Patients With Inflammatory Bowel Diseases Have Impaired Antibody Production After Anti-SARS-CoV-2 Vaccination: Results From a Panhellenic Registry.

BACKGROUND: Four EMA-approved vaccines against SARS-CoV-2 are currently available. Data regarding antibody responses to initial vaccination regimens in patients with inflammatory bowel diseases (IBD) are limited. METHODS: We conducted a prospective, controlled, multicenter study in tertiary Greek IBD centers. Participating patients had completed the initial vaccination regimens (1 or 2 doses, depending on the type of COVID-19 vaccine) at least 2 weeks before study enrolment. Anti-S1 IgG antibody levels were measured. Demographic and adverse events data were collected. RESULTS: We tested 403 patients (Crohn's disease, 58.9%; male, 53.4%; median age, 45 years) and 124 healthy controls (HCs). Following full vaccination, 98% of patients seroconverted, with mRNA vaccines inducing higher seroconversion rates than viral vector vaccines (P = .021). In total, IBD patients had lower anti-S1 levels than HCs (P < .001). In the multivariate analysis, viral vector vaccines (P < .001), longer time to antibody testing (P < .001), anti-TNFα treatment (P = .013), and age (P = .016) were independently associated with lower anti-S1 titers. Vedolizumab monotherapy was associated with higher antibody levels than anti-TNFα or anti-interleukin-12/IL-23 monotherapy (P = .023 and P = .032). All anti- SARS-CoV-2 vaccines were safe. CONCLUSIONS: Patients with IBD have impaired antibody responses to anti-SARS-CoV-2 vaccination, particularly those receiving viral vector vaccines and those on anti-TNFα treatment. Older age also hampers antibody production after vaccination. For those low-response groups, administration of accelerated or prioritized booster vaccination may be considered.

Thisis a multicenter study on IBD patients after COVID-19 vaccination and anti-S1 IgG antibody levels measurement. Patients with IBD have lower antibody responses than healthy controls, particularly those receiving viral vector vaccines and those on anti-TNFα or combination treatment.

Frequency and predictors of no treatment in anti-hepatitis C virus-positive patients at tertiary liver centers in Greece.

BACKGROUND/AIMS: Despite the improving efficacy of antiviral therapy, a significant proportion of chronic hepatitis C patients never start treatment. We determined the magnitude and reasons for no treatment in anti-hepatitis C virus (HCV)-positive patients visiting tertiary liver centers in Greece. MATERIALS AND METHODS: We retrospectively enrolled 1146 consecutive anti-HCV-positive patients who visited four physicians at two tertiary liver centers between 2002 and 2010. RESULTS: Treatment was initiated in 628 (55%) of the 1146 patients. In particular, 309 (27%) patients were lost to follow-up before HCV RNA testing. Independent predictors of no HCV RNA testing were first visit before 2007, parenteral drug use, and the treating physician. Of the 837 patients tested for HCV RNA, 768 (92%) were eligible for antiviral therapy, had detectable serum HCV RNA, and no contraindication to treatment. Among them, 140 (18%) patients were lost to follow-up before the initiation of treatment or refused antiviral therapy. Independent predictors of no treatment were the treating physician, absence of liver biopsy or transient elastography (odds ratio: 3.5, 95% confidence interval: 2.3-5.4, P<0.001), and normal compared with elevated alanine transaminase levels (odds ratio: 1.7, 95% confidence interval: 1.1-2.8, P=0.027). CONCLUSION: A significant proportion (>40%) of anti-HCV-positive patients visiting Greek tertiary liver centers do not receive antiviral therapy. Most of them are lost during the initial evaluation process, whereas the majority (>80%) of eligible patients who complete the initial evaluation eventually start antiviral therapy. The probability of treatment seems to be significantly associated with the treating physician, the alanine transaminase levels, and whether liver biopsy or transient elastography was performed.

An assessment of serum leptin levels in patients with chronic viral hepatitis: a prospective study.

BACKGROUND: The role of leptin in the course of liver disease due to chronic viral hepatitis (CVH) remains controversial. Our aims were to investigate the relationship between serum leptin concentrations and the severity of liver disease in a cohort of subjects with HBeAg negative chronic hepatitis B (CHB) and C (CHC) and to analyze the effect of body composition, the leptin system and insulin resistance together with viral factors on virologic response to antiviral treatment. METHODS: We studied 50 (36 men) consecutive patients suffering from biopsy-proven CVH due to HBV (n = 25) or HCV (n = 25) infection. Thirty-two (17 men) healthy volunteers served as controls. Levels of serum leptin and insulin were determined by immunoassays at baseline and at the end of the treatment. RESULTS: A significant association between serum leptin levels and the stage of hepatic fibrosis was noted; patients with cirrhosis presented higher serum leptin levels compared to those with lower fibrosis stage [CHB patients (17436 pg/ml vs 6028.5 pg/ml, p = 0.03), CHC patients (18014 pg/ml vs 4385 pg/ml, p = 0.05]. An inverse correlation between lower leptin levels and response to lamivudine monotherapy was noted in patients with CHB; those with a virologic response presented lower serum leptin levels (5334 vs 13111.5 pg/ml; p-value = 0.003) than non-responders. In genotype 1 CHC patients, insulin resistance played a significant role in the response to antiviral therapy. CONCLUSION: Our data clearly suggest that cirrhosis due to CHB or CHC is associated with higher leptin levels. Increased serum leptin levels represent a negative prognostic factor for response to lamivudine monotherapy in patients with CHB. In CHC patients insulin resistance strongly influences the response to antiviral treatment in patients infected with genotype 1.