EFFICIENCY OF TREATMENT FOR LATENT IRON DEFICIENCY IN PREGNANT WOMEN WITH CHRONIC PYELONEPHRITIS


Cite item

Full Text

Open Access Open Access
Restricted Access Access granted
Restricted Access Subscription or Fee Access

Abstract

Objective. To comparatively estimate the time course of changes in the functional, transport, and iron regulatory funds of iron metabolism in pregnant women with latent iron def iciency (LID) and chronic pyelonephritis treated and untreated with iron III hydroxide polymaltose complex. Subjects and methods. The trial enrolled 119 pregnant women, 52 of whom had LID and chronic pyelonephritis (Group 1) and 67 LID patients without urinary tract infection (UTI) (Group 2). According to the presence or absence of LID treatment, Group 1 and 2 patients were divided into subgroups: 1A) 24 pregnant women with chronic pyelonephritis and treated LID; 1B) 28pregnant women with chronic pyelonephritis and untreated LID; 2A) 31 pregnant women with non- UTI and treated LID; 2B) 36 pregnant women with non-UTI and untreated LID. The treatment or selective prevention of LID involved the use of iron preparations in the pregnant women with LID diagnosed by laboratory tests for iron metabolic parameters. Results. The time course of changes in the functional, transport, and iron regulatory funds of iron metabolism (hemoglobin, red blood cells, packed cell volume, red blood cell indices, serum iron, soluble transferrin receptors, iron transferrin saturation coefficient, erythropoietin (EPO), and its production adequacy ratio (PAR) was studied in the pregnant women with LID and chronic pyelonephritis treated and untreated with iron III hydroxide polymaltose complex. The efficiency of selective prevention of manifest iron deficiency (LID treatment in the pregnant women) depended on the level of endogenous EPO. In the pregnant women with LID and chronic pyelonephritis who had an EPO PAR of 40.8, the therapeutic efficiency was 70.9%, which was significantly lower than that (93.55%) in the LID patients without chronic pyelonephritis who had an EPO PAR of >0.8. Conclusion. LID treatment in the pregnant women prevents manifest iron deficiency, causing the incidence of placental insufficiency and fetal growth retardation to reduce.

Full Text

Restricted Access

About the authors

E. N KONOVODOVA

Acad. V.I. Kulakov Research Center of Obstetrics, Gynecology, and Perinatology; I.M. Sechenov First Moscow State Medical University

Email: kenzaen@rambler.ru

V. L TYUTYUNNIK

Acad. V.I. Kulakov Research Center of Obstetrics, Gynecology, and Perinatology

Email: tioutiounnik@mail.ru

N. A YAKUNINA

Acad. V.I. Kulakov Research Center of Obstetrics, Gynecology, and Perinatology

Email: doc-yakunina@yandex.ru

A. A PODYMOVA

I.M. Sechenov First Moscow State Medical University

Email: an-pod@yandex.ru

References

  1. Бурлев В.А. Воспалительный стресс: системный ангиогенез, белки острой фазы и продукты деструкции тканей у больных хроническим рецидивирующим саль-пингоофоритом. Проблемы репродукции. 2011; 5: 25—32.
  2. Бурлев В.А., Коноводова Е.Н., Орджоникидзе Н.В., Серов В.Н., Елохина Т. Б., Ильясова Н. А. Лечение беременных с латентным дефицитом железа. Российский вестник акушера-гинеколога. 2006; 1: 64—8.
  3. Коноводова Е.Н. Железодефицитные состояния у беременных и родильниц (патогенез, диагностика, про филактика, лечение): Автореф. дис.. д-ра мед. наук. М.; 2008: 46 с.
  4. Сухих Г.Т, ред. Беременность и роды при заболеваниях мочевыводящих органов. Орджоникидзе Н.В., Емельянова А.И., Панов В.О. и др. М.; 2009: 432 с.
  5. Румянцев А.Г., Морщакова Е.Ф., Павлов А.Д. Эритропоэтин в диагностике, профилактике и лечении анемий. М.; 2003: 447 с.
  6. Сухих Г.Т., Протопопова Т.Т., ред. Железодефицитные состояния у беременных и родильниц: Учебное пособие. Серов В.Н., Бурлев В.А., Коноводова Е.Н. и др. М.; 2009: 80 с.
  7. Хух Р., Брейман К. Анемия во время беременности и в послеродовом периоде. М.: Триада-Х; 2007: 73 с.
  8. Шехтман М.М. Акушерская нефрология. М.; 2000: 256 с.
  9. Allen L. Anemia and iron deficiency: effects on pregnancy outcome Am. J. Clin. Nutr. 2000; 71 (5): 1280—4.
  10. Gambling L., Andersen H., McArdle H. Iron and copper, and their interactions during development. Biochem. Soc. Trans. 2008; 36 (6): 1258—61.
  11. Gordon N. Iron deficiency and the intellect. Brain Dev. 2003; 25: 3—8.
  12. Haram K., Nilsen S., Ulvik R. Iron supplementation in pregnancy — evidence and controversies. Acta Obstet. Gynecol. Scand. 2001; 80: 683—8.
  13. Lozoff B. Iron deficiency and child development. Food Nutr. Bull. 2007; 28 (4): 560—71.
  14. Smiroldo S., Sacco S., Columbo F. et al. The role of infections in preterm labour. Book of abstracts 13th World Congress of Gynecological Endocrinology, Florence. Gynecol. Endocrinol. 2008; 24 (1): 158.
  15. Suominen P., Punnonen K, Rajamaki A., Irjala K. Serum transferrin receptor and transferrin receptor-ferritin index identify healthy subjects with subclinical iron deficits. Blood. 1998; 92 (8): 2934—9.

Supplementary files

Supplementary Files
Action
1. JATS XML

This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies