Arthritis & Rheumatism, Volume 62,
November 2010 Abstract Supplement

Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Atlanta, Georgia November 6-11, 2010.

Nonalcoholic Steatohepatitis as a Complication of Collagen Disease.

Takagi,  Kae, Kawaguchi,  Yasushi, Ota,  Yuko, Tochimoto,  Akiko, Fukazawa,  Chikako, Gono,  Takahisa, Katsumata,  Yasuhiro


Nonalcoholic fatty liver disease (NAFLD) is a silent disease, and is one of the most common causes of elevated liver enzymes. Nonalcoholic steatohepatitis (NASH) is distinguished from NAFLD by a liver biopsy revealing fatty change in the liver along with inflammation and damage. The development of NASH in collagen disease has been rarely reported. Our aims are to elucidate the frequency, clinical features, pathogenesis, and treatment of NASH associated with collagen disease.


A retrospective survey of collagen disease patients who were hospitalized and initially screened for NASH by identifying abnormalities in serum liver enzymes, and findings of severe fatty liver changes on abdominal computed tomography (CT) and ultrasound. NASH was confirmed by liver biopsy, and the clinical features of these patients before and after treatment were evaluated.


Five patients were identified with NASH (3 patients with systemic lupus erythematosus and 2 patients with Weber-Christian disease). Mean age was 33.8 ± 15.6 years old. Three of five patients showed increased BMI and high HOMA-R. All patients showed the increase levels of serum aminotransferase (AST/ALT). Before diagnosis of NASH, 4 patients had been treated by small amount of corticosteroid against collagen diseases. Fatty change was revealed by CT and/or US in all patients. Three cases having ALT level higher than 150IU/l, showed more prominent fatty change in CT grading. The Liver/spleen (L/S) ratio measured by CT were observed around 0.8 higher than 0.4. Pathological examination using liver biopsy specimens showed NASH in all 5 patients. Based on Brunt's classification, pathological score of two patients were Grade 2 and Stage 2, whereas the score were 1 in other three patients.

Table 1. Clinical characteristic

 case 1case 2case 3case 4case 5
collagen diseaseW-CW-CSLESLESLE
AST (IU/l)218821615175
ALT (IU/l)20526216014290
LDH (IU/l)958594720192230
gGTP (IU/l)34416710032157
ALP (IU/l)308234159146332
Tchol (mg/dl)223256172175121
HDL (mg/dl)195112NE37
LDL (mg/dl)12918879NE147
TG (mg/dl)393104405220262
Adiponectin (mg/ml)9.1729.46.5511.8
Leptin (ng/dl)11.120.824.414.719.3
Insulin (mU/ml)1.972.51758514.6
BS (mg/dl)62181108120118
HbA1C (%)66.55.5NENE
TNFa (pg/ml)
CT grade233NE1
CT L/S ratio0.80.410.38NE 
US (grade)23221
Pathology (grade)21112

In order to suppress the collagen disease activity, all patients were treated by higher amount of corticosteroid (prednisolone 20–40 mg/day) with and without immunosuppressive drugs such as cyclophosphamide, ciclosporin or mizoribine. In all patients, serum AST/ALT levels were remarkably turned to be normal in parallel with improvement of collagen disease activity within six months (AST: 117.4 ± 31.2 vs.26.0 ± 3.7, p < 0.05; ALT: 171.8 ± 29.1 vs.48.4 ± 16.7, p < 0.01). Furthermore, fatty liver change determined by CT and US were diminished. The average of L/S ratio before and after treatment was changed from 0.49 ± 0.26 to 1.22 ± 0.17 with statistically significant difference (p < 0.01). Although HOMA-R was improved in three cases, there were no significant changes in other risk factors including body weight and BMI before and after treatment.


NASH is relatively rare in collagen disease patients. Corticosteroid treatment with or without immunosuppressant drugs was effective for collagen disease as well as for NASH, suggesting that autoimmune factors are involved in the development of NASH associated with collagen disease.

To cite this abstract, please use the following information:
Takagi, Kae, Kawaguchi, Yasushi, Ota, Yuko, Tochimoto, Akiko, Fukazawa, Chikako, Gono, Takahisa, et al; Nonalcoholic Steatohepatitis as a Complication of Collagen Disease. [abstract]. Arthritis Rheum 2010;62 Suppl 10 :1666
DOI: 10.1002/art.29431

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