MENSTRUAL DISTURBANCE
Definition
Menstrual disturbance is classified as:
·
Amenorrhoea – absent menses for >6 months.
This can be fur-ther subdivided into primary amenorrhoea (failure of menarche –
the first appearance of periods– by age 16 years) or secondary amenorrhoea
(cessation of menstrual periods for >6 months in women who have previously
menstruated)
• Oligomenorrhoea
– reduced menstrual frequency to <9 peri-ods/year
• Polymenorrhoea
– frequent menstrual periods
• Menorrhagia
– heavy menstrual periods.
Polymenorrhoea and menorrhagia can relate to hypothyroidism but
usually reflect abnormal (dysfunctional) uterine bleeding (irregular bleeding,
which is more common in adolescents and women approaching the menopause, and
not caused by structural pathology). This is not considered further here as it
is not usually managed by endocrinologists in clinical practice.
Causes
The causes of primary amenorrhoea, secondary amenorrhoea and
oligomenorrhoea can be broadly divided into four groups:
1.
Premature ovarian failure.
2. Disordered gonadotrophin secretion
(hypogonadotrophic hypogonadism). This can be caused by hypothalamic–pituitary
disease (Chapter 5), including hyperprolactinaemia, or hypo-thalamic
amenorrhoea whereby low body weight (e.g. anorexia nervosa), intensive
exercise, prolonged psychological stress or systemic illness lead to suppressed
gonadotrophin pulsatility.
3.
Hyperandrogenic disorders, including
polycystic ovary syn-drome (PCOS; Chapter 26).
4.
Structural disease (e.g. uterine adhesions,
congenital absence of the uterus).
Assessment
History
Symptoms of oestrogen deficiency (flushes, vaginal dryness and
dyspareunia), androgen excess (hirsutism, acne), galactorrhoea, heavy exercise,
weight change, emotional stress and systemic illness should be looked for. It
is important to document the onset and duration of the menstrual disturbance.
Examination
This should include an evaluation of body habitus (e.g. anorexia
nervosa, Turner’s syndrome), hyperandrogenism, secondary sexual characteristics
(pubic and axillary hair, breast development), visual fields and anosmia.
Investigations
These should initially be based on measurement of oestradiol, FSH
and LH which will establish whether ovarian dysfunction is primary (raised
gonadotrophins) or secondary (low–normal gonadotrophins) (Figure 25.1). FSH and
LH should be measured in the follicular phase (days 0–5 of a period) to avoid
the FSH/LH surge which can give the false impression of raised gonadotrophins.
A pregnancy test may be indicated if the history is short, while a pelvic
ultrasound helps exclude structural abnormalities and can show altered ovarian
morphology (e.g. polycystic ovaries, ‘streak ovaries’ in Turner’s syndrome).
Other tests may subsequently be needed depending on clinical suspicion and the
pattern of the gonadotrophin results.
Treatment
Treatment is directed at the underlying cause (e.g. weight gain in
low body weight, dopamine agonists for prolactinomas). Oestrogen replacement
will improve symptoms of oestrogen deficiency and protect against decline in
bone mineral density. In women seeking pregnancy, fertility can be improved
with cause-specific treatment (Chapter 30).
Premature ovarian failure
This group of disorders are characterised by amenorrhoea,
oestrogen deficiency and raised gonadotrophins in women <40 years, due to
loss of ovarian follicular function. Causes include:
• Chromosomal
abnormalities (60%), especially Turner’s
syndrome
• Autoimmune
disease (20%)
• Iatrogenic
– following surgery, chemotherapy or radiotherapy
• Genetic.
Turner’s syndrome
This affects 1 in 2500 female births and results from complete or
partial absence of one X chromosome; the most common karyotype is 45 XO.
Affected patients are characterised by short stature and gonadal dysgenesis
(>90% have premature ovarian failure). Clinical features include webbing of
the neck, widened nipples, cubitus valgus and a short 4th metacarpal (Figure
25.2).
Management
Optimisation of growth and puberty
This is achieved through use of high dose GH and oestrogen
replacement. Oestrogen replacement is usually continued until an age at which
menopause would normally be expected to occur.
Screening for and seeking to prevent complications
Patients with Turner’s syndrome have an increased risk of
audiological (otitis media, sensorineural deafness), cardiac (hypertension,
coarctation of the aorta, bicuspid aortic valve, aortic dissection), renal
(congenital abnormalities), hepatic (raised liver enzymes, fatty liver
disease), metabolic (hypothyroidism, type 2 diabetes), skeletal (osteoporosis)
and neuropsychological (motor coordination, visuospatial) complications. These
should be screened for with annual measurement of body mass index (BMI), blood
pressure, HbA1c, thyroid function, liver and renal blood tests,
echocardiography every 3–5 years, and bone density and hearing tests every 5
years.
