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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
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 …
Contributors JY and YY contributed to the conception and design of the study; JY, TS and YY collected the clinical data; JY, TS, NY, NA, EI, AT, YH and YY analysed the results; JY, TS, NY, NA, DH, ST, MN, AC-R, EI, AK, YH and YY drafted and corrected the manuscript. All authors read and approved the final manuscript.
Funding This study was supported by a grant from the Practical Research Project for Rare/Intractable Diseases of the Japan Agency for Medical Research and Development (Grant No: JP19ek0109394 and JP19ek0109356) and a Health and Labour Sciences Research Grant on Rare and Intractable Diseases from the Ministry of Health, Labour and Welfare of Japan (Grant No: 19FC1007).
Competing interests None declared.
Patient consent for publication Not required.
Ethics approval This study was approved by the St. Marianna University School of Medicine Bioethics Committee (No 1646).
Provenance and peer review Not commissioned; externally peer reviewed.
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