Development of liver cirrhosis during azathioprine therapy for inflammatory bowel disease

Jihye Park; Jae Seung Lee; Mi Na Kim; Soo Jung Park; Jae Jun Park; Tae Il Kim; Jae Hee Cheon

doi:10.5217/ir.2026.00051

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Brief Communication Development of liver cirrhosis during azathioprine therapy for inflammatory bowel disease: Jihye Park^1,2,3, Jae Seung Lee^1,2, Mi Na Kim^1,2, Soo Jung Park^1,2,3, Jae Jun Park^1,2,3, Tae Il Kim^1,2,3, Jae Hee Cheon^1,2,3,4,5; DOI: https://doi.org/10.5217/ir.2026.00051
Published online: September 10, 2026

¹Department of Internal Medicine, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea

²Institute of Gastroenterology, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea

³Inflammatory Bowel Disease Center, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea

⁴Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea

⁵Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Korea

Correspondence to Jae Hee Cheon, Department of Internal Medicine, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, Korea. E-mail: GENIUSHEE@yuhs.ac

• Received: February 9, 2026 • Revised: May 25, 2026 • Accepted: June 14, 2026

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Azathioprine (AZT) remains a mainstay of maintenance therapy for inflammatory bowel disease (IBD) worldwide. However, adverse events associated with AZT are relatively common and are typically classified as either dose-dependent or dose-independent (idiosyncratic). Thiopurine-induced liver injury occurs in approximately 0.3% to 10% of patients. Several mechanisms have been proposed for thiopurine-induced liver injury, including acute hepatocellular hepatitis, cholestatic hepatitis (idiosyncratic), mixed hepatitis, nodular regenerative hyperplasia, and sinusoidal obstruction syndrome. Most cases of thiopurine-induced liver injury are benign and resolve spontaneously after drug discontinuation; however, in very rare instances, liver transplantation may be required [1]. Liver function tests every 3 to 4 months are recommended for patients with IBD receiving thiopurine maintenance therapy, but certain adverse effects may not be detected through blood tests alone [2]. Although liver cirrhosis related to AZT is rare, several case reports have documented its occurrence in patients with IBD. Despite being an exceptional complication of thiopurine therapy, liver cirrhosis can be fatal and warrants careful monitoring in the management of IBD.

The prevalence of liver cirrhosis in IBD has been reported to range from 1% to 2% in previous population-based studies. A recent analysis using the National Inpatient Sample database in the United States reported that liver cirrhosis was present in 1.67% of patients with IBD [3]. The identified causes of liver cirrhosis included alcoholic cirrhosis (24.2%), primary sclerosing cholangitis (5.2%), biliary cirrhosis (1.7%), toxic liver disease (0.21%), and unspecified cirrhosis (56.9%). Compared with patients without liver cirrhosis, those with liver cirrhosis had a higher mortality rate and greater hospitalization costs, indicating that liver cirrhosis adversely affects the outcomes of IBD [3]. Furthermore, a study conducted at Yale–New Haven Hospital from 2012 to 2020 reported that among 18 patients with both liver cirrhosis and IBD who were receiving biologic therapy, 72% had Crohn’s disease (CD), 28% had ulcerative colitis (UC), and 33% had decompensated liver cirrhosis [4]. The etiologies of liver cirrhosis in that study were primary sclerosing cholangitis (38.9%), nonalcoholic fatty liver disease (16.7%), and hepatitis C (16.7%) [4]. However, no prior study has specifically investigated the characteristics of AZT-related cirrhosis compared with controls.

In this study, we aimed to analyze differences in prior AZT use between patients with liver cirrhosis of known etiology and those with cirrhosis of unknown etiology. We also examined the clinical outcomes of both liver cirrhosis and IBD by comparing AZT-related cirrhosis with the control group.

We conducted a cross-sectional, case–control study at the IBD Clinic of Severance Hospital in Seoul, South Korea, between March 2005 and August 2025. Patients with liver cirrhosis and a concurrent diagnosis of IBD—including UC, CD, and intestinal Behçet’s disease (BD)—were identified using the hospital’s electronic medical record system. The inclusion criteria were as follows: (1) age 18 years or older, (2) a confirmed diagnosis of IBD based on clinical, endoscopic, radiological, and histological findings; (3) a confirmed diagnosis of liver cirrhosis according to clinical, laboratory, and radiological data; and (4) IBD diagnosed before liver cirrhosis. Of the 63 patients screened, 23 were excluded because of changes in final diagnosis or incomplete follow-up data, and 7 were excluded because liver cirrhosis had been diagnosed before IBD (Fig. 1). This study was approved by the Institutional Review Board of Severance Hospital, Yonsei University (IRB No: 4-2025-1129). The requirement for written informed consent was waived by the Institutional Review Board owing to the retrospective nature of the study.

The primary outcome was the difference in prior AZT use between patients with liver cirrhosis of known etiology and those with liver cirrhosis of unknown etiology. The secondary outcomes included (1) the clinical features of IBD in patients with possible AZT-associated cirrhosis and (2) the clinical characteristics of cirrhosis in patients with possible AZT-associated cirrhosis compared with those in the control group. For this analysis, the control group was defined as patients with liver cirrhosis of known etiology and patients with liver cirrhosis of unknown etiology who had no history of AZT use. The possible AZT-associated cirrhosis group was defined as patients with liver cirrhosis of unknown etiology who had a history of AZT use. We retrospectively collected the following data from the patients’ electronic medical records. The mean± standard deviation (SD) or median (range) was calculated for continuous variables, while categorical variables were expressed as frequencies and percentages, as appropriate. Independent Student t-tests (or Mann-Whitney U tests) were used to compare continuous variables, and chi-square tests (or Fisher exact tests) were used to compare categorical variables, as appropriate. The log-rank test was used to identify predictive factors associated with clinical outcomes of IBD and liver cirrhosis between the possible AZT-associated cirrhosis and the control group. All statistical analyses were performed using IBM SPSS Statistics for Windows, version 23.0 (IBM Corp., Armonk, NY, USA). A P-value <0.05 was considered statistically significant.

Between March 2005 and August 2025, 33 patients with IBD were diagnosed with liver cirrhosis at Severance Hospital, South Korea. A cirrhosis diagnosis is confirmed by combining clinical examinations, laboratory blood panels, and radiologic and/or elastography imaging at the hepatology department. Among these 33 patients, chronic hepatitis B was the most common etiology (n =10), followed by alcohol-related liver disease (n=4), nonalcoholic fatty liver disease (n=2), autoimmune hepatitis (n =2), and primary sclerosing cholangitis (n =2) after hepatology consultation. The etiology of liver cirrhosis remained unclear in the remaining 13 patients (Fig. 1). Among the 13 patients with an unknown etiology of liver cirrhosis, 10 (76.9%) had used AZT before the diagnosis of cirrhosis; this group was defined as having possible AZT-associated cirrhosis. Of the 20 patients with a known etiology of liver cirrhosis, 8 (40.0%) had used AZT prior to diagnosis.

In patients with possible AZT-associated cirrhosis, the condition developed after a mean duration of 53.3 ± 43.1 months of AZT use (range, 6–126 months; median, 32.5 months) at a mean dose of 70.0 ± 38.7 mg (range, 25.0–175.0 mg; median, 62.5 mg). However, there were no significant differences between the groups with known and unknown etiologies of liver cirrhosis in the duration of AZT use (53.3 ±43.1 months vs. 42.7 ± 37.2 months; P=0.591) or the maintenance dose of AZT (70.0 ± 38.7 mg vs. 81.3 ± 56.3 mg; P=0.622).

In the possible AZT-associated cirrhosis group, 7 patients (70.0%) had CD, 2 (20.0%) had intestinal BD, and 1 (10.0%) had UC (Table 1). A significant difference in IBD subtype distribution was observed between the possible AZT-associated cirrhosis group (CD 70.0%, BD 20.0%, UC 10.0%) and the control group (CD 30.4%, BD 34.8%, UC 34.8%; P=0.042). Compared with the control group, the mean age at IBD diagnosis was significantly lower in the possible AZT-associated cirrhosis group (30.9±12.6 years vs. 47.4±12.0 years; P=0.001). However, there was no significant difference in IBD duration between the 2 groups (222.5 ±79.1 months vs. 185.6 ±97.1 months; P= 0.299). Among patients with CD, the disease location did not differ between groups, but disease behavior was different in the possible AZT-associated cirrhosis group (inflammatory 0.0%, stricturing 42.9%, fistulizing 57.1%) than in the control group (inflammatory 85.7%, stricturing 0.0%, fistulizing 14.3%; P=0.005). In the control group, UC extent was categorized as proctitis (12.5%), left-sided colitis (62.5%), and pancolitis (25.0%).

There were no significant differences in IBD-related clinical outcomes analyzed using the log-rank test, including the use of biologic agents (50.0% vs. 26.1%; P=0.240), IBD-related surgery (50.0% vs. 30.4%; P=0.433), or IBD relapse (80.0% vs. 43.5%; P=0.070), between the possible AZT-associated cirrhosis group and the control group. Compared with the control group, the age at diagnosis of liver cirrhosis was significantly lower in the possible AZT-associated cirrhosis group (44.2 ±14.3 years vs. 56.1 ± 13.0 years; P=0.026) (Table 2). There were no significant differences in the duration of liver cirrhosis, the interval between IBD diagnosis and liver cirrhosis diagnosis, laboratory parameters, or Child–Turcotte–Pugh scores at both diagnosis and final follow-up between the possible AZT-associated cirrhosis group and the control group. Similarly, there were no significant differences in liver cirrhosis-related clinical outcomes analyzed using the log-rank test, including variceal bleeding (40.0% vs. 26.1%; P=0.444), decompensated cirrhosis (40.0% vs. 30.4%; P=0.696), hospitalization due to cirrhosis (40.0% vs. 34.8%; P=1.000), or mortality (10.0% vs. 4.3%; P=0.521) between the 2 groups.

In this study, prior AZT use was significantly more frequent in patients with liver cirrhosis of unknown etiology than in those with liver cirrhosis of known etiology among individuals with IBD. However, there were no significant differences in either the duration or the maintenance dose of AZT between the groups with known and unknown etiologies of liver cirrhosis. The higher frequency of AZT use in patients with liver cirrhosis of unknown etiology suggests the possibility of drug-induced cirrhosis. Moreover, the current results suggest an association rather than a clear causal relationship. This finding is consistent with a previous study reporting that liver stiffness, measured by transient elastography, was 5.2 kPa in IBD patients receiving thiopurines and 4.7 kPa in those not receiving thiopurines (P=0.07), although the difference was not statistically significant [5]. Furthermore, the absence of significant differences in AZT dose (mean, 70.0 mg) or duration of use (mean, 53.3 months) suggests that this adverse event may be mediated through a dose-independent mechanism.

We found a significant difference in IBD subtype distribution between the possible AZT-associated cirrhosis group (CD 70.0%, BD 20.0%, UC 10.0%) and the control group (CD 30.4%, BD 34.8%, UC 34.8%). Although possible AZT-associated cirrhosis is rare and our study had a small sample size with a retrospective observational design, which may limit generalizability, a previous study involving 37 patients with nodular regenerative hyperplasia secondary to AZT reported a similar distribution: 84% had CD and 16% had UC [6]. A systematic review and meta-analysis also demonstrated that CD was associated with a higher risk of nonalcoholic fatty liver disease compared with UC (risk ratio, 1.21; 95% confidence interval, 1.14–1.29; P<0.001) [7-9]. In another clinical study assessing liver fibrosis using transient elastography, 11 of 132 IBD patients had fibrosis, and 10 of these patients had CD [10]. Several mechanisms may explain the higher prevalence of possible AZT-associated cirrhosis in patients with CD. First, the use of immunosuppressive agents is generally higher in CD because of its transmural nature, increased relapse risk, and complications such as strictures and fistulas. Second, systemic inflammation is typically more severe in CD, and AZT may exacerbate hepatocellular injury through T-cell–mediated toxicity, thereby accelerating inflammatory liver damage and fibrosis. Third, both intestinal fibrosis in CD and hepatic fibrosis in cirrhosis share key profibrotic pathways, including transforming growth factor β1 (TGF-β1), platelet-derived growth factor, and extracellular matrix remodeling. Therefore, patients with CD may be more susceptible to AZT-induced hepatic fibrosis. Consistent with these mechanisms, stricturing and fistulizing phenotypes were more frequent than the inflammatory phenotype in the possible AZT-associated cirrhosis group compared with the control group in this study.

In our study, compared with the control cirrhosis group, the possible AZT-associated cirrhosis group included more patients diagnosed with IBD at a younger age and more patients with stricturing or penetrating CD. Patients with early-onset CD generally experience more extensive disease progression, more complicated disease behavior, and a higher frequency of bowel surgery compared with those with adult-onset or elderly-onset CD. Similarly, pediatric-onset UC is associated with a more aggressive phenotype, characterized by extensive disease at diagnosis and greater progression over time, compared with adult-onset or elderly-onset UC. The aggressive phenotype of early-onset IBD may increase the inflammatory burden, including elevated TGF-β1 and interleukin-13 levels, which may heighten hepatic susceptibility to AZT-induced fibrosis. Furthermore, patients with early-onset IBD typically begin immunosuppressive therapy earlier and continue it for a longer duration. Even with comparable cumulative thiopurine doses, patients with early-onset IBD may develop possible AZT-associated cirrhosis due to more severe immune dysregulation or an underlying genetic predisposition to autoimmune disease. Therefore, in patients with IBD diagnosed at a young age, and in those with stricturing or penetrating CD, more vigilant monitoring for possible AZT-associated cirrhosis is warranted during follow-up. In clinical practice, we should consider possible AZT-associated cirrhosis in the differential diagnosis list if we find nodular liver findings, thrombocytopenia, low albumin level, and/or increased prothrombin time.

There were no significant differences in IBD-related clinical outcomes, including the use of biologic agents, IBD-related surgery, or disease relapse, between the possible AZT-associated cirrhosis and control cirrhosis groups. Similarly, there were no significant differences in liver cirrhosis outcomes, such as variceal bleeding, decompensated liver cirrhosis, hospitalization, or mortality. Therefore, in patients with possible AZT-associated cirrhosis and IBD, both IBD and liver cirrhosis can be managed according to existing clinical guidelines.

Our study has several limitations. First, significant differences in baseline characteristics were observed between the 2 groups; caution is required in interpreting these results due to potential selection and information biases resulting from the retrospective study design. Second, the sample size was relatively small. Nevertheless, because possible AZT-associated cirrhosis is extremely rare in patients with IBD, our study is meaningful as the first to compare the clinical outcomes of possible AZT-associated cirrhosis and control cirrhosis. Third, although possible AZT-associated cirrhosis was defined as cirrhosis of unknown etiology in patients with a history of AZT use, the absence of liver biopsy confirmation and absence of liver stiffness measurement in some patients represents a potential limitation.

In conclusion, careful monitoring for possible AZT-associated cirrhosis is warranted in patients with IBD diagnosed at a young age and in those with severe CD behavior, even though the clinical outcomes of IBD and liver cirrhosis are comparable to those in the control group.

NOTES

Funding Source

The authors received no financial support for the research, authorship, and/or publication of this article.

Conflict of Interest

Park J and Cheon JH are editorial board members of the journal but were not involved in the peer reviewer selection, evaluation, or decision process of this article. No other potential conflicts of interest relevant to this article were reported.

Data Availability Statement

Data analyzed in this study are available from the corresponding author upon reasonable request.

Author Contributions

Conceptualization: Park J, Cheon JH. Data curation: Park J. Formal analysis: Park J. Resources: Lee JS, Kim MN, Park SJ, Park JJ, Kim TI. Software: Park J. Supervision: Cheon JH. Writ ing–original draft: Park J. Writing–review & editing: Lee JS, Kim MN, Park SJ, Park JJ, Kim TI, Cheon JH. Approval of final manuscript: all authors.

Fig. 1.

Study design and patient selection process. IBD, inflammatory bowel disease; LC, liver cirrhosis.

Table 1.

Comparison of Clinical Features of IBD between Patients with Possible AZT-Associated Cirrhosis and Those in the Control Group

Variable	Possible AZT-associated cirrhosis (n=10)	Control (n=23)	P-value
Male sex	8 (80.0)	14 (60.9)	0.430
Body mass index (kg/m²)	25.6 ± 6.5	23.0 ± 4.4	0.195
Diabetes mellitus	1 (10.0)	6 (26.1)	0.397
Age at diagnosis of IBD (yr)	30.9 ± 12.6	47.4 ± 12.0	0.001
Disease duration of IBD (mo)	222.5 ± 79.1	185.6 ± 97.1	0.299
Subtype of IBD			0.042
CD	7 (70.0)	7 (30.4)
BD	2 (20.0)	8 (34.8)
UC	1 (10.0)	8 (34.8)
Montreal classification of CD (n = 14)
Behavior			0.005
Inflammatory	0	6 (85.7)
Stricturing	3 (42.9)	0
Fistulizing	4 (57.1)	1 (14.3)
Location			0.268
Ileal	2 (28.6)	2 (28.6)
Colonic	0	2 (28.6)
Ileocolonic	5 (71.4)	3 (42.9)
Montreal classification of UC (n = 9)			0.216
Proctitis	0	1 (12.5)
Left-sided colitis	0	5 (62.5)
Pancolitis	1 (100.0)	2 (25.0)
Clinical outcomes of IBD
Use of biologic agents	5 (50.0)	6 (26.1)	0.240
IBD-related surgery	5 (50.0)	7 (30.4)	0.433
Disease relapse	8 (80.0)	10 (43.5)	0.070

Values are presented as number (%) or mean±SD. P-values compare the possible AZT-associated cirrhosis group with the control group.

IBD, inflammatory bowel disease; AZT, azathioprine; CD, Crohn’s disease; BD, Behçet’s disease; UC, ulcerative colitis; SD, standard deviation.

Table 2.

Comparison of Clinical Features of Cirrhosis between Patients with Possible AZT-Associated Cirrhosis and Those in the Control Group

Variable	Possible AZT-associated cirrhosis (n=10)	Control (n=23)	P-value
Age at diagnosis of cirrhosis (yr)	44.2 ± 14.3	56.1 ± 13.0	0.026
Disease duration of cirrhosis (mo)	60.9 ± 64.8	80.7 ± 65.9	0.430
Time from IBD diagnosis to cirrhosis (mo)	161.7 ± 101.5	104.8 ± 95.1	0.132
Laboratory findings at diagnosis of cirrhosis
Total bilirubin (mg/dL)	1.0 ± 0.3	1.1 ± 1.2	0.845
Albumin (g/dL)	4.1 ± 0.6	3.9 ± 0.8	0.485
Prothrombin time (INR)	1.1 ± 0.2	1.0 ± 0.1	0.357
Aspartate aminotransferase (IU/L)	35.6 ± 22.6	41.6 ± 26.9	0.558
Alanine aminotransferase (IU/L)	35.3 ± 44.8	30.9 ± 26.3	0.733
Gamma-glutamyl transferase (IU/L)	83.8 ± 83.6	161.0 ± 188.2	0.360
Triglycerides (mg/dL)	128.5 ± 35.1	138.6 ± 50.4	0.727
LDL-C (mg/dL)	112.8 ± 46.2	91.7 ± 57.4	0.558
HDL-C (mg/dL)	50.0 ± 8.9	50.2 ± 20.5	0.988
Glucose (mg/dL)	104.7 ± 21.7	116.7 ± 60.2	0.566
White blood cell count (/μL)	4,359 ± 1,147	6,281 ± 3,140	0.086
Platelet count (/μL)	142,556 ± 92,719	190,957 ± 84,555	0.167
Hemoglobin (g/dL)	12.5 ± 2.1	12.8 ± 2.4	0.726
C-reactive protein (mg/L)	2.5 ± 2.9	11.8 ± 23.6	0.249
CTP score at diagnosis			0.704
CTP A	9 (90.0)	20 (87.0)
CTP B	1 (10.0)	2 (8.7)
CTP C	0	1 (4.3)
CTP score at last follow-up			0.790
CTP A	7 (70.0)	16 (69.6)
CTP B	2 (20.0)	6 (26.1)
CTP C	1 (10.0)	1 (4.3)
Clinical outcomes of cirrhosis
Variceal bleeding	4 (40.0)	6 (26.1)	0.444
Decompensated cirrhosis	4 (40.0)	7 (30.4)	0.696
Hospitalization due to cirrhosis	4 (40.0)	8 (34.8)	1.000
Mortality due to cirrhosis	1 (10.0)	1 (4.3)	0.521

Values are presented as mean±SD or number (%). P-values compare the possible AZT-associated cirrhosis group with the control group.

AZT, azathioprine; IBD, inflammatory bowel disease; INR, international normalized ratio; LDL-C, low-density lipoprotein cholesterol; HDL-C, high-density lipoprotein cholesterol; CTP, Child–Turcotte–Pugh; SD, standard deviation.

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Development of liver cirrhosis during azathioprine therapy for inflammatory bowel disease

DOI: https://doi.org/10.5217/ir.2026.00051

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Development of liver cirrhosis during azathioprine therapy for inflammatory bowel disease

Fig. 1. Study design and patient selection process. IBD, inflammatory bowel disease; LC, liver cirrhosis.

Fig. 1.

Development of liver cirrhosis during azathioprine therapy for inflammatory bowel disease

Variable	Possible AZT-associated cirrhosis (n=10)	Control (n=23)	P-value
Male sex	8 (80.0)	14 (60.9)	0.430
Body mass index (kg/m²)	25.6 ± 6.5	23.0 ± 4.4	0.195
Diabetes mellitus	1 (10.0)	6 (26.1)	0.397
Age at diagnosis of IBD (yr)	30.9 ± 12.6	47.4 ± 12.0	0.001
Disease duration of IBD (mo)	222.5 ± 79.1	185.6 ± 97.1	0.299
Subtype of IBD			0.042
CD	7 (70.0)	7 (30.4)
BD	2 (20.0)	8 (34.8)
UC	1 (10.0)	8 (34.8)
Montreal classification of CD (n = 14)
Behavior			0.005
Inflammatory	0	6 (85.7)
Stricturing	3 (42.9)	0
Fistulizing	4 (57.1)	1 (14.3)
Location			0.268
Ileal	2 (28.6)	2 (28.6)
Colonic	0	2 (28.6)
Ileocolonic	5 (71.4)	3 (42.9)
Montreal classification of UC (n = 9)			0.216
Proctitis	0	1 (12.5)
Left-sided colitis	0	5 (62.5)
Pancolitis	1 (100.0)	2 (25.0)
Clinical outcomes of IBD
Use of biologic agents	5 (50.0)	6 (26.1)	0.240
IBD-related surgery	5 (50.0)	7 (30.4)	0.433
Disease relapse	8 (80.0)	10 (43.5)	0.070

Variable	Possible AZT-associated cirrhosis (n=10)	Control (n=23)	P-value
Age at diagnosis of cirrhosis (yr)	44.2 ± 14.3	56.1 ± 13.0	0.026
Disease duration of cirrhosis (mo)	60.9 ± 64.8	80.7 ± 65.9	0.430
Time from IBD diagnosis to cirrhosis (mo)	161.7 ± 101.5	104.8 ± 95.1	0.132
Laboratory findings at diagnosis of cirrhosis
Total bilirubin (mg/dL)	1.0 ± 0.3	1.1 ± 1.2	0.845
Albumin (g/dL)	4.1 ± 0.6	3.9 ± 0.8	0.485
Prothrombin time (INR)	1.1 ± 0.2	1.0 ± 0.1	0.357
Aspartate aminotransferase (IU/L)	35.6 ± 22.6	41.6 ± 26.9	0.558
Alanine aminotransferase (IU/L)	35.3 ± 44.8	30.9 ± 26.3	0.733
Gamma-glutamyl transferase (IU/L)	83.8 ± 83.6	161.0 ± 188.2	0.360
Triglycerides (mg/dL)	128.5 ± 35.1	138.6 ± 50.4	0.727
LDL-C (mg/dL)	112.8 ± 46.2	91.7 ± 57.4	0.558
HDL-C (mg/dL)	50.0 ± 8.9	50.2 ± 20.5	0.988
Glucose (mg/dL)	104.7 ± 21.7	116.7 ± 60.2	0.566
White blood cell count (/μL)	4,359 ± 1,147	6,281 ± 3,140	0.086
Platelet count (/μL)	142,556 ± 92,719	190,957 ± 84,555	0.167
Hemoglobin (g/dL)	12.5 ± 2.1	12.8 ± 2.4	0.726
C-reactive protein (mg/L)	2.5 ± 2.9	11.8 ± 23.6	0.249
CTP score at diagnosis			0.704
CTP A	9 (90.0)	20 (87.0)
CTP B	1 (10.0)	2 (8.7)
CTP C	0	1 (4.3)
CTP score at last follow-up			0.790
CTP A	7 (70.0)	16 (69.6)
CTP B	2 (20.0)	6 (26.1)
CTP C	1 (10.0)	1 (4.3)
Clinical outcomes of cirrhosis
Variceal bleeding	4 (40.0)	6 (26.1)	0.444
Decompensated cirrhosis	4 (40.0)	7 (30.4)	0.696
Hospitalization due to cirrhosis	4 (40.0)	8 (34.8)	1.000
Mortality due to cirrhosis	1 (10.0)	1 (4.3)	0.521

Table 1. Comparison of Clinical Features of IBD between Patients with Possible AZT-Associated Cirrhosis and Those in the Control Group

Values are presented as number (%) or mean±SD. P-values compare the possible AZT-associated cirrhosis group with the control group.

IBD, inflammatory bowel disease; AZT, azathioprine; CD, Crohn’s disease; BD, Behçet’s disease; UC, ulcerative colitis; SD, standard deviation.

Table 2. Comparison of Clinical Features of Cirrhosis between Patients with Possible AZT-Associated Cirrhosis and Those in the Control Group

Values are presented as mean±SD or number (%). P-values compare the possible AZT-associated cirrhosis group with the control group.