02260nas a2200409 4500000000100000008004100001260001300042653001500055653001000070653000900080653002200089653001500111653001000126653001100136653001100147653002100158653001900179653001200198653000900210653001600219653001800235653002200253653001500275653001300290653002200303653003200325100001600357700001500373700001500388700001400403245016100417856007800578300001000656490000800666520116200674022001401836 2002 d c2002 May10aAdolescent10aAdult10aAged10aAged, 80 and over10aBiomarkers10aChild10aFemale10aHumans10aInterferon-gamma10aInterleukin-1010aleprosy10aMale10aMiddle Aged10aMotor Neurons10aNeurons, Afferent10aRecurrence10aSteroids10aTreatment Outcome10aTumor Necrosis Factor-alpha1 aManandhar R1 aShrestha N1 aButlin C R1 aRoche P W00aHigh levels of inflammatory cytokines are associated with poor clinical response to steroid treatment and recurrent episodes of type 1 reactions in leprosy. uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1906406/pdf/cei0128-0333.pdf a333-80 v1283 a

Levels of leprosy antigen-induced interferon-gamma (IFN-gamma), tumour necrosis factor alpha (TNF-alpha) and interleukin-10 (IL-10) were measured in 96 leprosy patients with type 1 reactions (T1R) before, during and after a standard 12-week course of steroids. Peripheral blood mononuclear cells (PBMC) from leprosy patients with untreated T1R produced significantly more TNF-alpha than leprosy patients without T1R. Median levels of IFN-gamma and TNF-alpha in T1R patients fell during treatment with steroids; however, TNF-alpha levels increased as the steroid dose was reduced. Median IL-10 levels increased throughout the steroid treatment period and were associated strongly with TNF-alpha levels. Patients with high cytokine levels had a poorer recovery of sensory or voluntary muscle nerve function, a higher risk of reactivation of symptoms during steroid treatment, and a higher risk of another episode of T1R within 2 months of completing the steroid regimen. Rapid and effective reversal of the inflammatory process in T1R is critical to prevent permanent nerve damage from T1R and monitoring cytokine levels during treatment may be useful.

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