ABSTRACT Background: Patients with multiple sclerosis experience various disabilities, depending on the number and placement of lesions in the brain. Red blood cells with impaired membrane fluidity, as has been reported in patients with multiple sclerosis are known to be further targeted by phospholipase A2 during inflammatory activation. Objectives: The objective of the present study was therefore to investigate the haematological profile of patients with multiple sclerosis and to correlate this with their functional disability and inflammatory status. Methods: Differential full blood counts of 31 patients with multiple sclerosis and 30 age- and gender-matched control subjects were determined on a Beckman Coulter. The functional disability status of each patient was measured using the Kurtzke Expanded Disability Status Scale. C-reactive protein was determined on a Beckman auto-analyser. Results: The haemoglobin was significantly decreased in patients: 13.9 ± 1.40 g/dl, controls: 14.7 ± 1.60 g/dl, P = 0.01, while platelets were increased in patients: 292 ± 133 × 109/l, controls: 258 ± 88.0 × 109/l, P = 0.04. The number of red blood cells correlated inversely with the Kurtzke Expanded Disability Status Scale (R = –0.41; P = 0.02). Platelets correlated inversely with the haemoglobin (P = 0.04) and positively with Visual and Brainstem Scores (P < 0.01, P = 0.07 respectively), but inversely with the Sensory Score (P = 0.02). Conclusions: It is not clear from the results whether the compromised red blood cell profile in patients was due to unknown agents involved in the disease aetiology or from the resulting inflammatory responses, but the inverse correlation between the red blood cell count and the Kurtzke Expanded Disability Status Scale, a measure of neuronal function, suggested a relationship between red blood cell count and disease outcome. Furthermore, the inverse correlation of platelets with the haemoglobin suggested immunological involvement. Platelets, similar to white blood cells, supply fatty acids for pro-inflammatory eicosanoid synthesis.
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