The average person has 5 million hairs. Hair grows all over your body except on your lips, palms, and the soles of your feet. It takes about a month for healthy hair to grow half an inch. Most hairs grow for up to six years and then fall out. New hairs grow in their place.

Hair helps keep you warm. It also protects your eyes, ears and nose from small particles in the air. Common problem with the hair and scalp include hair loss, infections, and flaking.

Hair

Hair is a keratinous filament growing out of the epidermis. It is primarily made of dead, keratinized cells. Strands of hair originate in an epidermal penetration of the dermis called the hair follicle. The hair shaft is the part of the hair not anchored to the follicle, and much of this is exposed at the skin’s surface. The rest of the hair, which is anchored in the follicle, lies below the surface of the skin and is referred to as the hair root. The hair root ends deep in the dermis at the hair bulb, and includes a layer of mitotically active basal cells called the hair matrix. The hair bulb surrounds the hair papilla, which is made of connective tissue and contains blood capillaries and nerve endings from the dermis (Figure 5.11).

Just as the basal layer of the epidermis forms the layers of epidermis that get pushed to the surface as the dead skin on the surface sheds, the basal cells of the hair bulb divide and push cells outward in the hair root and shaft as the hair grows. The medulla forms the central core of the hair, which is surrounded by the cortex, a layer of compressed, keratinized cells that is covered by an outer layer of very hard, keratinized cells known as the cuticle. These layers are depicted in a longitudinal cross-section of the hair follicle (image), although not all hair has a medullary layer. Hair texture (straight, curly) is determined by the shape and structure of the cortex, and to the extent that it is present, the medulla. The shape and structure of these layers are, in turn, determined by the shape of the hair follicle. Hair growth begins with the production of keratinocytes by the basal cells of the hair bulb. As new cells are deposited at the hair bulb, the hair shaft is pushed through the follicle toward the surface. Keratinization is completed as the cells are pushed to the skin surface to form the shaft of hair that is externally visible. The external hair is completely dead and composed entirely of keratin. For this reason, our hair does not have sensation. Furthermore, you can cut your hair or shave without damaging the hair structure because the cut is superficial. Most chemical hair removers also act superficially; however, electrolysis and yanking both attempt to destroy the hair bulb so hair cannot grow.

The wall of the hair follicle is made of three concentric layers of cells. The cells of the internal root sheath surround the root of the growing hair and extend just up to the hair shaft. They are derived from the basal cells of the hair matrix. The external root sheath, which is an extension of the epidermis, encloses the hair root. It is made of basal cells at the base of the hair root and tends to be more keratinous in the upper regions. The glassy membrane is a thick, clear connective tissue sheath covering the hair root, connecting it to the tissue of the dermis.

Hair serves a variety of functions, including protection, sensory input, thermoregulation, and communication. For example, hair on the head protects the skull from the sun. The hair in the nose and ears, and around the eyes (eyelashes) defends the body by trapping and excluding dust particles that may contain allergens and microbes. Hair of the eyebrows prevents sweat and other particles from dripping into and bothering the eyes. Hair also has a sensory function due to sensory innervation by a hair root plexus surrounding the base of each hair follicle. Hair is extremely sensitive to air movement or other disturbances in the environment, much more so than the skin surface. This feature is also useful for the detection of the presence of insects or other potentially damaging substances on the skin surface. Each hair root is connected to a smooth muscle called the arrector pili that contracts in response to nerve signals from the sympathetic nervous system, making the external hair shaft “stand up.” The primary purpose for this is to trap a layer of air to add insulation. This is visible in humans as goose bumps and even more obvious in animals, such as when a frightened cat raises its fur. Of course, this is much more obvious in organisms with a heavier coat than most humans, such as dogs and cats.

Hair Growth

Hair grows and is eventually shed and replaced by new hair. This occurs in three phases. The first is the anagen phase, during which cells divide rapidly at the root of the hair, pushing the hair shaft up and out. The length of this phase is measured in years, typically from 2 to 7 years. The catagen phase lasts only 2 to 3 weeks, and marks a transition from the hair follicle’s active growth. Finally, during the telogen phase, the hair follicle is at rest and no new growth occurs. At the end of this phase, which lasts about 2 to 4 months, another anagen phase begins. The basal cells in the hair matrix then produce a new hair follicle, which pushes the old hair out as the growth cycle repeats itself. Hair typically grows at the rate of 0.3 mm per day during the anagen phase. On average, 50 hairs are lost and replaced per day. Hair loss occurs if there is more hair shed than what is replaced and can happen due to hormonal or dietary changes. Hair loss can also result from the aging process, or the influence of hormones.

Hair Color

Similar to the skin, hair gets its color from the pigment melanin, produced by melanocytes in the hair papilla. Different hair color results from differences in the type of melanin, which is genetically determined. As a person ages, the melanin production decreases, and hair tends to lose its color and becomes gray and/or white.

Nails

The nail bed is a specialized structure of the epidermis that is found at the tips of our fingers and toes. The nail body is formed on the nail bed, and protects the tips of our fingers and toes as they are the farthest extremities and the parts of the body that experience the maximum mechanical stress (Figure 5.13). In addition, the nail body forms a back-support for picking up small objects with the fingers. The nail body is composed of densely packed dead keratinocytes. The epidermis in this part of the body has evolved a specialized structure upon which nails can form. The nail body forms at the nail root, which has a matrix of proliferating cells from the stratum basale that enables the nail to grow continuously. The lateral nail fold overlaps the nail on the sides, helping to anchor the nail body. The nail fold that meets the proximal end of the nail body forms the nail cuticle, also called the eponychium. The nail bed is rich in blood vessels, making it appear pink, except at the base, where a thick layer of epithelium over the nail matrix forms a crescent-shaped region called the lunula (the “little moon”). The area beneath the free edge of the nail, furthest from the cuticle, is called the hyponychium. It consists of a thickened layer of stratum corneum.

Figure 5.13 Nails The nail is an accessory structure of the integumentary system.

Sweat Glands

When the body becomes warm, sudoriferous glands produce sweat to cool the body. Sweat glands develop from epidermal projections into the dermis and are classified as merocrine glands; that is, the secretions are excreted by exocytosis through a duct without affecting the cells of the gland. There are two types of sweat glands, each secreting slightly different products.

An eccrine sweat gland is a type of gland that produces a hypotonic sweat for thermoregulation. These glands are found all over the skin’s surface, but are especially abundant on the palms of the hand, the soles of the feet, and the forehead (Figure 5.14). They are coiled glands lying deep in the dermis, with the duct rising up to a pore on the skin surface, where the sweat is released. This type of sweat, released by exocytosis, is hypotonic and composed mostly of water, with some salt, antibodies, traces of metabolic waste, and dermicidin, an antimicrobial peptide. Eccrine glands are a primary component of thermoregulation in humans and thus help to maintain homeostasis.

Figure 5.14 Eccrine Gland Eccrine glands are coiled glands in the dermis that release sweat that is mostly water.

An apocrine sweat gland is usually associated with hair follicles in densely hairy areas, such as armpits and genital regions. Apocrine sweat glands are larger than eccrine sweat glands and lie deeper in the dermis, sometimes even reaching the hypodermis, with the duct normally emptying into the hair follicle. In addition to water and salts, apocrine sweat includes organic compounds that make the sweat thicker and subject to bacterial decomposition and subsequent smell. The release of this sweat is under both nervous and hormonal control, and plays a role in the poorly understood human pheromone response. Most commercial antiperspirants use an aluminum-based compound as their primary active ingredient to stop sweat. When the antiperspirant enters the sweat gland duct, the aluminum-based compounds precipitate due to a change in pH and form a physical block in the duct, which prevents sweat from coming out of the pore.

Sebaceous Glands

A sebaceous gland is a type of oil gland that is found all over the body and helps to lubricate and waterproof the skin and hair. Most sebaceous glands are associated with hair follicles. They generate and excrete sebum, a mixture of lipids, onto the skin surface, thereby naturally lubricating the dry and dead layer of keratinized cells of the stratum corneum, keeping it pliable. The fatty acids of sebum also have antibacterial properties, and prevent water loss from the skin in low-humidity environments. The secretion of sebum is stimulated by hormones, many of which do not become active until puberty. Thus, sebaceous glands are relatively inactive during childhood.

Hair serves a variety of functions, including protection, sensory input, thermoregulation, and communication. For example, hair on the head protects the skull from the sun. The hair in the nose and ears, and around the eyes (eyelashes) defends the body by trapping and excluding dust particles that may contain allergens and microbes. Hair of the eyebrows prevents sweat and other particles from dripping into and bothering the eyes. Hair also has a sensory function due to sensory innervation by a hair root plexus surrounding the base of each hair follicle. Hair is extremely sensitive to air movement or other disturbances in the environment, much more so than the skin surface. This feature is also useful for the detection of the presence of insects or other potentially damaging substances on the skin surface. Each hair root is connected to a smooth muscle called the arrector pili that contracts in response to nerve signals from the sympathetic nervous system, making the external hair shaft “stand up.” The primary purpose for this is to trap a layer of air to add insulation. This is visible in humans as goose bumps and even more obvious in animals, such as when a frightened cat raises its fur. Of course, this is much more obvious in organisms with a heavier coat than most humans, such as dogs and cats.

Short, long, curly, straight, up, down. Hair options can seem endless! Not all of what makes your hair look good comes from the outside, though. Good nutrition, physical activity, staying away from the sun, and other healthy habits can help your hair shine!

Here are some other tips for hair care:

If your hair is oily: Try washing your hair every day. You may also want to try shampoos that are made for oily hair. And stop using hair products that have oil in them, like pomades.

If your hair is dry: You may want to use a moisturizing shampoo made for dry hair. Also use a cream rinse or conditioner. You could also try shampooing less often.

If you see white flakes in your hair or on your shoulders: You most likely have dandruff. Try a dandruff shampoo. If it doesn’t help, your doctor may prescribe something stronger.

If you want to dye your hair:

• If possible, you might consider having a professional do this for you.
• If you are dyeing your hair at home, it’s best to get someone’s help.
• Follow the directions in the package carefully, especially any warnings.
• Do a test before using dye on your hair. Rub a tiny bit of the dye on the inside of your elbow or behind your ear. Leave it there for two days. If you get a rash, don't use the dye on your hair.
• Wear gloves when you apply dye.
• Talk with your doctor if your skin or scalp swells or gets itchy after using any hair product. Even natural products, such as henna dye, can cause an allergic reaction.

If you want to straighten your hair:

• If possible, you might consider having a professional do this for you.
• You can use a relaxer product at home, but it can burn your scalp if you use it the wrong way.
• It’s best not to try using a relaxer product by yourself. Get help to make sure you’ve put it on evenly and you get it all out when you’re through.
• Make sure to follow any directions, and don’t leave the straightener on too long.
• Keep in mind that straightening your hair can damage it. Try not to straighten it too often. Some hairdressers say around once every two months is okay.

If you want to make your hair curly:

• If you can, you might consider having a professional do this for you.
• You can use a permanent wave, or “perm” at home, but it’s a good idea to get help.
• Make sure to follow any directions, and don’t leave it on too long.

If you use hairdryers, curling irons, flat irons, or similar products: Be careful not to overuse them. Dryers and other products that use heat can dry out or break your hair. It’s a good idea to take a few days off from time to time.

If you swim in a pool a lot: Protect your hair from chlorine by wearing a swim cap or rinsing out your hair right after swimming. Soaking your hair with regular water before you put on your swim cap can also help.

Pili annulati is a hair disorder. In pili annulati, affected hair has a pattern of light and dark banding. People with pili annulati maydescribe their hair as "striped" or as having silvery beads. Pili annulati typically involves 20-80% of scalp hair, however it can involvefacial and body hair as well. Affected hairsmay be more prone to breakage. Pili annulati can present in infancy,childhood, or later in life. It can be seen withthe naked eye, however it may be more difficult to see in people withdark hair. Diagnosis is confirmed by polariscopic and/or electronmicroscopic examination of affected hairs. The condition runs in an autosomal dominant fashion in some families.Reduced penetrance and variable expression has been described. Sporadiccases have also been reported.

Pili torti is a rare hair condition characterized by fragile hair. In pili torti hair has a flattened shaft with clusters of narrow twists at irregular intervals. Some cases may be inherited in autosomal dominant or autosomal recessive patterns, while others are acquired. In the inherited form, symptoms tend to be present from early childhood. It can occur alone or as part of other diseases like ectodermal dysplasias, Menke disease, Bjornstand syndrome, or Bazex syndrome. Acquired cases of pili torti may be associated with anorexia nervosa, malnutrition, oral retinoid treatment, or inflammatory scalp conditions (e.g., cutaneous lupus erythematousus). If pili torti is detected, it is necessary to investigate possible neurological disorders, hearing loss, and defects in the hair, nails, sweat glands and teeth. There is no specific treatment for this condition, but it may improve spontaneously after puberty.

Either of two diseases resulting from fungal infection of the hair shafts. Black piedra occurs mainly in and on the hairs of the scalp and is caused by Piedraia hortae; white piedra occurs in and on the hairs of the scalp, beard, moustache and genital areas and is caused by Trichosporon species.

Monilethrix is a condition that affects hair growth. Its most characteristic feature is that individual strands of hair have a beaded appearance like the beads of a necklace. The name monilethrix comes from the Latin word for necklace (monile) and the Greek word for hair (thrix). Noticeable when viewed under a microscope, the beaded appearance is due to periodic narrowing of the hair shaft. People with monilethrix also have sparse hair growth (hypotrichosis) and short, brittle hair that breaks easily.

Affected individuals usually have normal hair at birth, but the hair abnormalities develop within the first few months of life. In mild cases of monilethrix, only hair on the back of the head (occiput) or nape of the neck is affected. In more severe cases, hair over the whole scalp can be affected, as well as pubic hair, underarm hair, eyebrows, eyelashes, or hair on the arms and legs.

Occasionally, the skin and nails are involved in monilethrix. Some affected individuals have a skin condition called keratosis pilaris, which causes small bumps on the skin, especially on the scalp, neck, and arms. Affected individuals may also have abnormal fingernails or toenails.

An inherited disorder of copper metabolism transmitted as an X-linked trait and characterized by the infantile onset of HYPOTHERMIA, feeding difficulties, hypotonia, SEIZURES, bony deformities, pili torti (twisted hair), and severely impaired intellectual development. Defective copper transport across plasma and endoplasmic reticulum membranes results in copper being unavailable for the synthesis of several copper containing enzymes, including PROTEIN-LYSINE 6-OXIDASE; CERULOPLASMIN; and SUPEROXIDE DISMUTASE. Pathologic changes include defects in arterial elastin, neuronal loss, and gliosis. (From Menkes, Textbook of Child Neurology, 5th ed, p125)

Hypotrichosis simplex is a rare form of hereditary hair loss without other abnormalities. Affected individuals typically show normal hair at birth, but experience hair loss and thinning of the hair shaft that starts during early childhood and progresses with age. Hypotrichosis simplex can be divided into 2 forms: the scalp-limited form and the generalized form, in which all body hair is affected. The progressive thinning of the hair shaft is a typical feature of androgenetic alopecia. Hypotrichosis simplex can be inherited either as an autosomal dominant or autosomal recessive trait. Some cases are caused by mutations in the APCDD1 gene on chromosome 18p11. To date, there is no treatment for this condition.

Hypertrichosis is defined as excessive hair growth anywhere on the body in either males or females. It is important to distinguish hypertrichosis from hirsutism, which is a term reserved for females who grow an excessive amount of terminal hairs in androgen-dependent sites.

There are several ways of classifying hypertrichosis. These are based on distribution (generalized vs. localized), the age of onset (congenital versus acquired), and the type of hair (vellus versus terminal).

Forms of generalized hypertrichosis include, but are not limited to, congenital generalized hypertrichosis (which is further divided into congenital hypertrichosis lanuginosa, universal hypertrichosis, and hypertrichosis universalis congenita), prepubertal hypertrichosis, acquired generalized hypertrichosis, and acquired hypertrichosis lanuginosa. They each differ in their etiology and clinical findings.

Forms of localized hypertrichosis include, but are not limited to, congenital localized hypertrichosis (congenital nevi, plexiform neurofibromas, Becker melanosis/nevus, nevoid hypertrichosis, spinal dysraphism, and the hair collar sign), localized hypertrichosis in hereditary and acquired systemic disease, and acquired localized hypertrichosis.

An understanding of lanugo, vellus, and terminal hair is integral in evaluating a patient with presumed hypertrichosis. Lanugo hair is fine, non-pigmented hair that covers the normal fetus. It is often several centimeters long. By the first few weeks of life, lanugo hair should be replaced by vellus hair on the body and terminal hair on the scalp. Vellus hair is lightly pigmented, fine, short hair, often referred to as “peach fuzz” that is found on the face, arms, stomach, and legs. Terminal hair is coarse, thick hair that is found on the scalp, underarms, and pubic area. In men, terminal hair is also found on the face. During puberty, vellus hair is replaced with terminal hair in androgen-dependent sites under the influence of testosterone.

Hirsutism means the growth of excessive male-pattern hair in women after puberty. It affects facial and body areas dependent on androgens, namely mustache and beard, pubic hair, buttocks, and thighs. It is a frequent reason for dermatological consultation. Hirsutism is the most common endocrine disorder affecting nearly 10% of women in the United States.

Irrespective of the cause, hirsutism can cause significant emotional stress and mental anguish. The key is to find the cause and address the cosmetic issue.

Etiology

The causes of hirsutism are variable. The condition may be of ovarian or adrenal origin, tumoral or not. The following are some examples.

Hyperandrogenic Hirsutism

Hirsutism is most often due to hyperproduction of androgens, of ovarian or adrenal origin. Hyperandrogenism of tumor origin, which is very severe, must be distinguished from non-tumor hyperandrogenism, which is often minimal or moderate.

Polycystic Ovary Syndrome (PCOS)

It represents the most common cause of hirsutism and causes about 75% of all cases. It affects 5% to 10% of women during their period of genital activity and 20% to 25% of adolescent girls. It is a heterogeneous and complex syndrome of unknown etiology characterized by the end of follicular maturation with an accumulation of small follicles under the cortex and hyperplasia of the ovarian stroma.

Hirsutism appears at puberty, accompanied by disturbances of the menstrual cycle, weight gain, dyslipidemia, insulin resistance, acne, and acanthosis nigricans. The patient reports spaniomenorrhea (prolongation of the cycle beyond 35 days), oligomenorrhea (less abundant menstruation), and infertility. The ovaries can be enlarged. Hypothyroidism or liver disease may be present.

Androgen-Secreting Tumors

Hyperandrogenism due to ovarian or adrenal tumors is rare. It is responsible for only 0.2% of all cases of hirsutism. These androgen-secreting tumors are autonomous, and therefore, do not depend on the hypothalamic-pituitary axis. Approximatively 50% of them are malignant, and in these cases, the plasma androgen levels are very high. They are also responsible for rapid-onset of virilization, hirsutism, and a pelvic or abdominal mass.

Non-classical Congenital Adrenal Hyperplasia (NCAH)

This is a common autosomal recessive disorder, caused by a partial 21-hydroxylase deficiency, and represents the most common adrenal etiology of hyperandrogenism. Its prevalence varies greatly according to the ethnicity of the patients. So it is more common in the Ashkenazi Jewish population (3.7%) and the Central European population (2%) and rare in Caucasians (0.1%). Like PCOS, NCAH can be expressed after the puberty by hirsutism, oligomenorrhea, acne, infertility, alopecia, and primary amenorrhoea.

Non-Hyperandrogenic Hirsutism

Medications

Many drugs can cause hirsutism: androgens, glucocorticosteroids, progestins, estrogen antagonists (clomiphene, tamoxifen), minoxidil, cyclosporine, danazol, diazoxide, phenytoin, D-penicillamine, and interferon.

It is important to know that hypertrichosis could also be caused by certain medications such as acetazolamide, phenytoin, latanoprost, streptomycin, psoralen, minoxidil, cyclosporine, and diazoxide.

Endocrinopathies

The responsibility of the endocrinopathies in the occurrence of hirsutism is rare, and other more specific symptoms and signs dominate the clinical picture:

• Cushing syndrome depends on adrenocorticotrophic hormone (ACTH). It can cause hirsutism, because of the stimulating nature of ACTH on the reticulated area that can cause excessive androgen secretion. The features of hypercorticism are often in the foreground.

• Hyperthyroidism or hypothyroidism is uncommonly a cause of isolated hirsutism.

• Hyperprolactinemia is manifested by amenorrhea, galactorrhea, infertility, and rarely hirsutism.

• Acromegaly is also a rare cause of isolated hirsutism.

Others Causes

Moderate hirsutism can be observed in pregnant women (physiological prolactin secretion) and postmenopausal women (relative hyperandrogenism due to the cessation of ovarian estrogen production).

Idiopathic Hirsutism

Idiopathic hirsutism defines the hirsutism that occurs in association with regular menses, normal ovarian morphology, and normal plasmatic androgen levels. It is a diagnosis of exclusion after elimination of other etiologies. It represents about 10% of all cases of hirsutism and 50% of cases of mild hirsutism. It may be due to hypersensitivity of the pilosebaceous follicle receptors to androgens and peripheral conversation induced by the 5-reductase of testosterone to dihydrotestosterone ten-fold more active on the follicle-sebaceous unit. This has genetic determinism and is frequently reported in women of East Indian and Mediterranean origin.

Epidemiology

The exact prevalence of hirsutism is not well known. It may be 10% or even higher than 50%. The psychological problem that this disease causes depends on ethnic and socio-cultural factors. Indeed, in some societies where the lack of hair is considered an important criterion of female beauty, minimal hirsutism could be considered a severe disorder, while much more pronounced hirsutism could be accepted in other societies.

Hirsutism appears to be most common in dark-skinned individuals. Hirsutism can occur in men but is difficult to recognize. In children, hirsutism is a sign of precocious puberty.

Hirsutism is also known to occur in women who discontinue the oral contraceptive pill and gain weight.

Pathophysiology

Hirsutism is an androgen-dependent disorder resulting from the interaction between circulating androgen levels and the sensitivity of the hair follicle to androgens. The skin can retain testosterone in a more active androgen, dihydrotestosterone (DHT) through a 5alpha-reductase enzyme of which there are two isoenzymes, types 1 (chromosome 5) and 2 (chromosome 2), present in the skin and the hair follicle. In addition, the skin and the pilosebaceous follicle have an androgen receptor (AR).

After exclusion of an exogenous intake of androgens, hirsutism results either from hypersecretion of androgens, from the ovary or the adrenal gland, or the increased cutaneous sensitivity of the skin to normal circulating levels of androgens. This last case is "idiopathic hirsutism."

History and Physical

The medical history is important. In the case of hirsutism of peripubertal and slow onset, it indicates primary hirsutism or non-tumoral secondary hirsutism. Late-onset or rapid progression, signs of virilization or high levels of hormones lead to adrenal (adenomas), ovarian (arrhenoblastoma), or pituitary (prolactinoma) tumors. Anamnesis of cycle disorders is an important indicator for secondary hirsutism (100% for tumors, 75% for polycystic ovaries, 0% to 25% for late adrenogenital syndrome).

The general characteristic is the sexual hair, whose density and properties change, especially in the middle areas of the body. Most often, the face, chest, areolas, white line, buttocks, sacrum, inner thighs, and external genitalia are affected. The severity of hirsutism can be quantified based on the Ferriman and Gallwey system, which evaluates nine areas of the body. For each, one assigns points from 1 to 4 are assigned according to the density of hair, ranging from the absence of hair to severe hirsutism. One can then calculate a total score; if it is greater than 7, the maximum being 36, it is considered abnormal. Other common symptoms associated with excess androgens are acne, menstrual irregularities, the temporal recession of the hairline and frontal alopecia.

Evaluation

The basic biological assessment is performed in the early follicular phase (third to the sixth day of the cycle, early morning, fasting) and after stopping possible oral contraception for two or three cycles unless a tumor cause is suspected. It comprises total testosterone, dehydroepiandrosterone sulfate (DHEAS), delta4-androstenedione (delta4A), luteinizing hormone (LH) / follicle-stimulating hormone (FSH), 17-hydroxyprogesterone (17-OHP), steroid hormone-binding globulin (SHBG). In the case of menstrual cycle disorder (amenorrhea, oligomenorrhea), the stimulating thyroid hormone (TSH) and prolactinemia (PRL) are included.

According to the clinical findings, one can add to the work up a short dexamethasone suppression test (Cushing syndrome), an adrenocorticotropic hormone (ACTH) stimulation test and a prolonged dexamethasone suppression test (late adrenogenital syndrome), a carbohydrate tolerance test or HOMA index (insulin resistance syndrome).

The diagnosis of idiopathic hirsutism is a diagnosis of exclusion. Approximately 15% to 50% of women suffering from hirsutism belong to this category. Its pathogenesis is then parallel to that of primary androgenetic alopecia.

Treatment / Management

Pharmacologic Treatment

Treatment of non-tumoral hirsutism still includes oral contraception. It inhibits by its progestogen the hypothalamic-pituitary axis, and thus the ovarian production of androgens; by its estrogen, it increases the SHBG. It is combined with an antiandrogenic treatment: flutamide, spironolactone, cyproterone acetate, finasteride are all used with variable but comparable results.

Oral contraceptives are the first treatment of choice as they suppress androgen production by the ovaries. However, they often do not work. In addition, for a female who desires a pregnancy, this treatment may not be ideal.

Spironolactone is known to block androgen receptors and is the second most common treatment. It can even be combined with an oral contraceptive. However, the improvement is slow and takes many months. Thus, compliance with spironolactone is low.

Finasteride is used to treat hirsutism and is preferred as it does not have any estrogenic or progesterone activity. However, it is not recommended in women of childbearing age as there is a risk of ambiguous genitalia in the fetus. Flutamide is another novel treatment, and while it does work, the medication is expensive and has the potential to cause liver damage.

Adrenal hyperandrogenism is slowed down by low dose corticosteroids, possibly associated with the treatments as mentioned earlier.

Fine hair growth can be inhibited by twice, daily topical application of eflornithine. Electrolysis is less used now except for coarse white hairs and also in cases of polycystic ovaries without insulin resistance.

Nonpharmacologic Treatment

As the effect of drug treatment that occurs only after 1 to 2 years, clinicians use the cosmetic approaches that are also appropriate for hypertrichoses: shaving, hair removal, discoloration by hydrogen peroxide, chemical depilation (p. thioglycolates). Fine hair growth can be inhibited by twice-daily topical application of eflornithine. Electrolysis is not used as often as in the past, except in the case of coarse white hairs. It has been replaced by long-term depilation with tools like depilatory lasers and various intense pulsed light devices.

Surgical Treatment

Surgical excision is necessary in the case of the tumoral process. Ovariectomy may be indicated for severe hyperandrogenism in menopausal or perimenopausal women.

Differential Diagnosis

Hypertrichosis is a diffuse increase of hair forming down in areas not dependent on androgens (often the cheeks and arms). It may be the consequence of an excess of glucocorticoids, the taking of certain drugs (phenytoin, penicillamine, ciclosporin, minoxidil, diazoxide), and systemic disorders (anorexia nervosa, hypothyroidism, porphyria, dermatomyositis). Hypertrichosis is often due to a familial or ethnic character and has a prepubertal onset.

Lanugo is a very thin, villous, and non-pigmented hair located anywhere on the body. Hypertrichosis is characterized by an excessive growth of hair affecting normally hairy areas in women.

Inflammation of follicles, primarily hair follicles.

Uncombable hair syndrome (UHS) is a rare disorder of the hair shaft of the scalp. It is usually characterized by silvery-blond or straw-colored hair that is disorderly; stands out from the scalp; and cannot be combed flat. It may first become apparent from 3 months of age to 12 years of age. Most cases are isolated, but in some cases it has been described in association with other diseases, such as ectodermal dysplasias, Bork syndrome and Angel-shaped phalangoepiphyseal dysplasia. The syndrome has been found to be caused by mutations in the genes PADI3, TGM3, and TCHH. These three genes code for proteins that are involved in hair shaft formation. The syndrome appears to be inherited in an autosomal recessive fashion; however, cases inherited in an autosomal dominant manner may also exist, as there are other genes involved in hair formation. The condition often spontaneously regresses in late childhood. Some published studies suggest that biotin may improve the condition.

Uncombable hair syndrome is a condition that is characterized by dry, frizzy hair that cannot be combed flat. This condition develops in childhood, often between infancy and age 3, but can appear as late as age 12. Affected children have light-colored hair, described as blond or silvery with a glistening sheen. The hair does not grow downward but out from the scalp in multiple directions. Despite its appearance, the hair is not fragile or brittle, and it grows at a normal or slightly slower rate. Only scalp hair is affected in uncombable hair syndrome.

For unknown reasons, this condition usually improves over time. By adolescence individuals with uncombable hair syndrome have hair that lies flat and has normal or nearly normal texture.

The prevalence of uncombable hair syndrome is unknown; at least 100 cases have been described in the scientific literature. There are likely more people who are undiagnosed because adults who seem unaffected may have had uncombable hair syndrome in childhood.

Superficial Staphylococcal Infections

S. aureus is often associated with pyoderma, skin infections that are purulent. Pus formation occurs because many strains of S. aureus produce leukocidins, which kill white blood cells. These purulent skin infections may initially manifest as folliculitis, but can lead to furuncles or deeper abscesses called carbuncles.

Folliculitis generally presents as bumps and pimples that may be itchy, red, and/or pus-filled. In some cases, folliculitis is self-limiting, but if it continues for more than a few days, worsens, or returns repeatedly, it may require medical treatment. Sweat, skin injuries, ingrown hairs, tight clothing, irritation from shaving, and skin conditions can all contribute to folliculitis. Avoidance of tight clothing and skin irritation can help to prevent infection, but topical antibiotics (and sometimes other treatments) may also help. Folliculitis can be identified by skin inspection; treatment is generally started without first culturing and identifying the causative agent.

In contrast, furuncles (boils) are deeper infections (Figure). They are most common in those individuals (especially young adults and teenagers) who play contact sports, share athletic equipment, have poor nutrition, live in close quarters, or have weakened immune systems. Good hygiene and skin care can often help to prevent furuncles from becoming more infective, and they generally resolve on their own. However, if furuncles spread, increase in number or size, or lead to systemic symptoms such as fever and chills, then medical care is needed. They may sometimes need to be drained (at which time the pathogens can be cultured) and treated with antibiotics.

When multiple boils develop into a deeper lesion, it is called a carbuncle (Figure). Because carbunclesare deeper, they are more commonly associated with systemic symptoms and a general feeling of illness. Larger, recurrent, or worsening carbuncles require medical treatment, as do those associated with signs of illness such as fever. Carbuncles generally need to be drained and treated with antibiotics. While carbuncles are relatively easy to identify visually, culturing and laboratory analysis of the wound may be recommended for some infections because antibiotic resistance is relatively common.

Proper hygiene is important to prevent these types of skin infections or to prevent the progression of existing infections.

Trichorrhexis nodosa is a disorder of the hair shaft characterized by easy breakability of hair and microscopically by nodes on the hair shaft 1. Trichorrhexis nodosa may be congenital or acquired. The more common acquired form results from repeated trauma to the hair shaft.

What is an ingrown hair?

An ingrown hair occurs when you cut a hair and it grows back into the skin, causing inflammation. It can happen anywhere on the body that hair is removed from, such as through shaving, tweezing, waxing or using hair removal cream.

Sometimes an ingrown hair can cause an infection around the hair follicle, known as folliculitis.

Common places for ingrown hairs are:

• men’s chins, cheeks and necks
• women’s legs, pubic areas and armpits
• buttocks

What are the symptoms of an ingrown hair?

The area around the ingrown hair can become swollen, red and itchy. It can become inflamed so that it is painful and looks like a pimple with pus. Ingrown hairs can form cysts (sacs of fluid beneath the skin) which can range from a small painless lump to a large, infected swelling.

What causes an ingrown hair?

There are 2 causes of ingrown hair.

1. Cutting a hair can force it back into its follicle.
2. Dead skin can clog the follicle, causing the hair to grow under the skin or re-enter its follicle or one nearby. The hair then grows inward instead of pushing through the surface of the skin.

You are more likely to get ingrown hairs if you have very curly or coarse hair. Cutting curly or coarse hair can lead to a type of ingrown hair called pseudofolliculitis or ‘razor bumps’ after shaving, tweezing or waxing hair in the area.

How is an ingrown hair treated?

Ingrown hairs often improve without treatment. It may help to stop shaving, tweezing, waxing or using hair removal cream until the condition improves.

Washing the area with a washcloth or soft toothbrush using a circular motion for several minutes can help release the hairs. You can also try inserting a sterile needle under the hair loop and pulling the ingrown end to the surface.

If the ingrown hair becomes infected, you may need an antibiotic cream from the doctor. In severe cases, oral antibiotics may be needed.

Talk to your doctor if you have a lot of ingrown hairs. There are medicines that can remove dead skin cells, reduce inflammation and treat infection.

Can ingrown hair be prevented?

You might be able to prevent ingrown hairs by:

• washing your skin with warm water and a mild facial cleanser
• exfoliating before you shave
• using a single blade or electric razor
• shaving in the direction of the hairs
• using shaving creams to cleanse the area

Alopecia areata is a common disorder that causes hair loss. "Alopecia" is a Latin term that means baldness, and "areata" refers to the patchy nature of the hair loss that is typically seen with this condition.

In most people with alopecia areata, hair falls out in small, round patches, leaving coin-sized areas of bare skin. This patchy hair loss occurs most often on the scalp but can affect other parts of the body as well. Uncommonly, the hair loss involves the entire scalp (in which case the condition is known as alopecia totalis) or the whole body (alopecia universalis). Other rare forms of alopecia areata, which have different patterns of hair loss, have also been reported.

Alopecia areata affects people of all ages, although it most commonly appears in adolescence or early adulthood. Hair loss occurs over a period of weeks. The hair usually grows back after several months, although it may fall out again. In some cases, unpredictable cycles of hair loss followed by regrowth can last for years. In addition to hair loss, some affected individuals have fingernail and toenail abnormalities, such as pits on the surface of the nails.

The hair loss associated with alopecia areata is not painful or disabling. However, it causes changes in a person's appearance that can profoundly affect quality of life and self-esteem. In some people, the condition can lead to depression, anxiety, and other emotional or psychological issues.