Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Ogechukwu Hannah Nnabude, MD

Alopecia is defined as the loss of hair regardless of the cause. It can occur anywhere on the body. The hair cycle consists of three phases: the anagen phase, which is the growth phase, the catagen phase, which is the resting phase, and the telogen phase, which is the shedding phase. This is the phase where hair falls out. Ninety percent of hair is in the anagen phase and the remaining ten percent are in the catagen phase and telogen phases. In the telogen phase, hair is going to recycle, and it starts growing again in the anagen phase.

The use of the word alopecia stretches back to the era of the Greek physician Hippocrates. Minoxidil and finasteride are the only FDA approved medications for treating alopecia. Hair transplant surgery originated in the 1900s and some of the major advancements in hair transplantation took place in Japan in the 1930s.

Alopecia is classified as either scarring or non-scarring. Over all, non-scarring alopecias tend to have better outcomes than scarring alopecias, which tend to be irreversible. The most common type is androgenetic alopecia. The majority of men start to lose hair in the third decade of life, while women begin to lose their hair in the fifth or sixth decade of life. As an individual ages, they will lose hair. Men more often lose hair in the front and the temporal regions of the scalp, while women tend to lose hair from the central area of the scalp. Also, female hair loss rarely results in complete baldness while male hair loss can end up with complete baldness. Males tend to retain hair at the posterior area of the scalp because the hair in this region is more resistant to the effects of androgenic hormones.

There are several pathophysiologic mechanisms responsible for alopecia, each related to the specific cause. For example, alopecia areata, is related with CD8+ T-cell autoimmunity, while androgenetic alopecia is related to the effects of androgen hormones on hair follicles.

Scarring alopecia is caused by numerous dermatologic factors, including glabrous skin (non-hairy), and is very difficult to diagnose and manage. Non-scarring alopecia is characterized by the absence of visible inflammation of the skin involved. Medications, endocrine diseases, infectious diseases, and autoimmune diseases can also cause hair loss.

There is a very wide list of diseases and conditions that can lead to alopecia. Proper history taking and physical examination, along with laboratory, microbiology, and in some cases, imaging studies, are helpful in narrowing down the diagnosis.

The epidemiology and demographics of alopecia varies by age, race, sex, and health status. Androgenetic alopecia is the most common cause of alopecia. Traction alopecia is seen most often in black populations and is associated with tight hair braids. Tinea capitis commonly seen in the pediatric population. Trichotillomania is more common in males among younger patients and females among adults.

There are multiple risk factors for alopecia including family history, medications, sex, age and illness. Androgenetic alopecia is more common in males and prevalence increases with age. People with a family history of hair loss are at greater predisposition to developing alopecia. Psychosocial stress, hormonal imbalance, and illness also increase the risk of alopecia.

The progression and severity of alopecia is based on the cause. Patients with alopecia are at increased risk of psychosocial complications such as anxiety and depression. In addition, these patients need to be evaluated for other medical conditions. Outcomes vary with the type of alopecia. Non-scarring alopecias such as androgenetic alopecia, anagen effluvium and early tinea capitis may be reversible while scarring alopecias such as traction alopecia and favus may not be reversible.

Biopsy, laboratory tests, trichoscopy, and hair pull test are some of the techniques used in diagnosis. MRI can be used in mycosis fungoides staging and is useful for alopecia mucinosa while microscopic testing and Wood’s lamp is useful for the diagnosis of fungal infection.

The diagnostic test of choice varies with the cause of alopecia. Biopsy, laboratory tests, trichoscopy, and hair pull test are some of the techniques used in diagnosis. MRI can be used in mycosis fungoides staging and is useful for alopecia mucinosa while microscopic testing and Wood’s lamp is useful for the diagnosis of fungal infection

The quantity, pattern, timing, and onset of hair loss can be important clues in narrowing down a diagnosis. For example. androgenetic alopecia affects the frontal hair line and crown of the hair while alopecia areata affects a small, round area of the scalp.

The presence of scarring, scaling or erythema are all helpful clues in determining the cause of the hair loss.

Some causes of alopecia may present with abnormal laboratory findings such as abnormal TSH, ESR or RPR levels.

There are no ECG findings associated with alopecia.

There are no X-ray findings associated with alopecia.

There are no echocardiogram or ultrasound findings associated with alopecia.

There are no CT scan findings associated with alopecia.

MRI is used in staging of mycosis fungoides. This is useful in the case of alopecia mucinosa.

Among all the imaging modalities, MRI is the most useful in mycosis fungoides staging. This is can be used in the case of alopecia mucinosa

There are tests that can be conducted outside of the laboratory that will help to confirm the diagnosis. Examples include potassium hydroxide test and biopsy

Currently, there are only two FDA-approved medical treatments for androgenetic alopecia and these are finasteride and minoxidil. Topical corticosteroids, immunosuppressants like cyclosporine Psoralen and ultraviolet A can all be used in the treatment of alopecia areata, topical antifungals can be used in tinea capitis.

Surgery is another option for the treatment of alopecia, although it is often seen as the last resort. it involves hair transplantation of hair follicles from one site to another.

Proper diet, hygiene, and avoidance can decrease the risk of developing certain types of alopecia such as tinea capitis and traction alopecia.

Treatment of underlying conditions such as hyperthyroidism, switching from medications that may cause hair loss such as beta blockers and certain antidepressants and avoidance offending agents such as certain types of hairstyles such as tight braids may limit further hair loss and, in some cases, reverse the hair loss.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Ogechukwu Hannah Nnabude, MD

The origin of the words uses to describe alopecia are of Greek and Celtic origin. Balding is often associated with enhanced social status and maturity. The term alopecia dates as far back as the time of Hippocrates. Minoxidil was not initially created for the treatment of alopecia and the idea of using finasteride in the treatment of alopecia was conceived by observing patients with a mutation in the 5-alpha-reductase enzyme. Hair transplantation began in the 19th century.

• The term alopecia (al-oh-PEE-she-uh) was used by physicians dating back to Hippocrates alopecia and is formed from the Greek αλώπηξ (alopex), meaning fox. The origin of this usage is because this animal sheds its coat twice a year. ^[1]
• The first use of the phrase alopecia areata is attributed to Polish physician John Jonston (1603–1675) in his book “Medicina Practica,” written in 1664. The term alopecia areata. (AA) was introduced by French physician Sauvages de Lacroix (1706–1767) in “Nosologia Methodica,” published in 1763. ^[1]
• The term bald probably comes from the word ball, a Celtic word which means “white patch” such as is sometimes seen on a horse’s head or the old English word balde, which means “white or pale”. ^[2]

• Minoxidil was initially produced for the management of refractory hypertension in the 1970s. ^[3] The effect of minoxidil on hair growth was first identified by Guinter Kahn. He observed and report hair growth on patients who were on the minoxidil patch and postulated their possible use for hair growth.
• Julianne Imperato-McGinley discovered smaller prostates and the absence of male patterned baldness in Caribbean males with a deficiency of 5-alpha-reductase, the enzyme required in the conversion of testosterone to dihydrotestosterone. These discoveries subsequently culminated into the development of finasteride, a 5-alpha-reductase inhibitor. ^{[4] [5] [6]}
• In 1897, Menahem Hodara succeeded in using scalp tissue harvested along with its intact blood supply from an unaffected region of the scalp to treat an area of the scalp scarred by favus. The foundations of the modern methods used in hair transplantation originated in the 1930s, ^[7] where Japanese surgeons replaced patchy regions of eyebrows or eyelashes using small grafts. However, this was not to treat baldness.
• Norman Orentreich pioneered the modern age of hair transplantation in the 1950s by successfully transplanting large amounts of hair. He experimented with using free donor grafts in the treatment of patients with male pattern baldness. The initial school of thought at that time was that hair transferred to an area affected by alopecia would do no better than the hair it replaced. However, Orentreich proved that the grafts were “donor dominant,” by showing that the transferred hairs thrived just as they would have at their previous location. ^[8]

The world is more accepting to men with baldness than women. In most parts of the world, baldness is considered to be less desirable and acceptable. However, majority of males and females with hair loss feel less desirable as a result of it. ^[9]

There are several famous people who are who have shaved heads including former soccer players and current soccer managers Pep Guardiola and Zinedine Zidane, former basketball player Michael Jordan and actors such as Bruce Willis, Vin Diesel, and Jason Statham.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ogechukwu Hannah Nnabude, MD

Alopecia can be subdivided into two main categories: non-scarring and scarring. Over all, non-scarring alopecia has a higher possibility of being reversible and having a better outcome while scarring alopecia is more likely to be irreversible and have a poorer outcome.

Alopecia may be classified according to the scarring into 2 subtypes/groups: non-scarring and scarring.
The six major categories of non-scarring alopecia are:

• Alopecia areata: this can affect any part of the body. When it affects only a portion of an area of the body, it is called alopecia areata. When it affects the entire site, it is called alopecia totalis. When it involves the whole body, it is called alopecia Universalis. The etiology is unknown, but it might be related to an autoimmune disease.^[1]

• Anagen effluvium: This is hair shedding that occurs during the anagen phase of the cell cycle. Seen in cancer patients who are receiving chemotherapeutic agents.

• Androgenetic alopecia: is a pattern of hair loss that is affected by hormones and genes.

• Telogen effluvium: results from shifting of hair growth cycle from the anagen phase towards the telogen phase. It may result from an illness like hypothyroidism or hyperthyroidism. Also, it can arise from stress like major surgery or severe psychological stress ^[2]. Other causes include drugs, crash diet, poor feeding. ^[3]

• ”’Tinea capitis”’: the classical kind of tinea capitis (black-dots) causes non-scarring hair loss, unlike other types like kerion and favus.

• Traumatic alopecia: This results from forceful traction of the hair. It is commonly seen in children and is similar to traction alopecia. Also, trichotillomania is a type of traumatic alopecia in which the patient pulls on his/her hair repeatedly. ^[4]

Scarring alopecia is divided into three major types:

• Alopecia mucinosa: This occurs when mucinous material accumulates in the hair follicles and the sebaceous glands. The mucinous material causes an inflammatory response that hinders the growth of hair.

• ”’Alopecia neoplastica”’: This occurs when there is metastatic infiltration of the scalp hair with malignant cells.

• ”’Tinea capitis”’: This is the inflammatory variety of tinea capitis (favus) or kerion, which is when the fungi cause abscess formation, which may culminate with scarring alopecia.

• Other causes of hair loss that occurs with scarring or inflammation include systemic lupus erythematosus, radiation therapy, and sarcoidosis. ^{[2] [5]} Diagnosis of hair loss is partly based on the areas affected. ^[5]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: José Eduardo Riceto Loyola Junior, M.D.[2]

Since alopecia has many different causes, the pathophysiologic mechanism for its development varies widely according to the cause. Alopecia areata, for example, is related with CD8+ T-cell autoimmunity, while androgenetic alopecia is related with androgen hormones effects’ on the hair follicle which leads to its miniaturization and hair loss. Tinea capitis on the other hand is an infectious disease that can damage the hair follicle and lead to definitive hair loss.

The most common causes for alopecia and its pathophysiology mechanism are briefly discussed below:

• The exact pathogenesis of alopecia areata is not fully understood.
• It has been theorized that T-cell-mediated autoimmunity must be involved in its development.
• The hair follicle typically has low levels of major histocompatibility complex expression, which provides protection from the immune system. It is believed that in alopecia Areata that protection is lost, resulting in a CD8+ T lymphocyte attack to the bulb of the hair, generating an inflammatory infiltrate in the peribulbar region of the hair follicle.^[1][2]
• Genes involved in the pathogenesis of alopecia areata include MCHR2 and MCHR2-AS1 which are related to the MHC pathway (melanin concentrating hormone).^[3]
• There is an association of alopecia Areata with other autoimmune diseases such as vitiligo, autoimmune thyroid disease, celiac disease, systemic erythematous, chronic atrophic gastritis which further reinforces its relationship with autoimmunity.^[4]

• Telogen effluvium is not a disease per se, but it is a common cause of hair loss due to a triggering event that increases the number of hair follicles that are in the catagen or telogen phase (shedding and resting phase) of the hair development cycle.
• It is of non-scarring type.
• There are many different events that can act as triggers for this condition, such as febrile diseases (malaria, HIV, tuberculosis), drugs (oral contraceptives, anticonvulsants, beta blockers, captopril antithyroid drugs and hypolipidemic drugs), thyroid diseases, organ dysfunction, nutritional (iron or zinc deficiency) or local factors such as hair dye.^[5]
• Telogen hairs are usually at least at 25% for the diagnosis of telogen effluvium to be made.^[6]

• Usually seen on children that pull their hair, the same mechanism as traction alopecia.
• May be associated with trichotillomania – a psychiatric condition in which the patient repeatedly pulls their hair.^[7]

• In androgenetic alopecia there is marked miniaturization of the hair follicle and disruption of the hair cycle.
• It is thought that in androgenetic alopecia the hair loss is the result of the shortening of the anagen phases of hair development and enlongation of the telogen phase that gradually takes place until the hair eventually doesn’t even leave the skin surface.^[8]
• The is also an increase in the period from the hair shedding to its regrowth.^[8]
• The miniaturization affects the hair follicle globally, including the dermal papilla which is essential for its maintenance.^[8]
• It is mediated by the presence of androgens, which is further reinforced by the fact that eunuchs do not bald.
• The molecular mechanism of action for the androgens such as testosterone and 5α-dihydrotestosterone (DHT) to act on the hair follicle is not fully understood.
• It is theorized that some genes that regulate the follicle cycling may be regulated by the presence of androgens and that the expression of such genes are related to the concentrations of androgen and androgen receptors in the follicle.^[8]
• It is also theorized through observation of families with androgenetic alopecia that these genes related to the disease may act in an autosomal dominant manner in men and autosomal recessive manner in women, though there is strong evidence for a polygenic mode of inheritance.
• Finasteride is used to treat androgenetic alopecia being a potent 5-alpha-reductase type-2 inhibitor, inhibiting the conversion of testosterone to DHT.

• Tinea capitais is caused by dermatophyte species that are able to invade keratinized tissues like the hair.
• It is usually transmitted via direct contact with organisms from other humans, animals, soil, or fomites.
• The dermatophyte infects the hair and grows towards the stratum corneum. It then affects the hair which becomes brittle and break.^[9]
• It may present with black dots, which is the non-inflammatory form of the disease, causing fracture of the hair. It also may present with intense inflammation which leads to follicular destruction, and may complicate with kerion, an abscess in the scalp, or favus, another inflammatory form in which there is a honeycomb destruction of the hair shaft. Both are severe forms of the disease.^[9]

• Anagen effluvium occurs mostly due to chemotherapy.
• Chemotherapeutic agents cause cessation of the hair growth during anagen phase, due to disruption of the cell cycle caused by the medication.^[9]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Ogechukwu Hannah Nnabude, MD

Scarring alopecia is caused by numerous dermatologic factors, including glabrous skin (non-hairy), and is very difficult to diagnose and manage. Non-scarring alopecia is characterized by the absence of visible inflammation of the skin involved. Endocrine abnormalities such as hypothyroidism and Cushing’s syndrome, medications such as allopurinol, warfarin and steroids, autoimmune diseases such as systemic lupus erythematosus, and infectious diseases such as syphilis and tinea capitis can also cause alopecia.

Severe emotional or physical stress may cause one-half to three-quarters of the hair on the scalp to shed in a type of alopecia called telogen effluvium. Shampooing, combing, or just stroking thee hair can lead to massive amounts of hair being detached from the scalp. This may occur to a noticeable degree weeks or even months after the stressful episode. The rate of hair loss often slows down after about 6 – 8 months.

Triggering factors may include:

• High fever or severe infection ^[1].
• Childbirth ^[2]
• Major surgery, major illness, sudden blood loss ^[2]
• Severe emotional stress ^[2]
• Crash diets, especially those that do not contain enough protein ^[3]
• A number of medications, including retinoids, anticoagulants ^[4], beta-blockers^[5], certain antidepressants ^[6], NSAIDs (including ibuprofen) and anticonvulsants ^[7] and trimethadione. ^[8]

Other possible causes of hair loss, especially if it is in an unusual pattern, include:

• Alopecia areata — bald patches that develop on the scalp, beard, and, possibly, eyebrows. Eyelashes may fall out as well.
• Anemia
• Autoimmune conditions such as systemic lupus erythematosus ^[9]
• Burns
• Certain infectious diseases such as syphilis
• Excessive shampooing and blow-drying
• Hormone changes
• Thyroid diseases ^[10]
• Nervous habits such as continual hair pulling or scalp rubbing
• Radiation therapy
• Tinea capitis (ringworm of the scalp)
• Tumor of the ovary or adrenal glands

Cardiovascular	Vasculitis
Chemical / poisoning	Selenium, thallium
Dermatologic	Acrokeratosis paraneoplastica of Bazex, alopecia cicatrisata, alopecia mucinosa, discoid lupus erythematosus, erythroderma, folliculitis, folliculitis decalvans, keratosis follicularis spinulosa decalvans cum op, perifolliculitis capitis abscedens et suffodiens, pseudopelade of Brocq, tufted folliculitis, Parry-Romberg syndrome
Drug Side Effect	Aclarubicin, actinomycin D, albendazole, amiodarone, antidepressants, Aprepitant, beta blockers [5], Bicalutamide, birth control pills, calcium channel blockers, cidofovir, clomifene, colchicine, combined oral contraceptive pill, Cyclophosphamide, Cytarabine, cytosine arabinoside, cytotoxic therapeutic agents, dabrafenib mesylate, Dacarbazine, Dactinomycin, danazol, daunorubicin, docetaxel, Doxorubicin Hydrochloride, eflornithine, Epirubicin hydrochloride, Epirubicin , Eribulin, etoposide, Febuxostat, Fluorouracil, Floxuridine, fluoxymesterone, gestrinone, heparin, hydroxychloroquine, idarubicin, ifosfamide, interferon alpha, Interferon alfa-2b , irinotecan hydrochloride, Ixabepilone, lamivudine, leflunomide, Leuprolide, Levoleucovorin, Levobunolol hydrochloride, lomustine, Megestrol, melphalan, mesalamine, methotrexate, methylphenidate, minocycline hydrochloride, Mitomycin, mitoxantrone, nabumetone, naltrexone, NSAIDs, Olsalazine, Oxandrolone, oxaliplatin, Oxaprozin, oxcarbazepine, paclitaxel, Palbociclib, pazopanib, Penicillamine, Pertuzumab, pixantrone, pramipexole, proguanil, repaglinide, retinoids, Sargramostim, Sodium aurothiomalate, sorafenib, stanozolol, Sulfasalazine, sulindac, Spironolactone, Temozolomide, teniposide, teriflunomide, testosterone, thiotepa, Tiagabine, topotecan, trabectedin, Tretinoin, tribavirin, valproic acid, vemurafenib, vincristine, Vinblastine, vismodegib
Ear Nose Throat	No underlying causes
Endocrine	Adrenal cortex insufficiency, hormone changes, hyperthyroidism, hypopituitarism, hypothyroidism, thyroid diseases
Environmental	No underlying causes
Gastroenterologic	Canada-Cronkhite syndrome
Genetic	Ablepharon macrostomia syndrome, Bazex-Dupre-Christol syndrome, biotinidase deficiency, BRESHECK syndrome, CARASIL, chondrodysplasia punctata 2, X-linked dominant, dermatopathia pigmentosa reticularis, Dubowitz syndrome, dwarfism-cerebral atrophy-keratosis follicularis syndrome, dystrophia myotonica type 2, epidermolysis bullosa with pyloric atresia, haemochromatosis, Hallermann-Streiff syndrome (HSS), Hay-Wells syndrome, hidrotic ectodermal dysplasia, holocarboxylase synthase deficiency, Hutchinson-Gilford progeria syndrome, hypohidrotic ectodermal dysplasia, autosomal dominant, hypohidrotic ectodermal dysplasia, autosomal recessive type, hypohidrotic ectodermal dysplasia, X-linked, hypotrichosis simplex, incontinentia pigmenti, junctional epidermolysis bullosa, non-Herlitz type, keratitis-ichthyosis-deafness syndrome, autosomal recessive, keratosis follicularis spinulosa decalvans cum ophiasi, lamellar ichthyosis type 2, Marie Unna hereditary hypotrichosis, monilethrix, myositis ossificans progressiva, orofaciodigital syndrome type 1, papular atrichia, proteus syndrome, pseudoprogeria syndrome, Rosselli-Gulienetti syndrome, Schopf-Schulz-Passarge syndrome, total congenital alopecia, vitamin D dependent rickets type 2a, Werner syndrome, Woodhouse-Sakati syndrome
Hematologic	Anemia, sudden blood loss
Iatrogenic	Major surgery, radiotherapy
Infectious Disease	Chagas disease, dissecting cellulitis, lepromatous leprosy, secondary syphilis, severe infection, shingles, tinea capitis, tinea favosa capitis, tuberculoid leprosy
Musculoskeletal / Ortho	Myotonic dystrophy
Neurologic	Parry-Romberg syndrome
Nutritional / Metabolic	Hypervitaminosis A, iron deficiency, vitamin H deficiency, zinc deficiency
Obstetric/Gynecologic	Child birth, pregnancy
Oncologic	Adrenal gland tumor, Cutaneous T-cell lymphoma, Ovarian tumor
Ophthalmologic	No underlying causes
Overdose / Toxicity	No underlying causes
Psychiatric	Severe emotional stress, trichotillomania
Pulmonary	No underlying causes
Renal / Electrolyte	No underlying causes
Rheum / Immune / Allergy	Alopecia areata, atopic dermatitis, autoimmune adrenalitis, lichen planopilaris, lichen planus, psoriasis, systemic lupus erythematosus, Vogt-Koyanagi-Harada syndrome
Sexual	No underlying causes
Trauma	Burns, traction alopecia
Urologic	No underlying causes
Dental	No underlying causes
Miscellaneous	Aging, crash diet, excessive blow-drying, excessive shampooing, high fever, major illness

• Ablepharon macrostomia syndrome
• Aclarubicin
• Acrokeratosis paraneoplastica of Bazex
• Actinomycin D
• Adenal gland tumor
• Adrenal cortex insufficiency
• Aging
• Albendazole
• Alopecia areata
• Alopecia cicatrisata
• Alopecia mucinosa
• Amiodarone
• Anemia
• Antidepressants
• Aprepitant
• Atopic dermatitis
• Autoimmune adrenalitis
• Bazex-Dupre-Christol syndrome
• Beta blockers ^[5]
• Biotinidase deficiency
• Birth control pills
• BRESHECK syndrome
• Burns
• Calcium channel blockers
• Canada-Cronkhite syndrome
• CARASIL
• Chagas disease
• Child birth
• Chondrodysplasia punctata 2, X-linked dominant
• Cidofovir
• Clomifene
• Colchicine
• Combined oral contraceptive pill
• Crash diet
• Cyclophosphamide
• Cutaneous T-cell lymphoma
• Cytarabine
• Cytosine arabinoside
• Cytotoxic therapeutic agents
• Danazol
• Daunorubicin
• Dermatopathia pigmentosa reticularis
• Discoid lupus erythematosus
• Dissecting cellulitis
• Docetaxel
• Doxorubicin Hydrochloride
• Dubowitz syndrome
• Dwarfism-cerebral atrophy-keratosis follicularis syndrome
• dystrophia myotonica type 2
• Eflornithine
• Epidermolysis bullosa with pyloric atresia
• Epirubicin hydrochloride
• Eribulin
• Erythroderma
• Etoposide
• Excessive blow-drying
• Excessive shampooing
• Fluoxymesterone
• Folliculitis
• Folliculitis decalvans
• Gestrinone
• Haemochromatosis
• Hallermann-Streiff syndrome (HSS)
• Hay-Wells syndrome
• Heparin
• Hidrotic ectodermal dysplasia
• High fever
• Holocarboxylase synthase deficiency
• Hormone changes
• Hutchinson-Gilford progeria syndrome
• Hyperthyroidism
• Hypervitaminosis A
• Hypohidrotic ectodermal dysplasia, autosomal dominant
• Hypohidrotic ectodermal dysplasia, autosomal recessive type
• Hypohidrotic ectodermal dysplasia, X-linked
• Hypopituitarism
• Hypothyroidism
• Hypotrichosis simplex
• Idarubicin
• Ifosfamide
• Incontinentia pigmenti
• Interferon alpha
• Irinotecan hydrochloride
• Iron deficiency
• Ixabepilone
• Junctional epidermolysis bullosa, non-Herlitz type
• Keratitis-ichthyosis-deafness syndrome, autosomal recessive
• Keratosis follicularis spinulosa decalvans cum op
• Keratosis follicularis spinulosa decalvans cum ophiasi
• Lamellar ichthyosis type 2
• Leflunomide
• Lepromatous leprosy
• Lichen planopilaris
• Lichen planus
• Major illness
• Major surgery
• Marie Unna hereditary hypotrichosis
• Melphalan
• Methotrexate
• Methylphenidate
• Mitoxantrone
• Monilethrix
• Myositis ossificans progressiva
• Myotonic dystrophy
• NSAIDs
• Orofaciodigital syndrome type 1
• Ovarian tumor
• Oxaliplatin
• Oxaprozin
• Paclitaxel
• Palbociclib
• Papular atrichia
• Parry-Romberg syndrome
• Pazopanib
• Perifolliculitis capitis abscedens et suffodiens
• Pixantrone
• Pregnancy
• Proguanil
• Proteus syndrome
• Pseudopelade of Brocq
• Pseudoprogeria syndrome
• Psoriasis
• Radiotherapy
• Retinoids
• Rosselli-Gulienetti syndrome
• Sargramostim
• Schopf-Schulz-Passarge syndrome
• Secondary syphilis
• Selenium
• Severe emotional stress
• Severe infection
• Shingles
• Sorafenib
• Stanozolol
• Sudden blood loss
• Systemic lupus erythematosus ^[9], dermatomyositis ^[11]
• Temozolomide
• Teniposide
• Teriflunomide
• Testosterone
• Thallium
• Thiotepa
• Thyroid diseases
• Tiagabine
• Tinea capitis
• Tinea favosa capitis
• Topotecan
• Total congenital alopecia
• Trabectedin
• Traction alopecia
• Tretinoin
• Tribavirin
• Trichotillomania
• Tuberculoid leprosy
• Tufted folliculitis
• Valproic acid
• Vasculitis
• Vemurafenib
• Vincristine
• Vismodegib
• Vitamin D dependent rickets type 2a
• Vitamin H deficiency
• Vogt-Koyanagi-Harada syndrome
• Werner syndrome
• Woodhouse-Sakati syndrome
• Zinc deficiency

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Ogechukwu Hannah Nnabude, MD

There is a very wide list of diseases and conditions that can lead to alopecia. Proper history taking and physical examination, along with laboratory, microbiology, and in some cases, imaging studies, are helpful in narrowing down the diagnosis. Alopecia can be caused by many different diseases. Some of the most well known and common causes are: androgenetic alopecia, alopecia areata, telogen effluvium, anagen effluvium, traction alopecia, and trichotillomania. Endocrine disorders such as hypothyroidism, hypoparathyroidism and Cushing’s syndrome as well as malnutrition and medications are also possible causes of alopecia.

Disease/Condition	Clinical presentation	Demographics/History	Diagnosis	Other notes
Androgenetic Alopecia [1] [2] [3]	Male pattern: The frontal hairline is thinner, hair loss occurs at the crown of the scalp, hair recession is seen at the temporal aspects of the scalp; Female pattern: Hair loss occurs at the crown of the scalp, however, the frontal hairline remains preserved.	Androgenetic alopecia is believed to have a worldwide prevalence of about 50,000 per 100,000 men and 15,000 per 100,000 women with post-menopausal women making up the majority.	Diagnosis is mostly clinical and is based on the pattern and absence of other explanations. Unlike in telogen effluvium, hair pull test shows a less than 20% telogen count.	It is the most common cause of hair loss.
Alopecia Areata [1] [4] [5] [6] [3] [7] [8] [9]	It presents with round patches of total hair loss with retained follicular ostia with the beard and scalp being the most frequently affected areas.	Alopecia areata has a prevalence of 100-200 per 100,000 individuals, and a risk of about 2% over an individual’s life. The mean age for diagnosis of alopecia areata is about 32 years in males and 36 years in females.	Close observation reveals the characteristic exclamation mark hairs. A hair pull test followed by trichogram shows telogen and pencil point shafts.	It is associated with several autoimmune diseases including thyroid disease, rheumatoid arthritis, inflammatory bowel disease, and vitiligo.
Telogen Effluvium [10] [11] [3]	There is a massive amount of hair shedding that is triggered by physiologic or psychologic stress.	Although considered to be a relatively common condition, the precise prevalence of telogen effluvium remains unknown. However, it is believed that it is more commonly seen in females than in males	Hair pull test followed by trichogram reveals numerous clubbed-shaped hairs; telogen count must exceed 20% for diagnosis.	It could be an acute self-limiting form triggered by stressors such as crash diets, childbirth, febrile illness, or psychological stress. It may be chronic and present in association with female pattern hair loss.
Anagen Effluvium [1]	There is diffuse hair loss and it is characterized by hair breakage that takes place in the anagen phase.	Associated with exposure to radiation, as in radiotherapy and cancer chemotherapy.	Trichoscopy would reveal the characteristic narrowing, fractured hair shafts with an absence of bulbs.	–
Trichotillomania [12] [13] [14] [15] [16] [1] [17] [18]	Presents with uneven broken hairs in the most frequently selected areas which are the scalp, eyebrows, eyelashes, body hair, facial hair, and pubic hair.	Based on the limited studies that have been done to determine the prevalence of trichotillomania among U.S. university students, Israeli adolescents, and older adults within the same community, the prevalence was shown to be between 500 per 100,000 to 2000 per 100,000. It usually starts around the age of 12–13 years It is more common in males during the childhood years while it is more common in females in the adult years.	Scalp inspection reveals uneven patches of hair loss with broken hairs that remain well attached to the skin. A characteristic finding that distinguishes trichotillomania from alopecia areata is that the affected areas are not totally devoid of hair shafts.	It occurs as a result of a lack of impulse control in which an individual pulls on hair.
Traction Alopecia [19] [1] [20] [21] [20]	Hair loss at regions of the scalp exposed to tension on hair follicles for a prolonged period of time in people who make tight hairstyles.	Traction alopecia is more commonly seen among black populations with females being affected more often than males at a rate of about 31,000-32,000 per 100,000 women compared to about 2,300 per 100,000 men. Traction alopecia is seen in about 18,000 per 100,000 girls between the ages of 5.4 to 14.3 years based on a study of African-American girls.	Mostly a clinical diagnosis based on hair loss at areas of the scalp where tension on the hair is highest.	Early detection and switching to more loose hairstyles may reverse the condition, however, with prolonged tension on the scalp destruction of the hair follicles will occur, causing the condition to become irreversible.
Chronic Cutaneous Lupus Erythematosus [22] [1]	Presents with an area with hair loss that gradually converts into scaly, thickened papules then into poorly-defined, variably-shaped plaques with atrophy, follicular plugging, telangiectasia, and depigmentation.	Black populations tend to have more serious disease. Cutaneous lupus erythematosus is more common in males than in females, with a ratio of about 59.4 per 100,000 versus 1.6 per 100,000.	Histological analysis after a hair pull test reveals a higher anagen count during active disease. Direct immunofluorescence may reveal granular C3 and IgG at the dermo-epidermal boundary which is found in greater than 70% of cases.	–
Tinea Capitis [23] [24] [25] [26] [27] [3]	Presents in diverse ways such as ordinary scaling without any obvious hair loss which is considered to be a seborrheic form, a crusted or pustular form that may be localized or diffuse, a ‘black dot’ type that is characterized by tiny black dots within regions of alopecia, an inflammatory mass called kerion, and a round, bald, scaly patch where the follicular ostia are filled with keratinous debris. A unique feature of tinea capitas is the presence of post-auricular and cervical lymphadenopathy.	It is more common in the pediatric population.	Potassium hydroxide preparation can be added to skin scrapings of affected areas in order to diagnose the condition. [1] Wood’s light can also be used in diagnosis as majority of Microsporum spp will appear bluish-green, occasionally dull yellow (Microsporum gypseum) and dull blue (Trichophyton schoenleinii).	In the U.S., under 5% of cases will show fluorescence. Possible complications of tinea capitas are kerion, an abscess in the scalp, or favus, another inflammatory form in which there is honeycomb destruction of the hair shaft. Both are severe forms of the disease and can cause permanent scarring.

• Adrenocortical insufficiency (primary or secondary)
• Anagen effluvium (anagen=growing hair)
• Cushing’s syndrome
• Diffuse hair thinning due to metabolic causes
• Hyperthyroidism
• Hypoparathyroidism
• Hypothyroidism
• Pituitary insufficiency
• Secondary syphilis
• Sheehan’s syndrome
• Telogen effluvium (telogen=resting hair)
• Temporary hair loss
  • Pregnancy
  • Malnutrition
    • Malabsorption
    • Protein deficiency
    • Tryptophan deficiency
    • Nontropical sprue
    • Vitamin A deficiency
    • Vitamin B deficiency
    • Vitamin D deficiency
    • Rickets
• Thyroiditis
• Trichotillomania

• Amyloidosis
• Chronic disciform lupus erythematosis
• Congenital defects
• Discoid Lupus Erythematosus
• Dissecting cellulitis
• Herpes zoster infection
• Infection
  • Favus
  • Typhoid Fever
  • Leptospirosis
  • Secondary syphilis
• Inflammatory dermatoses
• Lichen planopilaris
• Lymphoma
• Morphea
• Mycosis fungoides
• Neoplasm
• Neurodermatitis
• Physical or chemical agents:
  • ACE inhibitors
  • Allopurinol
  • Androgens
  • Anticoagulants ^[28]
  • Anticonvulsants ^{[29] [30]}
  • Antimycotic agents
  • Arsenic
  • Azathioprine
  • Beta blockers ^[31]
  • Borates
  • Cadmium
  • Chemotherapeutics
  • Chlorambucil
  • Cisplatin
  • Clofibrate
  • Cyclophosphamide
  • Cytarabine
  • Estrogens
  • Fluororacil
  • Gentamycin
  • Gold compounds
  • Heparins
  • Indomethacin
  • Levodopa
  • Linolic acid
  • Mercury and derivatives
  • Methotrexate
  • Niacin
  • Oral contraceptives
  • Propranolol
  • Retinoids
  • Salicylates
  • Selenium
  • Squalenes
  • Steroids
  • Thallium
  • Undecylenic acid
  • Vitamin A overdose
  • Warfarin
• Pseudofolliculitis barbae
• Psoriasis
• Sarcoidosis
• Scleroderma
• Systemic Lupus Erythematosus ^[32], dermatomyositis ^[33]

• Addison’s Disease
• Anemia
• Cancer
• Diabetes Mellitus
• Pneumonia
• Scarlet Fever
• Schmidt’s Syndrome
• Stress
  • Labor
  • Surgery
• Testicular feminization syndrome
• Turner’s Syndrome
• Typhoid fever
• Mechanical effects
  • Traction alopecia
  • Pressure alopecia (alopecia after extended bed rest)
  • Trichotillomania (compulsion to pull out one’s own hair)

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ogechukwu Hannah Nnabude, MD

The epidemiology and demographics of alopecia vary by the type of alopecia as well as the age, race, sex, hygiene, hair care habits, and health status of an individual. For example, in androgenetic alopecia, which has the highest prevalence of all the types of alopecia with about 50,000 per 100,000 men and 15,000 per 100,000 women worldwide, age and sex playing a role shown by the fact that men are more affected than women and post-menopausal women represent the highest proportion among females. In the case of alopecia areata, sex plays no role ^[1] but fair-skinned races are more commonly affected and the prevalence is about 100-200 per 100,000 individuals ^{[1] [2]}.

• Androgenetic alopecia is believed to have a worldwide prevalence of about 50,000 per 100,000 men and 15,000 per 100,000 women with post-menopausal women making up the majority. ^[3]
• Alopecia areata has a prevalence of 100-200 per 100,000 individuals, ^{[1] [2]} and a risk of about 2% over an individual’s life. ^{[1] [2]}. The mean age for diagnosis of alopecia areata is 32 years in males and 36 years in females based on a study of the population of Olmsted County, Minnesota which was done between 1990 to 2009 ^[4].
• Only limited studies on the prevalence of trichotillomania have been performed and these were done among U.S. university students, Israeli adolescents, and older adults within the same community. The prevalence was between 500 per 100,000 to 2000 per 100,000. ^{[5] [6] [7]}
• Traction alopecia is more commonly seen among black populations with females being affected more often than males at a rate of about 31,000-32,000 per 100,000 women compared to about 2,300 per 100,000 men. Traction alopecia was seen in 18,000 per 100,000 girls between the ages of 5.4 to 14.3 years based on a study of African-American girls. An 8-month old girl was the youngest reported case in the study. ^[8]
• Although considered to be a relatively common condition, the precise prevalence of telogen effluvium remains unknown. ^[9]

• The overall incidence of alopecia areata is approximately 20.2 per 100,000 person-years. ^[2]
• About 50,000 per 100,000 Caucasian males have androgenetic alopecia by the time they are 50 years old. This number rises to about 80,000 per 100,000 by the age of 70 years. ^[10]
• The incidence of cutaneous lupus erythematosus is about 4.2 per 100,000 individuals, with the incidence being higher in males. ^[11]

• Tinea capitis is more common among children and adolescents than in adults. ^[12]
• The risk of androgenetic alopecia increases with age. Up to 80,000 per 100,000 Caucasian men over the age of 70 years have androgenetic alopecia compared to 50,000 per 100,000 in Caucasian men who are 50 years.
• Although the link between age and risk of telogen effluvium is currently unclear, it has been observed that elderly women are more susceptible to telogen effluvium after sustaining severe trauma or bleeding, having a high fever, or going through psychological stress. ^[13] Studies have reported the incidence of telogen effluvium in children to be around 2.7%. ^[14]

• In telogen effluvium, women are at higher predisposition than men.
• Alopecia areata can occur in adults and children and distribution is about equal between the sexes ^[1].
• Traction alopecia is seen most commonly in females, the majority of whom are of African-American descent. ^[8]
• Cutaneous lupus erythematosus is more common in males than in females, with a ratio of about 59.4 per 100,000 versus 1.6 per 100,000. ^[11]

• Traction alopecia is seen most commonly in African-American females. This is likely as a result of certain hairstyles that are more predominantly made by African-Americans. ^[8]
• Caucasian males have the highest incidence of androgenetic alopecia. They are followed by Asian males, African-American males, and lastly, Native Americans and Eskimos. ^[10]
• Tinea capitis has a higher incidence among darker races. ^[15]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ogechukwu Hannah Nnabude, MD

Age, medications, sex, family history, and illness are all risk factors for alopecia. Androgenetic alopecia is more common in males and prevalence increases with age. People with a family history of hair loss are at a greater predisposition to developing alopecia compared to individuals who do not have a family history. Psychosocial stress, hormonal imbalance, and illness also increase the risk of alopecia.

• Some of the specific risk factors for alopecia are as follows:
  • Drugs
    • Anticoagulants such as heparin, warfarin ^[1]
    • Anticonvulsants such as [[valproic acid ^[2] and trimethadione. ^[3]
    • Antidepressants such as fluvoxamine and bupropion ^[4]
    • Beta-blockers such as nadolol ^[5]
  • Medical illness
    • Connective tissue disorders: SLE ^[6], dermatomyositis ^[7]
    • Hyper/hypothyroidism ^[8]
    • Nutritional deficiencies: iron, zinc, protein ^[9]
  • Poor hygiene which can predispose to tinea capitis ^[10]
  • Physiological and psychological stress which are associated with telogen effluvium ^[11]
  • Mechanical stressors such as tight braids which is associated with traction alopecia ^[12]
  • Chemicals and hair care products ^[13]
  • Male sex which is at increased risk of androgenetic alopecia ^[14]
  • Age of an individual is also a risk factor. For example, tinea capitis is more common in pediatric populations while the prevalence of androgenetic alopecia increases with age ^[15]
  • Family history of alopecia increases an individual’s predisposition to developing alopecia. ^[16]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ogechukwu Hannah Nnabude, MD

The severity and progression of alopecia are dependent on the cause. Patients with alopecia are at increased risk of psychosocial complications such as anxiety and depression. In addition, these patients need to be evaluated for other medical conditions. Outcomes vary with the type of alopecia.

The progression of alopecia depends on the type of alopecia an individual has. In some cases, it is irreversible as in alopecia mucinosa, alopecia neoplastica, and long-standing cases of tinea capitis. In other cases, it is reversible such as in anagen effluvium. In males with androgenetic alopecia, the hairline regression occurs mostly at the temporal areas bilaterally and vertex balding is also seen. In females with androgenetic alopecia, the frontal hairline is largely unaffected while in other areas, there is hair thinning ^{[1] [2]}. In telogen effluvium, it could take as much as 6 months for hair to begin growing again, and it often takes more time for the hair growth to be perceptible to the patient.

• In general, people with alopecia are at a greater risk of developing socio-psychological problems such as anxiety and depression as a result of hair loss.
• Other than progressive disease, complications of alopecia areata are inherent to the treatment of choice. However, a study revealed that alopecia areata may be associated with a greater risk of development of insulin resistance. ^[3]
• Tinea capitis can lead to irreversible hair loss if untreated, ridicule, and psychosocial impairment in children.
• If alopecia is secondary to another disease such as hypothyroidism, syphilis, Cushing syndrome, malnutrition or systemic lupus erythematosus, complications would be the same as the underlying disease.

• In telogen effluvium, recovery is usually good.
• Androgenetic alopecia is a progressive disease that tends to worsen with time. ^[4]
• In the majority of anagen effluvium cases, cessation of chemotherapy often leads to hair regrowth. However, it could take up as much as a few years to achieve a full recovery of hair. Less commonly, full recovery does not occur.
• In alopecia areata, about 34–50% of patients will recover spontaneously in 1 year or less with majority of them having recurring episodes of alopecia. Progression alopecia totalis or alopecia universalis occurs in 14–25% of patients and of those patients, complete recovery is seen in less than 10% of cases. The degree of hair loss and age of the patient at initial diagnosis may play a role in the outcome of the disease, with onset in childhood being associated with a poorer prognosis compared to a later age. ^[5] Patients with a positive family history of alopecia areata, presence of accompanying autoimmune disease and personal history of atopic diseases may also indicate poorer outcomes. ^[6]
• The prognosis of tinea capitis is excellent when patients are treated early. However, if left without treatment, patients may develop an abscess known as a kerion. This could lead to permanent hair loss.