Concurrent psoriatic arthritis and autoimmune hepatitis in a patient with psoriasis: a case report

Abstract

Background

Psoriasis is a chronic, autoimmune skin disorder that can be associated with systemic comorbidities, including psoriatic arthritis (PsA). The coexistence of psoriasis, PsA, and autoimmune hepatitis (AIH) is uncommon and may present diagnostic and therapeutic challenges. This case report highlights a patient with psoriasis who developed both PsA and AIH without prior immunosuppressive therapy.

Case presentation

A 57-year-old Palestinian woman with longstanding plaque psoriasis presented with worsening skin lesions, progressive arthralgia involving both knees and ankles, chronic inflammatory low back pain, and persistently abnormal liver biochemistry. She had been diagnosed with psoriasis at age 49, which had been resistant to various treatments, including topical corticosteroids and phototherapy. One year before presentation, the patient developed progressive arthralgia, particularly in the knees, ankles, and lower back. Physical examination revealed swollen joints and limited range of motion. Laboratory tests indicated elevated liver enzymes, and autoimmune panel results were positive for antinuclear antibodies (ANA) and anti-smooth muscle antibodies (ASMA), raising suspicion for autoimmune hepatitis. A liver biopsy confirmed type 1 AIH, characterized by lymphocytic infiltration and plasma cell predominance. Cyclosporine 100 mg daily was initiated, atorvastatin was discontinued, and the patient was monitored clinically and biochemically. After 6 weeks, psoriasis severity improved markedly, joint symptoms decreased, and liver enzyme levels normalized. No treatment-related adverse effects were documented during the reported follow-up period.

Conclusions

This case highlights the importance of considering autoimmune hepatitis in patients with psoriatic disease who develop persistent liver enzyme abnormalities, even in the absence of prior systemic immunosuppressive therapy. A multidisciplinary approach is important in such complex presentations, and cyclosporine may be a useful therapeutic option in selected patients requiring concomitant control of dermatologic, rheumatologic, and hepatic disease.

Introduction

Psoriasis is a chronic, autoimmune, hyperproliferative skin disorder that affects approximately 2–3% of the global population, with a significant number of patients experiencing moderate to severe forms of the disease. It is characterized by the formation of erythematous plaques covered with silvery scales, typically affecting the skin of the extremities, scalp, and trunk. The pathophysiology of psoriasis involves dysregulation of immune responses, primarily driven by T-cells that release pro-inflammatory cytokines, including interleukin-2 and tumor necrosis factor (TNF)-α, which promote keratinocyte proliferation and inflammation. Management of psoriasis includes topical treatments, phototherapy, and systemic therapies, with the latter being indicated for moderate to severe cases. The systemic agents most commonly used include acitretin, methotrexate (MTX), and cyclosporine, as well as biologic agents targeting specific immune pathways such as TNF-α [1–3].

Psoriatic arthritis (PsA), a common comorbidity in psoriasis patients, involves both peripheral and axial joint inflammation and often manifests with symptoms such as joint pain, swelling, and stiffness. PsA shares common immunological pathways with psoriasis, and its management typically includes non-steroidal anti-inflammatory drugs (NSAIDs), disease-modifying antirheumatic drugs (DMARDs), and biologic therapies targeting cytokines such as TNF-α, IL-17, or IL-23. Recent evidence also suggests that PsA may occur in approximately one-quarter of patients with psoriasis, emphasizing the clinical importance of screening for articular symptoms in these patients [1, 4].

In addition to these dermatologic and rheumatologic manifestations, patients with psoriasis may be at risk for developing other autoimmune disorders, including autoimmune hepatitis (AIH), a chronic inflammatory liver disease [5]. The association between psoriasis and AIH is not widely recognized, but available evidence suggests that AIH may occur in patients with psoriasis both in the absence of prior immunosuppressive therapy and, in some cases, after exposure to agents such as anti-TNF therapies [6, 7]. AIH is characterized by the presence of autoantibodies (such as antinuclear antibodies and anti-smooth muscle antibodies), elevated liver enzymes, and histological features of chronic liver inflammation, which, if left untreated, can lead to cirrhosis and liver failure. While corticosteroid therapy is the mainstay of AIH treatment, some cases may be resistant to steroids, necessitating alternative immunosuppressive treatments, including cyclosporine [8, 9].

Here, we present the case of a 57-year-old Palestinian woman with longstanding psoriasis who developed psoriatic arthritis and autoimmune hepatitis without prior exposure to immunosuppressive therapy. This rare presentation highlights the potential overlap of psoriasis, psoriatic arthritis, and autoimmune hepatitis and emphasizes the need for a multidisciplinary approach in managing complex cases. This case also underscores the potential role of cyclosporine as a treatment option for autoimmune hepatitis, as evidenced by the patient’s successful response to therapy.

Case presentation

A 57-year-old Palestinian woman presented with worsening plaque psoriasis, progressive pain and swelling involving both knees and ankles, chronic inflammatory low back pain, and persistently abnormal liver biochemistry identified during evaluation.

She had been diagnosed with cutaneous plaque psoriasis at the age of 49. Over the following years, lesions involving the upper and lower extremities and flexural areas remained active despite treatment with potent topical corticosteroids and approximately 50 sessions of phototherapy. During the year before presentation, she developed progressive arthralgia affecting both knees and ankles together with chronic low back pain that worsened after inactivity and improved somewhat with movement, raising concern for inflammatory arthritis.

Past medical and surgical histories were otherwise unremarkable. No known drug allergies were documented. Family and social histories were non-contributory. There was no prior exposure to systemic immunosuppressive therapy for psoriasis before the current evaluation.

Dermatologic examination showed extensive erythematous, well-demarcated scaly plaques involving the hands, feet, and flexural regions. Musculoskeletal examination demonstrated swollen and tender knees and ankles with reduced range of motion and Achilles tendon tenderness. The lower back pain had an inflammatory pattern. No scleral icterus, hepatomegaly, or stigmata of chronic liver disease were documented on examination (see Figs. 1, 2, 3).

Fig. 1.

Longitudinal ESR and CRP pattern over the years; the arrow indicates cyclosporine initiation

Fig. 2.

Longitudinal liver study pattern over the years; the arrow indicates cyclosporine initiation

Fig. 3.

Composite clinical photographs showing palmar and foot lesions before treatment (A and C) and after treatment (B and D)

Inflammatory markers were elevated, including erythrocyte sedimentation rate and C-reactive protein. Magnetic resonance imaging supported sacroiliac inflammatory involvement consistent with axial psoriatic arthritis. Representative magnetic resonance imaging of the sacroiliac joints demonstrating inflammatory involvement consistent with sacroiliitis is shown in Fig. 4. Liver function tests demonstrated persistent elevation of aminotransferases. Because these abnormalities persisted, additional evaluation was undertaken. Hepatitis B and hepatitis C testing was negative. Autoimmune serology showed positive antinuclear antibodies and anti-smooth muscle antibodies. Liver biopsy revealed portal lymphoplasmacytic inflammation with interface hepatitis, supporting type 1 autoimmune hepatitis. Representative histopathologic findings are shown in Fig. 5.

Fig. 4.

Coronal MRI of the sacroiliac joints. Coronal images demonstrate bilateral sacroiliac joint signal abnormalities

Fig. 5.

Liver biopsy histopathology showing features consistent with autoimmune hepatitis. A Lobular inflammatory activity. B Interface hepatitis with portal lymphoplasmacytic inflammation, including plasma cell-rich infiltrates

At presentation, competing explanations for the abnormal liver tests included medication-related hepatotoxicity, drug-induced autoimmune-like hepatitis, and viral hepatitis. Long-term atorvastatin exposure was considered, but persistent enzyme elevation together with positive antinuclear and anti-smooth muscle antibodies and biopsy findings of interface hepatitis with plasma cell-rich inflammation supported autoimmune hepatitis. Negative hepatitis B and C testing made active viral hepatitis less likely. Taken together, the clinical, serologic, and histologic findings supported concurrent psoriatic arthritis and autoimmune hepatitis in a patient with longstanding psoriasis.

Cyclosporine 100 mg daily was initiated. Atorvastatin was discontinued. Bezafibrate 400 mg daily was introduced for lipid management in the setting of liver dysfunction, and etoricoxib 90 mg was prescribed for symptomatic relief of arthralgia. No systemic corticosteroid was administered during the 6-week treatment interval described in this report.

The patient was monitored clinically and biochemically, including assessment of liver enzymes, renal function, blood pressure, and cyclosporine tolerance. After 6 weeks, psoriasis severity improved markedly, with the reported Psoriasis Area and Severity Index decreasing from 48 to 8. Joint swelling, tenderness, and inflammatory back pain also improved. Liver enzymes normalized, supporting biochemical response of the hepatic disease. No treatment-related adverse effects were documented during the reported follow-up period.

Timeline

(See Table 1)

Table 1.

Chronological timeline of the case

Time point	Key event
Age 49	Diagnosis of plaque psoriasis
Following years	Persistent cutaneous disease despite potent topical corticosteroids and approximately 50 phototherapy sessions
1 year before presentation	Progressive knee and ankle arthralgia and inflammatory low back pain developed
Presentation	Examination demonstrated active psoriasis and inflammatory musculoskeletal findings; inflammatory markers were elevated
Diagnostic workup	MRI supported sacroiliac inflammatory involvement; liver enzymes remained elevated; ANA and ASMA were positive; hepatitis B/C testing was negative
Liver biopsy	Biopsy supported type 1 autoimmune hepatitis
Treatment initiation	Cyclosporine 100 mg daily started; atorvastatin discontinued; bezafibrate and etoricoxib added
6-week follow-up	Cutaneous and joint symptoms improved; PASI decreased from 48 to 8; liver enzymes normalized

Investigations

(See Table 2)

Table 2.

Summary of major investigations and interpretation

Investigation	Finding	Interpretation
ESR and CRP	Elevated at presentation	Supported active systemic inflammation consistent with PsA activity
MRI sacroiliac joints	Inflammatory involvement reported	Supported axial psoriatic arthritis
AST/ALT/GGT	Persistently elevated before treatment; normalized after treatment	Prompted hepatic workup and later documented biochemical response
ANA	Positive	Supported autoimmune liver disease in the appropriate clinical context
ASMA	Positive	Supported type 1 AIH
Hepatitis B/C serology	Negative	Made active viral hepatitis less likely
Liver biopsy	Interface hepatitis with portal lymphoplasmacytic infiltration/plasma cells	Supported type 1 autoimmune hepatitis
PASI	48 before treatment; 8 after treatment	Documented marked clinical dermatologic improvement

Discussion

The coexistence of psoriasis, psoriatic arthritis (PsA), and autoimmune hepatitis (AIH) is a rare but clinically significant phenomenon, highlighting the complex interplay between dermatologic, rheumatologic, and hepatic autoimmune disorders. While psoriasis with PsA is well recognized, the additional occurrence of AIH is far less frequently reported. A review of the literature includes cases of AIH developing in patients with psoriasis both without prior immunosuppressive therapy and after exposure to biologic agents such as infliximab, suggesting that this association may reflect either a true autoimmune overlap or, in some cases, treatment-related liver injury [5–7].

In our patient, the diagnosis of AIH was suspected because of persistent elevation of liver enzymes in the setting of psoriasis and newly recognized PsA. Drug-related liver injury was considered, particularly given the history of atorvastatin use, but the persistence of abnormal liver biochemistry prompted further evaluation. Viral hepatitis B and C were excluded, while positive antinuclear antibodies and anti-smooth muscle antibodies increased the suspicion for AIH. The diagnosis was ultimately supported by liver biopsy, which demonstrated lymphocytic portal inflammation with plasma cell predominance and interface hepatitis, consistent with type 1 AIH. Taken together, these findings favored concomitant autoimmune hepatitis rather than viral hepatitis or a purely medication-related process.

Our case resembles the report by Jo et al., in which a patient with psoriasis developed AIH in the absence of prior immunosuppressive therapy. In contrast, Goujon et al. described AIH occurring after infliximab exposure, highlighting that not all cases arise through the same pathway. The present case is more similar to the former pattern, as the patient had not received methotrexate or biologic therapy before the diagnosis of AIH. This distinction is clinically relevant because it supports the possibility of a true autoimmune overlap rather than a solely drug-induced event [6, 7].

The exact pathophysiological mechanisms linking psoriasis, PsA, and AIH remain not fully elucidated. However, the concurrent occurrence of these conditions suggests a shared immunopathogenic pathway involving T-cell-mediated immune responses. In psoriasis and PsA, activated T-cells release pro-inflammatory cytokines, leading to keratinocyte proliferation and joint inflammation. Similarly, in AIH, aberrant T-cell responses target hepatocytes, resulting in liver inflammation and potential fibrosis. This commonality points to a dysregulated immune system as a central factor in the pathogenesis of these disorders [1, 10].

Management in such cases requires a multidisciplinary approach involving dermatology, rheumatology, and hepatology. In our patient, cyclosporine was selected because of its established role in the treatment of severe psoriasis and its reported use as an alternative immunosuppressive agent in selected cases of autoimmune hepatitis (AIH). Following treatment, improvement was observed in the patient’s skin lesions, joint symptoms, and liver enzyme abnormalities. This response should be interpreted cautiously, but it suggests that cyclosporine may be a reasonable option in carefully selected patients when concomitant control of dermatologic, rheumatologic, and hepatic disease is needed. In addition, targeted biologic therapies may be considered in selected complex cases; for example, ixekizumab has been reported to successfully treat psoriasis and progressive psoriatic arthritis in a patient with hepatitis B virus infection and end-stage kidney disease, although such options require careful assessment of comorbidities and hepatic safety. Regular monitoring of liver function, renal function, blood pressure, and drug safety remains essential [3, 8, 9, 11].

Conclusion

The concurrence of psoriasis, PsA, and AIH presents unique diagnostic and therapeutic challenges. This case highlights the need to consider autoimmune hepatitis in patients with psoriatic disease who develop persistent liver enzyme abnormalities, even in the absence of prior biologic or methotrexate exposure. Careful evaluation, including exclusion of competing causes and histopathologic confirmation when appropriate, is essential for timely diagnosis. A multidisciplinary approach may help guide individualized treatment and improve outcomes in such complex cases, and cyclosporine may be a useful therapeutic option in selected patients requiring concomitant control of dermatologic, rheumatologic, and hepatic disease.

Abbreviations

PsA

Psoriatic arthritis

AIH

Autoimmune hepatitis

PASI

Psoriasis Area and Severity Index

ANA

Antinuclear antibodies

ASMA

Anti-smooth muscle antibodies

CRP

C-reactive protein

ESR

Erythrocyte sedimentation rate

AST

Aspartate aminotransferase

ALT

Alanine aminotransferase

GGT

Gamma-glutamyl transferase

NSAIDs

Non-steroidal anti-inflammatory drugs

IL

Interleukin

TNF-α

Tumor necrosis factor-alpha

DMARDs

Disease-modifying antirheumatic drugs

MRI

Magnetic resonance imaging

FDA

Food and drug administration (not explicitly stated in the document, but common in medical literature)

Author contributions

Y.A., G.B., and N.A. contributed to drafting the manuscript. N.A. collected the patient data. M.A.S. critically reviewed the entire manuscript. All authors read and approved the final manuscript.

Funding

The authors have none to declare.

Data availability

No datasets were generated or analyzed during the current study.

Declarations

Ethics approval and consent to participate

Publishing of case reports in Palestine is not required to undergo any ethical approval by a committee according to the Palestinian Ministry of Health’s regulations; consent from patients is enough.

Consent for publication

Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors have none to declare.