HMGCR antibody-associated myopathy as a paraneoplastic manifestation of esophageal carcinoma
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Immune-mediated myopathies with antibodies may be triggered by statin exposure, but some patients with these disorders are statin-naive; thus, there are probably other etiologies.1 Several malignant tumors, including esophageal squamous cell carcinoma (ESCC), overexpress 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) protein.2 To date, the relationship between anti-HMGCR antibody–associated myopathy (HMGCR-M) and malignancy remains unclear.3,4 Here, we report a case of HMGCR-M in a patient with ESCC and paraneoplastic syndrome.
Footnotes
Supplemental data at Neurology.org
Author contributions: K.T.: study design and concept, data acquisition, analysis and interpretation, drafting the manuscript. K.H.: analysis and interpretation, data acquisition. Y.M.: analysis and interpretation, data acquisition, critical manuscript revision. H.N.: analysis and interpretation, data acquisition. Y.N.: analysis and interpretation, data acquisition. M. Koike: analysis and interpretation, data acquisition. S.N.: analysis and interpretation, data acquisition. Y.R.: analysis and interpretation, data acquisition. K.S.: analysis and interpretation, data acquisition, manuscript revisions. N.A.: analysis and interpretation, data acquisition, manuscript revision. M.I.: analysis and interpretation, data acquisition. Y.S.: analysis and interpretation, data acquisition. M.A.: analysis and interpretation, data acquisition. M. Katsuno: study supervision, critical manuscript revisions, data interpretation, study design and concept.
Study funding: Supported by KAKENHI grants from MEXT/JSPS, Japan (no. 26293206, 15K15337).
Disclosure: K. Tsujikawa reports no disclosures relevant to the manuscript. K. Hara is supported by KAKENHI Grant-in-Aid for Young Scientists B from JSPS, Japan (No. 15K1984). Y. Muro serves as an editorial board member of Immunopharmacology and Immunotoxicology and the Open Rheumatology Journal. He is supported by KAKENHI Grant-in-Aid for Scientific Research C from JSPS, Japan (No. 26461656). H. Nakanishi reports no disclosures relevant to the manuscript. Y. Niwa is supported by KAKENHI Grant-in-Aid for Young Scientists B from JSPS, Japan (No. 15K19878). M. Koike and S. Noda report no disclosures relevant to the manuscript. Y. Riku is supported by KAKENHI Grant-in-Aid for Young Scientists B from JSPS, Japan (No. 15K19483) and a grant from the Nitto Foundation. K. Sahashi is supported by KAKENHI Grant-in-Aid for Scientific Research C from JSPS, Japan (No. 26461268). N. Atsuta is supported by KAKENHI Grant-in-Aid for Scientific Research C from JSPS, Japan (No. 25461277). M. Ito is supported by KAKENHI Grant-in-Aid for Scientific Research C from JSPS, Japan (No. 25461313). Y. Shimoyama reports no disclosures relevant to the manuscript. M. Akiyama serves as a section editor of Journal of Dermatological Science and the Journal of Dermatology. He is supported by KAKENHI Grant-in-Aid for Scientific Research B from JSPS, Japan (No. 15H04887). M. Katsuno is supported by KAKENHI grants from JSPS, Japan (No. 26293206, 15K15337); a grant from Japan Agency for Medical Research and Development (No. 15ek0109025); and a grant from the Daiichi Sankyo Foundation of Life Science. Go to Neurology.org for full disclosures.
- Received December 26, 2015.
- Accepted in final form May 9, 2016.
- © 2016 American Academy of Neurology
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