sustained viral response. Before treatment, no factor was significantly associated with the nodal prevalence or size. The pretreatment nodal width (mean 5.3 vs. 3.6 mm; P=0.023) and the on-treatment nodal manifestations including a reduction in nodal width at 12 weeks of antiviral treatment (median; 1.05 vs. 0 mm, P=0.029) and a reduction of nodal volume at the end of treatment (24 weeks; median 0.62 vs. -0.01 ml, P=0.015) were significantly correlated with the sustained virologic response. A reduction of nodal width greater than 2.5 mm at 12 weeks always predicts sustained virologic response (100 vs. 77%; P=0.019). CONCLUSION Results confirm the high prevalence of perihepatic lymphadenopathy in patients with chronic hepatitis C. The use of the nodal width measurement in routine ultrasound follow-up may be a simpler early predictor of sustained virologic response during standard bi-therapy.

Acute exacerbations (AEs) of chronic hepatitis B (CH-B) are thought to be the result of breakdown of immune tolerance on the natural history of chronic hepatitis B virus (HBV) infection. Immune tolerance to HBV maintained in CH-B patients without hepatitis is under the control of the host's forkhead box p3-expressing regulatory T cells (Tregs). Its breakdown mimics the occurrence of autoimmune diseases. Severe AEs may lead to liver decompensation and mortalities. Consequently, AEs are currently the major therapeutic targets in patient treatment. In this study, we employed the SYFPEITHI scoring system to identify epitopes on HBV core antigen (HBcAg) for the construction of human leukocyte antigen class II tetramers to measure HBcAg-specific Treg frequencies (Tregf). Upregulation of Treg gene profiling accompanied by increased HBcAg-specific Tregf was detected in AE patients with sustained remission (SR) to anti-HBV therapy. Depletion of Tregs from peripheral blood mononuclear cells enhanced proliferation to HBcAg. HBcAg-specific Treg clones inhibited the killing capacity of cytotoxic T lymphocyte clones in an antigen-independent manner. A greater posttherapy increase in HBcAg-specific Tregf correlated with a higher SR rate to anti-HBV therapy. These results suggest that HBcAg-specific Tregs function as suppressor effectors and confer SR to anti-HBV therapy.

Sporadic cases of acute hepatitis E virus (HEV) infection with production of anti-HEV IgM have been reported occasionally in Taiwan despite no reported outbreaks in the past. This study was undertaken to determine whether serological markers correlated with virus detection. From 2002 to 2006, 72 reported cases of acute hepatitis E seropositive for anti-HEV IgM in Taiwan were enrolled for investigation. Acute phase serum samples were collected for detection of HEV RNA, HBV DNA, HCV RNA, and GBV-C RNA by PCR. The results showed that viral sequences of HEV, HBV, HCV and GBV-C were detected in 54 (75%), 21 (29.2%), 9 (12.5%), and 22 (30.6%) of cases, respectively. Acute hepatitis A co-infection was excluded in all patients because none were seropositive for anti-HAV IgM and, nine patients (12.5%) did not seroconvert to anti-HEV IgG. These results suggest that serum markers did not correlate completely with viremia in the diagnosis of acute HEV infection. Multiple viruses may co-infect with acute hepatitis E virus in Taiwan. Detection of hepatitis E viremia together with seropositivity for anti-HEV IgM and followed by seroconversion to anti-HEV IgG should be included in the diagnostic criteria for HEV infection.

Acute exacerbations (AEs) of chronic hepatitis B (CH-B) are accompanied by increased T cell responses to hepatitis B core and e antigens (HBcAg/HBeAg). Why patients are immunotolerant (IT) to the virus and why AEs occur spontaneously on the immunoactive phase remain unclear. The role of HBcAg-specific CD4+CD25+ regulatory T (Treg) cells in AE and IT phases was investigated in this study. The SYFPEITHI scoring system was employed to predict MHC class II-restricted epitope peptides on HBcAg overlapping with HBeAg that were used for Treg-cell cloning and for the construction of MHC class II tetramers to measure Treg cell frequencies (Treg f). The results showed that HBcAg-specific Treg f declined during AE accompanied by increased HBcAg peptide-specific cytotoxic T lymphocyte frequencies. Predominant Foxp3-expressing Treg cell clones were generated from patients on the immune tolerance phase, while the majority of Th1 clones were obtained from patients on the immunoactive phase. Treg cells from liver and peripheral blood of CH-B patients express CD152 and PD1 antigens that exhibit suppression on PBMCs proliferation to HBcAg. These data suggest that HBcAg peptide-specific Treg cells modulate the IT phase, and that their decline may account for the spontaneous AEs on the natural history of chronic hepatitis B virus infection.

To study the manifestations of perihepatic lymph nodes during the episode of acute hepatitis flare by point-of-care ultrasonography.One hundred and seventy-six patients with an episode of acute hepatitis flare (ALT value5 × upper normal limit) were enrolled retrospectively. Diagnosis of etiology of the acute hepatitis flare was based on chart records and serological and virological assays. The patients were categorized into two groups (viral origin and non-viral origin) and further defined into ten subgroups according to the etiologies. An ultrasonograpy was performed within 2 h to 72 h (median, 8 h). The maximum size of each noticeable lymph node was measured. Correlation between clinical parameters and nodal manifestations was analyzedEnlarged lymph nodes (width ≥ 5mm) were noticeable in 110 (62.5%) patients, mostly in acute on chronic hepatitis B (54.5%). The viral group had a higher prevalence rate (89/110 = 80.9%) and larger nodal size (median, 7 mm) than those of the non-viral group (21/66 = 31.8%; median, 0 mm) (P0.001 for both). Meanwhile, there were significant differences in the nodal size between acute and chronic viral groups (P0.01), and between acute hepatitis A and non-hepatitis A viral groups (P0.001). In logistical regression analysis, the nodal width still showed strong significance in multivariate analysis (P0.0001) to stratify the two groups. The area under the curve of ROC was 0.805, with a sensitivity of 80.9%, a specificity of 68.2%, positive predictive value of 80.92%, negative predictive value of 68.18%, and an accuracy of 76.14%.Point-of-care ultrasonography to detect perihepatic nodal change is valuable for clarifying the etiologies in an episode of acute hepatitis flare.