RESUMO
As we have argued before (Cooper et al, CCMRC, 1989) the association between chronic Trichuris colitis and linear growth retardation is specific: the variability in the degree of wasting, the pattern of post-treatment catch-up growth in which weight-for-height often remains constant or actually falls and the accelerated height velocity without a change in environment, all point to the existence of some endogenous growth-suppressing factor. A candidate for this factor is the cytokine and mediator of systemic inflammation tumour necrosis factor alpha (TNF), also known as cachectin. Thirteen children with the Trichuris dysentery syndrome had a mean height-for-age of -2.3 (SD 1.34) NCHS Z-scores. Plasma TNF was assayed by ELISA. 9/13 were positive (>20 pg ml-1). Values ranged from 0 to 99 pg/ml,-1, similar to those reported in acute but uncomplicated attacks of malaria. Controls: 10 paediatric surgery follow-up patients (height Z-score + 0.1) had plasma TNF < 20 pg ml-1; in 9 stunted but parasite-free children from the community (study of Grantham-Mcgregor) TNF was undetectable. Culture of colonic mucosal mononuclear cells from four of the Trichuris colitis children yielded higher concentrations of TNF in the supernatants than those of four non-Trichuris mild, non-specific colitis patients. This suggests that the source of the increased plasma TNF may be the lamina propria macrophages, increased in number in trichuriasis as we have already described (MacDonald et al, CCMRC. 1989) (AU)
