On pathology, distorted follicular anatomy is found, once again supporting the need for a dermatopathologist to read any scalp/hair biopsy. Treatment is a combination of patient realization of the habit, behavior modification, and therapy.
Additional use of pharmacologic agents should be decided on a case-by-case basis. If pharmacotherapy is indicated, clomipramine (Anafranil) is the first-line agent.3 Selective serotonin reuptake inhibitors have had limited success.
Alopecia areata is the most common nonscaring pattern of hair loss that presents as well-circumscribed areas of alopecia. In this hair-specific autoimmune disease, T-lymphocytes interact with follicular antigens. The clinician can differentiate alopecia areata from tinea capitis by the lack of scalp flaking. A simple fungal culture can confirm the diagnosis.
In an adult, a scalp tinea capitis infection is unlikely unless the patient works in a high-risk environment (e.g., an elementary school with a known outbreak) or is immunosuppressed. One out of five patients with alopecia areata report having a family member with the same condition.
Classically, alopecia areata presents as round or oval patches of nonscarred hair loss. Short exclamation-point hairs are often seen at the edges of the patch of hair loss. Other patterns of loss include ophiasis (a band of loss around the temporal and occipital scalp), alopecia totalis (loss of all scalp hair), and alopecia universalis (loss of all scalp and body hair).
Patients with alopecia areata may also experience such nail changes as ridges, pitting, brittleness, onycholysis, and koilonychia. Approximately 40% of patients with alopecia areata will have allergic rhinitis, atopic dermatitis, or asthma.4
Other associated diseases include autoimmune thyroid disease (e.g., Hashimoto’s thyroiditis, Graves’ disease), vitiligo, inflammatory bowel disease, HLA associations, and autoimmune polyendocrinopathy syndrome type 1. Type 1 diabetes is more prevalent in the relatives of persons with alopecia areata.
Typical treatment of alopecia areata involves a combination of intralesional corticosteroids (a concentration of 5 mg/mL of triamcinolone acetonide injected every four to eight weeks is usually sufficient), topical steroids, topical minoxidil, and oral biotin.
Bimatoprost ophthalmic solution (Latisse, Lumigan) is an option for eyelash loss and is used off-label for eyebrow regrowth. Treatment options for ophiasis, alopecia totalis, and alopecia universalis are extremely limited. Alopecia areata is most often chronic and relapsing.
Underlying Skin Conditions
Physical examination will typically reveal such underlying correctable skin conditions as seborrheic dermatitis or psoriasis. Both conditions may have the symptoms of itching and flaking and will impact such other body areas as the face, nasolabial folds, eyebrows, and ears.
Seborrheic dermatitis is more diffuse than psoriasis and can have a greasy yellow appearance, particularly on the face. Psoriasis is characterized by sharply marginated plaques with scale. Frequently, there is a family history of psoriasis. Plaques are often symmetric and are typically found on the elbows, knees, and groin.
Topical steroids are first-line agents for both conditions. Such steroid-sparing agents as ketoconazole shampoo (Nizoral) or cream (Ketozole, Nizoral) are effective for seborrheic dermatitis. For scalp psoriasis, consider OTC coal-tar shampoo and topical calcipotriene (Dovonex, Sorilux).
Underlying Endocrine Abnormalities
Hyperandrogenemia and thyroid dysfunction are the two most common underlying endocrine abnormalities that lead to hair loss in adult females. Patient history, other complaints, review of systems, and a physical examination all contribute to making this diagnosis. Laboratory workup confirms the diagnosis.
Thyroid dysfunction can be evaluated with TSH and T4 tests. Symptoms of hypothyroidism can include fatigue, weight gain, decreased appetite, cold intolerance, dry skin, muscle pain, joint pain, weakness in the extremities, depression, emotional lability, mental impairment, forgetfulness, impaired memory, inability to concentrate, constipation, paresthesias, nerve entrapment syndromes, blurred vision, decreased hearing, fullness in the throat, and hair loss.5 Typically, the hair loss associated with thyroid dysfunction is diffuse overall thinning with no scalp changes. The remaining hair can be dry, coarse, and lusterless.
Hyperandrogenic disorders include polycystic ovary syndrome (PCOS), adrenal or ovarian tumors, congenital adrenal hyperplasia, hyperprolactinemia, acromegaly, and Cushing syndrome. Signs of PCOS, the most common condition associated with hyperandrogenism, can include irregular menstrual cycle, amenorrhoea, impaired fertility, difficulty getting pregnant, miscarriage, seborrhea, excessive body hair, acne, and obesity.6
The pattern of hair loss seen with hyperandrogenism is typically diffuse and mimics that of androgenic alopecia. Treating hair loss in hyperandrogenic states or thyroid dysfunction requires addressing the underlying abnormality.
Cicatricial alopecia, also referred to as scarring alopecia, often results in permanent destruction of the hair follicle. In such cases, a scalp biopsy is almost always necessary to identify the form of cicatricial alopecia and to determine whether there is an underlying treatable condition, such as cutaneous lupus erythematosus (CLE).
This article originally appeared on Clinical Advisor