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Open Access

Clinical features of familial HAM/TSP

  • Satoshi Nozuma1,
  • Eiji Matsuura1Email author,
  • Toshio Matsuzaki2,
  • Osamu Watanabe1,
  • Ryuji Kubota2,
  • Shuji Izumo2 and
  • Hiroshi Takashima1
Retrovirology201411(Suppl 1):O7

Published: 7 January 2014


Infectious DiseaseCancer ResearchCerebrospinal FluidGenetic FactorSporadic Case

Some genetic factors are associated with the development of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). So far, there is a very few report about familial HAM/TSP. This study aimed to clarify the clinical features of familial HAM/TSP. We reviewed all patients with HAM/TSP, 784 in number, hospitalized to Kagoshima University Hospital from 1987 to 2012. Familial HAM/TSP cases (patients with one or more HAM/TSP patients in their family) were compared with 124 sporadic HAM/TSP cases (patients with no other HAM/TSP patient in their family) admitted in series for association of clinical features in an unmatched case-control design. As a result, 40 patients (5.1%) in total 784 were familial cases. In familial cases compared to sporadic cases, age of onset was earlier (41.3 year old vs. 51.6 year old, P<0.001), the number of acute progression cases was smaller (10.0 percent vs. 28.2 percent, p=0.019), motor disability grade was lower (4.0 vs. 4.9, p=0.043) in spite of longer duration of illness (14.3 years vs. 10.2 years, P=0.026), and duration between onset and time to use a wheelchair in daily life was longer (18.3 years vs. 10.0 years, P=0.025) significantly. Protein in cerebrospinal fluid (CSF) was significantly lower in familial cases (29.9 mg vs. 42.5 mg, p<0.001). HTLV-1 provirus load, anti-HTLV-1 antibody in serum and CSF, cells in CSF was not significantly different. Thus, we demonstrate familial HAM/TSP showing younger onset and slower progress than in sporadic cases. Our results suggest that some genetic factors might influence the incidence of familial HAM/TSP.

Authors’ Affiliations

Department of Neurology and Geriatrics, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima City, Kagoshima, Japan
Department of Molecular Pathology, Center for Chronic Viral Diseases, Kagoshima University, Japan


© Nozuma et al; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.