Masahide Hamaguchi, MD; Takao Kojima, MD; Noriyuki Takeda, MD; Takayuki Nakagawa, MD; Hiroya Taniguchi, MD; Kota Fujii, MD; Tatsushi Omatsu, MD; Tomoaki Nakajima, MD; Hiroshi Sarui, MD; Makoto Shimazaki, MD; Takahiro Kato, MD; Junichi Okuda, MD; Kazunori Ida, MD
Acknowledgments: The authors thank Chisato Nagata, MD, PhD (Department of Public Health, Gifu University, Gifu, Japan), for reviewing the manuscript and for assistance with the statistical analyses.
Grant Support: None.
Potential Financial Conflicts of Interest: None disclosed.
Requests for Single Reprints: Masahide Hamaguchi, MD, Department of Gastroenterology, Murakami Memorial Hospital, Asahi University, 3-23 Hashimoto-cho, Gifu 500-8523, Japan; e-mail, email@example.com.
Current Author Addresses: Drs. Hamaguchi, Kojima, Nakagawa, Taniguchi, Omatsu, Shimazaki, Kato, Okuda, and Ida: Department of Gastroenterology, Murakami Memorial Hospital, Asahi University, 3-23 Hashimoto-cho, Gifu 500-8523, Japan.
Drs. Takeda and Sarui: Department of Endocrinology and Metabolism, Murakami Memorial Hospital, Asahi University, 3-23 Hashimoto-cho, Gifu 500-8523, Japan.
Drs. Fujii and Nakajima: Molecular Gastroenterology and Hepatology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Hirokoji, Kawaramachi, Kamigyo-ku, Kyoto 602-8566, Japan.
Author Contributions: Conception and design: M. Hamaguchi, T. Kojima, N. Takeda.
Analysis and interpretation of the data: M. Hamaguchi, N. Takeda.
Drafting of the article: M. Hamaguchi, N. Takeda.
Critical revision of the article for important intellectual content: M. Hamaguchi, N. Takeda.
Final approval of the article: M. Hamaguchi, T. Kojima, N. Takeda, T. Nakagawa, H. Taniguchi, K. Fujii, T. Omatsu, T. Nakajima, H. Sarui, M. Shimazaki, T. Kato, J. Okuda, K. Ida.
Provision of study materials or patients: T. Kojima, J. Okuda, K. Ida.
Statistical expertise: M. Hamaguchi.
Administrative, technical, or logistic support: T. Kojima, N. Takeda, J. Okuda, K. Ida.
Collection and assembly of data: M. Hamaguchi, T. Kojima, N. Takeda, T. Nakagawa, H. Taniguchi, K. Fujii, T. Omatsu, T. Nakajima, H. Sarui, M. Shimazaki, T. Kato.
The frequent association of nonalcoholic fatty liver disease with components of the metabolic syndrome such as obesity, hyperglycemia, dyslipidemia, and hypertension is well known. However, no prospective study has examined the role of the metabolic syndrome in the development of this disease.
To characterize the longitudinal relationship between the metabolic syndrome and nonalcoholic fatty liver disease.
A prospective observational study.
A medical health checkup program in a general hospital.
4401 apparently healthy Japanese men and women, 21 to 80 years of age, with a mean body mass index (BMI) of 22.6 kg/m2 (SD, 3.0).
Alcohol intake was assessed by using a questionnaire. Biochemical tests for liver and metabolic function and abdominal ultrasonography were done. Modified criteria of the National Cholesterol Education Program Adult Treatment Panel III were used to characterize the metabolic syndrome.
At baseline, 812 of 4401 (18%) participants had nonalcoholic fatty liver disease. During the mean follow-up period of 414 days (SD, 128), the authors observed 308 new cases (10%) of nonalcoholic fatty liver disease among 3147 participants who were disease-free at baseline and who completed a second examination. Regression of nonalcoholic fatty liver disease was found in 113 (16%) of 704 participants who had the disease at baseline and who completed a second examination. Men and women who met the criteria for the metabolic syndrome at baseline were more likely to develop the disease during follow-up (adjusted odds ratio, 4.00 [95% CI, 2.63 to 6.08] and 11.20 [CI, 4.85 to 25.87], respectively). Nonalcoholic fatty liver disease was less likely to regress in those participants with the metabolic syndrome at baseline.
Ultrasonography may lead to an incorrect diagnosis of nonalcoholic fatty liver disease in 10% to 30% of cases and cannot distinguish steatohepatitis from simple steatosis. Self-reported alcohol intake may cause bias. Because all of the participants were Japanese, generalizability to non-Japanese populations is uncertain.
The metabolic syndrome is a strong predictor of nonalcoholic fatty liver disease.
Hamaguchi M, Kojima T, Takeda N, Nakagawa T, Taniguchi H, Fujii K, et al. The Metabolic Syndrome as a Predictor of Nonalcoholic Fatty Liver Disease. Ann Intern Med. 2005;143:722–728. doi: 10.7326/0003-4819-143-10-200511150-00009
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Published: Ann Intern Med. 2005;143(10):722-728.
Gastroenterology/Hepatology, Liver Disease, Obesity.
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