RESUMO
BACKGROUND: Whether clinical outcomes of acute cholangitis (AC) vary by etiology is unclear. AIM: To compare outcomes in AC caused by malignant biliary obstruction (MBO) and common bile duct stones (CBDS). METHODS: This retrospective study included 516 patients undergoing endoscopic retrograde cholangiopancreatography (ERCP) due to AC caused by MBO (MBO group, n = 56) and CBDS (CBDS group, n = 460). Clinical and laboratory parameters were compared between the groups. Propensity score matching (PSM) created 55 matched pairs. Confounders used in the PSM analysis were age, sex, time to ERCP, and technical success of ERCP. The primary outcome comparison was 30-d mortality. The secondary outcome comparisons were intensive care unit (ICU) admission rate, length of hospital stay (LOHS), and 30-d readmission rate. RESULTS: Compared with the CBDS group, the MBO group had significantly lower body temperature, percentage of abnormal white blood cell counts, and serum levels of aspartate aminotransferase, alanine aminotransferase, and creatinine. Body temperature, percent abnormal white blood cell count, and serum aspartate aminotransferase levels remained significantly lower in the MBO group in the PSM analysis. Platelet count, prothrombin time/international normalized ratio, and serum levels of alkaline phosphatase and total bilirubin were significantly higher in the MBO group. The MBO group had a significantly higher percentage of severe AC (33.9% vs 22.0%, P = 0.045) and received ERCP later (median, 92.5 h vs 47.4 h, P < 0.001). However, the two differences were not found in the PSM analysis. The 30-d mortality (5.4% vs 0.7%, P = 0.019), ICU admission rates (12.5% vs 4.8%, P = 0.028), 30-d readmission rates (23.2% vs 8.0%, P < 0.001), and LOHS (median, 16.5 d vs 7.0 d, P < 0.001) were significantly higher or longer in the MBO group. However, only LOHS remained significant in the PSM analysis. Multivariate analysis revealed that time to ERCP and multiple organ dysfunction were independent factors associated with 30-d mortality. CONCLUSION: MBO patients underwent ERCP later and thus had a worse prognosis than CBDS patients. Therefore, clinicians should remain vigilant in MBO patients with clinically suspected AC, and perform ERCP for biliary drainage as soon as possible.
RESUMO
Concurrent hepatitis B virus (HBV) and hepatitis C virus (HCV) infection is not uncommon as the two viruses shared the similar transmission routes. HCV is usually the dominant virus to suppress HBV, and HBV reactivation may occur during or after the course of anti-HCV treatment. By contrast, HCV reactivation after anti-HBV therapy in the concurrent HBV- and HCV-infected patients was rarely noted. Here, we reported the unusual viral evolutions of a patient with concurrent HBV and HCV infection, in whom HCV reactivation occurred during the entecavir therapy to rescue the severe HBV flare, while the following anti-HCV combination therapy with pegylated interferon and ribavirin elicited the second HBV flare despite sustained virological response to HCV infection, and further entecavir therapy healed the flare.
RESUMO
Background and Aims: Whether hepatitis C virus (HCV) reactivation occurs and how the viral load evolves in anti-HCV antibody-positive chronic hepatitis B (CHB) patients who underwent nucleos(t)ide analogue (Nuc) therapies remain unsolved. Methods: A cohort of 66 such patients was studied. Results: At the start of Nuc treatment (baseline), all patients had detectable hepatitis B virus (HBV) DNA levels (6.05 ± 1.88 log IU/mL), while HCV RNA levels (3.79 ± 1.43 log IU/mL) were detected (i.e., chronic hepatitis C (CHC)) in only 13 patients (19.7%). Following Nuc therapies, HBV DNA levels reached the nadirs at end of therapy (EOT) (6.05 ± 1.88 vs. 0.25 ± 0.99 log IU/mL, p < 0.0001) and relapsed at 6 months after EOT (6mEOT) at a level of 3.45 ± 2.64 log IU/mL compared with EOT (p < 0.0001). Among the 13 CHC patients, a non-significant decrease in HCV RNA was noted at EOT (3.52 ± 1.71 vs. 2.77 ± 2.63 log IU/mL, p = 0.166) but tended to decrease further at 6mEOT (2.77 ± 2.63 vs. 1.89 ± 2.06 log IU/mL, p = 0.063). Two of the thirteen CHC patients showed an increase in HCV-RNA ≥ 1 log10 IU/mL at EOT, and one of the fifty-three patients with undetectable HCV RNA at baseline (i.e., resolved past HCV infection) showed detectable HCV RNA at year 1 (3200 IU/mL) and year 2 (1240 IU/mL) following entecavir therapy. Conclusions: HCV reactivation did occur during HBV suppression, and the rate was 4.5% (3/66), 15.4% (2/13), and 1.9% (1/53), for all patients, CHC patients, and patients with resolved past HCV infection, respectively. The reverse HBV and HCV viral evolutions at 6mEOT indicate that HBV relapse may suppress HCV replication again.
