WESTPORT, CT (Reuters Health) Oct 25 - The pattern of interleukin-10 (IL-10) and tumor necrosis factor (TNF) production affects the risk of developing multiple sclerosis (MS), as well as the nature of the disease, according to a report in the October issue of the Annals of Neurology.
Immune-mediated inflammation plays a more important role in typical MS than in primary progressive MS, causing the authors to ponder whether cytokine production might play a role in the susceptibility to and outcome of MS.
Accordingly, Dr. Rudi G. J. Westendorp, from Leiden University Medical Center, in the Netherlands, and colleagues tested 50 patients with typical MS, 25 patients with primary progressive MS, 189 first-degree relatives and unrelated controls for their innate production of IL-10 and TNF.
Families of patients with typical MS had IL-10 production 12% lower than control families and 11% below families of patients with primary progressive MS, the authors report.
In contrast, TNF production in families of patients with typical MS was 10% higher than in control families and 20% higher than in families of patients with primary progressive MS, the report indicates.
Families with both low IL-10 and high TNF production faced a 4.2-fold increased risk of developing typical MS over that of families with high IL-10 and low TNF production, the researchers note, and an 8-fold increased risk of developing typical MS instead of primary progressive MS.
Disease progression in typical MS was not related to the level of production of IL-10 or TNF, the investigators observe.
"This study shows that typical MS is associated with an innate proinflammatory cytokine profile in contrast to primary progressive MS," the authors conclude.
"In our opinion," the researchers write, "this is the first evidence in human subjects that genetically determined cytokine production is related to the susceptibility for and outcome of MS."
"These observations," they believe, "give further support to the recently advocated view that primary progressive MS is a distinct form of MS and confirm the idea of heterogeneity in the pathogenesis of the disease."
Ann Neurol 2000;48:641-646.