Препараты железа и количество лейкоцитов

[HollisMP]

Здравствуйте.
Вопрос в том, влияет ли приём препаратов железа на количество лейкоцитов и фагоцитоз? Сегодня был спор с коллегой, где она опиралась на наличие работ, доказывающих достоверное снижение количества лейкоцитов и угнетение фагоцитоза вследствие приёма препаратов железа. Именно поэтому в нашем отделении препараты железа детям не даются, лечение ими только амбулаторное и на фоне полного здоровья. Не могу найти работ по данной теме в интернете. Помогите, пожалуйста, прояснить ситуацию.

[Dr.Vad]

IMMUNITY AND INFECTION
The relationship between iron deficiency and infection is complex (334,335 and 336). Iron deficiency clearly results in at least two abnormalities in the immune response: defective lymphocyte-mediated immunity and impaired bacterial killing by phagocytes. Evidence of defective cellular immunity includes as much as a 35% reduction in the number of circulating T cells. Both helper and suppressor T cells are affected (337). In addition, iron-deficient subjects do not respond as well as normal subjects to certain skin test antigens, such as to Candida, diphtheria, and Trichophyton. These abnormalities can be corrected by the administration of iron. No abnormalities have been noted in testing with tuberculin or dinitrochlorobenzene. Ribonucleotide reductase is an iron-containing enzyme required for the synthesis of DNA for cell division. Some authors have suggested that reduced levels of this enzyme might lead to impaired ability of the T cells to proliferate, thereby accounting for the defects in cell-mediated immunity, but others have reported changes in cytokine production in iron-deficient patients.
The nitroblue tetrazolium dye test of phagocyte function yielded abnormal results in iron-deficient children, and the abnormality could be corrected by iron administration (338,339). Furthermore, a decrease in the magnitude of the “oxidative burst” accompanying phagocytosis was observed (340). Finally, killing of several types of pathogenic bacteria by neutrophils was defective (338,341).
The sequence of changes in neutrophil function was studied as iron deficiency developed in rats. Myeloperoxidase activity was reduced to a greater extent and responded more slowly to iron therapy than did defects in the oxidative burst (342). Because the oxidative burst is considerably more important in bacterial killing than is myeloperoxidase, the observations suggest that the neutrophil conserves its most important function as the deficiency develops. The defect in the oxidative burst could be demonstrated only with the use of agents that induced phagocytosis; no defect was noted when the burst was stimulated by soluble agents. Thus, phagocytosis, rather than the oxidative burst itself, may be at fault.
Taken together, these abnormalities provide a basis for an expectation that resistance to infection may be impaired in iron deficiency. Conversely, considerable data suggest that iron deficiency and iron sequestration by binding proteins protect against infection by depriving the invading organisms of the metal. Thus, optimal immune function is highly dependent on iron balance; both iron-deficient and iron-overloaded hosts are at higher risk for infection.
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из главы Signs and Symptoms of Iron Deficiency

учебник-книга по гематологии для студентов и врачей Wintrobe's Clinical Hematology, 11th Edition, 2004.

[HollisMP]

Да, я тоже нашла, что именно дефицит железа приводит к данным изменениям, а не дача препаратов. Спасибо.