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Journal articles on the topic 'Hypothalamic amenorrhea'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

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1

Warren, Michelle P., and Joanna L. Fried. "HYPOTHALAMIC AMENORRHEA." Endocrinology and Metabolism Clinics of North America 30, no. 3 (September 2001): 611–29. http://dx.doi.org/10.1016/s0889-8529(05)70204-8.

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2

Keller, Jennifer L., and Kenneth Faber. "Hypothalamic Amenorrhea." Postgraduate Obstetrics & Gynecology 28, no. 21 (November 2008): 1–5. http://dx.doi.org/10.1097/01.pgo.0000337875.34050.5a.

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3

&NA;. "Hypothalamic Amenorrhea." Postgraduate Obstetrics & Gynecology 28, no. 21 (November 2008): 6. http://dx.doi.org/10.1097/01.pgo.0000337876.41673.71.

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4

Meczekalski, B., A. Tonetti, P. Monteleone, F. Bernardi, S. Luisi, M. Stomati, M. Luisi, F. Petraglia, and AR Genazzani. "Hypothalamic amenorrhea with normal body weight: ACTH, allopregnanolone and cortisol responses to corticotropin-releasing hormone test." European Journal of Endocrinology 142, no. 3 (March 1, 2000): 280–85. http://dx.doi.org/10.1530/eje.0.1420280.

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OBJECTIVE: Hypothalamic amenorrhea (HA) is a functional disorder caused by disturbances in gonadotropin-releasing hormone (GnRH) pulsatility. The mechanism by which stress alters GnRH release is not well known. Recently, the role of corticotropin-releasing hormone (CRH) and neurosteroids in the pathophysiology of HA has been considered. The aim of the present study was to explore further the role of the hypothalamic-pituitary-adrenal axis in HA. DESIGN: We included 8 patients (aged 23.16+/-1.72 years) suffering from hypothalamic stress-related amenorrhea with normal body weight and 8 age-matched healthy controls in the follicular phase of the menstrual cycle. METHODS: We measured basal serum levels of FSH, LH, and estradiol and evaluated ACTH, allopregnanolone and cortisol responses to CRH test in both HA patients and healthy women. RESULTS: Serum basal levels of FSH, LH, and estradiol as well as basal levels of allopregnanolone were significantly lower in HA patients than in controls (P<0.001) while basal ACTH and cortisol levels were significantly higher in amenorrheic patients with respect to controls (P<0.001). The response (area under the curve) of ACTH, allopregnanolone and cortisol to CRH was significantly lower in amenorrheic women compared with controls (P<0.001, P<0.05, P<0.05 respectively). CONCLUSIONS: In conclusion, women with HA, despite the high ACTH and cortisol levels and, therefore, hypothalamus-pituitary-adrenal axis hyperactivity, are characterized by low allopregnanolone basal levels, deriving from an impairment of both adrenal and ovarian synthesis. The blunted ACTH, allopregnanolone and cortisol responses to CRH indicate that, in hypothalamic amenorrhea, there is a reduced sensitivity and expression of CRH receptor. These results open new perspectives on the role of neurosteroids in the pathogenesis of hypothalamic amenorrhea.

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Podfigurna, Agnieszka, and Blazej Meczekalski. "Functional Hypothalamic Amenorrhea: A Stress-Based Disease." Endocrines 2, no. 3 (July 24, 2021): 203–11. http://dx.doi.org/10.3390/endocrines2030020.

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The aim of the study is to present the problem of functional hypothalamic amenorrhea, taking into account any disease and treatment, diagnosis, and consequences of this disease. We searched PubMed (MEDLINE) and included 38 original and review articles concerning functional hypothalamic amenorrhea. Functional hypothalamic amenorrhea is the most common cause of secondary amenorrhea in women of childbearing age. It is a reversible disorder caused by stress related to weight loss, excessive exercise and/or traumatic mental experiences. The basis of functional hypothalamic amenorrhea is hormonal, based on impaired pulsatile GnRH secretion in the hypothalamus, then decreased secretion of gonadotropins, and, consequently, impaired hormonal function of the ovaries. This disorder leads to hypoestrogenism, manifested by a disturbance of the menstrual cycle in the form of amenorrhea, leading to anovulation. Prolonged state of hypoestrogenism can be very detrimental to general health, leading to many harmful short- and long-term consequences. Treatment of functional hypothalamic amenorrhea should be started as soon as possible, and it should primarily involve lifestyle modification. Only then should pharmacological treatment be applied. Importantly, treatment is most often long-term, but it results in recovery for the majority of patients. Effective therapy, based on multidirectional action, can protect patients from numerous negative impacts on fertility, cardiovascular system and bone health, as well as reducing mental morbidity.

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6

Gordon, Catherine M. "Functional Hypothalamic Amenorrhea." New England Journal of Medicine 363, no. 4 (July 22, 2010): 365–71. http://dx.doi.org/10.1056/nejmcp0912024.

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7

Berga, Sarah L. "Functional hypothalamic amenorrhea." Current Opinion in Endocrinology & Diabetes 8, no. 6 (December 2001): 307–13. http://dx.doi.org/10.1097/00060793-200112000-00008.

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8

Warren, M. P., F. Voussoughian, E. B. Geer, E. P. Hyle, C. L. Adberg, and R. H. Ramos. "Functional Hypothalamic Amenorrhea." Obstetrical & Gynecological Survey 54, no. 8 (August 1999): 510–11. http://dx.doi.org/10.1097/00006254-199908000-00017.

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9

Ferin, M. "Stress and hypothalamic amenorrhea." Gynecological Endocrinology 10, sup4 (January 1996): 42–43. http://dx.doi.org/10.3109/09513599609116179.

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10

Guay, Andre T., Sudhir Bansal, and Mary Beth Hodge. "Possible hypothalamic impotencemale counterpart to hypothalamic amenorrhea?" Urology 38, no. 4 (October 1991): 317–22. http://dx.doi.org/10.1016/0090-4295(91)80143-u.

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11

Aurigemma, Nicole C. "Pathways To Functional Hypothalamic Amenorrhea." Medicine & Science in Sports & Exercise 50, no. 5S (May 2018): 95–96. http://dx.doi.org/10.1249/01.mss.0000535399.48422.29.

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12

Fourman, Lindsay T., and Pouneh K. Fazeli. "Neuroendocrine Causes of Amenorrhea—An Update." Journal of Clinical Endocrinology & Metabolism 100, no. 3 (March 1, 2015): 812–24. http://dx.doi.org/10.1210/jc.2014-3344.

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Context: Secondary amenorrhea—the absence of menses for three consecutive cycles—affects approximately 3–4% of reproductive age women, and infertility—the failure to conceive after 12 months of regular intercourse—affects approximately 6–10%. Neuroendocrine causes of amenorrhea and infertility, including functional hypothalamic amenorrhea and hyperprolactinemia, constitute a majority of these cases. Objective: In this review, we discuss the physiologic, pathologic, and iatrogenic causes of amenorrhea and infertility arising from perturbations in the hypothalamic-pituitary-adrenal axis, including potential genetic causes. We focus extensively on the hormonal mechanisms involved in disrupting the hypothalamic-pituitary-ovarian axis. Conclusions: A thorough understanding of the neuroendocrine causes of amenorrhea and infertility is critical for properly assessing patients presenting with these complaints. Prompt evaluation and treatment are essential to prevent loss of bone mass due to hypoestrogenemia and/or to achieve the time-sensitive treatment goal of conception.

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13

Boesgaard, Søren, Claus Hagen, Anders Nyboe Andersen, Henning Djursing, and Mogens Fenger. "Cortisol secretion in patients with normoprolactinemic amenorrhea." Acta Endocrinologica 118, no. 4 (August 1988): 544–50. http://dx.doi.org/10.1530/acta.0.1180544.

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Abstract. Patients with functional amenorrhea have raised central dopaminergic activity and opioid-mediated GnRH inhibition leading to inhibition of hypothalamic-pituitary-ovarian function. In the present study, basal serum cortisol and ACTH levels were measured in normoprolactinemic amenorrheic patients with (N = 14) and without (N = 7) insulin-dependent diabetes mellitus. Basal serum cortisol levels was significantly (P < 0.01) elevated in patients with normoprolactinemic amenorrhea compared with normal women. Basal serum cortisol was significantly (P < 0.02) elevated in amenorheic diabetic patients compared with menstruating diabetic women. In the amenorrheic groups both cortisol and ACTH levels increased significantly (P <0.01) after dopamine D-2 receptor blockade, whereas no hormonal changes occurred in the control groups. It is concluded that patients with normoprolactinemic amenorrhea have elevated basal serum cortisol, the reason probably being hypersecretion of corticotropin-releasing hormone. Secondly that dopaminergic blockade with metoclopramide stimulates ACTH and cortisol secretion in patients presumed to have raised dopaminergic activity.

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14

Schuiling, G. A., N. Valkhof, T. R. Koiter, and R. M. Lappöhn. "Differential effect of estrogen on pituitary responsiveness to GnRH in women with different forms of hypothalamic amenorrhea." Acta Endocrinologica 122, no. 5 (May 1990): 651–55. http://dx.doi.org/10.1530/acta.0.1220651.

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Abstract. The effect of treatment with estradiol valerate (6 days, 2-6 mg/day) on basal levels of LH and FSH and on response of LH and FSH levels to GnRH challenge (2 × 25 μg GnRH, iv) were investigated in women with "hypothalamic amenorrhea", but without other endocrine disorders. Three groups were studied: 11 women with primary amenorrhea, 10 women exhibiting secondary amenorrhea related with weight loss, and 7 women with normal weight and with amenorrhea persisting after a period of severe weight loss. Before treatment with estradiol valerate the estradiol concentrations in all women were at the lower limit of the follicular phase of a normal ovulatory cycle. In addition, there were no differences between the groups in basal LH and FSH levels and in responses to GnRH challenges. Treatment with estradiol valerate suppressed the basal levels of FSH but not of LH in all women. Estradiol did not affect the response to GnRH challenge in women with primary amenorrhea, weakly augmented the response in women with secondary amenorrhea associated with weight loss, and strongly increased the response in secondary amenorrheic women who had regained normal weight. The results are interpreted in the light of the well-established fact that estrogen augments the gonadotropin response only if the pituitary gland is not exposed to high concentrations of GnRH. It is hypothesized that the differential response to GnRH of the present patients after estrogen treatment reflects differences in GnRH exposure of the pituitary gland, with patients with primary amenorrhea having the highest level of GnRH exposure.

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15

Ghaffari, Firouzeh, Fatemeh Keikha, and Arezoo Arabipoor. "A Rare Case of Primary Amenorrhea with Two Etiologies, Hypothalamic Amenorrhea, Transverse Vaginal Septum, and No Hematocolpos." Case Reports in Obstetrics and Gynecology 2015 (2015): 1–3. http://dx.doi.org/10.1155/2015/989123.

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We reported a rare case of hypothalamic amenorrhea and transverse vaginal septum. A 28-year-old woman presented with primary amenorrhea and no complaint of abdominal pain. Laparoscopy revealed a small rudimentary uterus with streak ovaries and a vaginal pouch. The patient with diagnosis of Mayer-Rokitansky-Kuster-Hauser (MRKH) syndrome was subjected to a vaginoplasty in another fertility center. In our institute, after two courses of estrogen and progesterone, sonography revealed hematocolpos, while, under anesthesia, transverse vaginal septum was resected. Hysteroscopy revealed normal uterine cavity. She became pregnant 5 months postoperatively with controlled ovarian stimulation (COS) in conjunction with intrauterine insemination, and she has two healthy babies now. This case highlights the importance of careful evaluation of all primary amenorrheas. Clinicians should be aware of presence of more than one etiology which causes atypical presentations and accomplishes a systematic strategy for the evaluation of amenorrhea potential to avoid long-term side effects of a misdiagnosis.

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16

Koltun, Kristen J., Nancy I. Williams, Jennifer L. Scheid, and Mary Jane De Souza. "Discriminating hypothalamic oligomenorrhea/amenorrhea from hyperandrogenic oligomenorrhea/amenorrhea in exercising women." Applied Physiology, Nutrition, and Metabolism 45, no. 7 (July 2020): 707–14. http://dx.doi.org/10.1139/apnm-2019-0640.

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The mechanism underlying oligo/amenorrhea in exercising women is often presumed as hypothalamic inhibition secondary to energy deficiency; however, hyperandrogenism may provide an alternative mechanism in some exercising women. Our purpose was to compare reproductive, metabolic, and androgen profiles of exercising women with eumenorrheic, ovulatory menstrual cycles (n = 91), oligo/amenorrhea without evidence of hyperandrogenism (Oligo/Amen; n = 83), and oligo/amenorrhea with evidence of hyperandrogenism (Oligo/Amen-HA; n = 17), and determine the prevalence of oligo/amenorrhea with evidence of hyperandrogenism in exercising women. Self-reported menstrual history and quantification of daily estrogen and progesterone urinary metabolites determined reproductive status. Resting energy expenditure, body composition, and metabolic hormone concentrations determined metabolic status. Serum androgens and calculated free androgen index (FAI) determined androgen status. Groups were similar in age (22.4 ± 0.3 years), height (165.1 ± 0.5 cm), resting energy expenditure (1198.4 ± 12.0 kcal/day), and total triiodothyronine (85.0 ± 1.5 ng/dL) concentration. Oligo/Amen-HA had greater weight (60.0 ± 1.6, 56.1 ± 0.7 kg), body mass index (22.3 ± 0.4, 20.6 ± 0.2 kg/m2), percentage body fat (27.3% ± 1.4%, 24.4% ± 0.6%), fat mass (16.2 ± 1.0, 13.8 ± 0.4 kg), insulin (5.8 ± 0.7, 4.2 ± 0.3 μIU/mL), leptin (12.2 ± 2.3, 6.6 ± 0.7 ng/mL), FAI (6.1 ± 0.3, 1.7 ± 0.1), and luteinizing hormone/follicle-stimulating hormone (1.9 ± 0.3, 1.3 ± 0.2) compared with Oligo/Amen, respectively. In our sample, 17% of those with oligo/amenorrhea had concurrent hyperandrogenism. This study supports that oligo/amenorrhea in some exercising women is related to hyperandrogenism. Novelty Caution must be utilized when discriminating hypothalamic oligo/amenorrhea from hyperandrogenic oligo/amenorrhea. In our sample, 17% of those with presumed hypothalamic oligo/amenorrhea had concurrent hyperandrogenism. Exercise and/or mild energy deficiency may be protective against developing severe hyperandrogenic symptoms.

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17

Yen, Samuel S. C. "Female Hypogonadotropic Hypogonadism: Hypothalamic Amenorrhea Syndrome." Endocrinology and Metabolism Clinics of North America 22, no. 1 (March 1993): 29–58. http://dx.doi.org/10.1016/s0889-8529(18)30179-8.

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18

Marcus, Marsha D., Tammy L. Loucks, and Sarah L. Berga. "Psychological correlates of functional hypothalamic amenorrhea." Fertility and Sterility 76, no. 2 (August 2001): 310–16. http://dx.doi.org/10.1016/s0015-0282(01)01921-5.

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19

Ahima, Rexford S. "Body Fat, Leptin, and Hypothalamic Amenorrhea." New England Journal of Medicine 351, no. 10 (September 2, 2004): 959–62. http://dx.doi.org/10.1056/nejmp048214.

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20

Berga, Sarah L., and Lyda G. Girton. "The Psychoneuroendocrinology of Functional Hypothalamic Amenorrhea." Psychiatric Clinics of North America 12, no. 1 (March 1989): 105–16. http://dx.doi.org/10.1016/s0193-953x(18)30454-4.

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21

Warren, Michelle P., Claire C. Holderness, Valerie Lesobre, Raphaelle Tzen, Farnaz Vossoughian, and J. Brooks-Gunn. "Hypothalamic Amenorrhea and Hidden Nutritional Insults." Journal of the Society for Gynecologic Investigation 1, no. 1 (January 1994): 84–88. http://dx.doi.org/10.1177/107155769400100117.

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22

Collins, Taylor, and Krista L. Rompolski. "Hypothalamic Amenorrhea: Causes, Complications, & Controversies." Journal of Student Research 6, no. 1 (May 23, 2017): 24–32. http://dx.doi.org/10.47611/jsr.v6i1.288.

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Hypothalamic amenorrhea (HA) is considered a reversible condition characterized by the absence of menses for 3 months or more, due to suppressed secretions of gonadotropin releasing hormone affecting the entire hypothalamic-pituitary-ovarian axis. HA can be triggered by excessive stress, weight loss or excessive exercise, however, the etiology is still largely unknown. Serious, long-term complications include severe hypoestrogenism and infertility, in addition to a variety of hormonal aberrations. Hypoestrogenism also leads to diminished bone health, cardiovascular problems, and mood changes that lead to a higher prevalence of depression and anxiety. It is important that HA is diagnosed in a timely manner in order to begin therapeutic strategies that aim to resume menses and return to normal levels of circulating reproductive hormones. When attempts to resume menstruation naturally through lifestyle changes are unsuccessful, other pharmaceutical options are available. Treatment options range from estrogen-replacement therapy to the administration of gonadotropin releasing hormone, depending on the reproductive goals of the woman. More research is needed on novel treatments in order to determine the most effective standard of care.

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23

Strisanti, Ida Ayu Suptika. "AKUPUNKTUR TERAPI UNTUK MENURUNKAN LEVEL ANSIETAS PADA WANITA DENGAN WEIGHT LOSS RELATED AMENORRHEA: A PILOT STUDY." Jurnal Riset Kesehatan Nasional 4, no. 1 (June 25, 2020): 60. http://dx.doi.org/10.37294/jrkn.v4i1.227.

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ABSTRAKLatar Belakang: Weight loss related amenorrhea merupakan suatu kondisi amenorea yang disebabkan oleh disfungsi hypothalamus atau disebut juga dengan Functional Hypothalamic Amenorrhea (FHA). Ketika seorang wanita mengalami amenorea dalam jangka waktu yang relatif lama, tentunya kondisi ini akan mempengaruhi psikologis wanita tersebut. Oleh sebab itu, mengkaji kondisi psikis dari wanita yang menderita weight loss related amenorrhea dan membantu menurunkan level ansietasnya juga sangat di perlukan. Pilot study ini dilakukan untuk mengetahui efek dari akupunktur terapi untuk menurunkan level ansietas pada wanita dengan weight loss related amenorrhea.Metode: Sebanyak 15 orang wanita dengan diagnose weight loss related amenorrhea bersedia menjadi partisipan dalam pilot study ini. Seluruh partisipan mendapatkan 20 kali terapi yang dilakukan di Shanghai Research Institute of Acupuncture and Meridian, Shanghai-China. Zung Self-Rating Anxiety Scale (SAS) questionnaire digunakan dalam pilot study ini sebagai alat ukur terhadap level ansietas partisipan. Data yang didapatkan dalam study ini, dianalisa menggunakan paired-sample t-test dengan level signifikansi p≤0.05.Hasil: Terdapat penurunan yang signifikan pada hasil SAS partisipan dalam study ini. Sebelum terapi dilakukan, diperoleh hasil SAS sebesar 46.60±8.58 yang mengindikasikan ansietas sedang. Setelah menjalani 20 kali treatment, hasil SAS mengalami penurunan menjadi 41.80±3.07 (p<0.05), yang menunjukan ansietas dalam rentang normal.Kesimpulan: Hasil ini mengindikasikan bahwa akupunktur dapat dijadikan sebagai salah satu metode pengobatan untuk menurunkan level ansietas yang disebabkan oleh weight loss related amenorrhea.Kata kunci: Akupunktur, SAS, ansietas, weight loss related amenorrheaABSTRACTBackground: Weight loss related amenorrhea is a condition caused by dysfunction of the hypothalamic pituitary ovarian axis due to significant weight loss. Amenorrhea that caused by dysfunction of hypothalamic also known as Functional Hypothalamic Amenorrhea (FHA). When this amenorrhea last for long duration of time, it might involve our psychologist condition. This pilot study was conducted to investigate the effect of acupuncture to reduce anxiety level among women with weight loss related amenorrhea. Methods: Fifteen participants were enrolled in this pilot study. The participants received 20 sessions of acupuncture treatment and all of the treatment sessions was conducted in Shanghai Research Institute of Acupuncture and Meridian, Shanghai-China. Zung Self-Rating Anxiety Scale (SAS) questionnaire was used as a measurement tool to measure the anxiety level among participants. Paired-sample t-test was performed to analyze the data result, with significant p value ≤0.05. Results: Significant changes was found in mean score of SAS before and after treatment. It approximately 46.60 ± 8.58 before treatment and it decrease to 41.80 ± 3.07 after treatment (p<0.05). Conclusion: The result of this pilot study suggest that acupuncture is effective and it can be used as treatment method to reduce anxiety level among participants with weight loss related amenorrhea.Keywords: Acupuncture, SAS, anxiety, weight loss related amenorrhea

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24

Grinspoon, Steven, Karen Miller, Caryn Coyle, Judy Krempin, Catharina Armstrong, Sarah Pitts, David Herzog, and Anne Klibanski. "Severity of Osteopenia in Estrogen-Deficient Women with Anorexia Nervosa and Hypothalamic Amenorrhea1." Journal of Clinical Endocrinology & Metabolism 84, no. 6 (June 1, 1999): 2049–55. http://dx.doi.org/10.1210/jcem.84.6.5792.

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Reduced bone density is observed in over half of women with anorexia nervosa (AN), in whom the risk of fracture is significantly increased even at a young age. It is unknown to what extent low bone density in AN differs from other conditions of premenopausal osteoporosis and is related to estrogen deficiency and/or other factors, such as nutritional status. We therefore investigated bone loss in nutritionally replete and nutritionally deplete amenorrheic women by comparing patients with AN (n = 30) to age-matched subjects with hypothalamic amenorrhea (HA; n = 19) in whom duration of amenorrhea, prior estrogen use, and age of menarche were comparable. Healthy, age-matched, eumenorrheic women were studied as a control group (NL; n = 30). Weight and nutritionally dependent factors including (body mass index, 20.7 ± 0.3 vs. 16.7 ± 0.3 kg/m2; P < 0.0001), insulin-like growth factor I (270 ± 18 vs. 203 ± 17 ng/mL; P < 0.01), percent body fat (26% vs. 19%; P < 0.0001), and lean body mass (38.7 ± 1.1 vs. 34.3 ± 0.8, P < 0.01) were significantly different between the HA and AN groups, respectively. The bone densities of the anterior-posterior (AP) spine, total hip, and total body measured by dual energy x-ray absortiometry were reduced in both amenorrheic groups compared to those in control subjects, but were significantly lower in women with AN than in those with HA. The t scores for AP spine and hip were −1.80 ± 0.15 (AN), −0.80 ± 0.22 (HA), and 0.28 ± 0.19 sd (NL) for the AP spine and −1.62 ± 0.17 (AN), −0.51 ± 0.21 (HA), and 0.25 ± 0.16 (NL) for the total hip, respectively (P < 0.01 for all comparisons). Among the amenorrheic subjects, duration of amenorrhea, age of menarche, and N-telopeptide were inversely correlated with bone density at all sites, whereas body mass index, insulin-like growth factor I, lean body mass, and fat intake were positively correlated with bone density at all sites measured. In multivariate regression analyses, bone density was most significantly related to lean body mass (P= 0.05 and P = 0.03 for the spine and hip, respectively), but not to the duration of amenorrhea or other indexes of estrogen status among patients with AN. In contrast, bone density of the lumbar spine was significantly related to weight and duration of amenorrhea among patients with HA. These data demonstrate that the severity of osteopenia in AN is greater than that in patients with HA and is critically dependent upon nutritional factors in addition to the degree or duration of estrogen deficiency itself. Lean body mass, independent of the duration or severity of estrogen deficiency, is an important predictor of bone loss among women with AN.

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25

Torbati, Tina, Erika Dutra, and Chrisandra Shufelt. "Hypothalamic Amenorrhea and the Long-Term Health Consequences." Seminars in Reproductive Medicine 35, no. 03 (May 2017): 256–62. http://dx.doi.org/10.1055/s-0037-1603581.

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AbstractThe menstrual cycle is a reproductive vital sign and provides insight into hormonal imbalance as well as pregnancy. The significance of estrogen, however, extends beyond fertility and plays a role on tissues and organs throughout the body. Functional hypothalamic amenorrhea is a common form of secondary amenorrhea resulting in estrogen deficiency in young premenopausal women. While reversible, the cause of this disorder is related to psychological stress, excessive exercise, disordered eating, or a combination of these factors resulting in suppression of the hypothalamic–pituitary–ovarian axis. The resulting loss of estrogen has profound effects on many systems throughout the body, including cardiac, skeletal, psychological, and reproductive. Often, these young women are “walking well,” as they do not have bothersome symptoms of low estrogen and are unaware of the consequences of estrogen deficiency. This review focuses on the health consequences of hypothalamic amenorrhea, current research, and available treatment options.

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26

O'Donnell, Emma, John S. Floras, and Paula J. Harvey. "Estrogen status and the renin angiotensin aldosterone system." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 307, no. 5 (September 1, 2014): R498—R500. http://dx.doi.org/10.1152/ajpregu.00182.2014.

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The renin-angiotensin-aldosterone system (RAAS) is integrally involved in multiple cardiovascular physiological processes including arterial blood pressure (BP) regulation. Over activity of the RAAS has been implicated in the pathogenesis of a number of cardiovascular disease entities, including hypertension. Several lines of evidence suggest estrogen favorably modulates the RAAS. Conversely, estrogen deficiency due to menopause may contribute to over activity of the RAAS. Of importance, estrogen deficiency in women is not exclusive to the postmenopausal period. Functional hypothalamic amenorrhea is a reversible cause of premenopausal hypoestrogenemia. In contrast to postmenopausal women (PMW), premenopausal women with exercise-associated functional hypothalamic amenorrhea demonstrate decreased, not increased, resting BP compared with their estrogen-replete eumenorrheic counterpart. In this review we briefly examine the effects of estrogen status on the RAAS and present the hypothesis that the RAAS is altered in physically active women with functional hypothalamic amenorrhea.

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27

Tschugguel, Walter, and Sarah L. Berga. "Treatment of functional hypothalamic amenorrhea with hypnotherapy." Fertility and Sterility 80, no. 4 (October 2003): 982–85. http://dx.doi.org/10.1016/s0015-0282(03)01012-4.

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28

Stockman, J. A. "A Genetic Basis for Functional Hypothalamic Amenorrhea." Yearbook of Pediatrics 2012 (January 2012): 125–27. http://dx.doi.org/10.1016/j.yped.2011.06.033.

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29

SUH, B. Y., J. H. LIU, S. L. BERGA, M. E. QUIGLEY, G. A. LAUGHLIN, and S. S. YEN. "Hypercortisolism in Patients with Functional Hypothalamic-Amenorrhea." Obstetrical & Gynecological Survey 43, no. 11 (November 1988): 691–92. http://dx.doi.org/10.1097/00006254-198811000-00016.

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30

Warren, M. P., F. Voussoughian, E. B. Geer, E. P. Hyle, C. L. Adberg, and R. H. Ramos. "Functional Hypothalamic Amenorrhea: Hypoleptinemia and Disordered Eating." Journal of Clinical Endocrinology & Metabolism 84, no. 3 (March 1999): 873–77. http://dx.doi.org/10.1210/jcem.84.3.5551.

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31

Caronia, Lisa M., Cecilia Martin, Corrine K. Welt, Gerasimos P. Sykiotis, Richard Quinton, Apisadaporn Thambundit, Magdalena Avbelj, et al. "A Genetic Basis for Functional Hypothalamic Amenorrhea." New England Journal of Medicine 364, no. 3 (January 20, 2011): 215–25. http://dx.doi.org/10.1056/nejmoa0911064.

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32

Caronia, Lisa M., Cecilia Martin, Corrine K. Welt, Gerasimos P. Sykiotis, Richard Quinton, Apisadaporn Thambundit, Magdalena Avbelj, et al. "A Genetic Basis for Functional Hypothalamic Amenorrhea." Obstetrical & Gynecological Survey 66, no. 10 (October 2011): 618–19. http://dx.doi.org/10.1097/ogx.0b013e31822f94c4.

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RUIZ-ZAMBRANA, ALVARO, and SARAH L. BERGA. "A Clinician’s Guide to Functional Hypothalamic Amenorrhea." Clinical Obstetrics & Gynecology 63, no. 4 (October 2, 2020): 706–19. http://dx.doi.org/10.1097/grf.0000000000000573.

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SUH, B. Y., J. H. LIU, S. L. BERGA, M. E. QUIGLEY, G. A. LAUGHLIN, and S. S. YEN. "Hypercortisolism in Patients With Functional Hypothalamic-Amenorrhea*." Journal of Clinical Endocrinology & Metabolism 66, no. 4 (April 1988): 733–39. http://dx.doi.org/10.1210/jcem-66-4-733.

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GENAZZANI, A. D., F. RICCHIERI, C. LANZONI, C. STRUCCHI, and V. M. JASONNI. "Diagnostic and Therapeutic Approach to Hypothalamic Amenorrhea." Annals of the New York Academy of Sciences 1092, no. 1 (December 1, 2006): 103–13. http://dx.doi.org/10.1196/annals.1365.009.

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Liu, James H. "Hypothalamic amenorrhea: Clinical perspectives, pathophysiology, and management." American Journal of Obstetrics and Gynecology 163, no. 5 (November 1990): 1732–36. http://dx.doi.org/10.1016/0002-9378(90)91437-h.

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Genazzani, A. D., E. Chierchia, S. Santagni, E. Rattighieri, A. Farinetti, and C. Lanzoni. "Hypothalamic amenorrhea: From diagnosis to therapeutical approach." Annales d'Endocrinologie 71, no. 3 (May 2010): 163–69. http://dx.doi.org/10.1016/j.ando.2010.02.006.

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Anu Prasad, N. "AN OVERVIEW OF AMENORRHEA." Journal of Medical pharmaceutical and allied sciences 10, no. 3 (July 15, 2021): 2724–28. http://dx.doi.org/10.22270/jmpas.v10i3.1063.

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Abstract:

Amenorrhea is defined as the nonappearance of menstruation in women. Amenorrhea may be divided in to primary and secondary amenorrhea. Primary amenorrhea is caused due to anatomical, genetic, nutritional and other endocrine defects. Anatomical causes includes distal obstruction, MRKH and AIS. Primary Ovarian Insufficiency is the foremost causes of primary amenorrhea. The frequent causes of secondary amenorrhea are pregnancy. Other causes of secondary amenorrhea include PCOD, functional hypothalamic amenorrhea, POI. Depending upon the causes, the amenorrhea affected women should experiences the symptoms like hair loss, acne, excess facial hair, milky nipple discharge, etc along with the absence of menstruation. Amenorrhea is diagnosed using the patient laboratory data, pelvic ultrasonography, hysteroscopy. Management of amenorrhea is based upon its causes. PCOS patients is usually treated with regular exercise and healthy food diet. Amenorrhea is initially treated with hormonal therapy followed by hysterectomy. Regular intake of vitamin D and calcium is also recommended.

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Grosman-Rimon, Liza, Evan Wright, Danit Freedman, Erez Kachel, Sarah Hui, Iris Epstein, David Gutterman, and Sigal Eilat-Adar. "Can improvement in hormonal and energy balance reverse cardiovascular risk factors in athletes with amenorrhea?" American Journal of Physiology-Heart and Circulatory Physiology 317, no. 3 (September 1, 2019): H487—H495. http://dx.doi.org/10.1152/ajpheart.00242.2019.

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Abstract:

Female athletes display a high prevalence of hypothalamic amenorrhea as a result of energy imbalance. In these athletes with amenorrhea, decreased luteinizing hormone/follicule-stimulating hormone secretion leads to deficiency in endogenous estrogen. The severe estrogen deficiency in these athletes may increase cardiovascular risk similar to that in postmenopausal women. This review discusses the potential cardiovascular risk factors in athletes with amenorrhea as a result of hypoestrogenism, which include endothelial dysfunction and unfavorable lipid profiles. We also consider the potential to reverse the cardiovascular risk by restoring energy or hormonal imbalance along the reproductive axis in athletes with amenorrhea.

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Webb, S. M. "Circulating melatonin in hypothalamic amenorrhea: Cause or effect?" Gynecological Endocrinology 10, sup4 (January 1996): 37–38. http://dx.doi.org/10.3109/09513599609116177.

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Genazzani, A. D., F. Petraglia, L. Sgarbi, O. Gamba, A. Volpe, N. Surico, and A. R. Genazzani. "Chronobiological derangement of pituitary hormones in hypothalamic amenorrhea." Gynecological Endocrinology 10, sup4 (January 1996): 38–41. http://dx.doi.org/10.3109/09513599609116178.

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Chernukha, Chernukha G. E., Gusev D. V. Gusev, Tabeeva G. I. Tabeeva, and Prilutskaya V. Yu Prilutskaya. "Current principles of therapy for functional hypothalamic amenorrhea." Akusherstvo i ginekologiia 6_2018 (July 2, 2018): 11–17. http://dx.doi.org/10.18565/aig.2018.6.11-17.

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Chou, S. H., J. P. Chamberland, X. Liu, G. Matarese, C. Gao, R. Stefanakis, M. T. Brinkoetter, H. Gong, K. Arampatzi, and C. S. Mantzoros. "Leptin is an effective treatment for hypothalamic amenorrhea." Proceedings of the National Academy of Sciences 108, no. 16 (April 4, 2011): 6585–90. http://dx.doi.org/10.1073/pnas.1015674108.

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Meczekalski, Blazej, Agnieszka Podfigurna-Stopa, Alina Warenik-Szymankiewicz, and Andrea Riccardo Genazzani. "Functional hypothalamic amenorrhea: Current view on neuroendocrine aberrations." Gynecological Endocrinology 24, no. 1 (January 2008): 4–11. http://dx.doi.org/10.1080/09513590701807381.

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Chou, Sharon H., and Christos Mantzoros. "Bone metabolism in anorexia nervosa and hypothalamic amenorrhea." Metabolism 80 (March 2018): 91–104. http://dx.doi.org/10.1016/j.metabol.2017.10.009.

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Alexander, L. "Human Recombinant Leptin for Treatment of Hypothalamic Amenorrhea." MD Conference Express 11, no. 5 (August 1, 2011): 9. http://dx.doi.org/10.1177/155989771105003.

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Welt, Corrine K., Jean L. Chan, John Bullen, Robyn Murphy, Patricia Smith, Alex M. DePaoli, Aspasia Karalis, and Christos S. Mantzoros. "Recombinant Human Leptin in Women with Hypothalamic Amenorrhea." New England Journal of Medicine 351, no. 10 (September 2, 2004): 987–97. http://dx.doi.org/10.1056/nejmoa040388.

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BERGA, S. L., J. F. MORTOLA, L. GIRTON, B. SUH, G. LAUGHLIN, P. PHAM, and S. S. C. YEN. "Neuroendocrine Aberrations in Women With Functional Hypothalamic Amenorrhea*." Journal of Clinical Endocrinology & Metabolism 68, no. 2 (February 1989): 301–8. http://dx.doi.org/10.1210/jcem-68-2-301.

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Welt, Corrine K., Jean L. Chan, John Bullen, Robyn Murphy, Patricia Smith, Alex M. DePaoli, Aspasia Karalis, and Christos S. Mantzoros. "Recombinant Human Leptin in Women With Hypothalamic Amenorrhea." Obstetrical & Gynecological Survey 60, no. 2 (February 2005): 104–5. http://dx.doi.org/10.1097/01.ogx.0000151645.22134.0b.

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Lania, A., L. Gianotti, I. Gagliardi, M. Bondanelli, W. Vena, and M. R. Ambrosio. "Functional hypothalamic and drug-induced amenorrhea: an overview." Journal of Endocrinological Investigation 42, no. 9 (February 11, 2019): 1001–10. http://dx.doi.org/10.1007/s40618-019-01013-w.

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