Уважаемая Галина Афанасьевна!
Огромное спасибо за подробный ответ и предложения о возможных публикациях. Мне вообще не нравится спорить: стараюсь не принимать участия в них или сразу выхожу из него. Мне кажется, что мы с вами дискутируем и это всегда обоюдополезно для участвующих в целях получения более новой полной информации о состоянии медицины на текущий момент, поэтому можем ее продолжать в любом для Вас более удобном месте, просто пришлите мне ссылку.
Однако, хотя и первичный гипотиреоз и может быть ответственен за различные нарушения в месячном цикле, но отсутствуют (за исключением единичных наблюдений) данные, что он вызывает обильные кровевыделения на фоне нормальных цикличных менструаций.
В связи с тем, что распространенность железодефицита [не анемий!] (до 30-40% у женщин, свыше 50% у детей) с лихвой перекрывает таковую для гипотиреоза, логично было бы заключить, что если Fe-дефицит и не вызывает гипотиреоз, то все же существует высокая вероятность их сосуществования, что вы и можете наблюдать в Вашей клинике, опираясь на мою статистику и что гипотиреоз чаще выявляется у женщин, то несложно предугадать, что железодефицит выявится у каждой второй-третьей.
Более целесообразным на мой взгляд будет разместить на Вашем сайте перевод (не ошибусь, если скажу, что многие наши коллеги не понимают английского) уже опубликованных в мировой литературе статей, показывающих значимость железа в генезе и лечении гипофункции ЩЖ.
Mayo Clin Proc 2000 Feb;75(2):189-92 Anemia: a cause of intolerance to thyroxine sodium.
Shakir KM, Turton D, Aprill BS, Drake AJ 3rd, Eisold JF.
Department of Internal Medicine, National Naval Medical Center, Bethesda, Md., 20889-5600, USA.
Usual causes of intolerance to thyroxine sodium include coronary artery disease, advanced age, untreated adrenal insufficiency, and severe hypothyroidism. We describe 4 patients with iron deficiency anemia and primary hypothyroidism. After treatment with thyroxine sodium, these patients developed palpitations and feelings of restlessness, which necessitated discontinuation of the thyroid hormone. After the anemia was treated with ferrous sulfate for 4 to 7 weeks, they were able to tolerate thyroxine sodium therapy. Iron deficiency anemia coexisting with primary hypothyroidism results in a hyperadrenergic state. In such patients, we postulate that thyroid hormone administration causes palpitations, nervousness, and feelings of restlessness. Correction of any existing pronounced anemia in hypothyroid patients who are intolerant to thyroxine sodium therapy may result in tolerance to this agent.
Am J Clin Nutr 2002 Apr;75(4):743-8
Treatment of iron deficiency in goitrous children improves the efficacy of iodized salt in Cote d'Ivoire.
Hess SY, Zimmermann MB, Adou P, Torresani T, Hurrell RF.
Human Nutrition Laboratory, the Swiss Federal Institute of Technology, Zurich, Switzerland.
BACKGROUND: In many developing countries, children are at high risk of both goiter and iron deficiency anemia. Iron deficiency adversely affects thyroid metabolism and may reduce the efficacy of iodine prophylaxis in areas of endemic goiter. OBJECTIVE: The aim of this study was to determine whether iron supplementation in goitrous, iron-deficient children would improve their response to iodized salt. DESIGN: We conducted a randomized, double-blind, placebo-controlled trial in 5-14-y-old children in Cote d'Ivoire. Goitrous, iron-deficient children (n = 166) consuming iodized salt (10-30 mg I/kg salt at the household level) were supplemented with either iron (60 mg Fe/d, 4 d/wk for 16 wk) or placebo. At 0, 1, 6, 12, and 20 wk, we measured hemoglobin, serum ferritin, serum transferrin receptor, whole-blood zinc protoporphyrin, thyrotropin, thyroxine, urinary iodine, and thyroid gland volume (by ultrasonography). RESULTS: Hemoglobin and iron status at 20 wk were significantly better after iron treatment than after placebo (P < 0.05). At 20 wk, the mean reduction in thyroid size in the iron-treated group was nearly twice that in the placebo group (x +/- SD percentage change in thyroid volume from baseline: -22.8 +/- 10.7% compared with -12.7 +/- 10.1%; P < 0.01). At 20 wk, goiter prevalence was 43% in the iron-treated group compared with 62% in the placebo group (P < 0.02). There were no significant differences between groups in whole-blood thyrotropin or serum thyroxine at baseline or during the intervention. CONCLUSIONS: Iron supplementation improves the efficacy of iodized salt in goitrous children with iron deficiency. A high prevalence of iron deficiency among children in areas of endemic goiter may reduce the effectiveness of iodine prophylaxis.
Eur J Endocrinol 2002 Dec;147(6):747-53
Addition of microencapsulated iron to iodized salt improves the efficacy of iodine in goitrous, iron-deficient children: a randomized, double-blind, controlled trial.
Zimmermann MB, Zeder C, Chaouki N, Torresani T, Saad A, Hurrell RF.
The Human Nutrition Laboratory, Swiss Federal Institute of Technology, Seestrasse 72/PO Box 474, CH-8803 Ruschlikon, Switzerland. michael.zimmermann@ilw.agrl.ethz.ch
OBJECTIVE: In many developing countries, children are at high risk for both goiter and anemia. Iron (Fe) deficiency adversely effects thyroid metabolism and reduces efficacy of iodine prophylaxis in areas of endemic goiter. The study aim was to determine if co-fortification of iodized salt with Fe would improve efficacy of the iodine in goitrous children with a high prevalence of anemia. DESIGN AND METHODS: In a 9-month, randomized, double-blind trial, 6-15 year-old children (n=377) were given iodized salt (25 microg iodine/g salt) or dual-fortified salt with iodine (25 microg iodine/g salt) and Fe (1 mg Fe/g salt, as ferrous sulfate microencapsulated with partially hydrogenated vegetable oil). RESULTS: In the dual-fortified salt group, hemoglobin and Fe status improved significantly compared with the iodized salt group (P<0.05). At 40 weeks, the mean decrease in thyroid volume measured by ultrasound in the dual-fortified salt group (-38%) was twice that of the iodized salt group (-18%) (P<0.01). Compared with the iodized salt group, serum thyroxine was significantly increased (P<0.05) and the prevalence of hypothyroidism and goiter decreased (P<0.01) in the dual-fortified salt group. CONCLUSION: Addition of encapsulated Fe to iodized salt improves the efficacy of iodine in goitrous children with a high prevalence of anemia.
Int J Vitam Nutr Res 2002 Oct;72(5):296-9
The relation between serum ferritin and goiter, urinary iodine and thyroid hormone concentration.
Azizi F, Mirmiran P, Sheikholeslam R, Hedayati M, Rastmanesh R.
Endocrine Research Center, Shaheed Beheshti University of Medical Sciences, Tehran, I.R. Iran. azizi@erc-iran.com
OBJECTIVE: Many children are at high risk of both goiter and iron deficiency in Iran. Because iron deficiency may impair the efficacy of iodine supplementation, the aim of this study was to determine the relation between serum ferritin and goiter, urinary iodine, and thyroid hormones following iodized salt supplementation. DESIGN: A cross-sectional study of schoolchildren in 26 Iranian provinces. METHODS: In a national iodine deficiency disorders (IDD) monitoring program, 36,178 schoolchildren, approximately 1200 from each province, received goiter grading by WHO criteria. Urine and serum samples were collected from 2917 children and assayed for urinary iodine and serum ferritin, T4, T3, and thyroid-stimulating hormone (TSH) concentrations. RESULTS: Total goiter rates were 80 and 20% in children with ferritin concentrations < 10 mg/dL and > or = 10 mg/dL, respectively (p < 0.001). Increased serum T3 and decreased resin T3 uptake was present in those with lower serum ferritin levels; however, free T3 and T4 index, serum T4, and TSH were not significantly different between those with low and normal ferritin. CONCLUSION: Iron deficiency is associated with a high prevalence of goiter in Iranian schoolchildren.
Thyroid 2002 Oct;12(10):867-78
The impact of iron and selenium deficiencies on iodine and thyroid metabolism: biochemistry and relevance to public health.
Zimmermann MB, Kohrle J.
Laboratory for Human Nutrition, Swiss Federal Institute of Technology, Zurich, Switzerland.
Several minerals and trace elements are essential for normal thyroid hormone metabolism, e.g., iodine, iron, selenium, and zinc. Coexisting deficiencies of these elements can impair thyroid function. Iron deficiency impairs thyroid hormone synthesis by reducing activity of heme-dependent thyroid peroxidase. Iron-deficiency anemia blunts and iron supplementation improves the efficacy of iodine supplementation. Combined selenium and iodine deficiency leads to myxedematous cretinism. The normal thyroid gland retains high selenium concentrations even under conditions of inadequate selenium supply and expresses many of the known selenocysteine-containing proteins. Among these selenoproteins are the glutathione peroxidase, deiodinase, and thioredoxine reductase families of enzymes. Adequate selenium nutrition supports efficient thyroid hormone synthesis and metabolism and protects the thyroid gland from damage by excessive iodide exposure. In regions of combined severe iodine and selenium deficiency, normalization of iodine supply is mandatory before initiation of selenium supplementation in order to prevent hypothyroidism. Selenium deficiency and disturbed thyroid hormone economy may develop under conditions of special dietary regimens such as long-term total parenteral nutrition, phenylketonuria diet, cystic fibrosis, or may be the result of imbalanced nutrition in children, elderly people, or sick patients.
