Alopecia and Hirsutism - FMBR 2nd Edition

Educational Objectives

Program Objectives

Upon completing this educational activity, participants will be better able to:

1. Understand and appropriately respond to the wide range of medical and psychological issues frequently encountered by practicing family physicians.

2. Select relevant tests or diagnostic procedures for patients seeking care.

3. Utilize the best evidence-based knowledge to achieve optimal therapeutic goals.

4. Prescribe effective drugs and therapeutic procedures.

5. Integrate newly acquired knowledge into routine practice patterns.

After listening to this lecture and reading the accompanying summary, the clinician will be better able to:

1.  Define the categories of alopecia.

2. Assess treatment for alopecia.

3. Describe causes of hirsutism.

4. Compare treatments for hirsutism.

Summary

Alopecia And Hirsutism

Joel Heidelbaugh, MD, Clinical Associate Professor of Family Medicine and Urology; Director, Family Medicine Clerkship, University of Michigan Medical School, Ann Arbor

Key learning points: to define the basic categories of alopecia; to understand and appreciate the workup for alopecia; to understand the recommended treatments for alopecia; to know the basic characteristics of hirsutism; to understand the workup for hirsutism; to appreciate the recommended treatments for hirsutism

Alopecia

Androgenetic or androgenic alopecia: also known as male and female pattern baldness; the most common cause of hair loss; characterized by localized and systemic hair loss, which usually begins with the frontoparietal scalp and then the vertex scalp; male pattern baldness in females is indicative of androgen excess, and may be accompanied by hirsutism in mild cases and virilization in more serious cases; female pattern baldness similar but more diffuse, usually with incomplete baldness and maintenance of the frontal hairline

Alopecia areata: the second most common presentation of nonscarring alopecia; hair rapidly lost in a circular or oval patch, or less commonly, it may be diffuse, involving the entire scalp; may include facial or body hair and may be either episodic or persistent

Telogen effluvium: diffuse alopecia that follows a triggering event, including surgery, childbirth, emotional stress, hormonal fluctuations, or medication use; hair loss usually occurs about 3 months after the event and usually affects <50% of the scalp; recovery often complete once the triggering factor has resolved

Anagen effluvium: diffuse hair loss that occurs as a result of exposure to certain toxins; hair growth abruptly interrupted, leading to shedding of anagen hair after 1 to 4 weeks; rapidly affects 80% to 90% of the scalp; complete recovery can be expected once the triggering factor is removed

Traction alopecia: hair loss caused by a direct insult to the hair; associated with styling techniques such as using hot rollers or braiding; the pattern of hair loss may relate directly to the styling technique used; more common inblacks; may progress to scarring alopecia

Trichotillomania: a subtype of traction alopecia caused by self-inflicted hair loss, typically in the frontoparietal region and progressing backward; regrowth of up to 1 to 1.5 cm can occur, which may be visible before the hair is long enough to pull again

Cicatricial alopecia: also known as scarring alopecia, in which hair loss occurs with permanent destruction of hair follicles; often presents with inflammation arising from injury or disease; scalp lesions may be present; initially localized but may become diffuse in chronic presentations; scalp gradually scars and eventually becomes smooth, with no evidence of hair follicles; once scarring begins, hair loss is permanent

Tinea capitis: a fungal infection that causes hair to break off close to the scalp, leaving a “black dot effect”, often resulting from a secondary bacterial infection; scalp often pruritic; predominantly affects children, more commonly those of African descent

Alopecia neoplastica: presents with hard nodules or tumors, or with flat, unshaved skin with a loss of hair; can be secondary to primary skin cancer of the scalp or any type of metastatic tumor

Epidemiology: about 25% of men aged 25 years or older have some degree of clinically apparent and visible androgenetic alopecia; lifetime prevalence in men >40%; 2% to 3% of the general population develops alopecia areata; for trichotillomania, the ratio of women to men is estimated at 2.5:1

Alopecia workup: when evaluating patients with alopecia, taking a careful clinical history is essential; in patients who complain of increased hair shedding or loss, clinicians should investigate and document any potential triggers up to several months before the development of the hair loss; this includes medication or drug intake, systemic illness, pregnancy, or weight loss; gynecologic history important in women, and often hormonal evaluation is warranted, especially in women with androgenetic alopecia and a history of irregular menses; family history is also paramount for characterizing alopecia

Common etiologies: androgenetic alopecia often genetically determined; alopecia areata of unknown etiology, but autoimmune causes are suspected; for telogen effluvium, hypothyroidism and hyperthyroidism may be causes; nutritional deficiencies, specifically iron and zinc, and psychological stress play a role; for androgenetic alopecia, rare causes include testosterone or male hormone supplementation, as well as anabolic steroids or adrenal tumors; possible etiologies of cicatricial alopecia include physical trauma (eg, burns, radiation therapy), infections such as chronic staphylococcal folliculitis or (more rarely) tuberculosis or syphilis, and inflammatory or autoimmune disorders, such as discoid lupus erythematosus and pemphigoid or sarcoidosis

Primary prevention: cooling of the scalp can lead to contraction of blood vessels around the hair roots (may help prevent hair loss in patients undergoing chemotherapy); on physical examination, scalp should be evaluated, assessing for hair density in various regions of the scalp; potential for hair loss should be assessed by gently pulling on the hair to see how easily it releases from the scalp; dermoscopy may be useful, especially in cases of androgenetic alopecia, as this may reveal a differentiation in hair diameter of >20%; in early androgenetic alopecia, a brown or depressed halo-like appearance may occur at the follicular opening; in more advanced cases, yellow dots and sometimes a honeycombed or pigmented appearance can be appreciated in some exposed regions of the scalp

Diagnosis: generally for androgenetic alopecia, assessment of patient and family history is warranted, as well as an examination of the pattern of hair loss; diagnosis of alopecia areata follows a similar approach; in cases of telogen effluvium, patient history is important, as well as examination of the pattern of hair loss and demonstration of the pluck test (gentle pulling of the hair); a complete blood count to evaluate for anemia or lymphocytosis is warranted; for trichotillomania, patient history, examination, and pluck tests are helpful; for scarring alopecia or cicatricial alopecia, potassium hydroxide preparation for evaluation of fungal elements may be useful to rule out tinea capitis; genetics — while a genetic role is well known, the causative genes have not been identified; history of hormonal therapy — drugs that may cause hair loss include contraceptives that contain androgenic progestins and any hormonal treatments for menopause; testosterone replacement therapy may cause hair loss

Treatment for androgenetic alopecia: includes topical minoxidil, 2% for women and 5% for men; the 5-alpha-reductase inhibitor, finasteride, at a dose of 1 mg/day, may decrease hair loss; several recent studies have shown that finasteride at this dose may cause irreversible sexual side effects, specifically erectile dysfunction; topical minoxidil should be applied twice daily and used for at least 1 year before making any decision regarding its efficacy; hair transplantation is a commonly performed surgical option for hair restoration in men and women; with regard to hair transplantation, follicular unit hair transplantation is the gold standard because it preserves the natural architecture of the hair

Treatment for alopecia areata: the first episode may resolve spontaneously within a few weeks to months without any medical intervention; the severity of alopecia areata is important to note, as increased severity reduces the likelihood of complete hair regrowth; prognosis is worse in children; alopecia areata worsens over time, but most cases resolve spontaneously within a year; about 25% of patients with alopecia areata develop some type of total loss of scalp hair, such as alopecia totalis, or all body hair loss (such as alopecia universalis), that persists indefinitely; unfortunately, treatments aimed at hair regrowth do not change the course of the disease; these include pulsed high doses of oral or intravenous steroids, topical high-potency steroids under occlusion, topical immunotherapy, and photochemotherapy; long-term complete regrowth is typically seen in <20% of patients

Patchy alopecia areata: intralesional steroids, such as triamcinolone acetonide, are the most widely used treatments, with varying degrees of benefit; systemic steroids, dosed daily to monthly, are also widely used, with variable success

Treatment for telogen effluvium: possible causes of this condition should be explored; these include systemic underlying disease, use of illicit drugs, emotional stress, rapid weight loss, pregnancy and delivery, iron or vitamin D deficiency, interruption of current cycle of oral contraceptives, or underlying autoimmune disease; treatments should be aimed at identifying the cause and reversing it when possible

Treatment for cicatricial alopecia: can be either primary or secondary; diseases that primarily affect the hair follicle cause primary cicatricial alopecia, which may be either lymphocytic or neutrophilic, based on the type of inflammatory cell that predominates; the most common form of lymphocytic cicatricial alopecia causes fibrosing alopecia and is related to discoid lupus erythematosus; secondary cicatricial alopecia is caused by systemic disorders, including scleroderma, granulomatous inflammation such as sarcoidosis, or underlying neoplastic disease; to more specifically determine the etiology of cicatricial alopecia, pathologic evaluation should be conducted

Treatment for discoid lupus erythematosus of the scalp and lichen planopilaris: include topical steroids, often fluocinonide at 0% to 0.05% and clobetasol lotion or cream, as well as intralesional triamcinolone acetonide; oral corticosteroids, dosed at 1 mg/kg per day or 25 mg to 50 mg per day for 1 month can be helpful in the case of rapidly progressive disease; other potential therapeutic options include oral cyclosporine or hydroxyquinoline; mycophenolate mofetil and doxycycline have been shown to be efficacious in treating lichen planopilaris

Alopecia associated with metabolic diseases: alopecia is often associated with endocrine disorders, including hypopituitarism, hypoparathyroidism, diabetes mellitus, hyperprolactinemia, polycystic ovarian syndrome, and Cushing syndrome; the most common endocrine disorder seen in relation to alopecia is diabetes mellitus; alopecia has also been linked to dyslipidemia as well as underlying cardiovascular disease; association of hair loss with dyslipidemia is stronger in older individuals; a proven relationship between alopecia and insulin resistance may lead to dyslipidemia; alopecia, especially male pattern baldness, may be a marker for cardiovascular risk assessment; alopecia has reported as a side effect of statin drugs; alopecia has also been linked to gout; biologic therapies are being assessed for the treatment of alopecia

Hirsutism

Characteristics: defined as male pattern hair growth; hirsutism is a common problem among women; often benign and, in rare cases, it may be a sign of an underlying endocrinopathy or a hormonally-active neoplasm; broadly defined, but the common clinical definition refers to women with excessive growth of terminal hair in a male pattern, commonly on the face; using this definition, hirsutism is one of the most common endocrine disorders and may affect up to 10% of women in the United States; often related to the presence of abnormal androgen activity; may cause significant emotional stress in women, as they may view the condition as a loss of femininity; often characterized by hair that is dark, coarse, and potentially curly; while up to 10% of women in the US may be affected, true disease involving virilization is rare (affects approximately 1 in 100,000 women)

Role of ethnicity: familial hereditary hirsutism predominant form in whites; secondary hirsutism affects people of all races and ethnicities equally; familial or hereditary hirsutism common in various ethnic groups, including people of Middle Eastern, Mediterranean, Eastern European, East Indian, and Hispanic descent; the number of hair follicles is genetically determined and accounts for various racial and ethnic differences; the total number of follicles, including terminal hair on the upper lip, around the areola, and around the lower abdomen, influences the expression of hirsutism; dihydrotestosterone is the predominant androgen that acts on the hair follicle to produce terminal hair; the local production of dihydrotestosterone is determined by 5-alpha-reductase activity in the skin; differences in the activity of this enzyme may explain why women with similar testosterone levels may have different degrees of hirsutism

Common causes and risk factors: causes are both endogenous and exogenous; endogenous causes account for 95% of all cases of hirsutism, including heredity or familial hirsutism; idiopathic hirsutism diagnosed when no familial, drug, or pathologic cause identified; polycystic ovary syndrome is one of the most common causes of hirsutism, affecting up to 5% of women of reproductive age, and evident in nearly half of women with hirsutism; obesity also a common cause of hirsutism, as it may be associated with an increase in circulating free androgens and decrease in sex hormone-binding globulin; weight loss has been shown to decrease hirsutism

Rare causes of hirsutism: virilizing ovarian tumors — include arrhenoblastoma (the most common), adrenal rest tumors, Brenner tumors, hilar cell tumors, and granulosa cell tumors; onset often rapid; progression of virilization in hirsutism may be pronounced; other signs of virilization include frontal balding, deepening of the voice, clitoromegaly, and increased muscle development; adrenal tumors can also cause hirsutism, including conditions associated with congenital adrenal hyperplasia; autosomal recessive adrenal deficiency disorders most frequently encountered among Ashkenazi Jewish women; approximately 75% of women with Cushing syndrome exhibit some form of hirsutism; virilizing adrenal adenomas and adrenal carcinomas are rare but can also result in hirsutism

Exogenous causes of hirsutism: medications such as postmenopausal androgen therapy, anabolic steroids, and danazol (which is commonly used for endometriosis), oral contraceptives that contain norgestrel, and androgens that may be prescribed for breast cancer or aplastic anemia; other causes include pituitary adenomas, ectopic adrenocorticotropic hormone or corticotropin-releasing hormone production from carcinoid or other neoplasms, and pituitary adenomas that make excess prolactin and cause hyperprolactinemia

Hypertrichosis: a condition that results in an increase in total body hair; usually represents an adverse reaction to medications including phenytoin, glucocorticoids, minoxidil, or cyclosporine; hypertrichosis may also occur in patients with anorexia nervosa, malnutrition, hypothyroidism, porphyria, or dermatomyositis

Hirsutism workup: screening the general population is not recommended; hirsutism may be evident on routine physical examination; patients may also comment on their concerns; most causes of hirsutism not preventable; relative to diagnosis, most women experience slowly progressive mild hirsutism; family history of hirsutism and menses of female patients should by assessed; laboratory evaluation useful if suspicion of an androgen-secreting neoplasm is warranted; serum testosterone and dehydroepiandrosterone sulfate (DHEA sulfate) levels are used to rule out the potential for neoplasms of the ovary or adrenal gland; polycystic ovarian syndrome may be confidently diagnosed in a woman with hirsutism and irregular menses; may or may not include hyperprolactinemia and late onset congenital adrenal hyperplasia; in these cases, androgen-secreting tumors should be ruled out; patients with hirsutism and menstrual irregularities may be evaluated for partial 21-hydroxylase deficiency, especially if they are in a high-risk ethnic group; on physical examination, it is important to identify the location and distribution of the terminal hair; some terminal hair may be on the face, around the areola, on the abdomen, on the back, or on the shoulders; if a woman feels that she is developing a more masculine appearance, testosterone and DHEA sulfate levels should be obtained

Cushingoid syndrome: if patient describes a swelling on the posterior neck and upper thoracic spine, representative of the classic “buffalo hump,” evaluation for cushingoid syndrome should be conducted; other signs of Cushing syndrome include central obesity, proximal muscle weakness, striae, and acne; to evaluate for Cushing syndrome, 24-hour determination of urinary free cortisol and in some cases, an adrenocorticotropic (ACTH) stimulation test, should be obtained

Goals of treatment: aimed at ruling out underlying causes, specifically androgen-secreting neoplasms; if polycystic ovary syndrome, congenital adrenal hyperplasia, or Cushing syndrome is suspected, diagnostic testing should be performed and those patients should be referred to either a gynecologist or an endocrinologist; if no direct cause is determined, then treatment is often directed at reducing androgen production and blocking androgen action on peripheral tissues; pharmacotherapy usually starts with combination oral contraceptives, such as ethinyl estradiol and norgestimate, which are considered first-line therapy; these have been shown to reduce ovarian androgen secretion and increase sex hormone-binding globulin, reducing free testosterone levels; antiandrogens, such as spironolactone, have also been used effectively in combination with oral contraceptives; currently, spironolactone is the most commonly used antiandrogen in the US and is the only FDA-approved antiandrogen for treatment of polycystic ovary syndrome; flutamide and bicalutamide were previously used but found to be hepatotoxic; metformin and pioglitazone have also been shown to decrease androgen levels and have been used off label for treatment of polycystic ovary syndrome

Mechanical and cosmetic therapeutic options: physical removal of unwanted hair can include tweezing, shaving, waxing, the use of depilatory agents, lasers, and electrolysis, as well as other cosmetic options; no complete cure for hirsutism exists; can be improved through antiandrogen therapy and/or cosmetic therapies; for women who wish to conceive, pharmacotherapy should be discontinued and evaluation by a reproductive endocrinologist or a fertility specialist should be performed

Readings

Disclosures

For this activity, members of the faculty and planning committee reported nothing to disclose.

Acknowledgements

CME/CE INFO

Accreditation:

The Audio- Digest Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The Audio- Digest Foundation designates this enduring material for a maximum of 0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Audio Digest Foundation is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's (ANCC's) Commission on Accreditation. Audio Digest Foundation designates this activity for 0 CE contact hours.

Lecture ID:

FMBR170122

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.