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Effects of the Menstrual Cycle on Medical Disorders

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Effects of the Menstrual Cycle on Medical Disorders REVIEW ARTICLE Effects of the Menstrual Cycle on Medical Disorders Allison M. Case, MD; Robert L. Reid, MD xacerbation of certain medical conditions at specific phases of the menstrual cycle is a well-recognized phenomenon. We review the effects of the menstrual cycle on medical conditions, including menstrual migraine, epilepsy, asthma, rheumatoid arthritis, irritable bowel syndrome, and diabetes. We discuss the role of medical suppression of ovulationE using gonadotropin-releasing hormone agonists in the evaluation and treatment of these disorders. Peer-reviewed publications from English-language literature were located via MEDLINE or from bibliographies of relevant articles. We reviewed all review articles, case reports and series, and therapeutic trials. Emphasis was placed on diagnosis and therapy of menstrual cycle– related exacerbations of disease processes. Abrupt changes in the concentrations of circulating ovar- ian steroids at ovulation and premenstrually may account for menstrual cycle–related changes in these chronic conditions. Accurate documentation of symptoms on a menstrual calendar allows identification of women with cyclic alterations in disease activity. Medical suppression of ovula- tion using gonadotropin-releasing hormone agonists can be useful for both diagnosis and treat- ment of any severe, recurrent menstrual cycle–related disease exacerbations. Arch Intern Med. 1998;158:1405-1412 The menstrual cycle, an event that punctu- Several theories have been proposed to ates the lives of most women, may be asso- explain these menstrual cycle–related effects ciated with diverse physical, psychological, on existing disease processes, including fluc- and behavioral changes. Not surprisingly, it tuations in levels of sex steroids, cyclic alter- plays a significant role in women’s health and ations in the immune system, and changing disease. Conversely, menstrual cyclicity can perceptionsofdiseaseseveritybroughtabout be easily disrupted by disease, both physi- by premenstrual alterations in mood, as seen cal and psychological. in premenstrual syndrome. Exacerbation of certain medical con- ditions at specific menstrual cycle phases THE MENSTRUAL CYCLE is a well-recognized phenomenon. Accu- rate documentation of symptoms on a men- Normal menstrual cyclicity requires coordi- strual calendar allows identification of nation of the hypothalamus, pituitary gland, women with cyclic alterations in disease ac- and ovaries. Gonadotropin-releasing hor- tivity. The majority of these effects occur mone is released in a pulsatile fashion from during the luteal and menstrual phases of thehypothalamus.Itssecretionismodulated the cycle. Diseases most often affected are by a variety of neurotransmitters, including those characterized by relapsing and re- norepinephrine, serotonin, and endogenous mitting courses, and those that are easily opioids. Gonadotropin-releasing hormone triggered by external factors; for example, migraine, asthma, and epilepsy. This article is also available on our Web site: www.ama-assn.org/internal. From the Department of Obstetrics and Gynaecology, Queen’s University, Kingston General Hospital, Kingston, Ontario. ARCH INTERN MED/ VOL 158, JULY 13, 1998 1405 ©1998 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/23/2021 stimulates the release of follicle-stim- “add-back” therapy, similar to post- exist in prepubertal children.6,7 The ulating hormone and luteinizing hor- menopausal hormone replacement frequency of migraine headaches in mone from the anterior pituitary.1 therapy. Patients receiving gonado- women increases considerably af- The follicular phase, or the time tropin-releasing hormone agonists ter menarche.8-10 Sixty percent of of oocyte development before ovu- take a small dose of estrogen daily women with migraine link attacks lation, is marked by progressive (0.625-1.25 mg of conjugated estro- to menstruation. True menstrual mi- growth of an ovarian follicle. This gens or 1-2 mg estradiol). A proges- graine, however, occurs in the 8% to phase is characterized by estrogen se- tational agent (5 mg of medroxypro- 14% of women who experience mi- cretion, at first gradual, and then ex- gesterone acetate or 200 mg of oral graines exclusively at the time of ponential in the 5 to 6 days leading micronized progesterone) is admin- menstruation, and are virtually free up to ovulation. An abrupt transient istered on a cyclic schedule for 12 to of migraine at other times of the decline in estrogen level occurs co- 14 days every 1 to 3 months to in- cycle, with the exception of the small incident with ovulation. Recovery in duce a withdrawal bleed and mini- percentage of these women who ex- the luteal phase results from corpus mize the risk of endometrial hyper- perience a brief exacerbation asso- luteal production of estrogen and plasia.2,3 Sometimes the addition of ciated with ovulation.8,11 progesterone. a progestin will create symptoms at- Seventy percent to 90% of The lifespan of the corpus lu- tributable to the steroid itself, or may women with menstrual migraine ex- teum is fixed at approximately 12 exacerbate the preexisting medical perience improvement during preg- days. If fertilization of the ovum does condition. Since endometrial hyper- nancy, especially during the sec- not occur, the corpus luteum invo- plasia would be unlikely to develop ond and third trimesters.9,10,12,13 lutes, levels of estrogen and proges- with 6 months of unopposed use of These women may experience mi- terone fall dramatically, and men- estrogen, estrogen add-back may be graine attacks in the postpartum pe- struation occurs. Falling levels of used on its own during a brief (3-6 riod, associated with falling estro- ovarian hormones remove the nega- months) diagnostic trial. gen levels.14 Oral contraceptives have tive feedback from the pituitary gland In gynecology, gonadotropin- a variable effect on migraine, caus- and hypothalamus, and a new cycle releasing hormone agonists are used ing headaches to worsen, improve, of ovarian stimulation begins.1 to temporarily suppress ovarian ste- or show no change.15 Analogous to roid secretion to treat such condi- women with menstrual migraine, GONADOTROPIN-RELEASING tions as endometriosis, precocious some users of oral contraceptives HORMONE AGONISTS puberty, uterine leiomyomas, pre- experience headaches only during menstrual syndrome,4 and for pre- tablet-free or placebo days.16 Al- Gonadotropin-releasing hormone vention of menstruation in specific though the prevalence of migraine agonists are analogues of gonado- clinical situations (eg, thrombocyto- headaches decreases with advanc- tropin-releasing hormone, the hy- penia or leukemia).3 They can also be ing age, migraine can either regress pothalamic hormone that binds to used as diagnostic tools to confirm or worsen at menopause.17 specific receptors in the anterior pi- the relationship of the menstrual Migraines are vascular head- tuitary gland, stimulating the re- cycle to conditions such as premen- aches, associated with a vasocon- lease of gonadotropins. Gonadotro- strual syndrome and menstrual mi- strictive phase followed by vasodila- pin-releasing hormone agonists, by graine.3 If symptoms or cyclic exac- tation.18 Factors thought to trigger binding to gonadotropin-releasing erbations resolve with elimination of these vascular changes include ab- hormone receptors, cause an initial the ovarian cycle, a link to the men- normal platelet aggregation, altered increase in follicle-stimulating hor- strual cycle is confirmed. These pa- platelet content of serotonin, aber- mone and luteinizing hormone se- tients generally have excellent symp- rant neurotransmitter activity, and cretion, the so-called flare effect. Af- tomatic relief with continued use of central opioid disregulation.19-22 In ter about 1 week however, down- gonadotropin-releasing hormone menstrual migraine, estrogen with- regulation and desensitization of the agonists or after surgical oophorec- drawal is likely responsible for pituitary gland produces a hypogo- tomy. Gonadotropin-releasing hor- initiating some or all these vascular nadal state, sometimes likened to a mone agonists have also been used effects on intracranial vessels. Estro- “medical oophorectomy.”2 to treat a variety of medical condi- gen regulation of prostaglandin pro- Adverse effects of gonadotro- tions with severe, potentially life- duction may also be directly or indi- pin-releasing hormone agonist treat- threatening menstrual cycle– rectly involved with the pathogenesis ment are related to hypoestrogen- related exacerbations, examples of of menstrual migraine.11,23 ism, including hot flushes, headache, which are discussed in this review. Several investigators24-27 have vaginal dryness, and sleep distur- demonstrated an effect of estrogen bances. The adverse effect of great- MENSTRUAL MIGRAINE on the vasculature.It has been pro- est concern however, is accelerated posed that in women with men- bone loss, putting the patient at in- The evidence supporting a relation- strual migraine, estrogen may sen- creased risk for osteoporosis if con- ship between estrogen withdrawal sitize intracranial vessels, making tinued for prolonged periods (.6 and migraine headache is compel- these vessels more responsive to hor- months). This effect, and the hy- ling. Migraine headaches are 2 to 3 monal changes, leading to vasocon- poestrogenic symptoms, can be pre- times more common in women than striction associated with estrogen vented by the addition of
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