Patients with chronic hepatitis C have both higher prevalence of diabetes mellitus type 2 (T2DM) and increased cardiovascular risk compared to never infected people. Sustained viral response (SVR) achievement led to decreasing incidence and prevalence of T2DM during the interferon era of HCV treatment. Currently, direct-acting antiviral drugs (DAA) are the gold standard for treating HCV infection, while yielding SVR in nearly all patients. In chronic HCV patients with T2DM (prediabetes most likely too), DAA therapy is associated with both better fasting glucose and glycated hemoglobin (HbA1C) controls; thus reducing pharmacotherapy in a certain part of patients is possible. Papers mentioned in the review confirmed DAA role in both total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) increase. This alteration was accompanied by an increase in high-density lipoprotein cholesterol (HDL-C) and a decrease in triglycerides (TG) verified by most of the studies. However, the clinical significance of lipoprotein alterations caused by DAA therapy has not been explained yet. Moreover, DAA treatment of chronic hepatitis C improves hypertension control and atherosclerotic plaques. It is very likely that DAA therapeutic regimens will decrease both T2DM prevalence and cardiovascular risk in chronic hepatitis C patients; further research, however, is needed.

Background. Primary biliary cholangitis (PBC) is a chronic autoimmune cholestatic liver disease with wide ranges of reported incidence and prevalence. Aim. To map the incidence and prevalence of PBC in European countries from 2000 through 2020. Methods. Following PRISMA recommendations, we searched the Medline and Scopus databases for studies with information on either the incidence or prevalence of PBC. After data extraction, we used a random-effects model to estimate both the pooled annual incidence rate and pooled point-prevalence rate and performed subgroup analyses to identify components contributing to between-study heterogeneity. Results. We performed a qualitative and quantitative analysis of 18 studies. The pooled point-prevalence rate was 22.27 cases per 100,000 inhabitants (95% CI: 17.98–27.01), and the pooled annual incidence rate was 1.87 new cases per 100,000 inhabitants (95% CI: 1.46–2.34). In the subgroup analyses, we proved that a small part of the between-study heterogeneity is significantly associated with a history of being part of the Eastern Bloc.

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IgG4-related sclerosing cholangitis, a biliary manifestation of an IgG4-related disease, belongs to the spectrum of sclerosing cholangiopathies which result in biliary stenosis. It presents with signs of cholestasis and during differential diagnosis it should be distinguished from cholangiocarcinoma or from other forms of sclerosing cholangitis (primary and secondary sclerosing cholangitis). Despite increasing information and recently established diagnostic criteria, IgG4-related sclerosing cholangitis remains underdiagnosed in routine clinical practice. The diagnosis is based on a combination of the clinical picture, laboratory parameters, histological findings, and a cholangiogram. Increased serum IgG4 levels are nonspecific but are indeed a part of the diagnostic criteria proposed by the Japan Biliary Association and the HISORt criteria for IgG4-SC. High serum IgG4 retains clinical utility depending on the magnitude of elevation. Approximately 90% of patients have concomitant autoimmune pancreatitis, while 10% present with isolated biliary involvement only. About 26% of patients have other organ involvement, such as IgG4-related dacryoadenitis/sialadenitis, IgG4-related retroperitoneal fibrosis, or IgG4-related renal lesions. A full-blown histological finding characterized by IgG4-enriched lymphoplasmacytic infiltrates, obliterative phlebitis, and storiform fibrosis is difficult to capture in practice because of its subepithelial localization. However, the histological yield is increased by immunohistochemistry, with evidence of IgG4-positive plasma cells. Based on a cholangiogram, IgG-4 related sclerosing cholangitis is classified into four subtypes according to the localization of stenoses. The first-line treatment is corticosteroids. The aim of the initial treatment is to induce clinical and laboratory remission and cholangiogram normalization. Even though 30% of patients have a recurrent course, in the literature data, there is no consensus on chronic immunosuppressive maintenance therapy. The disease has a good prognosis when diagnosed early.

Objective: To identify pretreatment laboratory parameters associated with treatment response and to describe the relationship between treatment response and liver decompensation in patients with primary biliary cholangitis treated with ursodeoxycholic acid. Methods: We defined treatment response as both ALP ≤ 1.67 × ULN and total bilirubin ≤ 2 × ULN. Multiple logistic regression analyses were performed to adjust for confounding effects of sociodemographic variables. Results: Pretreatment total bilirubin ((TB); OR = 0.3388, 95%CI = 0.1671–0.6077), ALT (OR = 0.5306, 95%CI = 0.3830–0.7080), AST (OR = 0.4065, 95%CI = 0.2690–0.5834), ALP (OR = 0.3440, 95%CI = 0.2356–0.4723), total cholesterol ((TC); OR = 0.7730, 95%CI = 0.6242–0.9271), APRI (OR = 0.3375, 95%CI = 0.1833–0.5774), as well as pretreatment albumin (OR = 1.1612, 95%CI = 1.0706–1.2688) and ALT/ALP (OR = 2.4596, 95%CI = 1.2095–5.5472) were associated with treatment response after six months of treatment. Pretreatment TB (OR = 0.2777, 95%CI = 0.1288–0.5228), ALT (OR = 0.5968, 95%CI = 0.4354–0.7963), AST (OR = 0.4161, 95%CI = 0.2736–0.6076), ALP (OR = 0.4676, 95%CI = 0.3487–0.6048), APRI (OR = 0.2838, 95%CI = 0.1433–0.5141), as well as pretreatment albumin (OR = 1.2359, 95%CI = 1.1257–1.3714) and platelet count (OR = 1.0056, 95%CI = 1.0011–1.0103) were associated with treatment response after 12 months of treatment. Treatment response after 6 months of UDCA therapy is significantly associated with treatment response after 12 months of UDCA therapy (OR = 25.2976, 95% CI = 10.5881–68.4917). Treatment responses after 6 and 12 months of UDCA therapy decrease the risk of an episode of liver decompensation in PBC patients (OR = 12.1156, 95%CI = 3.7192–54.4826 and OR = 21.6000, 95%CI = 6.6319–97.3840, respectively). Conclusions: There are several pretreatment laboratory parameters associated with treatment response in patients with primary biliary cholangitis. Treatment response after six months is significantly associated with treatment response after 12 months of ursodeoxycholic acid (UDCA) therapy. Treatment responses after 6 and 12 months of UDCA decrease the risk of an episode of liver decompensation.

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