Published online Mar 27, 2026. doi: 10.4254/wjh.v18.i3.117367
Revised: January 27, 2026
Accepted: February 13, 2026
Published online: March 27, 2026
Processing time: 111 Days and 4.5 Hours
Autoimmune liver diseases, including autoimmune hepatitis, primary biliary cholangitis, and primary sclerosing cholangitis, have traditionally been regarded as disorders of young or middle-aged adults. However, the progressive aging of the global population has revealed a substantial and increasing number of cases diagnosed at ever older ages. Older adults frequently present with atypical or non-specific symptoms, are more likely to be diagnosed at advanced stages, and often exhibit a distinct biochemical profile compared with younger patients. In particular, the recent study by Delgado et al underscores these differences in late-onset autoimmune hepatitis, demonstrating a higher rate advanced fibrosis at presentation and diagnostic delay in elderly individuals. This editorial aims to highlight these observations, as these characteristics create unique diagnostic challenges and may negatively influence long-term outcomes. Treatment remains effective with standard first-line regimens; however, therapeutic decisions must be carefully individualized due to comorbidities, polypharmacy, and an increased vulnerability to treatment-related adverse events. Recognizing age-specific clinical patterns and adapting management strategies accordingly is essential to optimize care in this growing and frequently overlooked patient population.
Core Tip: Autoimmune liver diseases are increasingly relevant in older adults, with changing epidemiology and rising incidence, including presentation peaks in this age group. Clinical manifestations range from unusual presentations, acute liver failure, and acute hepatitis to more common indolent forms with minimal symptoms. Serologic testing does not differ from younger patients, but due to comorbidities, liver biopsy remains essential. First-line treatment generally does not change and is often effective, although older adults are more vulnerable to steroid-related complications and polypharmacy. Liver transplantation remains an option. However, this population is still understudied, and future research should incorporate comprehensive geriatric assessment.
- Citation: Hernández-Almonacid PG, Espejo-Amado JS, Marín-Quintero X. Autoimmune liver diseases in older adults: Clinical challenges and management considerations. World J Hepatol 2026; 18(3): 117367
- URL: https://www.wjgnet.com/1948-5182/full/v18/i3/117367.htm
- DOI: https://dx.doi.org/10.4254/wjh.v18.i3.117367
This editorial refers to "Impact of age on autoimmune hepatitis: A comparative study of patients diagnosed before and after sixty" by Delgado et al, 2025; https://doi.org/10.4254/wjh.v17.i12.110312.
Autoimmune liver diseases (AILD) are a group of disorders characterized by immune-mediated responses directed against hepatocytes and cholangiocytes[1]. This group included patients with autoimmune hepatitis (AIH), primary biliary cholangitis (PBC), and primary sclerosing cholangitis (PSC). Recently, overlapping syndromes and immunoglobulin G4 (IgG4)-related cholangitis have been recognized as additional entities on this spectrum. These diseases were classically considered conditions in young or middle-aged adults. However, the diagnosis of AILD in individuals aged > 60 years has significantly increased[2].
Demographic shifts and population ageing are global phenomena. By 2030, one in six individuals worldwide will be aged ≥ 60 years[3]. Older adults constitute a distinct clinical group with different disease behaviors, therapeutic needs, and outcomes compared with younger patients. They often present with a more insidious yet aggressive course, con
Delgado et al[9] provided important insights by identifying key differences in AIH among older adults. These findings offer a timely basis for examining the clinical challenges of AILD in elderly patients and outline the management considerations required for this growing population (Figure 1).
The study by Delgado et al[9] is a single-center retrospective cohort of adult patients with biopsy-confirmed AIH and ≥ 1 year of clinical follow-up. This is one of the largest series of studies conducted in Latin America. By analyzing de
The final cohort included 97 patients, approximately 40% of whom were aged > 60 years, highlighting the growing burden of this disease in the aging population. Older adults have a higher prevalence of metabolic and cardiovascular comorbidities, a more silent presentation with fewer classical symptoms, and lower transaminase and bilirubin levels. Despite the attenuated clinical profiles, these patients frequently present with ascites and advanced fibrosis. Importantly, this greater baseline severity did not result in a poorer treatment response, as older adults achieved biochemical outcomes comparable to those of younger patients, despite lower initial corticosteroid doses[9].
Although this study has limitations related to its retrospective, single-center design, moderate sample size, short follow-up period, and absence of key geriatric measures such as polypharmacy and frailty, it offers notable strengths. Considering the scarcity of regional data, the study population is valuable, and the diagnostic rigor is reinforced by the inclusion of exclusively biopsy-confirmed cases.
Therefore, this study makes a meaningful contribution by emphasizing the clinical and diagnostic features of late-onset AIH. These findings highlight the need for increased diagnostic suspicion of indolent presentations, frequent presence of advanced fibrosis at diagnosis in older adults, and influence of comorbidities that complicate therapeutic decision-making and outcomes.
Reports on AILD in older adults are limited; however, recent systematic reviews have shown an increasing incidence of AILD in older age groups[2,10]. Globally, AIH has an incidence of 1.37 and prevalence of 17.4 per 100000 individuals[11]. For PBC, pooled estimates reported an incidence of 1.76 and prevalence of 14.60 per 100000 individuals[12]. PSC data are scarce, with one large study reporting an incidence of 0.9 per 100000 individuals[13]. Age-specific patterns consistently revealed that older adults were most affected. The peak incidence of PBC occurs between the ages of 60 years and 79 years[12], mirroring AIH, in which presentation is most common after 60 years of age[11]. Overall, these data indicate a shift toward late-onset disease, highlighting the growing impact of population aging on AILD epidemiology.
Aging is a dynamic process that affects the tissues and organs at varying rates. Although the liver is believed to undergo minimal age-related changes, age-associated cellular and morphological alterations can lead to functional decline[14]. Senile atrophy, driven by reduced regenerative capacity, results in a 24%-37% decrease in liver weight along with re
Immunosenescence refers to the functional and quantitative remodeling of innate and adaptive immune cell popu
The primary challenge in the timely diagnosis of AILD in older adults is the wide variability in the clinical and serological phenotypes across populations. A systematic review by Chen et al[18] found that older adults are more often asy
Although AIH often has an indolent course, older adults may present with severe acute disease, with either de novo inflammation or exacerbation of an unrecognized chronic disease. In some studies, 41%-71% of older patients presented acutely, a pattern easily mistaken for drug-induced hepatotoxicity considering the high burden of polypharmacy[21]. The unusual symptoms include painless jaundice[22,23], hepatic encephalopathy[24], and acute liver failure[25]. Atypical features of PBC in older adults include initially normal liver test results[26], gastric antral vascular ectasia[27], recurrent hypoglycemic coma[28], and hemorrhage from a cholesterol embolus in the polyp[29]. These observations indicate that older adults may exhibit a broad and diverse clinical spectrum, reinforcing the need for a careful diagnostic evaluation.
The diagnostic criteria for AILD were the same for both the older and younger patients. In AIH, the autoantibody profile is similar across age groups, although the interpretation may be complicated by natural age-related autoantibodies that appear at low titers, have low affinity, and exhibit broad reactivity. Most older adults with AIH have type I disease, marked by ANA and anti-SM positivity with hypergammaglobulinemia, whereas < 4% have anti-LKM antibodies[21]. No age-specific serological patterns were identified for PBC or PSC. However, in PSCs, distinguishing the disease from IgG4-related sclerosing cholangitis, which is more common in older adults and more responsive to steroids, is essential, making serum IgG4 measurement a key step in evaluation[30].
The diagnostic landscape in older adults is complicated by the high prevalence of coexisting conditions such as metabolic dysfunction-associated steatotic liver disease (MASLD), viral hepatitis, drug-induced liver injury, and alcoholic liver disease, all of which commonly form part of the differential diagnosis in this population[4]. MASLD creates a complex ‘metabolic milieu’ that complicates clinical and biochemical monitoring; steatohepatitis may cause persistent aminotransferase elevations, potentially masking the biochemical response to immunosuppression or leading to an overestimation of AILD activity[31]. Histologically, this presents a diagnostic challenge as features such as macro
Overlapping phenomena between the different entities of AILD are not uncommon, with AIH-PBC Overlap syndrome being the most common type. Despite the lack of extensive epidemiological information, in some series, the mean age at presentation was 61 years, with a female predominance[34,35]. Furthermore, the age-related increase in extrahepatic autoimmune diseases poses an additional challenge to the diagnostic specificity. Sjögren’s syndrome and autoimmune thyroid disease are the most common; however, systemic lupus erythematosus, rheumatoid arthritis, ulcerative colitis, and Crohn’s disease are also frequent and may arise concurrently or even occur years following the diagnosis, reflecting the dynamic nature of the disease[31,36,37]. These diseases often generate non-specific autoantibody titers, reducing the positive predictive value of serological markers for AILD. This serological noise underscores the importance of a liver biopsy as an essential tool for establishing an accurate AILD diagnosis[4]. Notably, a wide range of metabolic and cardiovascular comorbidities shape the clinical landscape, influencing both the prognostic outlook and selection of therapeutic interventions.
AILD is associated with increased cancer risk; in PSC, the likelihood of cholangiocarcinoma, gallbladder cancer, and colon cancer is significantly elevated, whereas in AIH and PBC, the risk of hepatocellular carcinoma, especially within cirrhosis, is higher than that in the general population, reinforcing the need for appropriate oncologic surveillance[2,38].
Evidence comparing clinical outcomes across age groups in patients with AILD remains fragmented. Table 1 summarizes current studies evaluating these disparities, emphasizing the diagnostic challenges and phenotypic variations prevalent in the geriatric population[39-51].
| Ref. | Country | Total patients/elderly (%) | Comorbidities in the elderly | Biochemical profile | Serologic markers | Treatment response | Other characteristics |
| Autoimmune hepatitis | |||||||
| Czaja and Carpenter[39], 2006 | United States | n = 205/47 (23) > 60 years | AT (23%), RA (4%), SS (2%), SLE (2%) | No significant differences | No significant differences | 59% vs 61%; less steroid failure (5% vs 24%, P = 0.03) | Cirrhosis more common (33% vs 10%, P = 0.03); HLA-DR4 more frequent (47% vs 13%, P = 0.003) |
| Miyake et al[40], 2007 | Japan | n = 160/34 (21) > 65 years | 6 (18): CT, UC, GD, SS | Lower albumin; other labs similar | ANA/ASM 97% vs 94% (P = 0.53) | 95% vs 89% (P = 0.41) | Type II HLA: Frequency of DR2-DR4 was similar. Cirrhosis (F3-F4) more common in elderly (53% vs 30%, P = 0.014) |
| Morii et al[41], 2017 | Japan | n = 71/28 (39) > 70 years | SS, RA, CT | Lower albumin and cholesterol | Higher IgG and ANA titers (P = 0.02) | Both groups achieved remission | Fibrosis score similar |
| Baven-Pronk et al[42], 2018 | Netherlands | n = 359/73 (20.3) > 60 years | Higher autoimmune comorbidity (33% vs 20%, P < 0.05): CT, CD, UC, RA, SS, SLE | Lower ALAT (430 vs 670 IU/L, P < 0.001) | No significant differences | 81% vs 76% (P = 0.368) | Fewer acute onsets (10%), less jaundice (25%); no difference in cirrhosis |
| Díaz Ramírez et al[43], 2019 | Colombia | n = 214/29 (13.5) > 65 years | HBP (34.5%), dyslipidemia (20.7%), CVD (17.2%) | No significant differences | No significant differences | 83.9% vs 100% (P = 0.022) | Cirrhosis more common (55% vs 33%, P = 0.024); 1 elderly transplanted |
| Sonthalia et al[44], 2020 | India | n = 155/73 (20) > 60 years | DM, RA, CT | Higher ALAT and creatinine (P < 0.05) | ASM more common (45.5% vs 25.4%, P < 0.05) | 65.6% vs 51.5% | ACLF more frequent (39.4% vs 13.9%, P = 0.0024); cirrhosis more frequent (75.7% vs 56.6%, P = 0.045) |
| Dalekos et al[45], 2021 | Greece | n = 234/25 (10) > 70 years | CVD (72%), DM (32%) | Lower ALAT (P < 0.05) | No significant differences | 83.7% vs 88.9% (P = 0.566) | Cirrhosis more common (48% vs 27.3%, P = 0.03); no differences in presentation |
| Primary biliary cholangitis | |||||||
| Newton et al[46], 2000 | United Kingdom | n = 1023/397 (39) > 65 years | Not reported | No significant differences | No significant differences | Not evaluated | Similar clinical features; higher mortality (59% vs 33%, P = 0.001) |
| Muratori et al[47], 2008 | Italy | n = 234/49 (25) > 65 years | Not reported | Lower ALAT/ASAT (P = 0.0024) | No significant differences | Not evaluated | Elderly less symptomatic at diagnosis (26%, P = 0.02); male sex higher (40%, P = 0.002) |
| Franceschet et al[48], 2016 | Italy | n = 376/62 (16) > 65 years | Not reported | Lower ALAT, platelets, albumin | No significant differences | UDCA response similar (56.6% vs 67.7%, P = NS) | Higher mortality (41.9% vs 19.7%, P < 0.001) |
| Primary sclerosing cholangitis | |||||||
| Hirano et al[49], 2008 | Japan | n = 28/10 (25) > 50 years | UC | Not evaluated | Higher IgE in older group | Fewer liver transplants | Less CCA and less liver failure |
| Tanaka et al[50], 2014 | Japan | n = 197 PSC + 43 IgG4SC/98 (49) > 50 years | IBD | No significant differences | IgG and IgG4 similar in elderly vs young; IgG4-SC had higher IgG/IgG4; IgA higher in elderly PSC (P < 0.001) | Similar medical treatment; similar rate of stenting/balloon dilation; similar transplantation rates | Similar symptoms at presentation; 5-year survival 54.7% in elderly |
| Rupp et al[51], 2018 | Germany | n = 215/32 (15) > 50 years | IBD | Lower ALAT/ASAT (P = 0.03/0.05) | No significant differences | 6 elderly transplanted | CCA more frequent in elderly (12.5% vs 3.3%, P = 0.02); late onset associated with mortality; poorer transplant-free survival (10.5 years vs 20.8 years) |
The treatment of patients with AILD poses a significant challenge because of the frequent coexistence of multiple comorbidities, the high burden of polypharmacy, and the resulting risk of drug interactions, toxicity, and adverse effects. Additional difficulties arise in selecting and maintaining immunosuppressive therapy due to complications such as corticosteroid-induced osteoporosis[52], steroid-related psychosis, cognitive decline, delirium[53], increased cardio
Adding to this challenge is the scarcity of age-specific evidence, partly because of the exclusion of older adults from clinical trials and conditions more prevalent in this age group, such as chronic kidney disease, osteoporosis, cardio
Furthermore, osteoporosis is of particular interest. A key characteristic of glucocorticoid-induced osteoporosis is the rapid loss of bone mass (driven by increased bone resorption and reduced bone formation) together with an increased risk of fractures. It is estimated that within the first 3-6 months of therapy, the fracture risk is already significantly elevated, with reported incidences of up to 5.1% for vertebral fractures and 2.5% for non-vertebral fractures[59-61].
Three key points must be considered. First, the fracture risk is dose-dependent; even low doses such as 2.5 mg/day of prednisone are associated with an increased fracture risk[62]. Second, in patients receiving glucocorticoids, fractures tend to occur at higher bone mineral density (BMD) values compared with individuals not exposed to these medications[63-65], moreover, the underlying autoimmune disease itself should not be overlooked, as it contributes to a pro-inflammatory and pro-resorptive cytokine milieu and may be associated with malnutrition, weight loss, reduced functional capacity, and impaired mobility (factors that further predispose to the development of osteoporosis). Third, fracture risk assessment using the Fracture Risk Assessment Tool (FRAX) score, the main tool currently used to estimate fracture probability, tends to underestimate the risk when the total hip BMD is used, given that vertebral fractures are the predominant fractures in glucocorticoid users. These patients often exhibit spine-hip discordance in BMD; therefore, some authors have proposed adjustments to improve fracture risk estimation in this population[66]. Most clinical guidelines and expert consensus statements advocate the earlier initiation of therapy in high-risk patients. For example, the European Calcified Tissue Society and the International Osteoporosis Foundation recommend initiating treatment in patients with a ≥ 20% probability of fracture, a history of fragility fracture, those receiving prednisone doses ≥ 7.5 mg/day (or equivalent), or those with a T-score ≤ -1.5[67,68]. In contrast, the American College of Rheumatology recommends treatment initiation in patients with a history of fragility fracture, a T-score ≤ -2.5, a ≥ 10% probability of major osteoporotic fracture or ≥ 1% probability of hip fracture, and those receiving high-dose glucocorticoids, although specific dose thresholds are not clearly defined[69]. From our perspective, patients receiving glucocorticoids for > 3-6 months may benefit from earlier interventions. A T-score ≤ -1.5 appears to be a more appropriate threshold-considering the higher BMD at which fractures occur in this population-and a ≥ 10% risk of major osteoporotic fracture should be con
AIH is the condition under which the greatest amount of data is available for older adults. Most studies have employed standard corticosteroid therapy with or without azathioprine, as shown in a systematic review by Durazzo et al[70], in which the use of newer therapies was documented only in case series and reports that were excluded from formal analysis. This review evaluated 239 elderly patients, 151 of whom were candidates for immunosuppressive treatment. Of these, 87% received standard therapy, whereas the remaining 13% were treated with mycophenolate mofetil (MMF) in a single study[71]. One study has examined the effects of ursodeoxycholic acid (UDCA)[41].
The rates of complete or partial remission with standard therapy range from 90% to 95%[44,72,73], and are comparable to those reported in the general population[74]. Therapeutic failure was less frequent in older than in younger patients (9.1% vs 28.2%, P = 0.041; 5% vs 24%, P = 0.03)[39,75]. In the MMF study, the combined complete and incomplete response rates were 93.6%; however, this cohort included a higher proportion of patients with cirrhosis. Notably, 75% of the patients remained in remission for two years after treatment withdrawal. Fortunately, favorable therapeutic responses have been reported across different ethnic groups, with similar outcomes observed in Chinese and Caucasian cohorts[39,75].
Some studies have suggested lower relapse rates in older adults, such as a study by Al-Chalabi et al[73] (70% vs 42%, P = 0.002). Although standard therapy is highly effective, UDCA demonstrated a lower response rate, with only 50% of the patients achieving remission in a study by Morii et al[41].
In cases of incomplete response, guidelines recommend increasing corticosteroid and azathioprine doses before switching to second-line therapy[58,76], although this poses a challenge in older adults due to the higher risk of adverse effects and intolerance; therefore, we suggest considering the use of second-line agents rather than using higher doses of prednisolone. If second-line agents are required, options include MMF and tacrolimus. Although a few studies have specifically targeted older adults or provided geriatric subgroup analyses, evidence from the general population suggests a greater efficacy of tacrolimus in achieving remission in partial responders or in those with treatment failure (68.9% vs 59.6%), with comparable rates of adverse events (25.5% for MMF and 24.1% for tacrolimus). The most frequent side effects include neurotoxicity, gastrointestinal symptoms with tacrolimus, leukopenia, and gastrointestinal symptoms with MMF[77].
Regarding orthotopic liver transplantation in AIH, a European study reported five- and 10-year survival rates > 70%. However, age-stratified analyses showed better outcomes in younger recipients (78% in the 18-34 years group vs 61% in those aged > 50 years). This difference was attributed to the higher incidence of post-transplant infections in older patients (hazard ratio, 1.8; P = 0.002)[78]. Data from the European Liver Transplant Registry (1988-2016) showed that autoimmune cirrhosis accounted for 2% of all liver transplantation indications, totaling 2929 cases. The 10-year graft survival rate was 60%, and the patient survival rate was 68%. If the analysis were restricted to the past 15 years, these rates would have improved to 63% and 72%, respectively[79]. Age-stratified survival demonstrated a clear gradient; 75% for adults aged 18-45 years, 71% for those aged 46-60 years, 65% for those aged 60-70 years, and 60% for those aged > 70 years. Notably, the proportion of older transplant recipients has increased substantially, with adults aged > 60 years representing < 5% of liver transplant recipients in the 1980s and currently accounting for > 30%.
Regarding the treatment of PSC, a Japanese study involving 187 patients found no significant differences in the use of medical therapies between older and younger adults. In older and younger patients, UDCA was used in 76% and 77% of patients, bezafibrate in 19% and 20%, and prednisolone in 16% and 24% of patients, respectively. Endoscopic in
The Comprehensive Geriatric Assessment (CGA) is a multidimensional and dynamic appraisal process designed to assess the medical, functional, cognitive, and social capabilities and limitations of older adults. Rather than relying on chronological age, CGA serves as a framework to quantify biological reserves and predict critical outcomes, such as treatment-related toxicity and all-cause mortality[80,81]. CGA utilizes various domain-specific scales, including frailty indices such as the Liver Frailty Index and the Clinical Frailty Scale, which serve as the most robust predictors of mortality. Other essential domains include disease burden, typically assessed using the Charlson Comorbidity Index[81]; multidimensional tools such as the Multidimensional Prognostic Index integrate these parameters, offering superior prognostic precision by capturing the complex interplay between liver disease and geriatric status[80]; these assessments enable the classification of patients into fit (robust), vulnerable (pre-frail), and frail, offering a robust framework for individualized management and risk-stratified clinical decisions[82].
Establishing a CGA as a transversal pillar from the initial evaluation is crucial as it streamlines the entire clinical pathway in AILD. By stratifying patients into operational subgroups, this framework allows robust (fit) individuals to undergo standard, comprehensive diagnostic and therapeutic regimens, while identifying vulnerable (pre-frail) patients who may benefit from early, targeted interventions to preserve functional reserve. Conversely, in the frail population, the CGA prompts a critical reconsideration of aggressive management, shifting the focus toward safety, quality of life, and the avoidance of procedural futility[83,84]. This tailored approach informs high-stakes decisions, ranging from the intensity of immunosuppressive therapy to candidacy for liver transplantation, and facilitates the implementation of prehabilitation strategies aimed at improving or even reversing the frailty phenotype through nutritional and physical optimization[85]. Ultimately, efficient resource utilization can be achieved by minimizing unnecessary interventions and preventing treatment-related complications[81].
Despite the growing interest in AILD among older adults, important knowledge gaps persist. Most studies were retrospective and single-center, limiting external validity, and few systematically evaluated the influence of autoimmune, metabolic, or cardiovascular comorbidities on prognosis, fibrosis progression, or treatment response. The age cutoffs used to define older adults vary widely, further complicating the interpretation of the findings.
Dedicated cohorts and clinical trials with adequate representation of patients aged ≥ 70 years are needed, along with comprehensive geriatric assessments incorporating functional status, frailty, and polypharmacy, which are largely missing from the current research. Early diagnostic biomarkers, immune profiles related to immunosenescence, and the effects of frailty on outcomes should be prioritized. Evidence on liver transplantation and the eligibility criteria in older adults remains limited, representing an important area for future studies.
The peak incidence of AILD in patients aged > 60 years represents a significant epidemiological shift that demands a comprehensive approach. Clinicians must maintain a high index of suspicion because subtle clinical presentations often mask advanced underlying diseases. Considering the high prevalence of comorbidities, a low threshold for liver biopsy is essential to ensure diagnostic accuracy before therapy is initiated. Management must transition from age-based decisions to a frailty-centered framework, where integrating CGA is paramount for risk stratification, outcome prediction, and prevention of treatment-related futility. Furthermore, immunosuppressive therapy cannot be managed in isolation and must be strictly coupled with proactive preventive strategies that focus on cardiovascular optimization, bone health preservation, and the monitoring of infectious or cognitive complications. Ultimately, while standard therapies are effective, clinical success in older adults is measured not only by biochemical remission, but also by the preservation of functional reserve and quality of life.
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