eMedicine Specialties > Dermatology > Diseases of the Adnexa

Anagen Effluvium

Author: Robert A Schwartz, MD, MPH, Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Coauthor(s): Bryan D Seiff, MD, Staff Physician, Department of Ophthalmology, NY Presbyterian Hospital-Cornell; Pere Gascon, MD, PhD, Professor and Director, Division of Medical Oncology, Institute of Hematology and Medical Oncology, IDIBAPS, University of Barcelona Faculty of Medicine, Spain
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Updated: Sep 2, 2009

Introduction

Background

Normal human hairs can be classified according to the 3 phases of their growth cycle: anagen, catagen, and telogen. Anagen hairs are in a growing phase, during which the matrix cells of the hair follicle undergo vigorous mitotic activity. These hairs have long, indented roots covered with intact inner and outer root sheaths, and they are fully pigmented.

Toward the end of the anagen phase, the amount of pigment decreases at the base of the follicle, which expands to form a keratinized club. Then, the hair enters the catagen phase, a transitional phase in which mitotic activity decreases. The follicle separates from the dermal papilla and the capillary plexus and moves upward within its connective tissue sheath toward the epidermis. The resulting telogen hairs, or club hairs, are in a resting phase. These hairs have short, club-shaped roots that anchor them in the follicle. They lack root sheaths and show depigmentation of the proximal part of the shaft.

The hairs continue in this resting state until the follicle spontaneously reenters the anagen phase. At this point, the club hairs are forced out by growing hairs underneath them, and the cycle begins anew. The cycle is not synchronous throughout the scalp; patches of hair may be synchronized. The length of each phase of the cycle, as well as the length of the entire cycle, varies with the site and the age of the patient. In the scalp, for example, the average length of the anagen phase is 1000 days; that of the catagen phase, only a few days; and that of the telogen phase, 100 days. Of the 100,000 hairs on the average scalp, 10-15% are in the catagen or telogen phase at any time. Most hair follicles are in the anagen stage at any given time.

Pathophysiology

Hair loss can be classified according to the stage of the hairs shed. Telogen effluvium is defined as the early and excessive loss of normal club hairs from normal resting follicles in the scalp. This hair loss usually results from trauma to the normal hair as a result of a stressor such as parturition, surgery, or fever that causes an abnormally large percentage of hairs to move into the catagen and telogen phases. When anagen restarts 2-4 months later, the club hairs are pushed out and lost, causing a temporary diffuse thinning of the scalp hair.

Anagen effluvium occurs after any insult to the hair follicle that impairs its mitotic or metabolic activity. The hair loss is usually the result of an exposure to chemotherapeutic agents such as antimetabolites, alkylating agents, and mitotic inhibitors that are used to treat cancer, although it is not the only type of chemotherapy induced – hair loss in these patients.¹
 
The inhibition or arrest of cell division in the hair matrix can lead to a narrow, weakened segment of the hair shaft that is susceptible to fracture with minimal trauma. It can also result in complete failure of hair formation. The hair bulb itself may be damaged, and the hairs may separate at the bulb and fall out. Only actively growing anagen follicles are subject to these processes. This form of alopecia is more common and severe with combination chemotherapy than with the use of a single drug, and the severity is generally dose dependent. Anagen effluvium also occurs in persons with alopecia areata as the result of the inflammatory insult to the matrix.

The characteristic finding in anagen effluvium is the tapered fracture of the hair shafts. The hair shaft narrows as a result of damage to the matrix. Eventually, the shaft fractures at the site of narrowing.

Anagen effluvium is an uncommon symptom of pemphigus vulgaris.² The hair follicle is a preferential target for pemphigus autoantibodies because the desmosomal proteins are overexpressed in the follicular epithelium. The ensuing intercellular cleavage causes the anagen hairs in lesional and perilesional areas to fall out.

Clinical

History

• Patients present with diffuse hair loss after an exposure to drugs or toxic chemicals. Chemotherapeutic agents are most commonly responsible for hair loss. The most severe hair loss occurs in association with doxorubicin, the nitrosoureas, and cyclophosphamide. Hair loss usually begins 7-14 days after a single pulse of chemotherapy. The hair loss is clinically most apparent after 1-2 months.
• The patient's full dermatologic, systemic, and family histories should be obtained to rule out other causes of hair loss, including malnutrition, iron deficiency, endocrine and metabolic disorders, collagen disease, infections (eg, syphilis), and widespread skin disease.
• Anagen effluvium may be an uncommon symptom in a patient with pemphigus vulgaris.
• A variety of medications may cause hair loss, stimulate hair growth, or induce changes in hair shape and color. Drug-induced hair loss is usually a consequence of a toxic effect of the drug on the hair matrix. Although many drugs have been occasionally described to produce hair loss, the relationship between drug intake and hair loss has only been proven for a few agents. The type of hair loss (ie, telogen effluvium, anagen effluvium, or both) depends on the medication, its dosage, and patient susceptibility.

Physical

• Anagen effluvium is a nonscarring alopecia that leaves the follicular ostia intact.
• Most hair follicles are in the anagen stage at any given time; therefore, anagen alopecia affects a large percentage of the scalp.
• Some chemotherapeutic agents can also induce telogen effluvium.
• The combination of telogen effluvium and anagen effluvium can result in complete baldness.
• The diffuse alopecia of anagen effluvium can be distinguished from androgenetic alopecia, which is characterized by frontotemporal thinning followed by hair loss in the crown.
• The hair and scalp should be thoroughly inspected to rule out local disease.
  • Any erythema, scale, pustules, bogginess, sinus tract formation, or obliteration of the follicular openings should be noted.
  • Any of these findings may indicate another cause of the alopecia.

Causes

Chemotherapeutics used to treat cancer are the most common causes of anagen effluvium.^3,4,5

• The most severe alopecia is caused by doxorubicin, the nitrosoureas, and cyclophosphamide. Other causative agents include bleomycin, dactinomycin, daunorubicin, fluorouracil, and methotrexate.
• Other medications that can cause anagen effluvium include bismuth, levodopa, colchicine, and cyclosporine.
• Exposure to chemicals such as thallium, boron, and arsenic can precipitate anagen effluvium.
• Causes of anagen arrest also include radiation therapy, endocrine diseases, alopecia areata, cicatrizing disease, and trauma or pressure.
• Pemphigus vulgaris is reported to be a cause of anagen effluvium.

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