The hair follicle is a complex structure which produces the hair fiber consisting of a cortex, medulla, and cuticle (Figures 19-1 and 19-2). Hair follicles demonstrate the unusual ability to completely regenerate themselves. Hair grows, falls out, and then regrows. In the normal human scalp, up to 90% of hair follicles are in the growth phase called anagen, 1% in the transition phase catagen, and up to 10% in telogen or the loss phase. The anagen phase lasts approximately 3 years, catagen 2 to 3 weeks, and telogen 3 months.¹

Hair disorders are broadly grouped into the following categories:

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  The nonscarring alopecias associated with hair cycle abnormalities.

  
  
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  The scarring or cicatricial alopecias associated with inflammation and injury to the stem cell region of the hair follicle.

Hair loss is common and can occur with a variety of medical conditions. The workup of a patient with a hair disorder starts with a thorough history and physical examination as outlined in Tables 19-1 and 19-2, respectively.

The nonscarring hair disorders associated with abnormalities in the hair cycle include three very common hair disorders:

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  Androgenetic alopecia (AGA, with or without androgen excess)

  
  
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  Alopecia areata (AA)

  
  
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  Telogen effluvium (TE)

Androgentic alopecia occurs in genetically susceptible individuals in response to the conversion of testosterone to dihydrotestosterone (DHT) by 5-α reductase at the level of the hair follicle resulting in miniaturization and a shortened anagen phase of the hair cycle. AGA may be associated with hirsutism in women who have excess androgen production from the adrenal glands or ovaries or only in the end organ, the hair follicle.

Alopecia areata is an immune-mediated disease that targets the bulb region of anagen hair follicles resulting in a shortened anagen cycle. Telogen effluvium results when more follicles than usual transition to the telogen or loss phase of the hair cycle in response to a trigger. Two less commonly seen disorders of the hair cycle include hypertrichosis and generalized atrichia (absence of hair), a condition caused by a mutation in the hairless gene that results in normal hair follicle development but abnormal cycling in catagen. Hypertrichosis is defined as elongation of hair in nonandrogen-dependent areas and is commonly seen in patients treated with topical minoxidil or taking cyclosporine.

The scarring alopecias are characterized by lymphocytic, neutrophilic, or mixed inflammatory infiltrates that involve the bulge or stem cell region of the hair follicle, leading to fibrosis and permanent hair loss (Figure 19-1). The scarring alopecias may be primary or secondary as in the case of a burn or radiation injury, but in either case permanent loss of hair follicles occurs.

Hair loss may also occur with inherited or acquired structural hair abnormalities. When present, hair fibers break easily resulting in the chief complaint of “hair loss.”

Examination of the patient presenting with a hair disorder and the chief complaint of “hair loss” should focus on assessing the presence or absence of the following:

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  Vellus, indeterminate and terminal fibers ideally using scoring systems such as the Ludwig or Hamilton Norwood classification systems, or the Severity of AlopeciaScoring Tool (SALT score).^2–4 Vellus fibers are short, fine, light-colored, and barely noticeable. Terminal fibers are long, have a wider diameter, and are pigmented. Indeterminate fibers are somewhere in between vellus and terminal fibers.

  
  
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  Scale, erythema, folliculitis, scarring, or atrophy in the affected area.

  
  
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  Eyebrow, eyelash, or body hair loss.

  
  
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  Nail abnormalities, which if present can be a clue to an underlying medical problem associated with the chief complaint of hair loss.

  
  
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  Findings of androgen excess.

The following disorders are the most common causes of nonscarring alopecia.

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  Androgenetic alopecia: Male and female pattern alopecia

  
  
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  Alopecia areata

  
  
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  Telogen effluvium

Introduction

Androgenetic alopecia (AGA) in males is commonly called male pattern baldness and is the most common type of hair loss in men, affecting approximately 50% of Caucasian men by age 50.^5–7 AGA is characterized by the progressive miniaturization of terminal hairs or shortening of the anagen phase and transition to “baby” vellus fibers on the scalp in a characteristic distribution frequently classified using the Hamilton–Norwood Scale (Figure 19-3A). AGA is considered to be an androgen-dependent trait and the mode of inheritance polygenic with variable penetrance. Balding usually starts in the late teens or early twenties. However, approximately 10% of males will bald in a pattern that resembles female AGA.

Androgenetic alopecia in females is also commonly called female pattern baldness and can be classified using the Ludwig classification scale (Figure 19-3B). Classic AGA in women is also polygenic and androgen dependent with full expression usually by the mid-twenties. This pattern of alopecia may also occur in the perimenopausal and menopausal periods and may be a presenting feature of ovarian or adrenal gland abnormalities. A clinically useful classification system for women with pattern thinning is as follows:

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  Early onset

  
  
  
  
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    With androgen excess

    
    
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    Without androgen excess

  
  
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  Late onset

  
  
  
  
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    With androgen excess

    
    
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    Without androgen excess

Clinical Presentation

History

Patients usually report increased hair shedding and a noticeable decrease in hair density following one of the patterns described previously.

Physical Examination

Males may present with balding initially in the bitemporal regions, followed by the vertex region and when extensive, the two areas are no longer separated as demonstrated in Type VI Hamilton balding (Figure 19-3A). Males may also bald with the thinning process occurring from the anterior scalp to the vertex. Females present with thinning in the frontal scalp region accompanied by an increase in the part width and retention of the frontal hairline. Some patients will also exhibit a “Christmas tree” pattern in the anterior scalp region.

The Hamilton Norwood or Ludwig classification systems can be used to document the extent of the pattern alopecia, respectively (Figure 19-4A and B). The physical examination should focus on the areas noted in Table 19-2.

Laboratory Findings

Usually no laboratory studies are required in the evaluation and management of male AGA. Women who present with pattern alopecia should be evaluated for associated medical conditions or nutritional deficiencies. A summary of recommended laboratory tests is presented in Table 19-3.

Diagnosis and Differential Diagnosis

The diagnosis of male AGA is usually straightforward. The diagnosis of female AGA /female pattern alopecia may be slightly more complicated as pattern thinning is common in women with metabolic or nutritional disorders.

The differential diagnosis includes diffuse alopecia areata and telogen effluvium both of which will be discussed next. A scalp biopsy may be needed if there is difficulty making a diagnosis.

Management

Medical, surgical, cosmetic, and device treatments can be used to treat AGA. Medical treatments for male AGA include 5% topical minoxidil (Rogaine) in a foam or solution and finasteride (Propecia), an oral inhibitor of dihydrotestosterone (DHT) production. One ml of topical minoxidil should be applied twice daily to the affected area. Clinical response can vary with some men attaining significant hair regrowth while others experience only a reduction in hair loss. Treatment needs to be continued to maintain the result.