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Use of cerebrospinal fluid CXCL10 and neopterin as biomarkers in HTLV-1-associated myelopathy/tropical spastic paraparesis treated with steroids
  1. Junji Yamauchi1,
  2. Tomoo Sato1,
  3. Naoko Yagishita1,
  4. Natsumi Araya1,
  5. Daisuke Hasegawa1,
  6. Shuntaro Tsutsumi2,
  7. Misako Nagasaka2,3,
  8. Ariella Coler-Reilly2,
  9. Eisuke Inoue4,
  10. Ayako Takata5,
  11. Yasuhiro Hasegawa6,
  12. Yoshihisa Yamano1
  1. 1 Department of Rare Diseases Research, Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki, Japan
  2. 2 Department of Advanced Medical Innovation, St. Marianna University Graduate School of Medicine, Kawasaki, Japan
  3. 3 Department of Oncology, Karmanos Cancer Institute, Wayne State University, Detroit, Michigan, USA
  4. 4 Medical Informatics, St. Marianna University School of Medicine, Kanagawa, Japan
  5. 5 Department of Preventive Medicine, St. Marianna University School of Medicine, Kawasaki, Japan
  6. 6 Department of Neurology, St. Marianna University School of Medicine, Kawasaki, Japan
  1. Correspondence to Dr Yoshihisa Yamano, Department of Rare Diseases Research, Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki 2168512, Japan; yyamano{at}

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Human T-cell leukaemia virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) damages the spinal cord by chronic inflammation and causes progressive lower limb motor disability.1 Because the associated symptoms gradually progress over the years, it is challenging for clinicians to predict long-term functional prognosis and evaluate the treatment response. Recently, we proposed criteria for classifying disease activity in untreated patients.2 As per this classification, disease activity is classified as low, moderate or high based on the clinical course and concentrations of inflammatory cytokines C-X-C motif chemokine 10 (CXCL10) and neopterin in the cerebrospinal fluid (CSF). Although corticosteroids are widely used to slow disease progression,3 biomarkers for steroid-treated patients have not yet been validated. In the present study, we investigated whether these markers are associated with the progression of motor dysfunction in this population.

Materials and methods

This was a single-centre, retrospective cohort study of patients diagnosed with HAM/TSP based on the WHO criteria.4 Patients who were continuously treated with oral prednisolone (PSL) therapy and had the following data were enrolled: CXCL10 and neopterin concentrations in the CSF measured before and after the initiation of PSL therapy and serial data of the Osame motor disability score (OMDS) (online supplementary figure S1).5

Supplemental material


Patients visited St. Marianna University hospital every 1 to 3 months for treatment for HAM/TSP; motor disability was assessed using the OMDS at each visit. The PSL dose and the interval between the initiation of PSL therapy and CSF testing were not standardised. Oral PSL therapy was initiated at a median dose of 5.0 mg/day (IQR 3.0–5.0), and the dose was adjusted thereafter according to the symptoms (dose range 1.5–8.0 mg/day). The median time from …

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