Case 1 History
The patient is a 24-year-old female with a sudden-onset circumscribed oval area of alopecia on the temporal scalp. There is no associated erythema or scaling. Close examination reveals small hairs with proximal tapering at the edge of the area of involvement.
Microscopic Findings
Sections show a normal number of follicles that are uniformly miniaturized ( Fig. 9.1 ). There is an increased number of telogen and catagen follicles (∼25%) together with a peribulbar lymphocytic infiltrate.
Diagnosis
Alopecia Areata
Clinical Presentation
Alopecia areata (AA) is characterized by episodes of patchy circumscribed hair loss. The clinical course is unpredictable, and patches may regrow or progress to broader areas of involvement. Stress is a common self-reported clinical cofactor. Loss of all scalp hair is known as alopecia totalis, and loss of all scalp and body hair is known as alopecia universalis. AA may also present in diffuse fashion. In diffuse AA, uniform diffuse thinning is a common presentation.
Histopathology
Histopathologic changes of AA vary depending on chronicity. In active early disease, there is an inflammatory infiltrate centered on the follicular bulbs, which creates a pattern that has been likened to a swarm of bees (in this visual metaphor, the follicular bulb represents the hive). The infiltrate is largely composed of lymphocytes, but occasional eosinophils and plasma cells can also be present. Rarely, the infiltrate of AA is granulomatous. The infiltrate may damage the bulb, which results in pigment incontinence and trichomalacia (hair casts). As the disease progresses, the lymphocytic infiltrate converts the anagen hairs to catagen and telogen, and persistent disease results in miniaturized hairs. Sudden miniaturization results in the clinical appearance of so-called exclamation point hairs, which are typified by marked proximal thinning.
Differential Diagnosis
The differential diagnosis includes other common nonscarring alopecias ( Table 9.1 ). Key differences are highlighted in the table using our four key metrics. A more detailed description of these entities is also provided in Case 2.
| Alopecia Areata | Androgenetic Alopecia | Trichotillosis | Telogen Effluvium | |
|---|---|---|---|---|
| Follicular density | Mild reduction | Mild reduction | Normal but distorted | Normal |
| Size of follicles | Uniformly small | Small with prominence of sebaceous glands | Some small follicles | Some small follicles |
| Catagen and telogen percentage (normal, ∼15% or ∼9:1 anagen:catagen/telogen) | >25%; can be as high as 100% in active disease | Slight increase in telogen count (20%) | >25% | >25% |
| Inflammation | Peribulbar | Nonspecific perifollicular | Nonspecific perifollicular due to follicular damage | Hypoinflammatory or noninflammatory |
Case 2 History
A 48-year-old male presents with hair thinning on the vertex. There is also hair loss involving the bilateral temporal areas.
Microscopic Findings
Biopsy sections show a marked increase in small vellus-sized follicles (follicular miniaturization) that are largely in anagen phase ( Fig. 9.2 ). An increase in telogen phase follicles may be present. Fibrous tracts are apparent because of reduced follicular density. Sebaceous glands are prominent. A mild superficial perifollicular lymphohistiocytic infiltrate may be present as a nonspecific finding.
Diagnosis
Androgenetic Alopecia
Clinical Presentation
Androgenetic alopecia presents in males after puberty as bitemporal loss of hair with balding of the vertex scalp. In females, the onset is typically later than males, and there is diffuse thinning over the crown, with a stable frontal hairline. In both sexes, fine small hairs gradually replace terminal hairs.
Histopathology
Sections show an increased proportion of vellus-sized hairs with a resultant decrease in terminal hairs. As the hairs miniaturize, the bulbs retract to the dermis and may leave behind residual follicular stellae (also called fibrous streamers or tracts) in the subcutaneous tissue and lower dermis. There are increased telogen follicles, and a mild perifollicular lymphocytic infiltrate may be present superficially. Of note, sebaceous glands are intact and often prominent, and fibrosis is minimal or absent except in late protracted disease.
Differential Diagnosis
The differential diagnosis includes AA, telogen effluvium, and trichotillosis. Follicular miniaturization may also be seen in AA but is typically less common telogen effluvium or trichotillosis. AA shows characteristic peribulbar lymphocytic infiltrate, and trichotillosis shows frequent trichomalacia (see Table 9.1 ).
Telogen Effluvium
Clinical Presentation
The presentation of acute telogen effluvium can affect a patient at any age and presents as abrupt-onset hair shedding for 1 to 4 months over the entire scalp, with complete return to normal in most cases within 1 year. Telogen effluvium is often precipitated by stress (childbirth, surgery, infection, illness, nutritional deficiency, or psychological factors). Chronic telogen effluvium shows a longer course, with increased diffuse hair shedding for 6 months or longer, and can persist for years in some instances. A chronic effluvium may be induced by a medication.
Histopathology
Sections show normal or near-normal follicular density, and reductions in follicular size are attributable to the presence of telogen follicles ( Fig. 9.3 ). The number of telogen follicles tends to be larger in an acute effluvium in comparison with chronic involvement. Inflammation tends to be minimal.
