Hirsutism is excessive body hair on parts of the body where hair is normally absent or minimal. The word is from early 17th century: from Latinhirsutus meaning "hairy".[2] It usually refers to a male pattern of hair growth in a female that may be a sign of a more serious medical condition,[3] especially if it develops well afterpuberty.[4] Cultural stigma against hirsutism can cause much psychological distress and social difficulty.[5] Discrimination based on facial hirsutism often leads to the avoidance of social situations and to symptoms ofanxiety and depression.[6]
Hirsutism is usually the result of an underlyingendocrine imbalance, which may beadrenal,ovarian, orcentral.[7] It can be caused by increased levels ofandrogen hormones. The amount and location of the hair is measured by aFerriman–Gallwey score. It is different fromhypertrichosis, which is excessive hair growth anywhere on the body.[3]
Hirsutism affects between 5 and 15% of women across all ethnic backgrounds.[8] Depending on the definition and the underlying data, approximately 40% of women have some degree of facial hair.[9] About 10 to 15% of cases of hirsutism are idiopathic with no known cause.[10]
The causes of hirsutism can be divided into endocrine imbalances and non-endocrine etiologies. It is important to begin by first determining the distribution ofbody hair growth. If hair growth follows a male distribution, it could indicate the presence of increased androgens or hyperandrogenism. However, there are other hormones not related to androgens that can lead to hirsutism. A detailed history is taken by a provider in search of possible causes for hyperandrogenism or other non-endocrine-related causes. If the distribution of hair growth occurs throughout the body, this is referred to ashypertrichosis, not hirsutism.[11]
Idiopathic: When no other cause can be attributed to an individual's hirsutism, the cause is considered idiopathic by exclusion.[15] In these cases,menstrual cycles and levels of conventionally tested androgens (testosterone,androstenedione, anddehydroepiandrosterone sulfate) are normal.[19] Around 10 to 15% of women with hirsutism have idiopathic hirsutism.[10] Idiopathic hirsutism may be due to increased production ofdihydrotestosterone (DHT) in hair follicles and hence may actually still be due to hyperandrogenism.[10] It may be detectable by measurement of DHT or DHT metabolites.[10]
Rice et al. 2016 propose that idiopathic hirsutism is caused by epigenetic inheritance of discordant epigenetic markers. It is testable with current technology.[20]
PCOS is a condition characterized by excess androgens that can lead to hirsutism, irregular periods, and even infertility. The excess androgens can lead to disruptions in normal body hormones in thehypothalamic-pituitary-gonadal axis leading to these symptoms.[21] With PCOS, hair may grow on the face (like on the upper lip, chin, or jawline), chest, stomach, and back.[22]
Characterized by having two of three Rotterdam criteria:
Oligomenorrhea (fewer than eight menses in a year)
Clinical or biochemical evidence of hyperandrogenism
Cushing syndrome occurs when there is an endogenous or exogenous elevated levels of cortisol. One cause of endogenous Cushing syndrome is an adrenocorticotrophic hormone-secreting pituitary adenoma that is responsible for high secretion of not just cortisol but also androgens from the pituitary gland.[24]
Cushing syndrome has an apparent symptoms including: Hirsutism weight gain, extra fat build up around the face, abdominal striae, and irregular menstruation.[24]
CAH can be attributed to several enzymatic deficiencies but the most common is21-beta-hydroxylase. In CAH, a missing enzyme responsible for normal cortisol synthesis creates a build-up of androgen precursors. This precursor gets shunted to the androgen synthesis pathway leading to increased levels of androgen. Classical CAH is discovered at birth due to increased androgens during development causing ambiguous genitalia. Meanwhile, non-classical CAH is found in puberty presenting as anovulation.[19]
Can present similar to PCOS in non-classical CAH. Increase levels of 17-hydroxyprogesterone.[14][19]
Hirsutism is a clinical diagnosis of excessive androgenic, terminal hair growth.[25] A complete physical evaluation should be done prior to initiating more extensive studies, the examiner should differentiate between widespread body hair increase and male patternvirilization.[15] One method of evaluating hirsutism is theFerriman-Gallwey Score which gives a score based on the amount and location of hair growth.[26] The Ferriman-Gallwey Score has various cutoffs due to variable expressivity of hair growth based on ethnic background.[27][28]
Treatment of hirsutism is indicated when hair growth causes patient distress. The two main approaches to treatment are pharmacologic therapies targeting androgen production/action, and direct hair removal methods including electrolysis and photo-epilation. These may be used independently or in combination.[31]
Common medications consist of antiandrogens,insulin sensitizers, andoral contraceptive pills. All three types of therapy have demonstrated efficacy on their own, however insulin sensitizers are shown to be less effective than antiandrogens and oral contraceptive pills.[32] The therapies may be combined, as directed by a physician, in line with the patient's medical goals.Antiandrogens are drugs that block the effects ofandrogens liketestosterone anddihydrotestosterone (DHT) in the body.[13] They are the most effective pharmacologic treatment for patient-important hirsutism, however they haveteratogenic potential, and are therefore not recommended in people who are pregnant or desire pregnancy. Current data does not favor any one type of oral contraceptive over another.[32]
List of medications:
Bicalutamide: A pure antiandrogen.[33][34][35] It is effective similarly to flutamide but is much safer as well as better-tolerated.[33][34][35]
Cyproterone acetate: A dual antiandrogen andprogestogen.[39] In addition to single form, it is also available in some formulations of combined oral contraceptives at a low dosage (see below).[39] It has a risk ofliver damage.
Flutamide: A pure antiandrogen.[39] It has been found to possess equivalent or greater effectiveness than spironolactone, cyproterone acetate, andfinasteride in the treatment of hirsutism.[41][39] However, it has a high risk of liver damage and hence is no longer recommended as a first- or second-line treatment.[42][43][38][44] Flutamide is safe and effective.[36]
GnRH analogues: Suppress androgen production by the gonads and reduce androgen concentrations to castrate levels.[45]
Metformin: Insulin sensitizer. Antihyperglycemic drug used for diabetes mellitus and treatment of hirsutism associated with insulin resistance (e.g.polycystic ovary syndrome). Metformin appears ineffective in the treatment of hirsutism, although the evidence was of low quality.[36]
Lifestyle change, including reducing excessive weight and addressinginsulin resistance, may be beneficial. Insulin resistance can cause excessive testosterone levels in women, resulting in hirsutism.[47]
^Barth JH, Catalan J, Cherry CA, Day A (September 1993). "Psychological morbidity in women referred for treatment of hirsutism".J Psychosom Res.37 (6):615–9.doi:10.1016/0022-3999(93)90056-L.PMID8410747.
^Jackson J, Caro JJ; Caro G, Garfield F; Huber F, Zhou W; Lin CS, Shander D & Schrode K (2007). "The effect of eflornithine 13.9% cream on the bother and discomfort due to hirsutism".International Journal of Dermatology.46 (9). the Eflornithine HCl Study Group:976–981.doi:10.1111/j.1365-4632.2007.03270.x.PMID17822506.S2CID25986442.
^Blume-Peytavi U, Hahn S (Sep–Oct 2008). "Medical treatment of hirsutism".Dermatol Ther.21 (5):329–339.
^Ferriman, D.; Gallwey, J. D. (November 1961). "Clinical assessment of body hair growth in women".The Journal of Clinical Endocrinology and Metabolism.21 (11):1440–1447.doi:10.1210/jcem-21-11-1440.ISSN0021-972X.PMID13892577.
^Cheewadhanaraks, Sopon; Peeyananjarassri, Krantarat; Choksuchat, Chainarong (May 2004). "Clinical diagnosis of hirsutism in Thai women".Journal of the Medical Association of Thailand = Chotmaihet Thangphaet.87 (5):459–463.ISSN0125-2208.PMID15222512.
^abMüderris II, Bayram F, Ozçelik B, Güven M (February 2002). "New alternative treatment in hirsutism: bicalutamide 25 mg/day".Gynecological Endocrinology.16 (1):63–6.doi:10.1080/gye.16.1.63.66.PMID11915584.S2CID6942048.
^Giorgetti R, di Muzio M, Giorgetti A, Girolami D, Borgia L, Tagliabracci A (2017). "Flutamide-induced hepatotoxicity: ethical and scientific issues".Eur Rev Med Pharmacol Sci.21 (1 Suppl):69–77.PMID28379593.
^Mongioi, A.; Maugeri, G.; Macchi, M.; Calogero, A.; Vicari, E.; Coniglione, F.; Aliffi, A.; Sipione, C.; D'Agata, R. (February 1986). "Effect of gonadotrophin-releasing hormone analogue (GnRH-A) administration on serum gonadotrophin and steroid levels in patients with polycystic ovarian disease".Acta Endocrinologica.111 (2):228–234.doi:10.1530/acta.0.1110228.ISSN0001-5598.PMID3082098.
^Karakurt F, Sahin I, Güler S, et al. (April 2008). "Comparison of the clinical efficacy of flutamide and spironolactone plus ethinyloestradiol/cyproterone acetate in the treatment of hirsutism: a randomised controlled study".Adv Ther.25 (4):321–8.doi:10.1007/s12325-008-0039-5.PMID18389188.S2CID23641936.
^Taylor SI, Dons RF, Hernandez E, Roth J, Gorden P (December 1982). "Insulin resistance associated with androgen excess in women with autoantibodies to the insulin receptor".Ann. Intern. Med.97 (6):851–5.doi:10.7326/0003-4819-97-6-851.PMID7149493.
