Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_827_Библиотеки_им_академика_М_И_Перельмана

Evaluation of the effect of age on human hematopoiesis at the organ or cellular level demonstrates evidence of a dimin­ished reserve capacity. Abnormalities in function, not evi­denced in the basal state, become apparent in the stimulus-driven state. In addition to being lower, the aging response tends to be more variable. Given a comparable stress, hematologic abnormalities are likely to occur earlier and to be of greater severity in elderly than in younger per­sons. Thus, the rate of return of the hemoglobin level to nor­mal following phlebotomy may be blunted, and the ability to mount a granulocyte response to infection may be reduced. Data from earlier studies suggest that in the setting of severe infection, older patients may have normal or suppressed granulocyte counts. However, the precise definition of “elderly” and the impact of coexistent comorbidities and concomitant medications were not accounted for in these studies [3, 4]. Based on contemporary literature, it is true that a blunted hematopoietic response to different insults may be seen in the elderly [5, 6]. However, this can be overcome by the administration of exogenous growth factors [7, 8]. Furthermore, the relative contributions of age per se and age­related comorbidities to this suboptimal response are unclear. Several elegant animal studies have shown a reduced ability of the aged hematopoietic system to respond to a sustained insult [1]. Similar studies in humans are either not feasible or have been inconclusive. It is currently believed that HSC function in humans, though finite, is well in excess of human life span. Thus, diminutions in hematopoietic reserve capac­ity in aging humans may only be of clinical relevance in the presence of other comorbidities (occult or latent)1 or under conditions of extreme hematopoietic stress [1].