HTLV-I-ASSOCIATED MYELOPATHY - ANALYSIS OF 213 PATIENTS BASED ON CLINICAL-FEATURES AND LABORATORY FINDINGS

Citation
M. Nakagawa et al., HTLV-I-ASSOCIATED MYELOPATHY - ANALYSIS OF 213 PATIENTS BASED ON CLINICAL-FEATURES AND LABORATORY FINDINGS, Journal of neurovirology, 1(1), 1995, pp. 50-61
Citations number
69
Categorie Soggetti
Neurosciences,Virology
Journal title
ISSN journal
13550284
Volume
1
Issue
1
Year of publication
1995
Pages
50 - 61
Database
ISI
SICI code
1355-0284(1995)1:1<50:HM-AO2>2.0.ZU;2-8
Abstract
We studied the clinical features and laboratory findings in 213 patien ts with HTLV-I-associated myelopathy/tropical spastic paraparesis as d iagnosed in Kagoshima University Hospital. Some aspects of clinical fe atures in HTLV-I-associated myelopathy/tropical spastic paraparesis we re characterized by mode of HTLV-I transmission and age of onset. The patients with onset after 15 years old and no history of blood transfu sion before the onset of the disease (151 patients, group I) showed a shorter interval between the time of disease onset and that of inabili ty to walk. The patients with onset before 15 years old and without hi story of blood transfusion (21 patients, group II) had short stature a nd slow progression of the disease. The interval time and the progress ion of the disease in patients with history of blood transfusion befor e onset of disease (41 patients, group III) were in between those of t he above two groups. Patients whose ages of onset were older than 61 y ears old showed a faster progression than those with younger onset reg ardless of the mode of HTLV-I transmission. HTLV-I-associated myelopat hy/tropical spastic paraparesis patients often also showed other organ disorders such as leukoencephalopathy (69%), abnormal findings on che st X-ray (50%), Sjogren syndrome (25%) and arthropathy (17%). The pati ents with low anti-HTLV-I antibody titers in the cerebrospinal fluid ( 2X-8X by PA method) had an older age of onset on average, milder clini cal symptoms and lesser increase of neopterin in the cerebrospinal flu id than those in the high titer subgroup whose titers were higher than 1024X in cerebrospinal fluid regardless of the mode of HTLV-I transmi ssion. We speculate that the clinical course of HTLV-I-associated myel opathy/tropical spastic paraparesis mainly shows a slow progression wh ich consists of an initial progressive phase (probably an inflammatory phase) and a latter chronic phase, although some patients showed acut e/subacute onset and rapid progression.