Molecular Mimicry and Primary Biliary Cirrhosis: Premises Not Promises

Risk Factors and Comorbidities in Primary Biliary Cirrhosis: A Controlled Interview-Based Study of 1032 Patients *

“…This finding supports the hypothesis that infectious agents may break immunological tolerance in PBC. 26 Similarly, the increased prevalence and frequency of vaginal infections among female cases and the higher rate of tonsillectomy in all patients with PBC also support this hypothesis. Notably, the history for UTIs or vaginal infections reported by participants was not confirmed with laboratory data, perhaps because UTIs are often asymptomatic or minimally symptomatic, especially in women.…”

“…The model for sociodemographic and clinical candidate variables included sex, education level, body mass index (BMI) at age 25 (grouped as "high" [Ͼ30], "medium" [25][26][27][28][29][30], and "low" [Ͼ25]), indicators for whether the person had at least one vaccination (for chickenpox, hepatitis A, hepatitis B, diphteria-pertussis-tetanus, rubella, mumps, polio, small pox, or tuberculosis) and whether the person had had at least one urogenital condition (including pelvic or vaginal infection in women or any urinary tract infection in both sexes). Additionally, the following were considered to be possible explanatory variables: at least one first-degree family member (parent, sibling, or offspring) having PBC, systemic lupus erythematosus (SLE), arthritis, multiple sclerosis, Raynaud syndrome, Sjögren syndrome, scleroderma, polymyositis, autoimmune thyroid disease, or diabetes mellitus.…”

Experimental evidence on the immunopathogenesis of primary biliary cirrhosis

“…34,35 Epidemiological and experimental evidence, as well as animal models, supports the key role of environmental factors and, in particular, xenobiotics in the development of PBC.…”

Editorial: Recurrent primary biliary cirrhosis

“…However, features that make such a classification less satisfactory include a poor response to immunosuppression, no close association with the HLA phenotype associated with autoimmunity (HLA A1, B8 DR3), and no similar disease reported in children. Some 10 have suggested that PBC is triggered by an external factor (infectious or xenobiotic) that may either trigger an autoimmune process or, in some cases, e.g., hepatitis C viral infection or drug reactions, be associated with autoimmune phenomena. In immune-mediated drug reactions, the immune response is usually directed against the major drugmetabolizing enzyme (such as 1 of the family of cytochrome enzymes); in some autoimmune conditions associated with infection, molecular mimicry may be important.…”