Jorge E. Ferguson
The climacteric is defined as a transitory phase in a woman's life, between the ages of reproductive and non-reproductive capacity. Menopause, on the other hand, refers only to the cessation of menstruation and is considered complete after one year of amenorrhea. This fact occurs during the climacteric phase.
The climacteric is sometimes associated with certain symptoms, which is why it is called the climacteric syndrome.
The end of the fertility period occurs in three periods of unequal duration:
- Premenopause . It begins with the first irregularities and the dominant component is luteal insufficiency.
- Menopause . It corresponds to the cessation of menstruation and is determined by alterations in the hypothalamic-pituitary-ovarian axis and hypothalamic neurotransmitters.
- Postmenopause . Dominated by the long-term effects of estrogen deficiency.
Because the limits between each stage are poorly defined, some authors currently use the term perimenopause for the first two stages.
At the beginning of menarche there are approximately 500,000 oocytes in the ovary. In each menstrual cycle a variable amount of these are lost with their follicles, which leads to a gradual decrease in estrogens and inhibin. The reduction of inhibin increases the follicle-stimulating hormone (FSH) that would be the first laboratory finding of perimenopause; This causes rapid follicular development and the consecutive shortening of the cycles, that is, the first clinical manifestation.
As the number of follicles decreases, estrogen production continues to decrease, reaching levels that are not compatible with the induction of the sudden increase in luteinizing hormone (LH); in these circumstances ovulation ceases or becomes irregular.
Clinically, this circumstance is accompanied by irregular cycles, due to shortening of the luteal phase, or anovulatory cycles. When ovulation ceases completely, LH begins to rise and menopause occurs.
However, it is important to know that feedback mechanisms can cause readjustments between the pituitary and the ovary, provided that some follicles remain to respond, so that in some cases laboratory signs and clinical symptoms may normalize.
Although the menopausal ovary may be devoid of follicles, from whose cells the greatest amount of estrogens and progesterone come, it should be noted that many menopausal women are not completely estrogen-free.
Cells of the ovarian and adrenal stroma have the steroideogenic capacity to produce androstenedione. The conversion of this, at the peripheral level, to estrone constitutes the main source of estrogens at this age.
Therefore, even though menopausal women have an estrogen level lower than necessary to maintain reproductive function, this level is not negligible or non-existent.
Symptoms and signs
The climacteric symptoms derive from three main components: 1) diminishing ovarian activity, with the consequent hormonal deficiency that gives rise to the precursor and subsequent symptoms, related to the metabolic change in the affected terminal organ; 2) sociocultural factors, determined by the woman's environment, and 3) psychological factors, dependent on the woman's character.
The great variety of symptomatic pictures is the result of the interaction of these three components.
For years, one of the most frequent symptoms, suffocation, was given greater importance until it was shown that there are other structures that suffer from estrogen deficiency, but that need more time to manifest.
Currently we can divide these symptoms, according to the moment of appearance, into immediate and late.
Immediate manifestations . Vasomotor . Flushing is one of the most frequent and annoying climacteric. It can start in the years leading up to menopause and persist for several years afterward. It is described as a sensation of intense heat in the chest, neck and face, accompanied by perspiration, palpitations and anxiety and insomnia.
Although the main cause is the decrease in estrogen produced by the ovary, it is also currently postulated that there would be a supra-pituitary mechanism, through brain neurotransmitters that control the secretion of luteinizing hormone releasing hormone (LH-RH ). These substances released at the level of the nerve synapses are monoamines, dopamines, serotonin, norepinephrine, or also opioids and endorphins. Therefore, flushing would be a neurovascular phenomenon.
The loss of ovarian estrogens would act by disrupting the balance of brain neurotransmitters, which would affect two neighboring hypothalamic centers: 1) that of the LH-RH neurons, causing an increase in gonadotropics, and 2) that of thermoregulation, producing vasodilatation. cutaneous.
This symptom is observed in 80% of the menopausal women, although with a variable intensity, and it is very annoying in about 40%.
Other immediate symptoms . Menstrual irregularities, weight gain, asthenia, headaches, anxiety, forgetfulness, irritability, depressed state, sexual difficulties.
Late manifestations . They are those that become evident after a longer period of estrogen deficiency.
Trophic disorders . They are caused by urogenital atrophy, senile or atrophic vaginitis, dryness, burning, itching and eventual bleeding. Urological ailments in climacteric women can be very varied.
They will be determined by an atrophy of the epithelium of the urethra and the bladder trigone, which causes dysuria and urgency. At the level of the skin, a series of changes are also observed, such as dryness and cracking, which, although they can be attributed to age, would be reversible with estrogen therapy.
Cardiovascular disease . While cardiovascular and metabolic problems do occur. during menopause they should be considered as multifactorial, there are two facts that are indisputable.
The frequency of acute coronary accidents in women, which is lower than in men before this stage, tends to equalize after that age, which would be explained by a modification of the lipid profile due to the lack of estrogens.
Indeed, during climacteric, changes occur in plasma lipoproteins, with an increase in cholesterol bound to low-density lipoproteins (LDL-C) and a decrease in cholesterol bound to high-density lipoproteins (HDL-C). HDL-C is known to be a protective factor against coronary heart disease, while its decrease and the concomitant elevation of LDL-C levels are associated with an early incidence of coronary heart disease.
Other risk factors would be an increase in triglycerides and the fraction of very low density lipoproteins (VLDL).
Osteoporosis . This is the main cause of fracture in menopausal women. In the aging skeleton, there is a clear imbalance between the processes of bone resorption and formation. During menopause, bone resorption increases, with a corresponding loss of bone mass. Consequently, serum levels of Ca ++, phosphate and alkaline phosphatase would rise, with increased urinary Ca ++ excretion.
One of the main actions of estrogens on bone metabolism would be the regulation of bone resorption.
Although vasomotor alterations and menstrual irregularities are characteristic of this stage, the laboratory data will be those that will confirm the diagnosis of menopause.
The pituitary gonadotrophymes (FSH and LH) is so high. FSH values are usually around 100 mU / ml or more, while LH values are above 75 mU / ml.
These laboratory values should be evaluated in conjunction with the clinical picture, since LH levels can be equally elevated in the ovulatory phase of the cycle.
It is also important to remember that ovarian-hypothalamic-pituitary feedback mechanisms sometimes restore homeostasis, so that these abnormal laboratory values normalize for a short time and cycles reappear.
These events can also occur in patients with premature menopause. Therefore, it is advisable to monitor the woman for a year with repeated hormonal determinations.