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    Delayed menarche with normal pubertal growth

     

    Diagnosis

    Polycystic ovarian syndrome is a heterogeneous syndrome that usually presents during adolescence with unexplained hyperandrogenism and persistent anovulatory menstrual abnormality.8 In adolescents, it is characterized by hyperandrogenism and ovulatory dysfunction or abnormal uterine bleeding patterns. The exact etiology is unknown. It is one of the more common causes of elevated testosterone levels that was noted in this patient.

    Patients may present with acne, hirsutism, deepening of the voice, and androgenic alopecia, if hyperandrogenism is associated with their symptoms.8 An accurate diagnosis is a challenge because symptoms for PCOS can vary with race, age, weight, and medications. Adolescent patients pose particular diagnostic problems because characteristics of normal puberty often overlap with signs and symptoms of PCOS.

    There is currently a single indicator for hyperandrogenemia, which is identified as an elevated serum free testosterone caused by the bioactive portion of the serum testosterone that is the free fraction.9 The patient in this case presented with lack of menarche by more than 3 years after the onset of breast and pubic hair development and elevated free testosterone levels, which meets the criteria (Table 3).

    Epidemiology

    Polycystic ovarian syndrome is a common endocrine system disorder affecting 5% to 10% of women of reproductive age.7 In the United States, PCOS is the single most common endocrine cause of anovulatory infertility and is a risk factor for metabolic abnormalities.10

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    In a cross-sectional study with adolescent girls, it was determined that the majority of patients with PCOS were also diagnosed with hyperandrogenism and/or oligoanovulation: 69.6% and 67.6%, respectively.10 The study also associated PCOS with increased weight, demonstrating that adolescents with PCOS were substantially more likely to be moderately or extremely obese than those without PCOS.10,11

    Clinical studies suggest that the metabolic risk associated with PCOS is mostly due to obesity and that it does not independently increase the metabolic risk of adolescents.9

    Treatment and management

    Treatment for PCOS is a systematic approach directed at the underlying cause. The treatment also can be initialized depending on the patients’ complaints and goals. The priority in the adolescent with PCOS is treating menstrual irregularity and cutaneous manifestations of hyperandrogenism. Once PCOS is established in the adolescent, it is critical that screening for metabolic abnormalities is initiated.12

    Combined oral contraceptives (COCs) are the first-line medical treatment for adolescents because they normalize endometrial cycling, protecting against endometrial carcinoma and inhibiting ovarian function, and thereby normalizing serum androgens.4 Oral contraceptive pills (OCPs) decrease the LH levels and decrease androgen synthesis while increasing sex hormone-binding globulin levels and testosterone-binding globulin levels, thereby decreasing free testosterone.5

    Progesterone monotherapy is an alternative to COCs for those who are at risk for thromboembolic events or with contraindications for COCs. The disadvantage to this alternative is that irregular bleeding may persist and androgens are not well suppressed.12

    Lifestyle modifications are crucial in eliminating comorbidities related to obesity and insulin resistance. Diet, medication compliance, and exercise have shown 50% probability of improvement in menstrual cyclicity.12

    Discussion

    The Endocrine Society’s clinical guidelines define the appropriate criteria for the diagnosis of PCOS in the adolescent. These include an abnormal uterine bleeding pattern for age or gynecologic age persistent for 1 to 2 years (Table 3).13 Evidence of hyperandrogenism is also part of the diagnostic criteria and it includes persistent elevated testosterone, hirsutism, or acne.12

    Until the Endocrine Society's criteria were established, there were only the Rotterdam criteria for the diagnosis of PCOS that stated that 2 of the following 3 conditions should be present in women with PCOS:

    1. Absence of ovulation, irregular menstrual periods, or amenorrhea.

    2. Elevated levels of androgens (acne, excess body or facial hair).

    3. Confirmed polycystic ovaries.

    These criteria were problematic in adolescents because oligomenorrhea, acne, and multifollicular ovary morphology normally can be present in adolescent girls.13

    An ultrasound should not be used as a diagnostic criterion in adolescents because polycystic morphology is a common finding in the adolescent age group. An ultrasound should be used as a supportive method to help confirm the presence or absence of a thickened uterus and identify structural abnormalities.1 Pelvic ultrasounds are commonly ordered in the adult patient with PCOS to determine thickened uterus, ovarian volume, and number of follicles present. In the adolescent, increased ovarian volume and polycystic morphology is a common presentation outside of PCOS.

    Case resolution

    This patient met the criteria for PCOS based on the Endocrine Society’s clinical guidelines for the diagnosis of PCOS in adolescents.

    At this time, the decision was made to start with a progesterone challenge test to confirm anovulation versus inadequate estrogen or outflow tract obstruction. Positive withdraw bleeding confirms that there is a lack of ovulation. If the patient had no vaginal bleeding, then this could indicate inadequate estrogen or outflow tract obstruction. Medroxyprogesterone 10 mg daily was ordered for 10 days.

    Prior to treatment with OCPs, a bone age radiograph was also ordered to confirm that the patient had reached physical growth and development. It was obtained to assess whether the epiphyses had closed, and to ensure that the bone age correlated with the patient’s chronological age. Based on her height, weight, and sexual characteristics, her physicians did not anticipate a delay in bone age.11,13 Bone age needs to be considered when hormones such as estrogen are prescribed because the growth plate closes sooner in response to estrogen.

    The radiograph results confirmed that the patient’s bone age was consistent with her actual physical growth and development (Figure 2).

    At the 2-week follow-up, the progesterone challenge test was completed and the patient had vaginal bleeding. She was otherwise doing well. The option of OCPs was discussed and the decision was made to start the contraceptives. A discussion of diet and exercise as a way to normalize her menstrual cycles was initiated as well.

    The patient continued to do well on OCPs and continued with regular periods. Over the course of several months, and with appropriate lifestyle modifications, she lost 10 pounds.

    REFERENCES

    1. Klein DA, Poth MA. Amenorrhea: an approach to diagnosis and management. Am Fam Physician. 2013;87(11):781-788.

    2. Master-Hunter T, Heiman DL. Amenorrhea: evaluation and treatment. Am Fam Physician. 2006;73(8):1374-1382.

    3. Yildiz BO. Diagnosis of hyperandrogenism: clinical criteria. Best Pract Res Clin Endocrinol Metab. 2006;20(2):167-176.

    4. Scholes D, LaCroix AZ, Ichikawa LE, Barlow WE, Ott SM. Change in bone mineral density among adolescent women using and discontinuing depot medroxyprogesterone acetate contraception. Arch Pediatr Adolesc Med. 2005;159(2):139-144.

    5. Lanzo E, Monge M, Trent, M. Diagnosis and management of polycystic ovary syndrome in adolescent girls. Pediatric Annals. 2015;44(9):e223-e230.

    6. Trémollieres F. Impact of oral contraceptive on bone metabolism. Best Pract Res Clin Endocrinol Metab. 2013;27(1):47-53.

    7. Deligeoroglou E, Athanasopoulos N, Tsimaris P, Dimopoulos KD, Vrachnis N, Creatsas G. Evaluation and management of adolescent amenorrhea. Ann N Y Acad Sci. 2010;1205:23-32.

    8. Roe AH, Dokras A. The diagnosis of polycystic ovary syndrome in adolescents. Rev Obstet Gynecol. 2011;4(2):45–51.

    9. Rossi B, Sukalich S, Droz J, et al. Prevalence of metabolic syndrome and related characteristics in obese adolescents with and without polycystic ovary syndrome. J Clin Endocrinol Metab. 2008;93(12):4780-4786.

    10. Christensen SB, Black MH, Smith N, et al. Prevalence of polycystic ovary syndrome in adolescents. Fertil Steril. 2013;100(2):470-477.

    11. Nezi M, Christopoulos P, Paltoglou G, et al. Focus on BMI and subclinical hypothyroidism in adolescent girls first examined for amenorrhea or oligomenorrhea. The emerging role of polycystic ovary syndrome. J Pediatr Endocrinol Metab. 2016;29(6):693-702.

    12. Rosenfield RL. The diagnosis of polycystic ovary syndrome in adolescents. Pediatrics. 2015;136(6):1154-1165.

    13. Witchel SF, Oberfield S, Rosenfield RL, et al. The diagnosis of polycystic ovarian syndrome during adolescence. Horm Res Paediatr. 2015;83(6):376-389.

    Rachel S Dawson, DO, MPH, FAAP, FSAHM
    Dr Dawson is a pediatrician specializing in adolescent medicine at Baylor Scott & White Health, Killeen, Texas. She is director of the ...
    Rosa Cervantes, MSN, FNP
    Ms Cervantes is a family nurse practitioner in Fort Polk, Louisiana.

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