9 Nonandrogenetic Hair Loss

Kristen Lo Sicco, Lorena Avila, Eric L. Eisenberg, and Jerry Shapiro

Summary

This chapter encompasses the breadth of knowledge that is necessary to accurately identify and treat various types of scarring and nonscarring hair loss other than androgenetic alopecia. The importance of a thorough patient history and physical exam is highlighted in addition to adjunctive tools such as trichoscopy and lab evaluation. Hair transplantation is an option for many types of hair loss; however, caution must be taken when encountering cicatricial alopecia. Here the authors review the utility of hair restoration surgery for various nonandrogenetic alopecias, including potential risks when used to treat certain cicatricial alopecia.

A thorough history and detailed physical exam (PE), in addition to various serum laboratory investigations, will help accurately identify the cause of alopecia for the majority of patients (Box 9.1). A thorough history can aid the clinician in narrowing the potential cause(s) of alopecia. All hair loss patients should be questioned on the timing of their hair loss; gradual hair thinning over a period of years suggests androgenetic hair loss. In women with gradual thinning, it is important to inquire regarding menstruation, acne, and hirsutism to rule out polycystic ovary syndrome (PCOS). Sudden diffuse shedding after an emotional or a physical stressor suggests telogen effluvium (TE) and, less commonly, the diffuse type of alopecia areata (AA). Associated symptoms such as erythema, edema, crusting, pustule, and blister formation are important questions as these changes frequently occur in scarring disorders. In contrast, trichodynia—a complaint of scalp sensitivity or irritation—is nonspecific and may be associated with either scarring or nonscarring alopecia. Scalp burning, pain, and itch may be more commonly associated with various cicatricial alopecias, including lichen planopilaris (LPP), discoid lupus, central centrifugal cicatricial alopecia (CCCA), and dermatomyositis, and neutrophilic cicatricial alopecias including folliculitis decalvans, dissecting cellulitis (DC), and folliculitis keloidalis. Additionally, patients should be asked about general hair care and styling preferences that may contribute to alopecia, including regular use of blow dryers, hair straighteners, and tight braids.

Medical problems and medication use are a very important part of the history and often help toward determination of the cause of alopecia. The patient’s medical and surgical history over the 6 months prior to alopecia onset is important to elicit, as various intrinsic and extrinsic triggers of hair loss exist. Comorbid autoimmune disease, acute illnesses (including those with high fever), and dietary restrictions (including crash diets, rapid weight loss, and eating disorders) are often present in association with various alopecias. Recent surgeries, using either general anesthesia or local anesthesia for scalp-specific procedures, are potential triggers of nonscarring (TE) and cicatricial (pustular dermatosis of the scalp) alopecias. It is also important to be aware hormonal alterations that are potential triggers of TE, including pregnancy status or initiation and termination of birth control pill use.

Numerous medications are culprits of telogen, and less commonly anagen, and effluvium (Table 9.1).³ Fortunately, most medication-induced alopecias are nonscarring. However, various chemotherapeutic and biologic drugs have been associated with scarring hair loss.

Table 9.1 Drugs associated with hair loss

On PE, one should note the distribution and severity of hair loss, which will provide clues to the underlying etiology. For example, localized hair loss is usually seen in AA, whereas diffuse hair loss is more commonly associated with TE, metabolic disorders such as PCOS and the diffuse type of AA. Inspect areas of alopecia for the presence of broken-off, blunted hairs that can be seen in trichotillomania, and “exclamation point” hairs (short hairs whose proximal end is tapered and the distal end is broader) that occur in AA. Scarring is recognized by the absence of follicular ostia. In ambiguous cases, the use of a standard microscope, dermatoscope, or videomicroscope may help distinguish scarring from nonscarring alopecias without the aid of skin biopsies.

A hair pull test will aid in the assessment of current hair shedding. It is important to ask the patient if their hair was washed on the day of clinical evaluation as freshly washed hair often results in a falsely negative hair pull exam. The ability to pull more than five or six hairs when grasping approximately 60 hairs denotes a positive hair pull test. The hair tug test is an additional clinical examination that helps identify hair fiber fragility. The mid hair shaft is held with one hand and the distal hair shaft with the other, pulling away from the scalp with the distally placed hand. A positive hair tug test is a sign of hair breakage.^1,2

Serum laboratory examinations are often helpful unmask potential triggers of nonscarring alopecia. A thorough history and PE can help guide the clinician when choosing the appropriate serum tests. Testing for iron, zinc, and vitamin D deficiencies may be most beneficial for TE patients. Thyroid function tests and thyroid antibodies are useful for both AA and TE patients as thyroid dysfunction, autoimmune related or not, may be seen with these types of hair loss. Free and total testosterone and DHEAS (dehydroepiandrosterone sulfate) are important exams when evaluating for PCOS or other disorders of androgen excess such as an androgen-secreting neoplasm. Antinuclear antibody by indirect fluorescent antibody (to evaluate both the titer and pattern) and complement levels are necessary when a connective tissue disease such as lupus erythematosus is suspected (Table 9.2).

Table 9.2 Select laboratory tests in the investigation of hair loss

Though user dependent, dermoscopy of the scalp and hair, termed “trichoscopy,” is a noninvasive, rapid technique to aid in the diagnosis of various alopecias. Multiple structures may be visualized using trichoscopy, including hair shafts, follicular ostia, perifollicular epidermis, and blood vessels (Table 9.3).

Table 9.3 Trichoscopy: Structures and patterns

In the presence of a scarring alopecia, accurate diagnosis is usually established by obtaining a 4-mm punch biopsy at the advancing inflammatory border. Scarred regions should be avoided when selecting the biopsy location, as these areas are likely to show nonspecific changes. The biopsy should be performed in the direction of hair growth and penetrate into subcutaneous fat, yielding the optimal specimen for both vertical and horizontal sectioning. Vertical sectioning is important for examining features such as inflammatory infiltrates, scarring, and the presence of infectious organisms. Horizontal sectioning is important for determining the ratio of hair follicle stages (anagen vs. telogen) in addition to the presence of follicular miniaturization (terminal vs. vellus hairs).

9.3 Causes and Treatment of Hair Loss

The categories of hair loss are broadly classified as either cicatricial or noncicatricial. Cicatricial alopecia is caused by a heterogeneous group of conditions, most of which have scarring and atrophy as a common end point (Table 9.4 and Table 9.5). Clinically, this scarring is recognized by the absence of follicular ostia on shiny, atrophic skin. In contrast, noncicatricial alopecias demonstrate follicular ostia preservation on skin with normal reflectivity and thickness (Box 9.2, Table 9.6 and Table 9.7).

Table 9.4 Common causes of cicatricial alopecia

Table 9.5 Uncommon causes of cicatricial alopecia^{11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28}

Table 9.6 Common causes of noncicatricial alopecia

Table 9.7 Uncommon causes of noncicatricial alopecia^29–,33

9.3.1 Nonscarring

Metabolic Abnormalities

Vitamin and Mineral Deficiencies

Nutritional deficiencies play a controversial but potentially important role in various hair disorders.

In a mouse model, high doses of oral zinc have been shown to inhibit hair growth; yet, the same treatment can delay (but not prevent) the onset of chemotherapy-induced alopecia.9 Conditions such as acrodermatitis enteropathica, which results in severe zinc deficiency and is characterized by alopecia among other symptoms, are proof that zinc plays an important role for hair. In a recent study by Cheung et al, zinc deficiency was present in only 9.6% of their study population.⁹ Therefore, the clinician should consider zinc supplementation only if a deficiency exists. See Table 9.8 for zinc dosing suggestions.

Table 9.8 Laboratory evaluation and supplementation suggestions for hair loss (TE) patients with vitamin and mineral deficiencies

Iron deficiency: Some authors believe iron deficiency may be related to multiple nonscarring alopecias, including TE as well as AA and androgenetic alopecia. While causality has not been established, nor has iron supplementation been proven to impact hair growth,^10,11 many hair experts treat iron deficiency in the absence of anemia. When investigating iron deficiency with or without anemia, it is important to order a complete blood count (CBC) and ferritin as well as an iron panel as ferritin is an acute-phase reactant and may be elevated in the setting of infection, inflammation, or malignancy. It is important to investigate the underlying cause of iron-deficiency anemia, especially in the older patient population as gastrointestinal blood loss is an important cause of iron-deficiency anemia.

Thyroid Disease

Thyroid disease should also be considered in the evaluation of women with diffuse thinning and TE. Although data regarding the effect of thyroxine supplementation on TE is lacking, thyroid hormone has been proven to prolong the anagen phase.12 Given diffuse scalp involvement, the donor area may also be compromised, making hair transplantation difficult.

Polycystic Ovary Syndrome

Polycystic ovary syndrome is a disorder resulting in metabolic and reproductive abnormalities and affects up to 8% of women of child-bearing potential. It is characterized by the triad of (1) ultrasound evidence of polycystic ovaries, (2) chronic anovulation, and (3) hyperandrogenism. Additionally, other causes of hyperandrogenism and anovulation (i.e., androgen-secreting tumors, Cushing syndrome, and congenital adrenal hyperplasia) must be ruled out. Women with PCOS typically have irregular menses and increased androgen levels which lead to acne, hirsutism, and potentially androgenetic alopecia. In addition to decreasing the percentage of anagen hairs, androgens stimulate the conversion of scalp terminal hair follicles to vellus hair. An initial laboratory evaluation should include serum total and free testosterone, SHBG (sex hormone–binding globulin), DHEAS, prolactin, and a pelvic/transvaginal ultrasound. Female pattern androgenetic alopecia is the most common pattern of hair loss among women with PCOS and although less common, hair loss in a male pattern is also possible. Medical therapy such as spironolactone, finasteride, or cyproterone acetate, which either block androgen receptor binding or may inhibit 5-α-reductase activity, may result in improvement of alopecia after 6 to 12 months of therapy. If results are still unsatisfactory, hair transplantation to cosmetically significant regions may be helpful.^13,14

Effluviums

Telogen Effluvium

Telogen effluvium is one of the most common types of alopecia among presenting hair patients. Fortunately, it is a nonscarring alopecia and although it typically resolves by 6 months, chronic TE lasting over 6 months also occurs. Patients present with diffuse hair loss (usually <50% of scalp hair is shed) that typically begins around 3 months after a triggering event. The central part may be widened, with bitemporal thinning as well. Unlike androgenetic alopecia, TE is characterized by a positive hair pull test.

Often very alarmed by the excess hair shedding, patients may bring plastic bags of their shed hair (“hair bag sign”). The timing and causes of hair loss may differ depending on the type of TE. There are six types of TE: (1) immediate anagen release, (2) delayed anagen release, (3) immediate telogen release, (4) delayed telogen release, (5) short anagen phase, and (6) chronic TE (see Table 9.9).

Table 9.9 Telogen effluvium (TE)

As TE has numerous potential triggers, including medications, physiologic stressors, as well as nutritional, endocrinologic, and autoimmune disorders, a complete history and PE in addition to serum evaluation (see Table 9.10) are necessary to elucidate an underlying cause.

Table 9.10 Laboratory evaluation for patients with telogen effluvium

TE may unmask an underlying androgenetic alopecia, in which case hair loss can be progressive. Counseling is a vital component of therapy for TE patients. In the majority of cases, the natural history of TE includes 3 to 6 months of shedding before cessation and regrowth is noted at 3 to 6 months after trigger removal. However, significant regrowth may take 12 to 18 months. In addition to trigger removal, minoxidil is often employed given its effect on prolonging the anagen phase. Hair transplantation ideally should not be performed prior to resolution, as it is difficult to properly identify the regions of greatest cosmetic significance and areas of the donor with dormant follicles may be discarded as alopecic tissue. Hair transplantation may be necessary after the TE episode has resolved, especially in those with underlying androgenetic alopecia not responding to medical therapy.¹⁵

Anagen Effluvium

The anagen growth phase of hair is characterized by mitotic and metabolic activity. Any event, most often chemotherapy or radiotherapy to the head and neck, may cause the abrupt cessation or impairment of mitotic or metabolic hair follicle activity and subsequent proximal hair shaft weakening and breakage (either within the hair canal or complete failure of hair shaft formation). Given their effect against DNA replication, the most common chemotherapeutics to cause anagen effluvium include (1) antimetabolites, (2) alkylating agents, and (3) mitotic inhibitors. Less often, nutritional deficiency, immunobullous disease, AA, connective tissue disease, secondary syphilis, and toxin/medication exposures may cause anagen effluvium (see Table 9.11).

Table 9.11 Causes of anagen effluvium

Anagen effluvium is typically completely reversible, as the insult is only on the proliferating cells and the bulge stem cells (which are quiescent) are able to reinitiate follicle growth. Hair regrowth is apparent within 1 to 3 months of removal of the insult. Patients have a higher risk of permanent hair loss in the setting of bone marrow transplantation, Busulfan, and epidermal growth factor receptor inhibitor therapy and may ultimately require hair transplantation (assuming adequate donor hair is present).16

Loose Anagen Hair Syndrome

Loose anagen hair syndrome (LAHS) is a female-predominant genetic disorder likely resulting from premature and abnormal keratinization of the hair inner root sheath. This results in loose anagen hair which is easily and painlessly pulled from the scalp. LAHS primary affects light-haired children and less commonly adults. The scalp hair is typically short and dull and irregular alopecic patches occur as a result of easily plucked anagen hairs. On microscopic hair shaft examination, the loose anagen hair (which should comprise >50% of hairs on trichogram) lacks a sheath and has a characteristic “wrinkled sock” appearance. Most patients do not require surgical intervention as LAHS typically resolves spontaneously by adolescence or adulthood.

Autoimmune Disorders

Alopecia Areata

One of the most common hair disorders encountered in dermatology, AA, is an autoimmune, nonscarring form of hair loss. It typically presents with well-demarcated, coin-sized patches of noncicatricial alopecia scattered on an otherwise normal-appearing scalp, or in other hair-bearing regions (Fig. 9.1). Rarely, it presents with a large band-like patch of alopecia extending from bilateral temporal scalp to the occipital scalp (ophiasis pattern; Fig. 9.2), or with hair loss over the frontal and crown regions (sisaipho pattern). The diffuse form of alopecia may mimic TE; however, it is easily distinguished by the abrupt depigmentation of scalp hair, termed the “white overnight” phenomenon. In severe cases, hair loss affects the entire scalp (alopecia totalis), or the entire body (alopecia universalis).^17,18,19

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