1. Introduction
Autoimmune hepatitis is a chronic inflammatory disease of unknown etiology characterized by circulating antibodies, hypergammaglobulinemia, inflammatory changes in necrotic liver tissue, and a significant response to immunosuppressive therapy [1]. The pathogenesis, diagnosis, and treatment of autoimmune hepatitis continue to challenge physicians [2] because the disease has a variety of clinical phenotypes, and this diversity complicates its diagnosis and management [3]. Autoimmune hepatitis, in most cases, responds to immunosuppressive therapy, but if left untreated, it usually progresses to liver failure that requires transplantation [4, 5, 6]. So treatment should be done as soon as possible, which requires timely diagnosis. There are criteria for diagnosing autoimmune hepatitis, but sometimes there is a risk of misdiagnosis, even if standard diagnostic approaches are used. The diagnosis of autoimmune hepatitis and other liver disorders, such as Wilson disease, is challenging and important and should always be considered, especially when the response to primary treatment is insufficient [7]. Although the simultaneous occurrence of Wilson disease and autoimmune hepatitis is rare [8], both can present as acute or chronic hepatitis [9]. In other words, hepatocyte necrosis and exposure of intracellular antigens to the immune system are found in Wilson disease secondary to hepatocyte necrosis, which results in low antibody titers and may confuse diagnosis and differentiation between autoimmune hepatitis and Wilson disease [8, 10]. 
Wilson disease is an inherited disorder of copper metabolism that occurs with an excessive increase in the accumulation of copper in organs, such as the nervous system, liver, kidneys, and heart. A wide range of symptoms follows after damaging organs caused by copper deposition [11]. Wilson disease has been reported in different age groups from 3 to 50 years. The disease manifests as hepatic (about 40%), neurological (about 40%), mental (about 20%), and in rare cases (less than 10%), as hemolytic anemia. Hepatic manifestations include autoimmune hepatitis, recurrent jaundice, hepatitis, hepatic impairment, and chronic liver disease [12]. Wilson disease is a genetic disorder that can be successfully controlled if diagnosed and treated correctly and timely, but if left untreated, it can be fatal [11, 13, 14]. Early diagnosis and treatment, especially in acute liver failure, is important to protect against disease progression and cirrhosis or liver failure because prompt treatment allows serum copper to be removed and the patient to be stabilized to facilitate orthotopic liver rescue transplantation [13]. However, one of the challenges that clinicians face when managing patients with liver failure is the immediate reassurance of diagnosis of Wilson disease to facilitate patient survival because clinical manifestations of Wilson disease can vary widely. Sometimes due to the overlap of clinical manifestations of this disease with other diseases such as autoimmune hepatitis, its diagnosis becomes complicated and often delayed [15, 16, 17], resulting in unpleasant consequences. On the other hand, patients with acute liver failure due to autoimmune hepatitis, unlike patients with acute liver failure due to Wilson disease, may respond better to medical treatment with immunosuppressive agents, if diagnosed and treated promptly. This treatment can eliminate the need for liver transplants [18].
In general, in this group of patients who have Wilson disease and autoimmune hepatitis simultaneously, there are features of the patient, disease, and laboratory and histopathological studies that may be misleading. Therefore, identification of these features in rare patients who have both Wilson disease and autoimmune hepatitis is necessary for relevant specialists to adopt appropriate treatment [10].
A review of the available databases found that most studies on the simultaneity of Wilson disease and autoimmune hepatitis are case reports [7, 8, 9, 10, 15], and no systematic review study was found for a comprehensive review. Therefore, to obtain stronger and more reliable evidence in this field and due to the importance of correct and timely diagnosis and subsequent appropriate treatment of these two diseases to maintain patient survival, this study was conducted to determine features of the patient, disease, diagnostic studies, and therapeutic measures in cases of simultaneity of Wilson disease and autoimmune hepatitis so that the results could be an appropriate clinical guide for specialists.
2. Materials and Methods
The present systematic review study was conducted to review the comorbidity of autoimmune hepatitis and Wilson disease according to PRISMA (the Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines (2021). The research question in the present study was designed based on PICO (Patient/ Problem, Intervention, Comparison, and Outcome) components. The details of how to use PICO components, given that most of the studies were of the case report studies, are as follows:
P: Population/ Disease/ Problem: Patients with the simultaneity of Wilson disease and autoimmune hepatitis
I: Intervention: Therapeutic measures (dose, frequency, and duration), diagnostic tests (type and frequency), and risk factors for the simultaneity of Wilson disease and autoimmune hepatitis
C: Comparison: not applicable in this study
O: Outcome: Response to treatment (death, liver transplant, treated, etc.)
Data sources
To find evidence related to the study purpose objectives, Persian language databases, such as Barakat knowledge network system, SID, and Magiran, and international databases, such as Google Scholar, Web of Science, ProQuest, Springer, ScienceDirect, Medline via PubMed, and Scopus were searched with keywords specified in the title of the articles. The databases were searched with no time limit until the end of February 2016. In addition, the Civilica database was searched to find abstracts of articles presented at national and international congresses to include articles related to the purpose of the study. For a complete search, the final references of the obtained articles were also investigated. Two researchers conducted the search independently. The keywords specified for searching Persian and English language databases included “Wilson disease”, “hepatitis”, and “autoimmune”, which were used by MeSH strategy and Boolean operators (AND & OR). The search strategy is presented in Table 1.


Inclusion and exclusion criteria 
The inclusion criteria in the present review study included 1) the study was observational such as case report, case series, cross-sectional, group, and case-control studies, and 2) the study was published in Persian or English. The exclusion criteria included low-quality studies based on the score obtained from the checklist.
The quality of case report studies was evaluated using the instrument proposed by Murad et al. [19]. The instrument consists of eight questions in four dimensions, including selection, ascertainment, causality, and case report, each of which is given a score of 0 or 1. The maximum possible score for a study based on this instrument is eight. Of course, no cut-off point is considered for this instrument, and qualitative evaluation of the study and observance of the dimensions proposed in this instrument is considered more. In case of disagreement at all stages of primary and secondary screening, evaluation of article quality, and selection of studies, the third researcher was used to resolve existing differences and control bias.
The STROBE (the Strengthening the Reporting of Observational Studies in Epidemiology) statement checklist was also considered to assess the quality of observational studies, such as cross-sectional, cohort, and case-control studies. The STROBE checklist consists of 22 different sections and evaluates various aspects of the methodology, including sampling methods, measurement of variables, statistical analysis, adjustment of confounders, the validity and reliability characteristics of the tools used, and the objectives of the study. Each item is given a score of 0 or 1. In this checklist, the minimum score was considered 15.5 [17]. However, because the studies related to the purpose of the study were of the case report type, this checklist was not used, and the specific checklist pertaining to the case report studies was used.
Study selection
By searching databases, 218 studies were finally identified and reviewed after excluding duplicates during primary and secondary screening. So that in the first screening, titles and abstracts were reviewed; 15 articles remained after this stage. In the secondary screening, the full text of the articles was also evaluated by two researchers. At this stage, 5 articles were excluded from the review process due to inadequacy and ambiguity of information and publication in languages other than English or Persian. For example, one of the studies [17], despite reporting information on diagnostic tests and clinical manifestations of 10 patients (reporting information as a percentage and not reporting information on each case in detail), was excluded for reasons, such as not reporting the age of participants, diagnosis direction, treatment measures, and patient outcomes. Therefore, after this stage, 10 articles were evaluated in terms of quality. Because of the proper quality of the articles, no study was excluded, and finally, 10 studies entered the review process. The details are given in Figure 1. Data extraction
To extract information from studies, a checklist was designed that included the patient age and gender, reference, diagnosis direction (Wilson disease to autoimmune hepatitis or vice versa), clinical manifestations at primary diagnosis, preliminary diagnostic tests, primary therapeutic measures, duration of primary diagnosis to secondary diagnosis, clinical manifestations at secondary diagnosis, secondary diagnostic tests, secondary therapeutic measures, and outcomes. 
Finally, after extracting the data, the quantitative data obtained from studies, including patient age, and duration from primary to secondary diagnosis, were summarized and analyzed using descriptive statistics such as Mean±SD. Also, the qualitative data, including patient gender, diagnosis direction, and outcomes, were summarized and analyzed using descriptive statistics such as frequency (number and percentage).
3. Results
In the present study, 10 studies were included in the review process. The details of study selection are given in Figure 1. 
Study characteristics
Out of 10 studies, there were 8 case reports [7, 9, 10, 18, 20, 21, 22, 23], 1 opinion study [24], and 1 letter to the editor [25]. So that 6 case report studies, 1 opinion study, and the letter to the editor reported one case [9, 10, 18, 20, 22, 23, 24]. The other two studies reported two [21], and four cases [7], respectively.
In general, this review study reported information on 14 patients with comorbidity of Wilson disease and autoimmune hepatitis. The age range of patients was between 5 and 48 years, and the Mean±SD age of participants in the study was 19±11 years. Eight (57%) out of 14 participants were female. Diagnosis direction was autoimmune hepatitis to Wilson disease in 8 cases [7, 9, 21, 23, 24], and reverse in 3 cases [7, 20, 22]. In three cases [10, 18, 25], the simultaneity of Wilson disease and autoimmune hepatitis was considered from the beginning with no primary and secondary diagnosis. Finally, out of 8 patients [7, 15, 21, 23, 24] diagnosed with autoimmune hepatitis to Wilson disease, in two cases [9, 23], the primary diagnosis of autoimmune hepatitis was rejected. 
In another case [24], the primary diagnosis of autoimmune hepatitis was not rejected and remained. In three cases [7, 20, 22] with the diagnosis of Wilson disease to autoimmune hepatitis, in one case [22] primary diagnosis of Wilson disease was rejected. In another case [20], the primary diagnosis of Wilson disease was not rejected and remained. It should be noted that in other studies, no explanation was given regarding rejection or non-rejection of primary diagnosis. The duration from primary diagnosis to secondary diagnosis varied from one month to three years [7, 9, 20, 21, 24], although in some studies, this time has not been reported [22, 23].
Primary clinical manifestations reported in patients with early diagnosis of autoimmune hepatitis were nausea [9], vomiting [7], abdominal pain [7, 23], lethargy [9], fatigue, lethargy, skin rash, foot edema, pruritus [21], jaundice [21, 23], hepatomegaly [7], abdominal distension [23], and mild tremor [9]. Secondary clinical manifestations in patients with a secondary diagnosis of Wilson disease included severe encephalopathy, hand tremor [24], jaundice, ascites, advanced Cushing syndrome features [21], psychiatric (depression), and neurological symptoms (bradykinesia, gait disorders, visual acuity disorders) [7].
Primary clinical manifestations reported in patients with early diagnosis of Wilson disease included anorexia, weight loss, reduced concentration, aggressive behavior, epistaxis [20], fatigue, jaundice, dark urine, and pale stools [22]. Secondary clinical manifestation in patients with a secondary diagnosis of autoimmune hepatitis included jaundice [22].
Clinical manifestations in patients with the simultaneity of Wilson disease and autoimmune hepatitis (with no primary and secondary diagnosis) included nausea, vomiting, tea color urine [10], fever, jaundice, fatigue [25], coagulopathy, jaundice, ascites, and bilateral leg edema [18]. 
In almost all patients, diagnostic tests included complete blood count, kidney and liver function tests, prothrombin time, International Normalized Ratio (INR), and viral markers for hepatitis A, B, C, and E. More specific primary diagnostic tests in patients with primary diagnosis of autoimmune hepatitis and Wilson disease include cases, such as Anti-Nuclear Antibody (ANA) [7, 9, 10, 18, 20, 21, 22, 23, 24, 25], Anti-Mitochondrial Antibody (AMA) [10, 18, 20, 21, 23, 24, 25], Anti-Smooth Muscle Antibody (ASMA) [7, 9, 10, 18, 20, 21, 23, 25], anti-Liver Kidney Microsome (anti-LKM) [18, 23, 25], serum ceruloplasmin [7, 9, 10, 18, 20, 21, 24, 25], and 24-h urinary copper [7, 9, 10, 18, 20, 21, 22, 24, 25]. 
A summary of the most important results of the laboratory tests is given in Table 2.


Abdominal ultrasound was used as a diagnostic test in most studies [7, 9, 10, 17, 18, 20, 21, 23]. Liver biopsy was performed as a primary diagnostic test in patients with a primary diagnosis of autoimmune hepatitis [7, 21, 23, 24] and a secondary diagnostic test in patients with a primary diagnosis of Wilson disease [7, 20, 22]. Liver Magnetic Resonance Imaging (MRI) was used as a primary diagnostic test in a patient with a primary diagnosis of Wilson disease [22], abdominal MRI was used as a primary diagnostic test in a patient with a primary diagnosis of autoimmune hepatitis [24], and head MRI was used as a secondary diagnostic test in 2 patients with a secondary diagnosis of Wilson disease [7, 23]. Molecular genetic testing (DNA) was performed as a secondary diagnostic test in patients with a secondary diagnosis of autoimmune hepatitis [20] and a secondary diagnosis of Wilson [7, 24].
The drug treatments for patients with a primary diagnosis of autoimmune hepatitis included 5 cases of corticosteroid [7, 9, 21, 24] and 2 cases of corticosteroids and azathioprine [7, 21], followed by Wilson disease as a secondary diagnosis for this group of patients included 5 cases of d-penicillamine [7, 9, 21, 24], 1 case of azathioprine and zinc and 5-aminosalicylic acid [7] that this patient had Crohn’s disease. 
The drug therapies adopted for patients with a primary diagnosis of Wilson disease included one case of d-penicillamine with vitamin E and pyridoxine [20]. In another case with a primary diagnosis of Wilson disease, d-penicillamine was first prescribed, and a month later, steroids were added. Four weeks later, due to severe neutropenia, d-penicillamine was discontinued, and trientine was started. Six months later, trientine was gradually reduced, and zinc therapy was started. After 7 months, low-dose glucocorticosteroid therapy was resumed [7]. Drug therapies for patients with a secondary diagnosis of autoimmune hepatitis included 2 cases of corticosteroid therapy [20, 22].
The therapeutic measures for patients with the simultaneity of Wilson disease and autoimmune hepatitis (with no primary and secondary diagnosis) included prednisolone, azathioprine, d-penicillamine [10], prednisolone, and azathioprine [25]. A patient with Wilson disease and autoimmune hepatitis [18] received prednisolone and d-penicillamine along with several blood transfusions, vitamin K, diuretics, prophylactic antibiotics, and plasmapheresis, which resulted in liver transplantation due to no improvement. 
Liver transplantation was one of the successful therapeutic measures in which 3 patients [18, 21, 23] underwent liver transplantation, of which 2 [21, 23] out of 3 transplants were related to patients whose secondary diagnosis was Wilson disease. The patients’ condition improved in all cases after receiving treatment or transplantation. Other details are presented in Table 3.












4. Discussion
The present study was conducted to explore features of the patient, disease, diagnostic studies, and therapeutic measures in cases of Wilson disease and autoimmune hepatitis comorbidity. According to the results of the reviewed studies, in 8 cases [7, 9, 21, 23, 24], autoimmune hepatitis was the primary diagnosis, and Wilson disease was not diagnosed at first. In some cases, it seems that patients with Wilson disease have more convincing features of autoimmune hepatitis, and even primary treatment with immunosuppressive drugs may lead to relative improvement [21]. For example, in Gromny et al. study [24], increased aminotransferases, ANA positive, hypergammaglobulinemia, and negative viral markers were possible reasons for early diagnosis of autoimmune hepatitis. 
In another study [7], 3 patients with a primary diagnosis of autoimmune hepatitis were reported, so that in the first patient, possible reasons, such as ANA positive, high IgG, and liver cell fibrosis, led to the primary diagnosis of autoimmune hepatitis only. In the second patient, ASMA and ANA were positive and severe inflammation, and fibrosis of liver cells were the only causes of primary diagnosis of autoimmune hepatitis. However, six months after primary diagnosis of autoimmune hepatitis, serum ceruloplasmin levels, and mutations were detected in molecular genetic testing and psychiatric (depression) and neurological (bradykinesia, gait disorders, visual acuity disorders) symptoms led to the secondary diagnosis of Wilson disease. In the third patient in the above study [7], serum ceruloplasmin and urinary copper were normal at baseline, and primary diagnosis of autoimmune hepatitis was made based on ANA positive, periportal inflammation, and severe steatosis. 
In Santos et al. study [9], due to an increase in aminotransferases and bile enzymes, negative viral markers, ANA positive, and liver dysfunction, a primary diagnosis of autoimmune hepatitis was proposed. In Milkiewicz et al. study [21], an increase in aminotransferases and ASMA and ANA positive was one of the possible reasons for primary diagnosis of autoimmune hepatitis. Also, the clinical manifestations similar to autoimmune hepatitis and normal serum ceruloplasmin levels were possible reasons for the late diagnosis of Wilson disease. 
In general, for justifying primary diagnosis of autoimmune hepatitis only in the above studies [7, 9, 21, 24], it can be said that the presence of autoantibodies, hypergammaglobulinemia, increased aminotransferases and negative viral markers are among the criteria for autoimmune hepatitis diagnosis [15]. Therefore, the presence of any of the criteria in some patients with Wilson disease may be considered as misleading possible reasons for diagnosis. On the other hand, ANA and ASMA are recommended tests for diagnosing autoimmune hepatitis, but they are not specific because they can be diagnosed in children with other diseases, such as viral infections, celiac disease, and Wilson disease [18]. 
The role of antibodies in Wilson disease can be due to necrosis of liver cells or another disease as one of the primary features of its pathological mechanism [8, 9] that sometimes the presence of strong and prominent autoimmune features may lead to the exclusion of accurate screening for Wilson disease. Therefore, screening for Wilson disease should be considered, especially when a poor response to steroid therapy is seen in patients with autoimmune hepatitis. In this regard, diagnostic tests are suggested, such as serum ceruloplasmin, 24-h urinary copper, albumin level, molecular genetic testing (DNA), MRI, liver biopsy, and Kayser-Fleischer ring eye examination for more detailed evaluation and more accurate diagnosis. Regarding clinical manifestations, although most of the clinical manifestations of patients, such as nausea, vomiting, hepatomegaly, fatigue, and jaundice, overlap in two diseases and can be misleading, regarding symptoms such as psychiatric symptoms (depression) and neurological (bradykinesia, gait disorders, and visual acuity disorders) symptoms can also help diagnose Wilson disease. 
Liver transplantation was one of the therapeutic measures performed successfully for 3 patients [18, 21, 23]. However, 2 cases [21, 23] of 3 transplants were related to patients whose secondary diagnosis was Wilson disease. Therefore, early diagnosis of Wilson disease is very important because if diagnosis of Wilson disease is delayed, there is a possibility of liver transplantation. Therefore, correct evaluation and diagnosis in this group of patients is also important because if diagnosed early in patients with autoimmune hepatitis and Wilson disease, liver transplantation will usually be prevented. Thus, simultaneous administration of prednisolone, azathioprine, and d-penicillamine may improve the patient’s condition [10].
In some studies [7, 20, 22], Wilson disease was a primary diagnosis, and autoimmune hepatitis was not diagnosed. A possible reason for delayed diagnosis of autoimmune hepatitis is the result of diagnostic tests. In a study [7], the Kayser-Fleischer ring was seen on ocular examination, and changes in serum ceruloplasmin and 24-h urinary copper led to the primary diagnosis of Wilson disease only. In Dara et al. study [20], an increase in 24-h urinary copper and clinical manifestations, such as low concentration and aggressive behaviors of the patient, were among the possible reasons for primary diagnosis of Wilson disease only because patients with Wilson disease could refer with neurological disorders and psychiatric symptoms [13]. 
In general, for justifying the cause of primary diagnosis of Wilson disease in the other studies mentioned above [7, 20], it may be possible to point out significant cases for diagnosis of Wilson disease. For example, 24-h urinary copper is one of the tests considered for patients with Wilson disease. This test is abnormal in 80%-85% of untreated patients with Wilson disease, although abnormal copper metabolism may occur [25, 26]. During the review of studies in the present review, 24-h urinary copper was lower in studies with a secondary diagnosis of Wilson disease [7, 9, 21, 23, 24] than in studies with a primary diagnosis of Wilson disease [7, 20, 22], which probably is a factor of delayed diagnosis of Wilson disease. Kayser-Fleischer ring is also found in 50% of diagnoses of Wilson disease, but in some cases in Wilson disease, Kayser-Fleischer ring may not be present in the eye examination, and there is no history of neuropsychiatric symptoms. Low ceruloplasmin levels are seen in most patients with neurological Wilson disease, but it may be within the normal range in about half of patients with liver Wilson disease [27]. In view of the above, screening for autoimmune hepatitis in patients with a primary diagnosis of Wilson disease should be considered. In this regard, it is suggested to perform diagnostic tests such as serological tests, ANA, ASMA, AMA [7, 9, 10, 18, 20, 21, 23], Anti-LKM, complement level, gamma globulin, IgG, albumin, molecular genetic tests (DNA), MRI, and liver biopsy for more accurate assessments and diagnosis.
5. Conclusion
In general, the comorbidity of Wilson disease and autoimmune hepatitis is uncommon but important. In the presence of symptoms in these patients, comorbidity of these two diseases should be considered. Additional assessments such as serum ceruloplasmin, 24-h urinary copper 24, molecular genetic testing (DNA), MRI, serological tests, ANA, ASMA, AMA, anti-LKM, complement level, gamma globulin, IgG, albumin, Kayser-Fleischer ring eye examination, and liver biopsy for correct diagnosis should be considered. Regarding clinical symptoms, psychiatric (depression) and neurological symptoms (bradykinesia, gait disorders, and visual acuity disorders) can help diagnose Wilson disease so that appropriate treatment can be proposed. If appropriate treatment is started for the disease with a diagnosis of Wilson or autoimmune hepatitis, but the response to treatment is insufficient, it is better to consider the simultaneous occurrence of two diseases or the initial misdiagnosis. 
The limitations of the present study were the impossibility of performing meta-analysis due to heterogeneity in the results of diagnostic tests that lacked exactly equal kits and therapeutic measures. Access to articles published in other languages (except Persian and English) was also a limitation. It is suggested to conduct further studies to obtain stronger and more credible evidence in this field.

Ethical Considerations
Compliance with ethical guidelines
This study was approved by the Ethics Committee of the Isfahan University of Medical Sciences (Code: IR.MUI.MED.REC.1400.115).

Funding
This study was supported by the Deputy of Research and Technology of Isfahan University of Medical Sciences (Grant number: 54805).

Authors' contributions
Conceptualization and supervision: Peiman Nasri and Fatemeh Famouri; Methodology: Peiman Nasri and Fatemeh Famouri, Seyed Esmaeil Hosseini-Kordkhyli; Investigation, writing  original draft, and writing  review & editing: All authors; Data collection: Seyed Esmaeil Hosseini-Kordkhyli, Azar Jafari-Koulaee, Silva Hovsepian; Hossein Saneian, Majid Khademian; Data analysis: Peiman Nasri and Fatemeh Famouri; Funding acquisition and Resources: Peiman Nasri, Seyed Esmaeil Hosseini-Kordkhyli.

Conflicts of interest
The authors declared no conflict of interest.

Acknowledgements
We would like to express our gratitude to the honorable Deputy of Research and Technology of Isfahan University of Medical Sciences for their support of this project.


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