Management of secondary amenorrhoea

GENITAL TRACT ABNORMALITIES Asherman's syndrome

Asherman's syndrome is a condition in which intrauter-ine adhesions prevent normal growth of the endometrium

Table 39.5 Classification of secondary amenorrhoea

Uterine causes Ovarian causes

Hypothalamic causes (hypogonadotrophic hypogonadism)

Pituitary causes

Causes of hypothalamic/ pituitary damage

(hypogonadism)

Systemic causes

Asherman's syndrome Cervical stenosis Polycystic ovary syndrome Premature ovarian failure (genetic, autoimmune, infective, radio/chemotherapy) Weight loss Exercise Chronic illness Psychological distress Idiopathic

Hyperprolactinaemia Hypopituitarism Sheehan's syndrome Tumours (craniopharyngiomas, gliomas, germinomas, dermoid cysts) Cranial irradiation Head injuries Sarcoidosis Tuberculosis

Chronic debilitating illness Weight loss

Endocrine disorders (thyroid disease, Cushing's syndrome etc.)

Table 39.6 The aetiology of secondary

amenorrhoea in 570 patients attending

an

endocrine clinic (Balen et al. 1993).

Polycystic ovary syndrome

36.9%

Premature ovarian failure

23.6%

Hyperprolactinaemia

16.9%

Weight-related amenorrhoea

9.8%

Hypogonadotrophic hypogonadism

5.9%

Hypopituitarism

4.4%

Exercise-related amenorrhoea

2.5%

[27]. This may be the result of a too vigorous endometrial curettage affecting the basalis layer of the endometrium or adhesions may follow an episode of endometritis. It is thought that oestrogen deficiency increases the risk of adhesion formation in breastfeeding women who require a puerperial currettage for retained placental tissue. Typically amenorrhoea is not absolute, and it may be possible to induce a withdrawal bleed using a combined oestrogen/progestagen preparation. Intrauterine adhesions may be seen on a hysterosalpingogram (HSG) (Fig. 39.2). Alternatively, hysteroscopic inspection of the uterine cavity will confirm the diagnosis and enable treatment by adhesiolysis. The adhesions bridge the anterior and posterior walls of the uterine cavity and are usually avascular, although may contain vessels, muscle and even endometrium. Following surgery, a 3-month course of cyclical progesterone/oestrogen should be given. Some clinicians insert a foley catheter into the uterine cavity for 7-10 days post-operatively [28], or an intrauterine contraceptive device for 2-3 months [29], to prevent recurrence of adhesions.

In a series of 292 infertile women who were thought to have intrauterine adhesions, as detected by HSG, 46% conceived without treatment but only 53% delivered a live infant and 13% had placenta accreta [30]. It has been suggested that the pregnancy rates after hysteroscopic treatment of intrauterine adhesions depends upon the degree of the initial problem [31] being 93% for mild and 57% for severe disease. The outcome of the pregnancy would appear to depend upon the post-treatment contour of the uterine cavity.

Cervical stenosis

Cervical stenosis is an occasional cause of secondary amenorrhoea. It was relatively common following a traditional cone biopsy for the treatment of cervical intraep-ithelial neoplasia. However, modern procedures such as laser or loop diathermy have less post-operative cervical complications [32]. Treatment for cervical stenosis consists of careful cervical dilatation.

OVARIAN CAUSES OF SECONDARY AMENORRHOEA Polycystic ovary syndrome See earlier sections.

Premature ovarian failure. Ovarian failure by definition, is the cessation of periods accompanied by raised gonadotropin level prior to the age of 40 years. It may occur at any age. The exact incidence of this condition is unknown as many cases go unrecognized, but estimates vary between 1 and 5% of the female population. Studies of amenorrhoeic women report the incidence of premature ovarian failure to be between 10 and 36%.

Chromosomal abnormalities are common in women with primary amenorrhoea. Hague et al. [33] found chromosomal abnormalities in 70% of patients with primary amenorrhoea and in 2-5% of women with secondary amenorrhoea due to premature ovarian failure. Ovarian failure occurring before puberty is usually due to a chromosomal abnormality, or a childhood malignancy that required chemotherapy or radiotherapy. Adolescents who loose ovarian function soon after menarche, are often found to have a Turner's mosaic (46XX/45X) or an X-chromosome trisomy (47, XXX) (also see Plate 39.1, facing p. 562). There are some genetic anomalies that run in families with premature ovarian failure (POF), although these are not assessed in routine clinical practice.

Overall, the most common cause of POF is autoimmune disease; with infection, previous surgery, chemo- and radiotherapy also contributing ovarian autoantibodies can be measured and have been found in up to 69% of cases of POF. However, the assay is expensive and not readily available in most units. It is therefore important to consider other autoimmune disorders, and screen for autoantibod-ies to the thyroid gland, gastric mucosa parietal cells and adrenal gland if there is any clinical indication.

Prior to the absolute cessation of periods of true premature ovarian failure, some women experience an intermittent return to menses, interspersed between variable periods of amenorrhoea. Gonadotropin levels usually remain moderately elevated during these spontaneous cycles, with plasma FSH levels of 15-20 i^/l. This occult ovarian failure, or resistant ovary syndrome, is associated with the presence of primordial follicles on ovarian biopsy, and pregnancies are sometimes achieved, although the ovaries are usually resistant to exogenous gonadotropins as they are to endogenous hormones. It is probable that reports of pregnancy in women with POF represent cases of fluctuating ovarian function rather than successes of treatment [34].

It is, however, possible to achieve pregnancy by oocyte donation, as part of in vitro fertilization treatment. Experimental work in animals has succeeded in transplanting primordial follicles into irradiated ovaries, with subsequent ovulation and normal pregnancy [35]. The prospect of transplantation of cryopreserved ovarian tissue is coming close to fruition in humans and should soon offer the chance of fertility to women who have received radiotherapy or chemotherapy.

The diagnosis and consequences of premature ovarian failure require careful counselling of the patient. It may be particularly difficult for a young woman to accept the need to take oestrogen preparations that are clearly labelled as being intended for older postmenopausal women, while at the same time having to come to terms with the inability to conceive naturally. The short- and long-term consequences of ovarian failure and oestrogen deficiency are similar to those occurring in the fifth and sixth decade. However, the duration of the problem is much longer and therefore hormone replacement therapy is advisable to reduce the consequences of oestrogen deficiency in the long term.

Younger women with premature loss of ovarian function have an increased risk of osteoporosis. A series of 200 amenorrhoeic women between the ages of 16-40 demonstrated a mean reduction in bone mineral density of 15% as compared with a control group and after correction for body weight, smoking and exercise [36]. The degree of bone loss was correlated with the duration of the amenor-rhoea and the severity of the oestrogen deficiency rather than the underlying diagnosis, and was worse in patients with primary amenorrhoea compared with those with secondary amenorrhoea. A return to normal oestrogen status may improve bone mass density, but bone mineral density is unlikely to improve more than 5-10% and it probably does not return to its normal value. However, it is not certain if the radiological improvement seen will actually reduce the risk of fracture, as remineralization is not equivalent to the restrengthening of bone. Early diagnosis and early correction of oestrogen status is therefore important.

Women with POF have an increased risk of cardiovascular disease. Oestrogens have been shown to have beneficial effects on cardiovascular status in women. They increase the levels of cardioprotective HDL but also total triglyceride levels, while decreasing total cholesterol and low-density lipoprotein (LDL) levels. The overall effect is of cardiovascular protection.

The HRT preparations prescribed for menopausal women are also preferred for young women. The reason for this is that even modern low dose combined oral contraceptive (COC) preparations contain at least twice the amount of oestrogen that is recommended for HRT, in order to achieve a contraceptive suppressive effect on the hypothalamic-pituitary axis. HRT also contains 'natural' oestrogens rather than the synthetic ethinyloestradiol that is found in most COCs.

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Responses

  • jens werfel
    Can loop diathermy treatments cause pof?
    6 years ago

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