andpublication, it has been published continuously since 1979. Pediatrics in Review is owned, published, Pediatrics in Review is the official journal of the American Academy of Pediatrics. A monthly
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LMenstrual Disorders in theAdolescent: AmenorrheaMargaret M. Polaneczky, MD* and Gail B. Slap, MDt
This is the first of a two-pan article about menstrual disorders in the
adolescent. The second part, on dysmenorrhea and dysfunctional uterinebleeding, will appear in the March 1992 issue of Pediatrics in Review.R.J.H.
FOCUS QUESTIONS1. What is the difference between
primary and secondary
amenorrhea?
2. What are the symptoms ofhypothalamic amenorrhea andhow are they treated?
3. What is the appropriate
laboratory evaluation of secondary
amenorrhea?
4. What is the diagnostic approach to
patients who have primaryamenorrhea?
PIR Quiz-CME CreditThe American Academy of Prescribed hours per issue by rate cover.) To receive CMEPediatrics is accredited by the the American Academy of credit on the 1992 annual creditAccreditation Council for Con- Family Physicians. (Terms of summary, you must be enrolledtinuing Medical Education to approval: Beginning date Jan- in PREP or subscribe to Pediat-
sponsor continuing medical ed- aury 1992. Enduring Materials rics in Review and return theucation for physicians. As an are approved for 1 year, with PIR Quiz Card by February 28,organization accredited for con- option to request renewal. For 1993. PIR Quiz Cards receivedtinuing medical education, specific information, please after this deadline will be re-completion of the PIR Quiz consult the AAFP Office of corded in the year it is re-meets the criteria for 2 hours of Continuing Medical Education.) ceived; with cards from thecredit, per issue, of the Amen- The questions for the PIR 1992 PIR journals, acceptedcan Academy of Pediatrics’ quiz are located at the end of through December 31, 1994.PREP Education Award. each article in this issue. Each The PIR quiz card is bound
The American Academy of question has a SINGLE BEST into the January issue. Corn-Pediatrics designates this contin- ANSWER. To obtain credit, plete the quizzes in each issueuing medical education activity record your answers on the PIR and send it to: American Acad-for 2 credit hours, per issue, in Quiz Card found in the January erny of Pediatrics, PREP Of-Categoiy 1 of the Physician’s issue, and return the card to the fice, P0 Box 927, Elk GroveRecognition Award of the Amer- Academy. (PREP group partici- Village, IL 60009-0927.ican Medical Association. pants will receive the PIR Quiz The correct answers to the
This program has been re- Card and Self-Assessment questions in this issue appearviewed and is acceptable for 2 Credit Reply Sheet under sepa- on the inside front cover.
Pediatrics iii Review Vol. 13 No. 2 Februa,y 1992 43
The menstrual history is an integralpart of the evaluation of the adoles.cent female. Abnormal menstrualflow or timing may be the first signof systemic illness or sexually trans-mitted disease. Amenorrhea may sig-nal an endocrine or genetic disorderor may suggest structural abnormali-
ties of the genital tract. Most impor.tantly, any abnormality in menstru-ation should alert the clinician to thepossibility of pregnancy.
Normal Menstrual CycleThe average age of menarche in the
United States is 12.8 years andranges from 9 to 16 years. Menarcheusually occurs 2 to 2.5 years afterbreast budding and 1 year after thegrowth spurt. Consequently, the ab-sence of menarche at 15 years of agemay be normal in an adolescent whojust passed her growth spurt but ab-normal in an adolescent who com-pleted puberty 2 years earlier. Mostearly menstrual cycles are anovula.tory. As a result, menses in theyoung adolescent often are irregularand may be prolonged or heavy.Dysmenorrhea and premenstrual
ARTICLE
symptoms tend to accompany ovula-tory cycles and, therefore, are morecommon in the older adolescent.
Regular ovulatory cycles usuallyare established within 1 to 2 years ofmenarche. Although normal cyclelength ranges from 21 to 45 days, thelength for a given individual is fairlyconstant. Normal menstrual flowlasts 2 to 7 days and usually is heavi-est on the first and second days. Theaverage blood loss during a normalmenstrual period is 30 to 40 mL.
Primary Amenorrhea
Primary amenorrhea, or delayedmenarche, is defined as any one ofthe following: 1) the absence of men-arche by 16 years of age in the pres-ence of normal pubertal growth anddevelopment; 2) the absence of men-arche by 14 years of age in the ab-
sence of normal pubertal growth anddevelopment; or 3) the absence ofmenarche 2 years after completedsexual maturation.
INITIAL EVALUATION
A complete history and physical ex-amination is the most important stepin evaluating the adolescent who hasprimary amenorrhea. Particular atten-tion should be focused on pubertalmilestones. The history should in-elude questioning about maternal age
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44 Pediatrics in Review Vol. 13 No. 2 February 1992
ADOLESCENT MEDICHIEMenstrual Disorders
at menarche, gestational complica-tions and medications, childhood de-velopment, chronic systemic illness,nutrition, and family history of ge-netic anomalies. Physical examina-tion should be meticulous andinclude charting of height, weight,and sexual maturation rating; com-plete neurologic examination, includ-ing the cranial nerves; examinationof the skin, hair, and genitalia forsigns of hirsutism or virilization; pal-pation of the thyroid; and palpationof the abdomen and groin formasses.
Pelvic examination, if done in asensitive manner, need not be a trau-matic experience. At absolute mini-mum, a careful examination of theexternal genitalia must be performed.Use of the speculum should be pre-ceded by digital vaginal examinationto avoid injuring the patient with anabsent vagina or an outflow obstruc-tion. If a normal vagina and cervixare present, microscopic examinationof the cervical mucus may help clar-
ify the degree of estrogen stim-ulation. Bimanual examination,followed by ultrasonographic exami-nation of the pelvis, if necessary,will establish the presence or absenceof a uterus and ovaries.
DIFFERENTIAL DIAGNOSIS ANDMANAGEMENT
Patients who have primary amenor-rhea can be divided into four groups,depending on pubertal maturation andinternal genitalia (Figure 1).
No breast development-Intact uterus
These individuals lack ovarian estro-gen but have normal development ofthe Mullerian system during fetallife. The differential diagnosis in-cludes gonadal dysgenesis, hypothal-amic-pituitary disorder, and geneticdefects in ovarian steroid production.Measurement of the serum levels offollicle stimulating hormone (FSH)and luteinizing hormone (LH) willdifferentiate patients who have gona-dal (ovarian) dysgenesis and abnor-
Jmal steroid production from thosewho have hypothalamic or pituitarydisorders. Chromosomal analysis isindicated when FSH and LH levelsare high.
Gonadal dysgenesis is the mostcommon cause of primary amenor-rhea. It usually is due to Turner syn-drome (45,XO kaiyotype) or someother abnormality in X chromosomestructure or number. The ovaries failto develop, leaving remnant fibrousbands called gonadal streaks. Patientswho have gonadal dysgenesis aresexually immature, amenorrheic, andhave high FSH and LH levels (hyper-gonadotropic hypogonadism). Indi-viduals who have Turner syndromeoften have other stigmata, such asshort stature, webbed neck, or chestand limb abnormalities. Patients whohave mosaic Turner syndrome orother X chromosome abnormalitiesmay be phenotypically normal exceptfor sexual immaturity.
Gonadal dysgenesis also may oc-cur in individuals who have normal
THypogonadotropic hypogonadism
Breasts (-)
Uterus (+)
Lesions of the central nervous system
Kailman syndrome
Pituitary gonadotropic deficiencies
(eg, chronic disease, anorexia nervosa)
Breasts (+)
Uterus (-)
Gonadal dysgenesis
45,XO (Turner syndrome)
Other X chromosome variants
Pure XX or XY
gonadal dygenesisGonadal enzyme deficiency
Breasts (-)
Uterus (-)
Karoytype (XY)
Breasts (+)
Uterus (+)
Cyclic pain
Absent
�1Hypothalmic-pituitary-ovarian axis
disturbance (evaluate as
secondary amenorrhea)
FIGURE 1. Diagnostic approach to patients who have primaty amenorrhea. Adapted from Maschak CA, Kletzky OA, Davajan V. Mishell DRJr. Clinical and laboratoty evaluation of patients with primaty amenorrhea. Obstet Gynecol. 1981;5 7: 71 9. Reprinted with pennission from the
American College of Obstetrics and Gynecology.
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Any abnormality in menstruationshould alert the clinician to the
possibility of pregnancy.
Pediatrics in Review Vol. 13 No. 2 February 1992 45
----=�
ADOLESCENT MEDICINEMenstrual Disorders
karyotypes. Genetic males and fe-males who have gonadal dysgenesiswill be phenotypically female be-cause, in the absence of testosterone,gender development is female. In thegenetic male, the gonadal streaksmust be removed because of the riskof malignancy.
Individuals who have gonadal dys-genesis are almost universally sterile,and hormonal replacement should beinitiated during early adolescence.However, these patients do have in-tact uteri and may be able to bearchildren after donor oocyte implanta-tion and hormonal support.
Patients who have primary amen-orrhea due to hypogonadotropic hy-pogonadism have normal ovaries butlack hypothalamic or pituitary stim-ulation of the ovaries. FSH and LHlevels will be low or low-normal.These patients are genetically andphenotypically female but are sex-ually immature. Care must be takento exclude both tumors of the centralnervous system (CNS) and congenitaldefects in the production of gonado-tropin releasing hormone (GnRH).The most common CNS tumors pro-ducing primary amenorrhea are pitui-tary adenomas andcraniopharyngiomas. Hypothalamicdefects in GnRH production may oc-cur as the result of abnormal hypo-thalamic development. When thisoccurs in association with anosmiaand facial abnormalities, it is calledKallmann syndrome. Hypogonado-tropic hypogonadism also may be as-sociated with systemic disease,exercise, psychological stress, or an-orexia nervosa. (These diagnoses arediscussed in detail in the section onsecondary amenorrhea.)
Abnormal steroidogenesis due to17-aipha-hydroxylase deficiency is arare disorder that results in the inabil-ity of the ovary to produce estrogen.It occurs in chromosomally normalfemales with structurally normal ova-ries and uterus. These patients alsohave a defect in adrenal steroid pro-
duction resulting in hypertension andhypokalemia. The diagnosis shouldbe considered in patients who havehypergonadotropic hypogonadism,normal female karyotypes, and nor-mal female genitalia.
Normal breast development-Absentuterus
Individuals in this category are phe-notypically female. Pelvic examina-tion, however, reveals an absent orshortened vagina and an absentuterus. The diagnosis at this point iseither androgen insensitivity (testicu-lar feminization) or Mullerianagenesis.
Patients who have testicular femin-ization are chromosomally male (XY)and have normal male gonads thatproduce normal male levels of testos-terone, yet they appear phenotypi-cally female. This is due to a geneticX-linked defect in androgen-receptorfunction with resultant end-organ in-sensitivity to androgen. The Wolifianducts fail to develop, and the exter-nal genitalia develop as female in theabsence of testosterone stimulation.Because the male gonad is still ableto produce Mullerian inhibiting fac-tor, the Mullerian ducts regress andfemale internal genitalia do not de-velop. Internally, these individualshave normal male gonads and fibrousMullerian remnants. The low levelsof endogenous gonadal and adrenalestrogens, unopposed by androgen,result in breast development. Becauseof target end-organ androgen insensi-tivity, axillary and pubic hair issparse or absent. Confirmatory labo-ratory studies include male levels ofserum testosterone and male chromo-somes. The gonads, which may beeither intraabdominal or inguinal,should be removed because there is a20% incidence of malignancy. Estro-gen replacement should be initiatedfollowing surgery.
Approximately 15% of cases ofprimary amenorrhea are due to Mul-lerian agenesis (Rokintansky-Kuster-
Hauser syndrome). These patients arechromosomally and phenotypicallyfemale but have anomalous develop-ment of the Mullerian system. Con-sequently, the vagina and uterus failto develop normally. Ovaries arepresent; breast development, steroidproduction, axillary hair, and pubichair are normal. Renal anomalies oc-cur in 15% to 40% of patients, andskeletal abnormalities occur in 12%.Cardiac and other congenital abnor-malities also are increased in fre-quency. Chromosomal studies shouldbe performed to confirm the normalxx chromosomal complement and toexclude rare forms of incompleteandrogen insensitivity or pseudoher-maphroditism. Once the diagnosis ismade, a functioning vagina usuallycan be created by the use of vaginaldilators or by vaginoplasty. Hor-monal therapy is not necessary.
No breast development-Absent uterus
This rare combination occurs in ge-netic males (XY) whose gonads pro-duce Mullerian inhibiting factor butinsufficient testosterone to induce thedevelopment of male internal and ex-ternal genitalia. Phenotypic gender,therefore, is female. The lack of tes-tosterone is due to a gonadal enzymedeficiency or to early gonadal regres-sion (“vanishing testes”). Laboratoryevaluation reveals a male karyotype,low androgen levels, and high gonad-otropin levels. Treatment includessurgical removal of the gonads andestrogen replacement.
Normal breast development-Intactuterus
Individuals in this category are phe-notypically normal females whoundergo normal Mullerian develop-ment and normal pubertal progres-sion. They can be presumed to havenormal female kaiyotypes. Thecauses of the amenorrhea include va-ginal outlet obstruction (eg, imperfor-ate hymen, transverse vaginalseptum) and disturbances in the hy-pothalamic-pituitary-ovarian axis.The management of patients in thislatter group is identical to that of pa-tients who have secondary amenor-rhea.
Secondary Amenorrhea
Secondary amenorrhea is defined asthe absence of menstruation for atleast three cycles or at least 6 months
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46 Pediatrics in Review Vol. 13 No. 2 February 1992
in females who have already estab-lished menstruation. Although men-ses often are irregular in youngadolescents, they should stabilizewithin 1 to 2 years of menarche.Amenorrhea occurring more than 18months after menarche should beconsidered abnormal and warrantsinvestigation.
Pregnancy always must be in-cluded in the differential diagnosis ofsecondary amenorrhea. Sensitivequestioning need not imply inherentdistrust or disbelief of the adolescentwho denies sexual activity. Instead,
it acknowledges the strong sociocul-tural pressures that may lead an ado-lescent to give an inaccurate sexual
history.Once pregnancy has been ex-
cluded, evaluation of secondary
amenorrhea focuses on the hypothala-mic-pituitary-ovarian axis. This be-gins with a complete history andphysical examination (Figure 2).
INITIAL EVALUATION
Maintenance of normal menses re-quires adequate body fat composi-tion. Because weight loss or failureto gain weight is a common sign ofillness during adolescence, secondaryamenorrhea may be an indication ofpoor nutrition, stress, or systemic ill-ness. Common diseases presentingduring adolescence that may be asso-
ciated with secondary amenorrhea in-clude anorexia nervosa, inflammatorybowel disease, diabetes mellitus, thy-roid disease, and pituitary adenomas.The history,therefore,should includequestioning about caloric intake, diet-
ing, weight fluctuation, bowel habits,exercise, medication and drug use,headache, visual change, and galac-
torrhea. Family history of menstrualirregularities, eating disorders, diabe-tes, and thyroid disease also may be
helpful.The physical examination should
begin with measurement of heightand weight and an assessment ofbody habitus. Common stigmata ofanorexia nervosa include cachexia,lanugo, parotid enlargement, brady-cardia, hypotension, and hypother-mia. Fundoscopic examination, gross
visual fields, and examination of thecranial nerves should be done as partof an initial screening for a pituitary
lesion. Breast examination should in-clude an attempt to elicit galactor-rhea. If light microscopy of the
FIGURE 2. Evaluation of secondary amenorrhea. CT, computed tomography; DHEA-S, dehydroepiandrosterone sulfate; LH, luteinizinghormone; MRI, magnetic resonance imaging; TEST, testosterone; TSH, thyroid stimulating hormone. Modified from Speroff L, Glass RH,
Kase NG. Clinical Gynecologic Endocrinology and Infertility. 4th ed. Baltimore, MD: Williams and Wilkins; 1989:178
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Menses often are irregular duringearly adolescence but should
stabilize within 2 years ofmenarche.
Pediatrics in Review Vol. 13 No. 2 February 1992 47
expressed fluid reveals fat lobules, itconfirms that the discharge is breastmilk and suggests stimulation of thebreast by high prolactin levels. Thehair, skin, and external genitalia
should be inspected for evidence ofandrogen excess (eg, hirsutism, clito-romegaly, male escutcheon). The ab-
domen should be palpated for ten-derness, masses, or signs of preg-nancy. A rectal examination for fis-sures, fistulae, skin tags, or occult
blood also should be done.
On pelvic examination, the vaginalmucosa and cervical mucus may help
define the degree of estrogen stim-ulation. Estrogenic mucus is clear,watery, distensible, and reveals fern-
ing on light microscopy. Bimanualand rectovaginal examination shouldbe done in all patients presentingwith unexplained secondary amenor-rhea to evaluate uterine and ovariansize and to screen for pelvic masses.
The minimum laboratory evalua-tion of secondary amenorrhea in-cludes a pregnancy test (serum orurine level of human chorionic go-nadotropin), thyroid function studies,and serum prolactin level. Prolactin
should be measured even in the ab-sence of galactorrhea because onlyone third of patients who have ele-vated levels will have galactorrhea. Itis estimated that 5% to 10% of pa-tients who have both amenorrhea andelevated serum prolactin levels havepituitary adenomas, while 25% ofthose with amenorrhea, galactorrhea,and high prolactin levels have adeno-mas. It should be remembered that
mild elevations in the serum prolactinlevel usually are due to medication,breast stimulation, stress, hypothy-roidism (due to stimulation of the pi-tuitary by thyroid releasinghormone), or other extraneous fac-tors. The first elevation should beevaluated by comparison with a sec-ond sample drawn in a relaxed, fast-ing state. Persistently high prolactinlevels (>100 ng/mL) are associatedwith tumors and mandate radiologic
evaluation of the pituitary via com-puted tomography or magnetic reso-nance imaging.
If the physical examination revealssigns of androgen excess, serum lev-els of dehydroepiandrosterone sulfate(DHEA-S) and testosterone should bemeasured. The differential diagnosisof hirsutism-virilization and oligome-
norrhea includes polycystic ovariansyndrome (PCOS), ovarian tumors,
congenital adrenal hyperplasia (C-21hydroxylase deficiency), adrenal tu-mors, and Cushing syndrome.DHEA-S levels > 700 ng/mL and tes-tosterone levels > 90 p.g/mL requirefurther investigation. This may in-dude measurement of a serum 17-hydroxyprogesterone level, adrenal
suppression testing, and computed to-mography or magnetic resonance im-aging of the abdomen and pelvis.
PROGESTERONE CHALLENGE
After excluding pregnancy, hypothy-roidism, and pituitary adenoma as the
cause of secondary amenorrhea, thenext step in the evaluation is admin-istration of a progesterone challenge.The purpose of this is twofold. First,
withdrawal bleeding following expo-sure to exogenous progesterone es-tablishes the presence of a normaluterus. Second, withdrawal bleedingindicates that the endometrium has
been primed by endogenous estrogenand, thus, implies ovarian function.Oral medroxyprogesterone acetate isadministered in a dose of 5 to 10 mgdaily for 5 to 10 days. If complianceis of concern, 200 mg of progester-one suspended in oil can be given asa single intramuscular injection.
Positive withdrawal bleeding
The occurrence of bleeding, howeverminimal, 2 to 7 days after concluding
the progesterone regimen constitutespositive withdrawal bleeding and es-tablishes the presence of anovulation.The most common cause of anovula-
tion in a postmenarchal adolescent isPCOS. This disorder is characterizedby amenorrhea or oligomenorrhea,
hirsutism, infertility, and often obes-ity. When spontaneous bleeding oc-curs in association with PCOS, ittends to be unpredictable and often is
prolonged or heavy (ie, dysfunctionaluterine bleeding). Oligomenorrhea or
ADOLESCENT MEDICINEMenstrual Disorders
secondary amenorrhea is variable inits onset and duration.
The fundamental defect character-izing PCOS probably is not locatedin the ovary. Instead, it is probablythe result of inappropriate signals
along the hypothalamic-pituitary-ovarian axis. It has been suggestedthat exaggerated adrenarche andobesity, resulting in high levels of
extraglandular estrogen, lead to pos-itive feedback on LH secretion andnegative feedback on FSH secretion.This is reflected in a high LH-to-FSHratio ( > 2). The elevated LH levelleads to hyperplasia of the ovarianstroma and theca cells and increasedovarian production of androgens. Pe-ripheral aromatization of the andro-gens to estrogens then perpetuate the
anovulation.Treatment of PCOS attempts to in-
terrupt this cycle. Use of a combined
estrogen-progestin oral contraceptivehelps control hirsutism, regulates
menses, and is well-tolerated by mostadolescents. Although a strong oral
progestin formulation (ie, levonorges-trol) is useful in controlling dysfunc-tional uterine bleeding, a lowerstrength, nonandrogenic progestin
formulation (ie, norothindrone)should be considered for long-termuse in the hirsute patient. If the ado-lescent prefers not to use an oral con-traceptive, progesterone should beadministered every 3 months in theabsence of spontaneous menses toprotect against the long-term risk ofendometrial hyperplasia.
The hirsutism associated withPCOS also may respond to anti-an-drogens such as spironolactone. The
effectiveness of spironolactone is re-lated to dosage. An initial dose of150 to 200 mg daily is recom-mended, with subsequent tapering toa maintenance dose of 25 to 50 mg.
Oral contraceptives containing ges-todene and norgestimate are expected
to be approved by the FDA in 1992.These nonandrogenic, potent proges-
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tins may prove to be the optimal for-mulation for the hirsute patient withPCO.
Negative withdrawal bleeding
If the patient fails to bleed after theprogestin challenge, either the uterusis abnormal or there has been insuffi-cient endogenous estrogen to primethe endometrium. A combined oralestrogen-progestin regimen should re-sult in bleeding if the endometrium isnormal.
If no bleeding occurs after the es-trogen-progestin regimen, Ashermansyndrome may have occurred as a re-sult of uterine instrumentation,trauma, or infection. The resultingformation of intrauterine scarring(synechiae) causes amenorrhea.
In the adolescent who has a nor-mal vagina and uterus and no riskfactors for intrauterine scarring, theestrogen-progestin challenge can beeliminated and a hypoestrogenic statecan be presumed to exist. Serum go-nadotropin levels then should bemeasured. High serum levels of go-nadotropins (FSH and LH) indicateovarian failure (hypergonadotropichypogonadism). Karyotype testingshould be performed on patients withpresumed ovarian failure to rule outTurner mosaicism or other chromo-somal abnormalities. The presence ofany portion of a Y chromosome man-dates gonadectomy to eliminate therisk of malignant transformation ofthe gonad. Ovarian failure also mayresult from autoimmune disease,chemotherapy, or radiation.
Low serum levels of gonadotropinspoint to a defect in the hypothalamusor pituitary (hypogonadotropic hypo-gonadism or hypothalamic amenor-rhea). Although the incidence ofpituitary tumors is low in the absenceof galactorrhea or an elevated serumprolactin, radiologic evaluationshould be considered in cases whereno obvious cause for hypothalamicdysfunction can be found. Hypothala-mic amenorrhea comprises a hetero-geneous group of disorders asdiscussed previously, including sys-temic illness, anorexia nervosa, exer-cise-induced amenorrhea, andstressful situations (eg, going awayto school). It is believed that stressleads to alterations in hypothalamicGnRh secretion, possibly due to ele-
vated beta-endorphin levels. Short-term treatment includes reassurance,counseling, and watchful waiting. Ifthe amenorrhea persists, estrogen re-placement is indicated. This is bestaccomplished with a combined estro-gen-progestin oral contraceptive. Analternative regimen for the adolescentwho is not sexually active is a conju-gated estrogen (0.625 to 1 .25 mgdaily on days 1 to 25) and medroxy-progesterone acetate (10 mg daily ondays 16 to 25). Menses usually oc-curs at the end of each cycle.
Exercise-induced amenorrhea prob-ably is due to a complex interplay ofdecreased body fat and stress. Ath-letes who have body fat below thetenth percentile for age are likely todevelop amenorrhea. High-energyoutput and stress may act indepen-dently of body fat in inducing amen-orrhea because menses often returnduring nontraining intervals, evenwhen body fat remains unchanged.Elevated prolactin levels also havebeen observed in some amenorrheicathletes during peroids of intense ex-ercise. The simplest way to treat ex-ercise-induced amenorrhea is todecrease the amount of exercise. Ifthe amenorrhea persists, estrogenreplacement therapy should beinstituted.
Anorexia nervosa is a special caseof hypothalamic amenorrhea. Al-though the mechanisms of amenor-rhea are similar to those of exercise-induced amenorrhea (ie, low bodyfat, stress, beta-endorphin release),the complex psychological and mcdi-cal problems associated with anorexianervosa are difficult to manage. Ateam approach employing psychiatriccounseling, close medical supervi-sion, nutritional consultation, andhormonal replacement provides thebest outcome.
There is increasing evidence thatosteoporosis associated with chronicestrogen deficiency may begin duringthe adolescent years. For this reason,
estrogen replacement therapy shouldnot be delayed until adulthood in the
patient who has well-established hy-pogonadism. Progesterone should beadministered with the estrogen tominimize the risk of endometrial car-cinoma. When such a combined regi-men is used, the benefits appear tofar outweigh the risks.
SUGGESTED READINGAmerican College of Obstetrics and
Gynecology. Amenorrhea. Technical
Bulletin. 1989;128:1-7Chihul Hi, London SN. Menstrual cycle
disorders. Obstet Gynecol Clin North Am.
1990;17:275-481Coupey SM. Common menstrual disorders.
Pediatr Clin North Am. 1989;36:551-571Droegemueller W, Herbst AL, Mishell DR,
Stenchever MA. Comprehensive
Gynecology. 1st ed. St. Louis, MO: CVMosby Co; 1987
Emans SJH, Goldstein DP. Pediatric and
Adolescent Gynecology. 3rd ed. Boston,MA: Little, Brown and Company; 1990
Farber M, ed. Congenital anomalies of theparamesonephric ducts. Semin Repro
