Патофизиологические особенности развития функциональной гипоталамической аменореи у пациенток с нервной анорексией
Патофизиологические особенности развития функциональной гипоталамической аменореи у пациенток с нервной анорексией
Чернуха Г.Е., Гусев Д.В., Табеева Г.И., Прилуцкая В.Ю. Патофизиологические особенности развития функциональной гипоталамической аменореи у пациенток с нервной анорексией. Гинекология. 2018; 20 (1): 16–22.
DOI: 10.26442/2079-5696_20.1.16-22
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Chernukha G.E., Gusev D.V., Tabeeva G.I., Prilutskaia V.Yu. Pathophysiological features of development of functional hypothalamic amenorrhea in patients with anorexia nervosa. Gynecology. 2018; 20 (1): 16–22.
DOI: 10.26442/2079-5696_20.1.16-22
Патофизиологические особенности развития функциональной гипоталамической аменореи у пациенток с нервной анорексией
Чернуха Г.Е., Гусев Д.В., Табеева Г.И., Прилуцкая В.Ю. Патофизиологические особенности развития функциональной гипоталамической аменореи у пациенток с нервной анорексией. Гинекология. 2018; 20 (1): 16–22.
DOI: 10.26442/2079-5696_20.1.16-22
________________________________________________
Chernukha G.E., Gusev D.V., Tabeeva G.I., Prilutskaia V.Yu. Pathophysiological features of development of functional hypothalamic amenorrhea in patients with anorexia nervosa. Gynecology. 2018; 20 (1): 16–22.
DOI: 10.26442/2079-5696_20.1.16-22
Энергетический дефицит является результатом недостаточного поступления энергии по сравнению с ее высокими расходами. Развитие дефицита энергии часто связано со стремлением похудеть, строгой диетой, а также с беспокойством женщины о своем весе вместе с изменением пищевого поведения. Результатом расстройств приема пищи в комплексе со снижением массы тела является нервная анорексия, сопровождающаяся энергетическим дефицитом. Физиологические изменения, происходящие на фоне хронического энергетического дефицита, способствуют включению компенсаторных механизмов сохранения энергии для обеспечения жизненно важных физиологических функций. К наиболее частым метаболическим изменениям относят гиполептинемию на фоне снижения процентного содержания жировой ткани, снижение трийодтиронина, а также повышение концентраций грелина, пептида YY и нейропептида Y. Эффект энергетических и метаболических изменений приводит к подавлению гипоталамо-гипофизарно-яичниковой оси, секреции гонадотропин-рилизинг-гормона с последующим подавлением высвобождения лютеинизирующего и фолликулостимулирующего гормонов. Подавление гипоталамо-гипофизарно-яичниковой оси приводит к хроническому дефициту эстрогенов, что сопровождается развитием функциональной гипоталамической аменореи.
Ключевые слова: нервная анорексия, аменорея, расстройства приема пищи, лептин.
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The energy deficit is the result of insufficient energy intake compared to its high costs. The development of energy deficiency is often associated with the desire to lose weight, a strict diet, as well as the woman's concern about her weight along with a change in eating behavior. The result of eating disorders in combination with a decrease in body weight is anorexia nervosa, accompanied by an energy deficit. Physiological changes occurring against a background of chronic energy deficiency contribute to the inclusion of compensatory mechanisms of energy conservation to provide vital physiological functions. The most frequent metabolic changes include hypoleptinemia in the presence of a decrease in the percentage of fat tissue, a decrease in triiodothyronine, and an increase in the concentrations of ghrelin, peptide YY and neuropeptide Y. The effect of energy and metabolic changes leads to suppression of the hypothalamic-pituitary-ovarian axis, gonadotropin releasing hormone secretion, with the subsequent suppression of the release of luteinizing and follicle stimulating hormones. The suppression of the hypothalamic-pituitary-ovarian axis leads to chronic estrogen deficiency, which is accompanied by the development of functional hypothalamic amenorrhea.
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2. Practice Committee of the American Society for Reproductive Medicine Current evaluation of amenorrhea. Fertil Steril 2006; 86: S148.
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10. Berga SL, Girton LG. The psychoneuroendocrinology of functional hypothalamic amenorrhea. Psychiatr Clin North Am 1989; 12: 105–16.
11. Dundon CM, Rellini AH, Tonani S et al. Mood disorders and sexual functioning in women with functional hypothalamic amenorrhea. Fertil Steril 2010; 94 (6): 2239–43.
12. Berga S, Loucks T. Use of cognitive behavior therapy for functional hypothalamic amenorrhea. Ann N Y Acad Sci 2006; 1092: 114–29.
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17. Cumella EJ, Wall AD, Kerr-Almeida N. MMPI-2 in the inpatient assessment of women with eating disorders. J Pers Assess 2000; 75 (3): 387–403.
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22. Walsh BT, Kaplan AS, Attia E et al. Fluoxetine after weight restoration in anorexia nervosa: a randomized controlled trial. JAMA 2006; 295 (22): 2605.
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25. Gorwood P, Ades J, Bellodi L et al. The 5-HT(2A) -1438G/A polymorphism in anorexia nervosa: a combined analysis of 316 trios from six European centres. Mol Psychiatry 2002; 7 (1): 90–4.
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27. Kaye W. Neurobiology of anorexia and bulimia nervosa. Physiol Behav 2007.
28. Kaye WH, Frank GK, McConaha C. Altered dopamine activity after recovery from restricting-type anorexia nervosa. Neuropsychopharmacology 1999; 21 (4): 503–6.
29. Bergen AW, Yeager M, Welch RA et al. Association of multiple DRD2 polymorphisms with anorexia nervosa. Neuropsychopharmacology 2005; 30 (9): 1703–10.
30. Bachner-Melman R, Lerer E, Zohar AH et al. Anorexia nervosa, perfectionism, and dopamine D4 receptor (DRD4). Am J Med Genet B Neuropsychiatr Genet 2007.
31. Ando T, Komaki G, Naruo T et al. Possible role of preproghrelin gene polymorphisms in susceptibility to bulimia nervosa. Am J Med Genet B Neuropsychiatr Genet 2006; 141 (8): 929–34.
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35. Luo E, Stephens SB, Chaing S et al. Corticosterone blocks ovarian cyclicity and the LH surge via decreased kisspeptin neuron activation in female mice. Endocrinology 2016; 157 (3): 1187–99.
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37. Breen KM, Davis TL, Doro LC et al. Insight into the neuroendocrine site and cellular mechanism by which cortisol suppresses pituitary responsiveness to gonadotropin-releasing hormone. Endocrinology 2008; 149: 767–73.
38. Oakley AE, Breen KM, Clarke IJ et al. Cortisol reduces gonadotropin-releasing hormone pulse frequency in follicular phase ewes: in uence of ovarian steroids. Endocrinology 2009; 150: 341–9.
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40. Frisch RE, McArthur JW. Menstrual cycles: Fatness as a determinant of mini- mum weight for height necessary for their maintenance or onset. Science 1974; 185: 949–51.
41. Miller KK, Grinspoon S, Gleysteen S et al. Preservation of neuroendocrine control of reproductive function despite severe undernutrition. J Clin Endocrinol Metab 2004; 89: 4434–8.
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1. Pettersson F, Fries H, Nillius SJ. Epidemiology of secondary amenorrhea. I. Incidence and prevalence rates. Am J Obstet Gynecol 1973; 117 (1): 80–6.
2. Practice Committee of the American Society for Reproductive Medicine Current evaluation of amenorrhea. Fertil Steril 2006; 86: S148.
3. Hoek HW, van Hoeken D. Review of the prevalence and incidence of eating disorders. Int J Eat Disord 2003; 34 (4): 383–96.
4. Wakeling A. Epidemiology of anorexia nervosa. Psychiatry Res 1996; 62 (1): 3–9.
5. Stoving RK, Hangaard J, Hansen-Nord M, Hagen C. A review of endocrine changes in anorexia nervosa. J Psychiatr Res 1999; 33: 139–52.
6. Franko DL, Keshaviah A, Eddy KT et al. A longitudinal investigation of mortality in anorexia nervosa and bulimia nervosa. Am J Psychiatry 2013; 170: 917–25.
7. Roux H, Blanchet C, Stheneur C et al. Somatic outcome among patients hospitalised for anorexia nervosa in adolescence: disorders reported and links with global outcome. Eat Weight Disord 2013; 18: 175–82.
8. Roux H, Chapelon E, Godart N. Epidemiology of anorexia nervosa: a review. Encephale 2013; 39: 85–93.
9. Giles DE, Berga SL. Cognitive and psychiatric correlates of functional hypothalamic amenorrhea: a controlled comparison. Fertil Steril 1993; 60: 486–92.
10. Berga SL, Girton LG. The psychoneuroendocrinology of functional hypothalamic amenorrhea. Psychiatr Clin North Am 1989; 12: 105–16.
11. Dundon CM, Rellini AH, Tonani S et al. Mood disorders and sexual functioning in women with functional hypothalamic amenorrhea. Fertil Steril 2010; 94 (6): 2239–43.
12. Berga S, Loucks T. Use of cognitive behavior therapy for functional hypothalamic amenorrhea. Ann N Y Acad Sci 2006; 1092: 114–29.
13. Bomba M, Gambera A, Bonini L et al. Endocrine profiles and neuropsychologic correlates of functional hypothalamic amenorrhea in adolescents. Fertil Steril 2007; 87: 876–85.
14. Nappi R, Facchinetti F. Psychoneuroendocrine correlates of secondary amenorrhea. Arch Womens Ment Health 2003; 6: 83–9.
15. Garner DM, Olmsted MP, Polivy J. Development and validation of a multidimensional eating disorder inventory for anorexia nervosa and bulimia. Int J Eat Disord 1983; 2: 15–34.
16. Pop-Jordanova N. MMPI for personality characteristics of patients with different diseases. Pril (Makedon Akad Nauk Umet Odd Med Nauki) 2015; 36 (1): 153–64.
17. Cumella EJ, Wall AD, Kerr-Almeida N. MMPI-2 in the inpatient assessment of women with eating disorders. J Pers Assess 2000; 75 (3): 387–403.
18. Nozaki T, Motoyama S, Arimura T et al. Psychopathological features of anorectic patients who dropped out of inpatient treatment as assessed by the Minnesota multiphasic personality inventory. Biopsychosoc Med 2007; 1: 15.
19. Grice DE, Halmi KA, Fichter MM et al. Evidence for a susceptibility gene for anorexia nervosa on chromosome 1. Am J Hum Genet 2002; 70 (3): 787–92.
20. Kaye WH, Weltzin TE, Hsu LK, Bulik CM. An open trial of fluoxetine in patients with anorexia nervosa. J Clin Psychiatry 1991; 52 (11): 464–71.
21. Kaye WH, Nagata T, Weltzin TE et al. Double-blind placebo-controlled administration of fluoxetine in restricting- and restricting-purging-type anorexia nervosa. Biol Psychiatry 2001; 49 (7): 644–52.
22. Walsh BT, Kaplan AS, Attia E et al. Fluoxetine after weight restoration in anorexia nervosa: a randomized controlled trial. JAMA 2006; 295 (22): 2605.
23. Bergen AW, van den Bree MB, Yeager M et al. Candidate genes for anorexia nervosa in the 1p33-36 linkage region: serotonin 1D and delta opioid receptor loci exhibit significant association to anorexia nervosa. Mol Psychiatry 2003; 8 (4): 397–406.
24. Brown KM, Bujac SR, Mann ET. Further evidence of association of OPRD1 & HTR1D polymorphisms with susceptibility to anorexia nervosa. Biol Psychiatry 2007; 61 (3): 367–73.
25. Gorwood P, Ades J, Bellodi L et al. The 5-HT(2A) -1438G/A polymorphism in anorexia nervosa: a combined analysis of 316 trios from six European centres. Mol Psychiatry 2002; 7 (1): 90–4.
26. Gutiérrez B, Bellón JÁ, Rivera M et al. The risk for major depression conferred by childhood maltreatment is multiplied by BDNF and SERT genetic vulnerability: a replication study. J Psy Neurosci 2015; 40 (3): 187–96.
27. Kaye W. Neurobiology of anorexia and bulimia nervosa. Physiol Behav 2007.
28. Kaye WH, Frank GK, McConaha C. Altered dopamine activity after recovery from restricting-type anorexia nervosa. Neuropsychopharmacology 1999; 21 (4): 503–6.
29. Bergen AW, Yeager M, Welch RA et al. Association of multiple DRD2 polymorphisms with anorexia nervosa. Neuropsychopharmacology 2005; 30 (9): 1703–10.
30. Bachner-Melman R, Lerer E, Zohar AH et al. Anorexia nervosa, perfectionism, and dopamine D4 receptor (DRD4). Am J Med Genet B Neuropsychiatr Genet 2007.
31. Ando T, Komaki G, Naruo T et al. Possible role of preproghrelin gene polymorphisms in susceptibility to bulimia nervosa. Am J Med Genet B Neuropsychiatr Genet 2006; 141 (8): 929–34.
32. Chernukha G.E., Tabeeva G.I., Gusev D.V. Kisspeptin i reproduktivnaia sistema. Ginekologiia i endokrinologiia. 2017; 3 (132): 72–7. [in Russian]
33. Caronia L et al. A Genetic Basis for Functional Hypothalamic Amenorrhea. N Engl J Med 2011; 364: 215–25.
34. Gunnar M, Quevedo K. The neurobiology of stress and development. Annu Rev Psychol 2007; 58: 145–73.
35. Luo E, Stephens SB, Chaing S et al. Corticosterone blocks ovarian cyclicity and the LH surge via decreased kisspeptin neuron activation in female mice. Endocrinology 2016; 157 (3): 1187–99.
36. Boyar RM, Hellman LD, Roffwarg H et al. Cortisol secretion and metabolism in anorexia nervosa. N Engl J Med 1977; 296 (4): 190–3.
37. Breen KM, Davis TL, Doro LC et al. Insight into the neuroendocrine site and cellular mechanism by which cortisol suppresses pituitary responsiveness to gonadotropin-releasing hormone. Endocrinology 2008; 149: 767–73.
38. Oakley AE, Breen KM, Clarke IJ et al. Cortisol reduces gonadotropin-releasing hormone pulse frequency in follicular phase ewes: in uence of ovarian steroids. Endocrinology 2009; 150: 341–9.
39. Frisch RE. Fatness, menarche, and female fertility. Perspect Biol Med 1985; 28: 611–33.
40. Frisch RE, McArthur JW. Menstrual cycles: Fatness as a determinant of mini- mum weight for height necessary for their maintenance or onset. Science 1974; 185: 949–51.
41. Miller KK, Grinspoon S, Gleysteen S et al. Preservation of neuroendocrine control of reproductive function despite severe undernutrition. J Clin Endocrinol Metab 2004; 89: 4434–8.
42. Tinahones FJ, Martinez-Alfaro B, Gonzalo-Marin M et al. Recovery of menstrual cycle after therapy for anorexia nervosa. Eat Weight Disord 2005; 10: e52–e55.
43. Golden NH, Jacobson MS, Schebendach J et al. Resumption of menses in anorexia nervosa. Arch Pediatr Adolesc Med 1997; 151: 16–21.
44. Al-Dakhiel Winkler L, Stampe Frølich J, Schulpen M, Klinkby Støving R, Body Composition and Menstrual Status in Adults With a History of Anorexia Nervosa – At What Fat Percentage is the Menstrual Cycle Restored? Int J Eat Disord 2016.
45. El Ghoch M, Calugi S, Chignola E et al. Body fat and menstrual resumption in adult females with anorexia nervosa: a 1-year longitudinal study. 2016 J Hum Nutr.
46. Arimura C, Nozaki T, Takakura S et al. Predictors of menstrual resumption by patients with anorexia nervosa. Eat Weight Disord 2010; 15, e226–e233.
47. Zhang Y, Proenca R, Maffei M et al. Positional cloning of the mouse obese gene and its human homologue. Nature 1994; 372: 425–32.
48. Jin L, Zhang S, Burguera BG et al. Leptin and leptin receptor expression in rat and mouse pituitary cells. Endocrinology 2000; 141: 333–9.
49. Chan JL, Heist K, DePaoli AM et al. The role of falling leptin levels in the neuroendocrine and metabolic adaptation to short-term starvation in healthy men. J Clin Invest 2003; 111: 1409–21.
50. Thong FS, McLean C, Graham TE. Plasma leptin in female athletes: relationship with body fat, reproductive, nutritional, and endocrine factors. J Appl Physiol 2000; 88: 2037–44.
51. Kyle UG, Schutz Y, Dupertuis YM, Pichard C. Body composition interpretation. Contributions of the fat-free mass index and the body fat mass index. Nutrition 2003; 19: 597–604.
52. Laughlin GA, Yen SS. Hypoleptinemia in women athletes: absence of a diurnal rhythm with amenorrhea. J Clin Endocrinol Metab 1997; 82: 318–21.
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ФГБУ «Национальный медицинский исследовательский центр акушерства, гинекологии и перинатологии им. акад. В.И.Кулакова» Минздрава России. 117997, Россия, Москва, ул. Академика Опарина, д. 4
*c-galina1@yandex.ru
V.I.Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology of the Ministry of Health of the Russian Federation. 117997, Russian Federation, Moscow, ul. Akademika Oparina, d. 4
*c-galina1@yandex.ru