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September 01, 1999; 53 (4) Article

Clinical and laboratory features of primary progressive and secondary progressive MS

Khurram Bashir, John N. Whitaker
First published September 1, 1999, DOI: https://doi.org/10.1212/WNL.53.4.765
Khurram Bashir
From the Department of Neurology and the Center for NeuroimmunologyUniversity of Alabama at Birmingham; and Neurology and Research Services of the Birmingham Veterans Medical Center (Dr. Whitaker), Birmingham, AL.
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John N. Whitaker
From the Department of Neurology and the Center for NeuroimmunologyUniversity of Alabama at Birmingham; and Neurology and Research Services of the Birmingham Veterans Medical Center (Dr. Whitaker), Birmingham, AL.
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Clinical and laboratory features of primary progressive and secondary progressive MS
Khurram Bashir, John N. Whitaker
Neurology Sep 1999, 53 (4) 765; DOI: 10.1212/WNL.53.4.765

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Abstract

Objective: To compare the clinical and laboratory features of primary progressive (PP) and secondary progressive (SP) MS, to evaluate the role of CSF and urine myelin basic protein-like material (MBPLM) in differentiating PP from SP MS, and to assess the utility of urine MBPLM as a surrogate marker of disease activity in progressive MS.

Background: The current categorization of subtypes of MS is based solely on clinical and temporal characteristics of the disease. Laboratory markers are needed that can differentiate reliably the subtypes of MS and serve as surrogate markers of disease progression.

Methods: Clinical and paraclinical data of 51 PPMS and 140 SPMS patients were reviewed retrospectively. CSF and urine MBPLM were measured using a double-antibody radioimmunoassay.

Results: PPMS was more likely to present with progressive myelopathy (p ≤ 0.001) after the age of 40 years (p = ≤0.001), and it affected men relatively more often than SPMS (male-to-female ratio, 1:1.7 versus 1:3.2 respectively). Ambulatory assistance was required by PP patients more often and earlier than in those with SPMS. The incidence of abnormal CSF, evoked potential, and cranial MRI studies was similar in the two groups. Spinal cord MRI abnormalities were noted significantly more often in SP disease. There was an insignificant trend of higher CSF MBPLM in SPMS compared with PPMS. Urine MBPLM and MBPLM/creatinine were significantly higher in SPMS than in PPMS. However, the values of urine MBPLM and MBPLM/creatinine at the initial visits of patients with PPMS and SPMS were not significantly different. Urine MBPLM/creatinine was significantly higher in both PPMS and SPMS compared with normal control subjects. No correlation was found between urine MBPLM and disease duration or between urine MBPLM and clinical disability. There was no correlation between urine MBPLM/creatinine and either disease duration or clinical disability.

Conclusions: These findings provide additional evidence of the differences in PPMS and SPMS, notably in the associated changes in MBPLM in urine, and also suggest a possible role for urine MBPLM in identifying patient cohorts. The high urine MBPLM levels in progressive MS patients indicate a potential role of this marker for assessing responsiveness to therapeutic interventions.

  • Received September 28, 1998.
  • Accepted in final form April 3, 1999.
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