Sexually Transmitted Diseases - I. I. Mavrov 2005

Climacteric
Female Climacteric

The cessation of reproductive function during a woman's climacteric period triggers age-related changes across other Organs and systems, limiting the body's adaptive capacity and laying the groundwork for psychoemotional, autonomic, and metabolic-endocrine disorders, as well as cardiovascular, respiratory, and other systemic diseases. Concurrently with damaging mechanisms, the body mobilizes compensatory processes aimed at preserving vitality, maintaining homeostatic stability, and increasing life expectancy.

The natural course of the climacteric period is frequently complicated by a distinct symptom complex known as climacteric syndrome (CS). According to various authors (E. M. Vikhlyayeva, V. P. Smetnyk, 1980; N. M. Tkachenko, 1987, et al.), the prevalence of CS ranges from 26 to 48%. It is characterized by neuropsychiatric, vasomotor, and metabolic-endocrine disturbances that arise against the backdrop of physiological Aging, often leading to a decline or even complete loss of a woman's working capacity. Clinical and laboratory analyses reveal varying levels of impairment in The Cardiovascular system and Central Nervous system, alongside disruptions in cortico-subcortical interactions, which determine the Specific features of psychoemotional and autonomic-vascular disorders.

Climacteric syndrome is a multifactorial condition influenced by hereditary and environmental factors, as well as the somatic health of the body prior to the onset of the climacteric period. However, one should not underestimate The Significance of such criteria as socioeconomic status, marital status, having children, the health of family members, and professional capacity. Evidently, The impact of adverse factors during the transitional period merely acts as a triggering moment that exposes pre-existing hypothalamic pathology against the Background of the age-related restructuring of the complex autonomic-humoral-hormonal system.

Consequently, There is a disruption in the regulatory axis comprising higher cerebral centers, the Hypothalamus, the Pituitary Gland, the Ovaries, and the Uterus, which functionally interact via positive and negative feedback loops. During the climacteric period, control over the normal Menstrual cycle is the first to fail within this system, originating at the level of specialized Brain Neurons. These neurons, as is well known, receive environmental information and convert it into neurohumoral signals transmitted to the neurosecretory Cells of the hypothalamus. Hypothalamic cells secrete gonadotropin-releasing hormone (GnRH) and thyrotropin-releasing hormone (TRH), which regulate the release of prolactin from the pituitary gland.

Upon release from hypothalamic cells, releasing factors travel via the local vascular network of the hypothalamo-pituitary portal system directly to the anterior pituitary. At the anterior pituitary level, GnRH stimulates the secretion and release of glycoprotein gonadotropins, namely LH and FSH. These two Hormones are transported to the ovaries via the bloodstream: FSH stimulates follicular GROWTH AND DEVELOPMENT, while LH regulates steroidogenesis. To ensure a normal menstrual cycle, the levels of these gonadotropins must be maintained in a strictly defined proportion. Driven by FSH and LH, the ovaries produce estrogens and progesterone. During menopause, estradiol synthesis drops sharply, whereas gonadotropin levels become noticeably elevated.

The underlying causes of CS may include age-related changes in specific hypothalamic centers or estrogen deficiency. Notably, fluctuations in estrogen levels hold greater significance in the Pathogenesis of CS than absolute estrogen deficiency. At the same time, changes within the Reproductive System do not play a decisive role in the onset of CS, given that declining sex hormone secretion and elevated gonadotropins are also observed in uncomplicated menopause and following surgical oophorectomy, without The Development of pathological syndromes.

Functional inadequacy within the higher regulatory centers of the Autonomic nervous system may result from METABOLISM/18.html">The Influence of various genetic factors. Family studies have shown that the incidence of CS among first- and second-degree relatives exceeds 30%; There are also reports of simultaneous onset of menopause and CS in twins. Thus, in cases where thorough and comprehensive investigations fail to identify the cause of CS, the potential impact of genetic factors should be considered.

Among the various causes of this condition, an unfavorable premorbid background is frequently cited (difficult living conditions, prolonged starvation in childhood and adolescence, high incidence of infectious diseases, severe extragenital pathologies, TRAUMATIC BRAIN INJURIES, prolonged psychotraumatic situations, etc.). However, the impact of adverse factors during the transitional period should be viewed as a contributing factor that brings out pre-existing hypothalamic pathology against the backdrop of age-related Changes in the autonomic-humoral-hormonal system.

Alterations in the functional state of the hypothalamus trigger a range of metabolic-endocrine and trophic disorders (Osteoporosis, weight gain, dystrophic changes in the vulva, senile colpitis, trigonitis, Cystalgia, etc.). The Structural and functional connectivity of the hypothalamus with other brain formations—most notably the Limbic System and reticular formation, which serve as the neural substrate for emotional and motivational behavior—along with changes in their functional state, forms The basis of the emotional and psychiatric disorders observed in patients with CS (tearfulness, irritability spells, feelings of fear and anxiety, impaired Memory and Attention, intolerance to auditory and olfactory stimuli, etc.).

Patients with moderate and severe forms of CS exhibit elevated Blood ACTH levels, a clear correlation between the degree of increased TSH production and CS severity, and altered LH/FSH ratios. An increase in T3 levels against a background of unchanged T4 levels, elevated cortisol levels, and—in nearly 25% of patients—increased aldosterone and testosterone secreted by the Adrenal Glands are also noted. These indicators of central and peripheral neuroendocrine function point to a lack of coordinated activity in CS.

The climacteric period coincides with the onset of cellular and systemic aging: with the onset of menopause, female fertility is lost, the incidence of non-communicable diseases rises, pathological weight gain occurs, Temperature regulation resistance decreases, osteoporosis develops, degenerative changes occur in the cardiovascular system, and Sleep patterns are disrupted, among other changes.

Clinical manifestations include irregular menstrual cycles followed by complete cessation, involution of the uterus and secondary sex characteristics, and a gradual decline in libido. Many women experience no subjective Complaints during menopause, passing through this transition completely asymptomatically.

Menstrual irregularities generally fall into two categories: very short menstrual cycles, or cycles characterized by increased intervals between periods and a reduced volume of blood loss. In some postmenopausal patients—typically six months or more after their last menstruation—vaginal bleeding may occur. This symptom always warrants a thorough clinical investigation.

The cessation of menstruation is a critical turning point that may exacerbate a woman's fear of losing her youth and the inevitable approach of old age. The most characteristic symptoms during this period include hot flashes, fatigue, nervousness, sweating, headaches, insomnia, irritability, joint and Muscle pain, dizziness, palpitations, and a "pins and needles" sensation. However, the most distressing symptoms of CS include depression, memory impairment, weight gain, bone fragility, and dyspareunia.

A decline in ovarian function generally does not affect sexual desire and activity, which can persist into advanced old age. Loss of libido upon the onset of menopause is typically associated with other factors. Various psychological reactions to the onset of menopause are observed: patients may actively adapt to it, react passively, or exhibit signs of nervousness, depression, and anxiety.

CS can also manifest prominently in younger individuals, such as following the sudden cessation of ovarian function due to castration (surgical, chemical, medical, or radiation-induced). It is frequently accompanied by elevated blood pressure (climacteric Hypertension), perineal and vulvar pruritus, psychological disturbances, and other symptoms.

The diverse and numerous symptoms of CS are categorized into three groups: neurovegetative, metabolic-endocrine, and psychoemotional. However, in clinical practice, one frequently encounters various overlapping manifestations, and categorizing pathological symptoms into a specific group is not always straightforward. Diseases of various organs and systems arising during a woman's transitional age are frequently attributed by specialists to the climacteric period. Nonetheless, determining whether these conditions are directly related to menopause or independent of it is often challenging. Early and late symptoms of CS, as well as typical subjective and objective manifestations, are also distinguished.

Neurovegetative disorders. Autonomic-vascular disorders are observed in 30–45% of women with CS. The frequency of the most characteristic symptoms is as follows: hot flashes in 90.7%, hyperhidrosis in 81%, blood pressure fluctuations in 55.7%, headaches in 48.3%, pronounced discomfort in 38%, sleep disturbances in 28.6%, cardiac pain in 24.7%, general weakness and decreased working capacity in 22.8%, chills in 11.4%, and sympathoadrenal crises in 10.6% of patients.

Neuropsychiatric disorders occupy a prominent place in the clinical picture of the disease. It has been established that in 75% of patients, autonomic-vascular and psychoemotional disorders occur simultaneously, while in 25% they appear after a short interval (3–6 months). Psychoemotional disorders typically emerge before menopause or within the first year following its onset, whereas vasomotor reactions often become dominant within a year post-menopause and persist for an average of up to 5 years thereafter.

Asthenoneurotic syndrome is observed in 13.1% of patients. Against the background of asthenia, patients exhibit tearfulness, irritability spells, feelings of fear and anxiety, intolerance to auditory and olfactory stimuli, and depression. Paroxysmal blood pressure elevations occur under various conditions (at rest, during activity, or during psychological agitation). Between paroxysms, blood pressure remains normal.

Metabolic-endocrine disorders are caused by both general age-related changes in metabolic processes and the heightened reactivity of certain organs and Tissues to physiological age-related hypoestrogenism, manifested as dystrophic changes in the vulva, senile colpitis, trigonitis, and cystalgia. In the pre- and postmenopausal periods, patients may experience dyspareunia, dryness, and a burning sensation in the vulvovaginal region.

Extragenital estrogen-deficient states. With the onset of menopause, patients may experience "dry" Conjunctivitis, laryngitis, and dry Mouth. Facial Hair growth, lowering of the vocal pitch, osteoporosis, weight gain, and alterations in homeostatic systems are also noted.

Early specific symptoms of CS. Vasomotor symptoms occur in 75% of postmenopausal women. They are characterized by intermittent vasodilation followed by vasoconstriction. The exact mechanism behind hot flashes remains unclear. Evidently, they are associated with the release of adrenaline, which is controlled by the central nervous system. During hot flashes, levels of dehydroepiandrosterone, androstenedione, cortisol, and progesterone increase. A correlation has been noted between pulsatile LH release and the onset of hot flashes.

Hot flashes are characterized by a sensation of a wave of heat spreading throughout the entire body or in localized areas, frequently centered around the HEAD and Neck. Patients may also complain of severe nocturnal sweating. Although a link between LH surges and hot flashes has been established, it should be noted that they also occur in women following hypophysectomy. Presumably, the centers controlling LH secretion and thermoregulation are located in close anatomical proximity, and/or a central mechanism simultaneously initiates both processes (G. Mulley et al., 1977).

During the first two years following menopause, alongside vasomotor instability, women experience atrophic changes in the genital tract, most notably the development of atrophic vaginitis. As a consequence of oophorectomy, this condition is noted in 20% of patients. Patients with atrophic vaginitis may lack complaints of dyspareunia, presenting solely with mucous discharge, vaginal burning, or itching.

Following the onset of menopause, approximately 20% of women experience Urinary Tract complications, namely atrophic urethritis (in both acute and chronic forms) and cystitis. Patients with acute urethritis complain of frequent urination and dysuria, whereas those with chronic urethritis report difficulty initiating urination and nocturia.

Urinary symptoms are associated with atrophic changes in the epithelium of the Urethra and Urinary Bladder, as well as a decrease in the elasticity of the pelvic support structures for the uterus, bladder, and urethra. Cytological examination of smears from the Vagina and distal urethra has revealed that in 10% of postmenopausal women, urethral smears contain cornified cells, reflecting a normal level of tissue estrogenization; in 70%, parabasal and intermediate cells are present, indicating reduced (yet not absent) estrogenic stimulation; and in 20%, only parabasal cells are found, signaling true atrophy.

Late symptoms of climacteric syndrome primarily include osteoporosis (detected in 10% of patients), which manifests as a deficiency in normally mineralized bone mass. Its main underlying causes are easily identified clinically: estrogen deficiency, a sedentary lifestyle, and hyperadrenocorticism. Osteoporosis is more common in women with a slender build, a family History of the condition, and a lack of physical activity. Factors potentially linked to postmenopausal osteoporosis also include impaired calcium metabolism and others.

The acceleration of bone mass reduction in women is closely correlated with declining ovarian function. Prior to menopause, no significant bone loss is observed. This relationship is confirmed by the reduction in bone mass seen two years after oophorectomy in premenopausal women. Following the natural cessation of ovarian function, bone loss proceeds at a rate of 3% annually during the first few years, and subsequently at 1–2%. By the age of 65, bone density in 50% of women approaches a value corresponding to two standard deviations below the premenopausal mean.

Bone loss occurs much more rapidly and extensively in trabecular bone than in cortical bone. Consequently, bone density decreases earlier in the vertebrae than in the tubular bones, which explains the characteristic physical appearance of elderly women with pronounced osteoporosis (loss of height, significant cervical Kyphosis). Osteoporosis poses a major health hazard for women. After the age of 45, pathological fractures of the hip and wrist occur more frequently As a result of minor trauma or even spontaneously.

Patients in the late postmenopausal period may complain of back and joint pain associated with osteoporosis.

Cardiovascular complications occupy a notable place in the Clinical presentation of climacteric syndrome. Pre-menopausal women exhibit a lower incidence of CORONARY Heart DISEASE compared to men of the same age, suggesting that estrogens are a key protective factor. Clearly, functioning ovaries provide protection against the development of coronary heart disease. By age 60, the risk of severe cardiovascular disease in women is three times lower than in men.

After age 50, arterial hypertension is detected more frequently in women than in men. Furthermore, disruptions in Cholesterol and triglyceride levels following the onset of menopause have been well documented. Elevated blood lipid levels and hypertension presumably contribute to the atherosclerotic process.

Some women develop urticaria and facial edema accompanied by vasomotor rhinitis, alongside intolerance to various medications and foods. Skin changes may be generalized or restricted to the external genitalia. Patients report decreased skin elasticity and suppleness, as well as an increased fragility and tendency to injury. Dryness of the skin and/or pruritus are frequently observed, particularly in the vulvar region.

In some cases, cystocele, rectocele, and prolapse of internal genital organs occur due to the weakening of pelvic floor support structures. Some patients note that their breasts lose firmness and decrease in size, while the nipples and areolae become less prominent. In such women, the uterus and ovaries are significantly reduced in size; the external os of the cervix nearly merges with the vaginal fornices, the cervix shrinks, and its canal may become stenosed. Urethral stenosis and wart-like growths on the urethral walls are occasionally observed.

Diagnosis is straightforward and based on characteristic subjective complaints and medical history. To understand the genesis of various clinical variants of climacteric syndrome, an in-depth examination of the central nervous, neuroendocrine, autonomic, and cardiovascular systems is required, enabling targeted Pathogenetic Therapy.

Comparing the course and onset of the disease, evaluating pathological symptoms, assessing social and mental status, and accounting for extragenital conditions make it possible to determine the form and severity of climacteric syndrome, as well as to forecast its prognosis.

General and gynecological history plays a crucial role. Its findings assist in diagnosing atypical forms of climacteric syndrome and often directly indicate a link between the onset of pathological symptoms and the onset of menopause. It is essential to consider The Nature and efficacy of prior treatments, as well as the status of the homeostatic system. In cases of hypertension, the time of its onset and the specific Features of the climacteric period should be clarified.

In severe, protracted cases of climacteric syndrome, craniography is performed to rule out a pituitary adenoma.

If menstrual rhythm persists in women over 55 or resumes in postmenopause, an examination is indicated to rule out a hormonally active feminizing ovarian tumor. To this end, endometrial biopsy or Curettage of the uterine mucosa is performed. The detection of endometrial hyperplasia resulting from heightened estrogenic stimulation is most characteristic of these tumors, which are typically unilateral.

In the presence of obesity and sympathoadrenal crises, Differential diagnosis must be conducted to exclude Diabetes Mellitus, hypothyroidism, hypothalamic syndrome, and pheochromocytoma. The character of cardiac pain, ECG findings, and nitroglycerin and obzidan tests help differentiate climacteric cardiopathy from coronary heart disease. Increased libido, hirsutism, hypertrichosis, and a deeper voice tone in the postmenopausal period may indicate The Emergence of a hormonally active defeminizing ovarian tumor.

Treatment. It has long been believed that treating climacteric syndrome is unnecessary, as it is a transient condition that eventually undergoes spontaneous regression. However, clinical observations and experimental studies demonstrate the necessity of comprehensive treatment for such patients, not only to achieve an immediate therapeutic effect but also to prevent osteoporosis, atherosclerosis, Metabolic Disorders, and other complications.

The approach to treating patients with climacteric syndrome must be determined individually, taking into account the pathogenesis of the disease, clinical manifestations, severity, and duration. The patient’s age, the phase of the climacteric period, the presence of extragenital diseases, the timing of their onset, and specific Clinical Features are all taken into account. In some cases, it is necessary to determine the CHARACTERISTICS OF THE climacteric period in female relatives of the First and Second degrees.

Currently, the treatment of patients with climacteric syndrome comprises several stages: 1) non-pharmacological therapy, 2) non-hormonal pharmacotherapy, and 3) hormone therapy. This division is somewhat conventional, as severe forms of climacteric syndrome often require all three therapeutic modalities, meaning patient management is comprehensive in nature.

The First stage of treatment recommends a rational regimen of work, rest, and Nutrition, along with physiotherapy, therapeutic exercise, climatotherapy, balneotherapy, electrotherapy, and acupuncture.

Physiotherapeutic treatment modalities affect The Nervous System and help alleviate subjective complaints. These Methods are combined with psychotherapy, vitamin therapy (Vitamins A, B, C, E), and a specific hygienic and dietary regimen: prescribing a low-calorie diet rich in vegetables and fruits, while restricting CARBOHYDRATES, animal fats, salt, and fluids.

Special emphasis is placed on therapeutic exercise. Morning exercises should be performed daily (15–20 min), supplemented by therapeutic gymnastics three times a week for 30 minutes. Group exercise sessions with musical accompaniment are beneficial. Climatotherapy and aerotherapy in all their forms are indicated for all patients. For vasomotor disorders, various Water-cure Procedures exert a favorable effect: saline-alkaline or conifer baths followed by a shower, as well as oxygen baths (every other day) or radon baths. These treatments have been shown to reduce irritability and sweating, mitigate hot flashes affecting the head and face, and improve overall well-being. For hypertension of climacteric origin, iodine-bromine and radon baths are recommended. Wet wraps, especially at night, have a beneficial effect on insomnia.

Electrotherapy is highly effective. Recommended procedures include a galvanic collar with calcium chloride, novocaine, or bromine (for headaches and dizziness); transorbital Electrophoresis; cervicofacial electrophoresis; and electrosleep (cerebral electrotherapy). These methods reduce heightened irritability in menopausal women by enhancing inhibitory processes in both the Cerebral Cortex AND subcortical structures. Acupuncture is prescribed in combination with other therapeutic modalities.

During the Second Stage, to normalize the functional state of the central and autonomic nervous systems, sympatholytic agents are indicated—specifically reserpine and obzidan—along with stugeron, which reduces sympathicotonia and exhibits antihistaminic activity. When parasympathetic reactions predominate, anticholinergic agents (belladonna tincture) and antihistamines (tavegil, suprastin) are effective, as are medications that exert a depressant effect on autonomic and emotional excitability (belloïd, bellaspon/bellataminal). Vitamins B, B₆, and E are used to normalize homeostatic changes. ATP is prescribed to improve Nerve Impulse transmission from the Vagus nerve to The Heart and to reduce the impact of the sympathoadrenal division of the autonomic nervous system on the myocardium.

For psycho-emotional disorders, depression, and hypochondriacal syndrome, neurotropic agents (such as tazepam), tranquilizers, neuroleptics (frenolon), and psychotropic stimulants (nootropic, cerebrolysin, aminalon) are utilized.

At the Third Stage, if one or two courses of combined non-hormonal treatment fail to produce the desired effect, therapy transitions to hormone replacement, often combined with the aforementioned modalities.

Depending on the clinical presentation of climacteric syndrome, estrogens, progestins, combined estrogen-progestin preparations, or a combination of estrogens and androgens may be indicated. Estrogens have been established to alleviate vasomotor symptoms, vaginal dryness, and urinary frequency, relieve insomnia, reduce irritability, improve memory, and enhance overall well-being. They are successfully used for the Prevention of osteoporosis.

Long-term estrogen therapy may cause adverse effects, including breast tenderness, fluid retention, weight gain, and endometrial Cancer. Estrogen use is contraindicated in patients with estrogen-dependent tumors, impaired hepatic metabolism, and thromboembolic disorders.

The optimal estrogen treatment regimen should account for the following factors: the concentration of biologically active estrogens in peripheral blood and tissues must not exceed premenopausal levels; and The Use of minimal doses should ensure adequate biological activity in target organs.

According to V. P. Smetnik (1990), in cases of severe estrogen deficiency symptoms, atrophic vaginitis, conjunctivitis, laryngitis, or cystalgia, hormone therapy should be initiated with pure estrogens (1 ml of a 0.1% oil solution of estradiol dipropionate; 1 ml of a 0.05% oil solution of estrone or folliculin; ethinyl estradiol, 0.05 mg; estriol, 0.5 mg).

Currently, pure oral estrogens are typically prescribed in an intermittent regimen (3 weeks of intake followed by a 7–10 day break, for 2–3 courses) or in a cyclical regimen, where progestins are administered after estrogens. The intermittent Nature of the treatment courses and the subsequent administration of progestins are aimed at mitigating their proliferative effects on target organs (uterus, Mammary Glands).

For moderate to severe forms of climacteric syndrome in the absence of estrogen deficiency symptoms (such as osteoporosis or senile colpitis), combination therapy is recommended, including electroanalgesia and microdoses of combined estrogen-progestin hormones (Bisecurin, Non-Ovlon). Patients with a cyclic course of climacteric syndrome are prescribed pure progestins (Norkolut, Premarin-Nor, progesterone, pregnin). For osteoporosis, pure estrogens alone or in combination with androgens are indicated.

Prevention of climacteric syndrome should begin long before a woman reaches the transitional age and should include the timely treatment of disorders across various Organ Systems, as well as the proper management of work, rest, and nutrition. The development and severity of climacteric syndrome depend on the reserve capacity of the hypothalamic region and the body's somatic status.