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Limitations of a single-point evaluation of anti-MDA5 antibody, ferritin, and IL-18 in predicting the prognosis of interstitial lung disease with anti-MDA5 antibody-positive dermatomyositis

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Abstract

Autoantibodies against melanoma differentiation-associated gene 5 (MDA5) are important serological markers in dermatomyositis (DM) with rapidly progressive interstitial lung disease (ILD). Recent studies noted that anti-MDA5 antibody (anti-MDA5ab), ferritin, and IL-18 are useful biomarkers for evaluating the responses to treatment and the status of ILD in anti-MDA5ab-positive DM. In this study, we further studied the importance of anti-MDA5ab levels and of ferritin and IL-18 concentrations in our patients. These biomarkers could be sometimes useful for evaluating ILD status and/or predicting the prognosis in patients with anti-MDA5ab-positive DM with several exceptional cases. A single-point evaluation of anti-MDA5ab levels and of ferritin and IL-18 concentrations has limitations in predicting the prognosis of ILD with DM. We consider that the timing of initial therapy and the anti-MDA5ab isotype, in addition to the patient’s age, are also crucial factors for predicting the prognosis.

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Acknowledgments

This work was supported by grants from the Ministry of Education, Culture, Sports, Science and Technology of Japan (23591618 to YM and 23249058 to MA) and by a grant from the Ministry of Health, Labour and Welfare of Japan (to YM).

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Authors and Affiliations

  1. Division of Connective Tissue Disease and Autoimmunity, Department of Dermatology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan

    Yoshinao Muro, Kazumitsu Sugiura & Masashi Akiyama

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  1. Yoshinao Muro
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  2. Kazumitsu Sugiura
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  3. Masashi Akiyama
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Correspondence to Yoshinao Muro.

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Muro, Y., Sugiura, K. & Akiyama, M. Limitations of a single-point evaluation of anti-MDA5 antibody, ferritin, and IL-18 in predicting the prognosis of interstitial lung disease with anti-MDA5 antibody-positive dermatomyositis. Clin Rheumatol 32, 395–398 (2013). https://doi.org/10.1007/s10067-012-2142-x

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  • DOI: https://doi.org/10.1007/s10067-012-2142-x

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