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Albert J Czaja

Publications and source records attributed to Albert J Czaja.

At least 19 recordsLinked to original sources
PubMed2007

Autoimmune liver disease and rheumatic manifestations.

PURPOSE OF REVIEW: To review studies that clarify the rheumatic manifestations of autoimmune hepatitis, elucidate shared pathogenic pathways, and encourage innovative site-specific therapies. RECENT FINDINGS: Autoimmune hepatitis has clinical manifestations, serological markers, pathogenic mechanisms, genetic predispositions, and therapies similar to the rheumatic diseases. The rheumatic manifestations may mask the underlying liver disease and vice versa. Variations in clinical phenotype and outcome for the autoimmune liver diseases may reflect host-specific and region-specific factors, and defects in counter-regulatory suppressor functions by regulatory T cells may facilitate cell-mediated cytotoxicity and autoreactivity. Mixed syndromes with hallmark features of one disease in another probably reflect a genetic predisposition for immune expression that is shared among the diseases. Mycophenolate mofetil, budesonide, rapamycin, and 6-thioguanine are promising treatments, and de-novo autoimmune hepatitis after liver transplantation suggests that the calcineurin inhibitors may have paradoxical effects on self-tolerance. SUMMARY: Clinical phenotypes of autoimmune hepatitis commonly include rheumatic manifestations that can mask the liver disease. Defects in counter-regulatory functions enhance cell-mediated cytotoxicity, and pharmacological interventions that promise site-specific actions affecting immunocyte differentiation and proliferation are feasible.

Autoantibodies↗
PubMed2006

Evidence of a genetic basis for the different geographic occurrences of liver/kidney microsomal antibody type 1 in hepatitis C.

Antibodies to liver/kidney microsome type 1 occur in Italian patients with hepatitis C, but rarely develop in North American patients. Our goals were to compare the frequencies of the HLA markers associated with autoimmune expression in Italian and North American patients with chronic hepatitis C and to determine genetic bases for regional differences in antibody production. HLA B8, DR3, DR4, DR7, DR11, DR13, DQ2, and the B8-DR3-DQ2 haplotype were determined by microlymphocytotoxicity and polymerase chain reaction in 105 Italian patients (50 with microsomal antibodies), 100 North American patients (none with microsomal antibodies), and Italian and North American healthy control subjects. Italian patients with microsomal antibodies differed from North American patients without these antibodies by having a higher frequency of HLA DR7 (54% vs. 27%, P=0.002). HLA DR7 occurred more frequently in seropositive Italian patients than in seronegative counterparts (54% vs. 11% P < 0.0001), Italian healthy control subjects (54% vs. 29%, P=0.0009), and North American healthy control subjects (54% vs. 19%, P < 0.0001). The frequency of HLA DR7 was similar in North American patients and controls (27% vs. 19%, P=0.2), but it was lower than in Italian controls (19% vs. 29%, P=0.059). Seropositive Italian patients had a lower frequency of HLA DR11 than seronegative Italian patients and Italian controls (18% vs. 34%, P=0.07, and 18% vs. 35%, P=0.02, respectively). In contrast to seropositive Italian patients, North American patients had HLA DR4 (30% vs. 12%, P=0.02), HLA DR13 (29% vs. 10%, P=0.01), and the B8-DR3-DQ2 haplotype (23% vs. 6%, P=0.01) more often. Similarly, HLA DR4 and the B8-DR3-DQ2 phenotype were more frequent in North American patients than in Italian controls (30% vs. 16%, P=0.005, and 23% vs. 7%, P=0.00002, respectively). HLA DR7 is associated with the development of microsomal antibodies in Italian patients with chronic hepatitis C. The lower frequency of HLA DR7 in North America could contribute to the rarity of these antibodies in this region. HLA DR11 may be protective against the development of microsomal antibodies in Italian patients, whereas HLA DR4, HLA DR13, and the B8-DR3-DQ2 haplotype may be protective in North American patients.

Adult↗
PubMed2006

Thiopurine methyltransferase deficiency and azathioprine intolerance in autoimmune hepatitis.

Thiopurine methyltransferase deficiency has been associated with intolerance to azathioprine. Our goals were to assess the frequency of enzyme deficiency in autoimmune hepatitis and correlate deficiency states with azathioprine intolerance. Eighty-six patients receiving azathioprine (50-150 mg daily) were evaluated for enzyme activity and azathioprine-related complications. Their findings were compared to 89 similarly treated but untested patients. Thirteen patients (15%) had low thiopurine methyltransferase levels (11.4+/- 0.9 U/ml RBC; range, 3.5-14.9 U/ml RBC). Azathioprine intolerance occurred as commonly in patients with normal or above normal enzyme levels as in patients with below normal levels (12% versus 15%, p = 0.7). Patients treated without enzyme testing had the same frequency of complications (9% versus 13%, p = 0.5) as tested patients. We conclude that routine screening of blood thiopurine methyltransferase levels has a low yield for identifying individual patients at risk for azathioprine toxicity during conventional low dose therapy for autoimmune hepatitis.

Adult↗
PubMed2006

Autoimmune hepatitis--approach to diagnosis.

CONTEXT: Autoimmune hepatitis has diverse features that can delay its diagnosis and the institution of potentially lifesaving corticosteroid therapy. OBJECTIVE: Review the clinical, laboratory, and histologic features of autoimmune hepatitis and promulgate routine application of its codified diagnostic criteria. DATA SOURCES: Reference lists and MEDLINE. STUDY SELECTION: All clinically pertinent published observations that indicate the diversity of manifestations and pitfalls in diagnosis. DATA EXTRACTION: Findings that had common clinical relevance and the potential to confuse the diagnosis or delay institution of therapy were selected. DATA SYNTHESIS: Autoimmune hepatitis can present acutely and have histologic features of centrilobular zone 3 inflammation. Many patients may be asymptomatic, but they frequently have severe or advanced disease and typically develop symptoms later. Autoantibodies are reflective of immune-mediated mechanisms, but they are not diagnostic, pathogenic, or even required for the diagnosis. Genetic factors affect susceptibility, clinical phenotype, and treatment outcome, and they may be clues to indigenous etiologic agents. Autoimmune hepatitis can recur or develop de novo after liver transplantation, and it should be considered in all transplanted patients with allograft dysfunction. Diagnostic criteria have been codified, and a scoring system quantifies the strength of the diagnosis and accommodates atypical or deficient features. CONCLUSION: Autoimmune hepatitis is an important diagnosis to consider in all patients with chronic hepatitis of undetermined cause.

Algorithms↗
PubMed2006

Distinctive clinical phenotype and treatment outcome of type 1 autoimmune hepatitis in the elderly.

Autoimmune hepatitis is classically a disease of young women. Our aims were to determine its occurrence, clinical phenotype, and outcome in elderly patients and contrast findings to young adults. Two-hundred-and-five white North American adults with definite type 1 autoimmune hepatitis were grouped according to age at presentation and the groups compared. Forty-seven patients (23%) were aged > or = 60 years (median age, 68 years), and 31 patients (15%) were aged < or = 30 years (median age, 25 years). The patients > or = 60 years had a higher frequency of cirrhosis at presentation than the patients < or = 30 years (33% versus 10%, P = .03). They also had thyroid or rheumatic diseases more commonly (42% vs. 13%, P = .006). HLA DR3 occurred more frequently in the patients < or = 30 years than in those > or = 60 years (58% vs. 23%, P = .004), and HLA DR4 occurred more often in the patients > or = 60 years (47% vs. 13%, P = .003). Patients aged > or = 60 years failed corticosteroid treatment less commonly than those aged < or = 30 years (5% vs. 24%, P = .03). Autoimmune hepatitis occurred in patients aged 18-30 years (15%), 31-39 years (15%), 40-49 years (21%), 50-59 years (25%), and > or = 60 years (23%). Differences in age distribution, HLA frequencies, and treatment outcome occurred after age > or = 40 years. In conclusion, elderly patients have a greater frequency of cirrhosis at presentation and HLA DR4 than patients < or = 30 years, and they have a lower occurrence of treatment failure. Transitions in clinical and genetic phenotypes occur after age > or = 40 years. Genetic susceptibilities may favor etiologic factors that are age-related.

Adolescent↗
PubMed2006

Frequency and significance of antibodies to cyclic citrullinated peptide in type 1 autoimmune hepatitis.

OBJECTIVES: Determine the frequency, clinical phenotype, and prognostic implications of antibodies against cyclic citrullinated peptides in patients with type 1 autoimmune hepatitis. METHODS: Three hundred and ninety-five serum samples from 179 patients were tested by enzyme-linked immunosorbent assay, and findings correlated with clinical and histological features, frequency of HLA DR3 and DR4, and treatment outcome. RESULTS: Twenty patients (11%) had antibodies against cyclic citrullinated peptides. Seropositivity was associated with a higher frequency of rheumatoid arthritis (RA) (25 vs. 0%, P < 0.001). Patients with antibodies against cyclic citrullinated peptides also had a significantly greater occurrence of histological cirrhosis at presentation (47 vs. 20%, P = 0.01) and death from hepatic failure than seronegative patients (25 vs. 9%, P = 0.04). Cirrhosis at presentation occurred more commonly in the patients with antibodies against cyclic citrullinated peptides and RA than in the other patients (100 vs. 21%, P = 0.005). CONCLUSIONS: Antibodies against cyclic citrullinated peptides occur in a subgroup of patients with type 1 autoimmune hepatitis who have a greater occurrence of cirrhosis at presentation and death from hepatic failure. Their presence with RA at accession characterizes a subgroup with cirrhosis.

Adolescent↗
PubMed2006

Autoimmune liver disease.

PURPOSE OF REVIEW: To review studies that improve the diagnosis and treatment of autoimmune hepatitis and presage new drug and molecular site-specific interventions. RECENT FINDINGS: Autoimmune hepatitis can present as acute or chronic hepatitis and as allograft dysfunction after liver transplantation. Elderly patients have an indolent but aggressive disease that responds well to corticosteroid therapy, and human leukocyte antigen DR4 characterizes this population. Geographic and ethnic factors influence clinical phenotype and behavior, and defects in T-regulatory cells may enhance cell-mediated cytotoxicity. Treatment response is the best index of prognosis, and normalization of serum aminotransferase abnormalities prevents disease progression. Mycophenolate mofetil, budesonide, rapamycin, and 6-thioguanine have been effective in small clinical experiences. De-novo autoimmune hepatitis can occur in adults and children after liver transplantation, and rapamycin may be an effective treatment. SUMMARY: Autoimmune hepatitis has a global distribution and diverse clinical manifestations. Phenotypes are affected by regional and ethnic factors which may provide clues to the etiologic agents. Defects in counter-regulatory functions enhance cell-mediated cytotoxicity, and interventions that promise site-specific actions affecting immunocyte differentiation and proliferation are now feasible. Autoimmune hepatitis must be considered in all patients with acute and chronic hepatitis and in all cases of allograft dysfunction after liver transplantation.

Autoantibodies↗
PubMed2006

Clinical and HLA phenotypes of type 1 autoimmune hepatitis in North American patients outside DR3 and DR4.

AIMS: To determine the clinical phenotype and outcome of patients with definite type 1 autoimmune hepatitis, who lack human leukocyte antigen (HLA) DR3 and DR4, and to assess the importance of HLA DR7 and DR13. METHODS: Two hundred and seven adult patients were typed for DR3, DR4, DR7, and DR13 by DNA-based techniques. One hundred and two blood donors constituted a normal population. RESULTS: Twenty-six patients lacked DR3 and DR4 (13%). Treatment failure occurred more commonly in these individuals than in the 68 patients with DR4 (20% vs. 3%, P = 0.03), and relapse after drug withdrawal was less frequent than in the 84 patients with DR3 (55% vs. 87%, P = 0.03). HLA DR13 occurred more often than in those with DR3 (54% vs. 15%, P = 0.0002) or DR4 (54% vs. 12%, P = 0.00005), and it was more frequent than in normal adults (54% vs. 22%, P = 0.003), including those without DR3 or DR4 (54% vs. 27%, P = 0.03). HLA DR7 was not associated with susceptibility or outcome. CONCLUSIONS: White North American patients who lack DR3 and DR4 respond differently to corticosteroid treatment than patients with classical HLA phenotypes. HLA DR13 is common in these adult patients, and it may affect treatment outcome.

Adrenal Cortex Hormones↗
PubMed2006

Clinical significance of HLA DRB103-DRB104 in type 1 autoimmune hepatitis.

BACKGROUND: HLA DRB1*03-DRB1*04 combines both susceptibility factors for type-1 autoimmune hepatitis. AIMS: Determine whether this phenotype is a risk factor for autoimmune hepatitis in white North American patients, assess its associations with clinical features and treatment outcome, and determine whether alleles within this phenotype affect prognosis. METHODS: One hundred and ninety-eight patients with type 1 autoimmune hepatitis and 102 normal adults were evaluated. HLA typing was performed by DNA-based techniques. RESULTS: Twenty-eight patients had HLA DRB1*03-DRB1*04, and the frequency was higher than in normal subjects (14% vs 4%, OR 4.0%, 95% CI 1.4-11.8, P = 0.01). Patients with DRB1*03-DRB1*04 relapsed less frequently than patients with DRB1*03 (1.3 +/- 0.3 vs 2.1 +/- 0.2, P = 0.04), but they otherwise had outcomes similar to patients with other phenotypes. Patients with DRB1*03-DRB1*04 who had 3-4 alleles encoding lysine at position DRbeta71 within the class II molecule of the major histocompatibility complex developed cirrhosis more commonly (75% vs 9%, P = 0.05) and had a higher frequency of hepatic-related death or liver transplantation (40% vs 0%, P = 0.04) than patients with fewer alleles. CONCLUSIONS: HLA DRB1*03-DRB1*04 is a risk factor for type-1 autoimmune hepatitis, and its impact on outcome relates to the diversity of DRB1*04 alleles that encode a critical motif.

Adolescent↗
PubMed2005

Treatment challenges and investigational opportunities in autoimmune hepatitis.

New drugs and advances in molecular biology afford opportunities to upgrade the treatment of autoimmune hepatitis. The aims of this study were to define treatment problems, identify possible solutions, and stimulate investigations to improve patient care. A clinical subcommittee of the International Autoimmune Hepatitis Group reviewed current management difficulties and proposed corrective actions. The assessment of new front-line and salvage therapies for adults and children were given top priority. Cyclosporine and mycophenolate mofetil were endorsed as drugs worthy of rigorous study in severe disease, and budesonide was endorsed for study as front-line therapy in mild disease. Diagnostic criteria and treatment regimens for children required codification, and pharmacokinetic studies were encouraged to develop optimal dosing schedules based on therapeutic ranges. Collaborative efforts were proposed to help understand racial, geographical, and genetic factors affecting outcome and to establish definitions and therapies for variant syndromes and graft dysfunction after transplantation. The development of experimental animal models was deemed essential for the study of site-specific molecular interventions, and gene therapy was endorsed as a means of bolstering reparative processes. In conclusion, evolving pharmacological and technical advances promise to improve the treatment of autoimmune hepatitis, and investigations of these advances are timely, feasible, and necessary.

Gastroenterology↗
PubMed2005

Autoantibodies in autoimmune liver disease.

Autoantibodies indicate an immune reactive state, but in liver disease they lack pathogenicity and disease specificity. Antinuclear antibodies, smooth muscle antibodies, antibodies to liver/kidney microsome type 1, antimitochondrial antibodies, and perinuclear antineutrophil cytoplasmic antibodies constitute the standard serological repertoire that should be assessed in all liver diseases of undetermined cause. Antibodies to soluble liver antigen/liver pancreas, asialoglycoprotein receptor, actin, liver cytosol type 1, nuclear antigens specific to primary biliary cirrhosis, and pore complex antigens constitute an investigational repertoire that promises to have prognostic and diagnostic value. These autoantibodies may emerge as predictors of treatment response and outcome. Antibodies to histones, doubled-stranded DNA, chromatin, and lactoferrin constitute a supplemental repertoire, and they support the immune nature of the liver disease. Final diagnoses and treatment strategies do not depend solely on serological markers. Autoantibodies are floating variables, and their behavior does not correlate closely with disease activity. There are no minimum levels of significant seropositivity, especially in children. Over-interpretation is the major pitfall in the clinical application of the serological results. New autoantibodies will emerge as the search for target antigens and key pathogenic pathways continues.

Autoantibodies↗
PubMed2005

Empiric therapy of autoimmune hepatitis with mycophenolate mofetil: comparison with conventional treatment for refractory disease.

GOAL: To assess the outcomes of empiric therapy with mycophenolate mofetil in patients with autoimmune hepatitis. BACKGROUND: Mycophenolate mofetil is a purine antagonist that selectively inhibits immunocyte proliferation, and its empiric use in autoimmune hepatitis has been stimulated by small clinical experiences. STUDY: Eight patients received mycophenolate mofetil (0.5-3 g daily) for 19 +/- 7 months as frontline therapy or after adverse responses to conventional corticosteroid treatment. Seventeen patients who had been treated with high-dose corticosteroid regimens after treatment failure constituted a historical comparison population. RESULTS: Five of the 8 patients receiving mycophenolate mofetil and all 17 patients who had been treated with the conventional corticosteroid regimens for treatment failure responded to therapy. The frequency of response (62% vs. 100%, P = 0.02) was lower during longer intervals of treatment (19 +/- 7 months vs. 6 +/- 1 months, P = 0.02) in the patients receiving mycophenolate mofetil. None receiving mycophenolate mofetil resolved their laboratory abnormalities, whereas 6 patients in the comparison group improved to normal tests (0% vs. 35%, P = 0.1). Histologic resolution did not occur in 4 patients sampled during treatment, and successive specimens in 2 patients showed progressive fibrosis. Corticosteroids could not be withdrawn in the patients treated with mycophenolate mofetil, whereas discontinuation was possible in 7 patients in the comparison group (0% vs. 41%, P = 0.06). CONCLUSIONS: Mycophenolate mofetil did not induce laboratory resolution, prevent progressive fibrosis, or allow corticosteroid withdrawal. Clinical trials are needed to evaluate its role and target population.

Adrenal Cortex Hormones↗
PubMed2005

Autoimmune liver disease.

PURPOSE OF REVIEW: This review aims to demonstrate how recent insights into disease behavior and mechanisms and the availability of new drugs can be assimilated into evolving concepts of diagnosis and treatment. RECENT FINDINGS: Autoimmune hepatitis has a global distribution, and its clinical manifestations are similar in different regions. Concurrent immune diseases are common, and immunoglobulin A nephropathy may explain ascites in some patients. Subclinical celiac disease can cause cryptic liver dysfunction or be associated with autoimmune hepatitis. A fulminant presentation that is associated with de novo rather than exacerbated pre-existent disease is possible, and these patients may have centrilobular zone 3 necrosis. Bile duct injury as a background histologic finding should not change the diagnosis or therapy, and the clinical significance of autoantibodies can be determined only by examination of liver biopsy tissue. Molecular mimicry may be important in breaking self-tolerance, and a murine model based on DNA immunization with self-antigens supports this hypothesis. Corticosteroid therapy reduces or prevents hepatic fibrosis, and noninvasive techniques promise to facilitate the development of treatments that enhance this effect. Mycophenolate mofetil is a possible salvage therapy that requires clinical trial, and liver transplantation has a 5-year patient survival of 78% but is frequently followed by recurrent disease and acute rejection. SUMMARY: Autoimmune hepatitis should be considered in all patients with acute or chronic liver disease. Therapy can reduce or prevent fibrosis. The new immunosuppressive drugs should undergo clinical trial before empiric use. Animal models promise to identify key pathogenic sites that can be targeted by therapies.

Hepatitis, Autoimmune↗
PubMed2005

Anti-tRNP(ser)sec/SLA/LP autoantibodies. Comparative study using in-house ELISA with a recombinant 48.8 kDa protein, immunoblot, and analysis of immunoprecipitated RNAs.

BACKGROUND: Antibodies against tRNP((ser)sec) (ribonucleoproteins, RNP) have been described in our laboratory as markers of poor outcome in type 1 autoimmune hepatitis (AIH). The antigenic protein has been sequenced and cloned as a 48.8 kDa protein and identified with soluble liver antigen (SLA) and liver-pancreas (LP) antigen. The aim of this paper was to determine the best assay by which to detect these antibodies in type 1 AIH. METHODS: A simple and reliable enzyme linked immunoassay based on prokaryotically expressed protein was compared with an immunoblot assay using prokaryotically- and eukaryotically-expressed proteins and an assay based on immunoprecipitated RNAs from HeLa cell extracts. Eighty-one sera from 58 patients with type 1 AIH, 168 sera from patients with autoimmune diseases or chronic hepatitis C, and 60 sera from healthy subjects were similarly tested. RESULTS: The specificity of the assays was 100%, but the frequency of seropositivity was higher in the assay based on immunoprecipitated RNAs (44.4%) than in the enzyme-linked immunosorbent assay (ELISA) (16%) and the immunoblot assay with prokaryotically (12.34%) and eukaryotically (14.8%)-expressed protein. There were no clinical differences between the patients positive by ELISA, immunoblot assay, or immunoprecipitated RNAs. CONCLUSIONS: These results suggest that the analysis of the immunoprecipitated RNAs is the most useful, sensitive and specific method to detect anti-tRNP((ser)sec)/SLA/LP autoantibodies.

Autoantibodies↗
PubMed2004

Progressive fibrosis during corticosteroid therapy of autoimmune hepatitis.

Hepatic fibrosis and cirrhosis are possible consequences of corticosteroid-treated autoimmune hepatitis. Our aims were to determine the frequency of progressive fibrosis and the factors associated with this progression. Two hundred seventy-seven liver tissue specimens that had been obtained from 73 patients were interpreted in batch under code by a single pathologist. Fibrosis scores and histological activity indices were determined using the Ishak scoring system, and worsening fibrosis scores were correlated with clinical features, laboratory findings, and treatment responses. Fibrosis scores increased (2.3 +/- 0.4 points to 4.2 +/- 0.4 points; P <.0001) in 18 patients (25%) during 79 +/- 13 months. Only five patients (7%) developed cirrhosis, and 55 patients (75%) had stable (16 patients) or decreased (39 patients) fibrosis scores. Human leukocyte antigen (HLA) DR3/DR4 occurred more frequently in patients with progressive fibrosis than others (23% vs. 2%; P =.03). Patients with progressive fibrosis had higher histological activity indices at last follow-up than patients with stable or reduced fibrosis (3.2 +/- 0.7 vs. 1.7 +/- 0.2; P =.01), and these indices worsened more commonly during therapy (17% vs. 2%, P =.04). Relapse, treatment failure, and incomplete response did not affect progression of fibrosis. In conclusion, fibrosis progresses in only a minority of patients during corticosteroid therapy. Progression is associated with HLA DR3/DR4 and worsening histological activity. Exacerbations or persistence of disease activity does not increase disease progression after treatment has been instituted.

Disease Progression↗
PubMed2004

Decreased fibrosis during corticosteroid therapy of autoimmune hepatitis.

BACKGROUND/AIMS: Reduction in hepatic fibrosis and reversibility of cirrhosis has been described in chronic liver disease. Our goal was to determine changes in fibrosis and the frequency of histological cirrhosis in corticosteroid-treated autoimmune hepatitis (AIH). METHODS: Three hundred twenty-five liver specimens from 87 treated patients were reviewed in batch under code by one pathologist and graded by the Ishak method. RESULTS: Fibrosis scores improved (3.4+/-0.2 versus 2.6+/-0.2, P=0.0002) during 63+/-6 months, and histological activity indices decreased concurrently (6.8+/-0.5 versus 2.1+/-0.2, P<0.0001). Fibrosis scores improved in 46 patients (53%) during 57+/-7 months and did not progress in 23 patients during 62+/-12 months. The fibrosis score improved more commonly in patients who had improvement in the histological activity indices than in others (61 versus 32%, P=0.02), and the frequency of histological cirrhosis decreased from 16% (14 patients) to 11% (10 patients). CONCLUSIONS: Fibrosis commonly improves or does not progress during corticosteroid therapy of AIH, and histological cirrhosis may disappear. Improvements in fibrosis are associated with suppression of inflammatory activity. Improvement or prevention of fibrosis may be a common but unheralded advantage of corticosteroid therapy.

Adrenal Cortex Hormones↗
PubMed2004

Frequency and significance of antibodies to Saccharomyces cerevisiae in autoimmune hepatitis.

Our aims were to determine the frequency of antibodies to Saccharomyces cerevisiae in autoimmune hepatitis and assess associations with concurrent mucosal diseases, genetic factors, and corticosteroid response. Seropositivity was determined by enzyme immunoassay in 385 samples obtained from 178 patients. Antibodies to Saccharomyces cerevisiae were detected in 49 patients (28%), and serum levels of immunoglobulin A were higher in seropositive patients (410 +/- 35 versus 321 +/- 20 mg/dL; P = 0.02). Individuals with and without antibodies were not otherwise distinguished by concurrent mucosal diseases, laboratory findings, or outcomes. Antibodies to tissue transglutaminase occurred more commonly in seropositive patients (16 versus 4%; P = 0.008), but this association was lost when corroborating serological criteria for celiac disease were sought. We conclude that antibodies to Saccharomyces cerevisiae are common in autoimmune hepatitis. They may be associated with non-disease-specific immune responses, but they do not define individuals with a distinctive clinical phenotype, associated mucosal diseases, or treatment outcome.

Adolescent↗