STUDY - Technical - New Dacian's Medicine
Hirsutism
and Virilization
Translation Draft
I have to shoot hard today because I'm going to be able to complete the group of urogenital disorders...
Hirsutism, the male type of hair growth in women, is a common problem, but difficult to address. Hair distribution and growth in normal people is under complex genetic and endocrine control, so there is considerable variability in hair growth among normal men and women.
Consequently, abnormal hair growth is difficult to define. Some patients seek medical attention for what the doctor may consider an insignificant cosmetic defect. Others, due to personal and cultural differences, may not be disturbed by surprising degrees of hirsutism. The central problem in dealing with these patients is the separation of those rare situations, in which hirsutism is a manifestation of a serious and curable disease, from the majority of hirsute women to whom excess hair is mainly a cosmetic problem.
Let's first address the elements related to the control of normal hair growth and
distribution. I'll start with the endocrine control approach. Androgens are determined by the major hair distribution in both sexes. There are three circulating androgens in women: dehydroepiandrosterone, produced in the adrenal, androstendion which is produced equally in the adrenal and ovary and testosterone, which is both secreted by the ovary and adrenal and formed in the extraglandular tissue of the circulating dehydroepiandrosterone and androstendion.
The production of androgens from the adrenal is regulated primarily by adrenocorticotropin, while ovarian androgenic secretion is regulated by the luteinizing hormone (LH). These different androgens should be converted into testosterone (or dihydrotestosterone) before binding to the androgenic receptor of the target cells and inducing an androgenic response. Thus, adrenal androgens virilize only to the extent that they serve as precursors to testosterone and dihydrotestosterone.
Several types of relationships can be defined between hair growth and androgens in normal individuals. The growth of eyelashes, eyebrows and body hair is not dependent on androgens. Axial and pubic hair is sensitive to small amounts of androgens, hair growth in these regions starting at the time of adrenarha under the control of adrenal androgens and is approximately equal in men and women. Hair growth in certain regions, such as the face, upper pubic triangle, chest and ears, is more typical in men and appears to require higher levels of androgen produced in the testicles.
Finally, the scalp hair shows androgenically mediated regression. The reason why different regions of the body respond differently to the same or similar androgen is unknown. The metabolism of androgens may differ in different places. The hair follicle, like other androgenic targets, requires the conversion of testosterone to dihydrotestosterone to express androgenic action and hair follicles in all regions of the body perform this conversion.
Moreover, the same receptor that is essential for androgenic action in other cells, mediates the effects of dihydrotestosterone in the hair follicle. Genetic disorders with normal testosterone production, but with the absence of androgenic receptor, manifest with deficiency or absence of hair of the axis, pubic, facial, trunk and limbs. Regional differences in androgenic hair responsiveness in normal individuals may also be the consequence of regional differences in the amount of androgenic receptors in the hair follicle.
As for genetic factors, despite similar hormonal levels, hair distribution varies between individuals and between different ethnic and racial groups. White son of a blind man with dark hair and dark skin of any sex tend stares to be more hirsulate than blondes or with light skin. Asians, American Indians and blacks are on average less hirsuass than whites. Asians have reduced facial and body hair except for the axillary and pubic regions, and American Indians, in addition, rarely develop alopecia. The heterogeneity of hair types also exists within a family. The hair type inheritance is complex and probably polygenic in nature.
Other factors would be represented by aging, which is an essential condition for some types of hair development. For example, in men, hair on the torso and extremities often increases for several years after maximum levels of plasma androgens have been reached. Conversely, androgen loss may not result in decreased normal hair growth in men or complete cancellation of hirsutism in women. The woman in the first trimester of pregnancy usually has an increase in hair on her face, extremities and breasts. Menopause is often associated with hair loss in the pubic, axillary and extremity regions, while facial hair growth intensifies in postmenopausal women. These changes cannot be explained solely by changes in the levels of androgens.
Let's move now on to pathological hair growth and distribution. A central consideration in the evaluation of women with hirsutism is also the presence of signs of virilization or defeminization, as such signs suggest marked androgenic excess. In patients with hyperproduction of androgens, signs of defeminization, such as menstruation disorders, are much more common than virilization.
However, the presence or absence of obvious virilization should be interpreted with caution for at least two reasons. First, the signs of virilization (clitoromegalia, baldness, hair tightening, hirsutism) indicate an androgenic excess at some point in the patient's life, but do not necessarily mean that the active disease is present at the time of evaluation. It is necessary to measure plasma androgenic levels and/ or production rate to determine whether androgenic excess is active. Secondly, severe hyperandrogenization may exist in the absence of clear virilization, i.e. at the same level of androgenic production and clitoregaliline may be present in one patient and in another not.
Then it is necessary to realize some diagnostic considerations. Excessive hair growth can be caused by drugs that exert their effects independently of androgens and do not produce defeminization or virilization. Such drugs include phenytoin, minoxidil, diazoxide, cyclosporin and hexachlorobenzene, hair growth produced by these agents generally having the character of fine hair on the body. Androgens produce hirsutism, as well as virilization. Some synthetic progestogens have androgenic activity.
Now the tumors are in place. The rapid onset of hair growth, with or without accompanying signs of french virilization, suggests a neoplastic source of androgens. Such tumors include adenoma and adrenal carcinoma, ovarian tumors like adrenoblastoma that directly secrete androgens and Krukenberg tumors of the ovary that stimulate surrounding ovarian stromal tissue to produce excess androgens.
The most common cause of ovarian hyperandrogenism is polycystic ovary disease. This condition has a wide spectrum of manifestations that range from discrete hirsutism to amenorrhea and virilization. The remarkable feature for diagnosis is the puberty installation of chronic anovulation and hirsutism. Enlarged cystic ovaries, obesity and amenorrhea (Stein-Leventhal syndrome) are present in only half or less of women with this disorder and should not be present for diagnosis. The fundamental anomaly in polycystic ovary disease is not fully understood, but elevated levels of plasma LH cause increased androgenic secretion by stromal and tecal cells of the ovary.
There's a few things to be said about attenuated forms of adrenal hyperplasia. The adrenal gland may be the source of androgenic excess in the absence of a tumor. Hereditary defects in adrenal steroidogenesis (congenital adrenal hyperplasia) can produce virilization and each may occur in a late-onset form in which hirsutism or virilization and irregular cycles occur at the expected time of puberty or in adulthood. Clinical presentation in these cases is not usually distinguished from polycystic ovary disease.
The deficiency of 21-hydroxylase with delayed onset is the most common attenuated form of congenital adrenal hyperplasia and was most intensively studied, its incidence in the general population of hirsute, oligomereic women, being of the order 1-5%. The presence of elevated plasma levels of adrenal androgens (such as dehydroepiandrosterone-sulphate) or suppressible hyperandrogenism in dexamethasone does not necessarily imply that hyperandrogenization is due to a specific adrenal steroidogen defect, but these findings may be useful as therapeutic orientation.
In many women with hirsutism, an accurate diagnosis cannot be made, having to do with idiopathic hirsutism. The term idiopathic hirsutism applies to women with signs of androgenic excess, but with normal menstruation, normal-sized ovaries, without evidence of a tumor of the adrenal or ovary and normal adrenal function. The slight increase in androstendion and plasma testosterone is common in such women and the rate of testosterone production is increased, although to a lesser degree than patients with polycystic ovary disease.
Experience with antiandrogens cyproterone acetate and flutamine indicates that this form of hirsutism is androgenically mediated, as therapy results in improvement. Women with idiopathic hirsutism may constitute the extreme end of the normal series of androgenic production or a real pathological subgroup. Some women with a presumptive diagnosis of hirsutism actually have a mild or onset form of polycystic ovary disease, but in many hirsutism is not accompanied or followed by signs of ovarian dysfunction. If these women are just the extremes of a normal limit of androgenic production, then their hirsutism is mainly a cosmetic defect.
Let's move on to the diagnostic evaluation now! The decision on when to make a complex diagnostic assessment depends on several factors. Such an assessment is appropriate for all women with hirsutism accompanied by virilization (if it should be performed in women with isolated hirsutism, it depends on the severity, distribution and rate of hair growth). Anamnesis is taken with particular attention to the ingestion of drugs and to details of the development of puberty and the history of menstruation and their relationship with the onset of excessive hair growth.
The physical examination is directed towards establishing the sites of androgen-dependent hair growth (pubic, axilary, facial, on the torso and extremities) and assessing the signs of virilization that correlate with the high levels of androgenic hyperproduction and increase suspicion for androgen-producing neoplasms.
Such signs include larynx width (thickening of the voice), temporary baldness, clitoregalalia and increased muscle mass of the scapular belt. Signs of cortisone excess (plethora, centripetal obesity, striae and dorsocervical and supraclavicular fat packs) should also be sought. Pelvic examination should include the search for palpable ovarian masses. laboratory tests include measurement of serum androgens and, when indicated, radiography of the ovaries and adrenal glands.
Basal measurements of dehydroepiandrosterone-sulphate greater than 22 micromoles/ l or serum testosterone above 7 nmol/ l suggest neoplastic sources of androgenic excess (serum testosterone levels within normal limits are harder to interpret because total levels in women do not necessarily reflect free or unbound hormone levels when testosterone-binding globulin is either increased or low).
Suspected Cushing syndrome should be evaluated if a screening test (such as renal excretion of free cortisone or dexamethasone "overnight" suppression test) is abnormal. Diagnosis of polycystic ovary disease is made on the basis of anamnesis and clinical features in a woman with chronic anovulation. Women may be screened for late onset adrenal hyperplasia through the short ACTH stimulation test and 17-hydroxyprogesterone plasma measurement.
Treatment, in the case of drug-induced hirsutism and neoplastic disease of the ovaries or adrenals is clear, represented by stopping the administration of drugs or removal of the tumor. The defects of adrenal steroidogenesis are treated with glucocorticoids to suppress excess ACTH and inhibit adrenal androgenic secretion. In most cases (polycystic ovary disease, as well as idiopathic hirsutism), both cosmetic treatment and suppression of androgenic production or its action at the receptor level are necessary.
Cosmetic therapy is oriented towards masking or removing hair from exposed areas of the skin. Small amounts of hair can be bleached (discolored) with perhydrol. Methods of hair removal are classified in depilators (hair removal from the surface of the skin) or epilators (removal of hair intact with root). depilating techniques include shaving and chemical methods. shaving has no adverse effects on the rate of growth or tightening of the hair (although blunt heads may feel rough), but shaving of regions other than armpits or feet is unacceptable to most women.
Chemical dipilators are effective for limited areas of hair removal and are generally safe if used correctly. The most effective depilators are mercaptan derivatives, such as tioglycolic acid, which reduce difulid bonds in the peptide chains of keratin. The hair fiber swells and softens to a consistency that can be washed off the skin. Great care should be taken in their application to avoid skin irritation due to the alkalinity of these preparations.
Temporary epilation can be obtained by plucking (useful only for insulated brushes), wax treatment or the use of epilators. The heavens are melted and applied to the skin. When the wax cools and hardens, it is plucked, removing the thread with it. The procedure is relatively painful and the best results can be obtained by exercise or at the beauty salon. Permanent epilation can only be achieved by electrolysis. Treatments are expensive and time-consuming, and success depends on the skills of the person performing this operation.
During cosmetic treatment, attempts to suppress androgenic hyperproduction may also be matched. Treatment with combined contraceptive pills suppresses androgenic ovarian secretion, when restoring fertility is not an objective. To minimize adverse effects, oral contraceptives should contain progestogen with the lowest androgenic side effects (such as desogestrel or norgestimate) and estrogens at the lowest effective doses.
Women over 35 years of age who smoke and those with hypertension, history of thromboembolic diseases, impaired liver function or suspected estrogen-dependent neoplasm should not be treated with oral contraceptives. The combination of oral contraceptives and luteinizing hormone-releasing hormone analogues offers no additional advantage over exclusive oral contraceptives. Suppression of androgenic adrenal hyperproduction can be obtained with low doses of dexamethasone and is most useful in the late-onset 21-hydroxylase deficiency.
Antagonization of androgenic effects in the hair follicle is the basis of antiandrogen treatment. Ciprotheron-acetate has been used successfully, but is not widely used. Flutamide, the antagonist of the androgenic receptor, is also effective, but it can cause liver failure and it will be avoided. Spironolactone has a dual action of blocking androgenic receptors and inhibiting androgenic production and is useful as an alternative therapy. Cimetidine also binds to androgenic receptors and acts as an androgenic antagonist, but does not have a general benefit in the treatment of hirsutism.
Finasteride, a 5alpha-reductase inhibitor, has been successfully used for this purpose, but can cause toxic effects if it crosses the placenta. If pharmacological therapy is undertaken, the patient should be advised to seek a 6-month treatment for an appropriate efficacy assessment. Even when treatment is long-lasting, the spectacular reversal of hair growth is unlikely to be achieved by interfering with synthesis or androgenic action. Such hormonal manipulations can stop or slow the rate of hair growth, but superfluous hair must handle cosmetic treatment.
That's it!
I have to shoot hard today because I'm going to be able to complete the group of urogenital disorders...
Hirsutism, the male type of hair growth in women, is a common problem, but difficult to address. Hair distribution and growth in normal people is under complex genetic and endocrine control, so there is considerable variability in hair growth among normal men and women.
Consequently, abnormal hair growth is difficult to define. Some patients seek medical attention for what the doctor may consider an insignificant cosmetic defect. Others, due to personal and cultural differences, may not be disturbed by surprising degrees of hirsutism. The central problem in dealing with these patients is the separation of those rare situations, in which hirsutism is a manifestation of a serious and curable disease, from the majority of hirsute women to whom excess hair is mainly a cosmetic problem.
Let's first address the elements related to the control of normal hair growth and
distribution. I'll start with the endocrine control approach. Androgens are determined by the major hair distribution in both sexes. There are three circulating androgens in women: dehydroepiandrosterone, produced in the adrenal, androstendion which is produced equally in the adrenal and ovary and testosterone, which is both secreted by the ovary and adrenal and formed in the extraglandular tissue of the circulating dehydroepiandrosterone and androstendion.
The production of androgens from the adrenal is regulated primarily by adrenocorticotropin, while ovarian androgenic secretion is regulated by the luteinizing hormone (LH). These different androgens should be converted into testosterone (or dihydrotestosterone) before binding to the androgenic receptor of the target cells and inducing an androgenic response. Thus, adrenal androgens virilize only to the extent that they serve as precursors to testosterone and dihydrotestosterone.
Several types of relationships can be defined between hair growth and androgens in normal individuals. The growth of eyelashes, eyebrows and body hair is not dependent on androgens. Axial and pubic hair is sensitive to small amounts of androgens, hair growth in these regions starting at the time of adrenarha under the control of adrenal androgens and is approximately equal in men and women. Hair growth in certain regions, such as the face, upper pubic triangle, chest and ears, is more typical in men and appears to require higher levels of androgen produced in the testicles.
Finally, the scalp hair shows androgenically mediated regression. The reason why different regions of the body respond differently to the same or similar androgen is unknown. The metabolism of androgens may differ in different places. The hair follicle, like other androgenic targets, requires the conversion of testosterone to dihydrotestosterone to express androgenic action and hair follicles in all regions of the body perform this conversion.
Moreover, the same receptor that is essential for androgenic action in other cells, mediates the effects of dihydrotestosterone in the hair follicle. Genetic disorders with normal testosterone production, but with the absence of androgenic receptor, manifest with deficiency or absence of hair of the axis, pubic, facial, trunk and limbs. Regional differences in androgenic hair responsiveness in normal individuals may also be the consequence of regional differences in the amount of androgenic receptors in the hair follicle.
As for genetic factors, despite similar hormonal levels, hair distribution varies between individuals and between different ethnic and racial groups. White son of a blind man with dark hair and dark skin of any sex tend stares to be more hirsulate than blondes or with light skin. Asians, American Indians and blacks are on average less hirsuass than whites. Asians have reduced facial and body hair except for the axillary and pubic regions, and American Indians, in addition, rarely develop alopecia. The heterogeneity of hair types also exists within a family. The hair type inheritance is complex and probably polygenic in nature.
Other factors would be represented by aging, which is an essential condition for some types of hair development. For example, in men, hair on the torso and extremities often increases for several years after maximum levels of plasma androgens have been reached. Conversely, androgen loss may not result in decreased normal hair growth in men or complete cancellation of hirsutism in women. The woman in the first trimester of pregnancy usually has an increase in hair on her face, extremities and breasts. Menopause is often associated with hair loss in the pubic, axillary and extremity regions, while facial hair growth intensifies in postmenopausal women. These changes cannot be explained solely by changes in the levels of androgens.
Let's move now on to pathological hair growth and distribution. A central consideration in the evaluation of women with hirsutism is also the presence of signs of virilization or defeminization, as such signs suggest marked androgenic excess. In patients with hyperproduction of androgens, signs of defeminization, such as menstruation disorders, are much more common than virilization.
However, the presence or absence of obvious virilization should be interpreted with caution for at least two reasons. First, the signs of virilization (clitoromegalia, baldness, hair tightening, hirsutism) indicate an androgenic excess at some point in the patient's life, but do not necessarily mean that the active disease is present at the time of evaluation. It is necessary to measure plasma androgenic levels and/ or production rate to determine whether androgenic excess is active. Secondly, severe hyperandrogenization may exist in the absence of clear virilization, i.e. at the same level of androgenic production and clitoregaliline may be present in one patient and in another not.
Then it is necessary to realize some diagnostic considerations. Excessive hair growth can be caused by drugs that exert their effects independently of androgens and do not produce defeminization or virilization. Such drugs include phenytoin, minoxidil, diazoxide, cyclosporin and hexachlorobenzene, hair growth produced by these agents generally having the character of fine hair on the body. Androgens produce hirsutism, as well as virilization. Some synthetic progestogens have androgenic activity.
Now the tumors are in place. The rapid onset of hair growth, with or without accompanying signs of french virilization, suggests a neoplastic source of androgens. Such tumors include adenoma and adrenal carcinoma, ovarian tumors like adrenoblastoma that directly secrete androgens and Krukenberg tumors of the ovary that stimulate surrounding ovarian stromal tissue to produce excess androgens.
The most common cause of ovarian hyperandrogenism is polycystic ovary disease. This condition has a wide spectrum of manifestations that range from discrete hirsutism to amenorrhea and virilization. The remarkable feature for diagnosis is the puberty installation of chronic anovulation and hirsutism. Enlarged cystic ovaries, obesity and amenorrhea (Stein-Leventhal syndrome) are present in only half or less of women with this disorder and should not be present for diagnosis. The fundamental anomaly in polycystic ovary disease is not fully understood, but elevated levels of plasma LH cause increased androgenic secretion by stromal and tecal cells of the ovary.
There's a few things to be said about attenuated forms of adrenal hyperplasia. The adrenal gland may be the source of androgenic excess in the absence of a tumor. Hereditary defects in adrenal steroidogenesis (congenital adrenal hyperplasia) can produce virilization and each may occur in a late-onset form in which hirsutism or virilization and irregular cycles occur at the expected time of puberty or in adulthood. Clinical presentation in these cases is not usually distinguished from polycystic ovary disease.
The deficiency of 21-hydroxylase with delayed onset is the most common attenuated form of congenital adrenal hyperplasia and was most intensively studied, its incidence in the general population of hirsute, oligomereic women, being of the order 1-5%. The presence of elevated plasma levels of adrenal androgens (such as dehydroepiandrosterone-sulphate) or suppressible hyperandrogenism in dexamethasone does not necessarily imply that hyperandrogenization is due to a specific adrenal steroidogen defect, but these findings may be useful as therapeutic orientation.
In many women with hirsutism, an accurate diagnosis cannot be made, having to do with idiopathic hirsutism. The term idiopathic hirsutism applies to women with signs of androgenic excess, but with normal menstruation, normal-sized ovaries, without evidence of a tumor of the adrenal or ovary and normal adrenal function. The slight increase in androstendion and plasma testosterone is common in such women and the rate of testosterone production is increased, although to a lesser degree than patients with polycystic ovary disease.
Experience with antiandrogens cyproterone acetate and flutamine indicates that this form of hirsutism is androgenically mediated, as therapy results in improvement. Women with idiopathic hirsutism may constitute the extreme end of the normal series of androgenic production or a real pathological subgroup. Some women with a presumptive diagnosis of hirsutism actually have a mild or onset form of polycystic ovary disease, but in many hirsutism is not accompanied or followed by signs of ovarian dysfunction. If these women are just the extremes of a normal limit of androgenic production, then their hirsutism is mainly a cosmetic defect.
Let's move on to the diagnostic evaluation now! The decision on when to make a complex diagnostic assessment depends on several factors. Such an assessment is appropriate for all women with hirsutism accompanied by virilization (if it should be performed in women with isolated hirsutism, it depends on the severity, distribution and rate of hair growth). Anamnesis is taken with particular attention to the ingestion of drugs and to details of the development of puberty and the history of menstruation and their relationship with the onset of excessive hair growth.
The physical examination is directed towards establishing the sites of androgen-dependent hair growth (pubic, axilary, facial, on the torso and extremities) and assessing the signs of virilization that correlate with the high levels of androgenic hyperproduction and increase suspicion for androgen-producing neoplasms.
Such signs include larynx width (thickening of the voice), temporary baldness, clitoregalalia and increased muscle mass of the scapular belt. Signs of cortisone excess (plethora, centripetal obesity, striae and dorsocervical and supraclavicular fat packs) should also be sought. Pelvic examination should include the search for palpable ovarian masses. laboratory tests include measurement of serum androgens and, when indicated, radiography of the ovaries and adrenal glands.
Basal measurements of dehydroepiandrosterone-sulphate greater than 22 micromoles/ l or serum testosterone above 7 nmol/ l suggest neoplastic sources of androgenic excess (serum testosterone levels within normal limits are harder to interpret because total levels in women do not necessarily reflect free or unbound hormone levels when testosterone-binding globulin is either increased or low).
Suspected Cushing syndrome should be evaluated if a screening test (such as renal excretion of free cortisone or dexamethasone "overnight" suppression test) is abnormal. Diagnosis of polycystic ovary disease is made on the basis of anamnesis and clinical features in a woman with chronic anovulation. Women may be screened for late onset adrenal hyperplasia through the short ACTH stimulation test and 17-hydroxyprogesterone plasma measurement.
Treatment, in the case of drug-induced hirsutism and neoplastic disease of the ovaries or adrenals is clear, represented by stopping the administration of drugs or removal of the tumor. The defects of adrenal steroidogenesis are treated with glucocorticoids to suppress excess ACTH and inhibit adrenal androgenic secretion. In most cases (polycystic ovary disease, as well as idiopathic hirsutism), both cosmetic treatment and suppression of androgenic production or its action at the receptor level are necessary.
Cosmetic therapy is oriented towards masking or removing hair from exposed areas of the skin. Small amounts of hair can be bleached (discolored) with perhydrol. Methods of hair removal are classified in depilators (hair removal from the surface of the skin) or epilators (removal of hair intact with root). depilating techniques include shaving and chemical methods. shaving has no adverse effects on the rate of growth or tightening of the hair (although blunt heads may feel rough), but shaving of regions other than armpits or feet is unacceptable to most women.
Chemical dipilators are effective for limited areas of hair removal and are generally safe if used correctly. The most effective depilators are mercaptan derivatives, such as tioglycolic acid, which reduce difulid bonds in the peptide chains of keratin. The hair fiber swells and softens to a consistency that can be washed off the skin. Great care should be taken in their application to avoid skin irritation due to the alkalinity of these preparations.
Temporary epilation can be obtained by plucking (useful only for insulated brushes), wax treatment or the use of epilators. The heavens are melted and applied to the skin. When the wax cools and hardens, it is plucked, removing the thread with it. The procedure is relatively painful and the best results can be obtained by exercise or at the beauty salon. Permanent epilation can only be achieved by electrolysis. Treatments are expensive and time-consuming, and success depends on the skills of the person performing this operation.
During cosmetic treatment, attempts to suppress androgenic hyperproduction may also be matched. Treatment with combined contraceptive pills suppresses androgenic ovarian secretion, when restoring fertility is not an objective. To minimize adverse effects, oral contraceptives should contain progestogen with the lowest androgenic side effects (such as desogestrel or norgestimate) and estrogens at the lowest effective doses.
Women over 35 years of age who smoke and those with hypertension, history of thromboembolic diseases, impaired liver function or suspected estrogen-dependent neoplasm should not be treated with oral contraceptives. The combination of oral contraceptives and luteinizing hormone-releasing hormone analogues offers no additional advantage over exclusive oral contraceptives. Suppression of androgenic adrenal hyperproduction can be obtained with low doses of dexamethasone and is most useful in the late-onset 21-hydroxylase deficiency.
Antagonization of androgenic effects in the hair follicle is the basis of antiandrogen treatment. Ciprotheron-acetate has been used successfully, but is not widely used. Flutamide, the antagonist of the androgenic receptor, is also effective, but it can cause liver failure and it will be avoided. Spironolactone has a dual action of blocking androgenic receptors and inhibiting androgenic production and is useful as an alternative therapy. Cimetidine also binds to androgenic receptors and acts as an androgenic antagonist, but does not have a general benefit in the treatment of hirsutism.
Finasteride, a 5alpha-reductase inhibitor, has been successfully used for this purpose, but can cause toxic effects if it crosses the placenta. If pharmacological therapy is undertaken, the patient should be advised to seek a 6-month treatment for an appropriate efficacy assessment. Even when treatment is long-lasting, the spectacular reversal of hair growth is unlikely to be achieved by interfering with synthesis or androgenic action. Such hormonal manipulations can stop or slow the rate of hair growth, but superfluous hair must handle cosmetic treatment.
That's it!
Have a good day, everyone!
Dorin, Merticaru