Chapter 50.

Menstrual Disorders and Pelvic Pain

Hypergonadotropic Hypogonadism
Ovarian failure is considered premature when it occurs in women <40 years old and accounts for 10% of secondary
amenorrhea. Primary ovarian insufficiency (POI) has generally replaced the terms premature menopause and premature ovarian
failure in recognition that this disorder represents a continuum of impaired ovarian function. Ovarian insufficiency is associated
with the loss of negative-feedback restraint on the hypothalamus and pituitary, resulting in increased FSH and LH levels. FSH is
a better marker of ovarian failure as its levels are less variable than those of LH. As with natural menopause, POI may wax and
wane, and serial measurements may be necessary to establish the diagnosis.
Once the diagnosis of POI has been established, further evaluation is indicated because of other health problems that may be
associated with POI. For example, POI occurs in association with a variety of chromosomal abnormalities, including Turner
syndrome, autoimmune polyglandular failure syndromes, radio- and chemotherapy, and galactosemia. The recognition that early
ovarian failure occurs in premutation carriers of the fragile X syndrome is important because of the increased risk of severe
mental retardation in male children with FMR1 mutations. In the majority of cases, however, a cause for POI is not determined.
Hypergonadotropic hypogonadism occurs rarely in other disorders, such as mutations in the FSH or LH receptors. Aromatase
deficiency and 17 -hydroxylase deficiency are associated with elevated gonadotropins with hyperandrogenism and
hypertension, respectively. Gonadotropin-secreting tumors in women of reproductive age generally present with high, rather
than low, estrogen levels and cause ovarian hyperstimulation or dysfunctional bleeding.
Treatment: Hypo- and Hypergonadotropic Causes of Amenorrhea
Amenorrhea almost always is associated with chronically low levels of estrogen, whether it is caused by hypogonadotropic
hypogonadism or ovarian insufficiency. Development of secondary sexual characteristics requires gradual titration of estradiol
replacement with eventual addition of progestin. Symptoms of hypoestrogenism can be treated with hormone replacement
therapy or oral contraceptive pills. Patients with hypogonadotropic hypogonadism who are interested in fertility require treatment
with pulsatile GnRH or exogenous FSH and LH, whereas patients with ovarian failure can consider oocyte donation, which has a
high chance of success in this population.
Polycystic Ovarian Syndrome (PCOS)
PCOS is diagnosed on the basis of a combination of clinical or biochemical evidence of hyperandrogenism, amenorrhea or
oligomenorrhea, and the ultrasound appearance of polycystic ovaries. Approximately half of patients with PCOS are obese, and
abnormalities in insulin dynamics are common, as is metabolic syndrome. Symptoms generally begin shortly after menarche and
are slowly progressive. Lean patients with PCOS generally have high LH levels in the presence of normal to low levels of FSH
and estradiol. The LH/FSH ratio is less pronounced in obese patients in whom insulin resistance is a more prominent feature.
Treatment: Polycystic Ovarian Syndrome
A major abnormality in patients with PCOS is the failure of regular, predictable ovulation. Thus, these patients are at risk for the
development of dysfunctional bleeding and endometrial hyperplasia associated with unopposed estrogen exposure. Endometrial
protection can be achieved with the use of oral contraceptives or progestins (medroxyprogesterone acetate, 5–10 mg, or
prometrium, 200 mg daily for 10–14 days of each month). Oral contraceptives are also useful for management of
hyperandrogenic symptoms, as is spironolactone, which functions as a weak androgen receptor antagonist. Management of the
associated metabolic syndrome may be appropriate for some patients (Chap. 242). For patients interested in fertility, weight
control is a critical first step. Clomiphene citrate is highly effective as a first-line treatment, with or without the addition of
metformin. Exogenous gonadotropins can be used by experienced practitioners.

PELVIC PAIN
The mechanisms that cause pelvic pain are similar to those which cause abdominal pain (Chap. 13) and include inflammation of
the parietal peritoneum, obstruction of hollow viscera, vascular disturbances, and pain originating in the abdominal wall. Pelvic
pain may reflect pelvic disease per se but also may reflect extrapelvic disorders that refer pain to the pelvis. In up to 60% of
cases, pelvic pain can be attributed to gastrointestinal problems, including appendicitis, cholecystitis, infections, intestinal
obstruction, diverticulitis, and inflammatory bowel disease. Urinary tract and musculoskeletal disorders are also common causes
of pelvic pain.
Approach to the Patient: Pelvic Pain
A thorough history that includes the type, location, radiation, and status with respect to increasing or decreasing severity can
help identify the cause of acute pelvic pain. Specific associations with vaginal bleeding, sexual activity, defecation, urination,
movement, or eating should be specifically sought. A careful menstrual history is essential to assess the possibility of pregnancy.
Determination of whether the pain is acute versus chronic and cyclic versus noncyclic will direct further investigation (Table 50-
1). However, disorders that cause cyclic pain occasionally may cause noncyclic pain, and the converse is also true.
Table 50-1 Causes of Pelvic Pain

Acute Chronic
Cyclic pelvic pain Premenstrual symptoms

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