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Anagen Effluvium

  • Author: Robert A Schwartz, MD, MPH; Chief Editor: Dirk M Elston, MD  more...
Updated: Jun 21, 2016


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 re-enters 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. 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; the catagen phase lasts only a few days; and the telogen phase lasts 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. This process is different from chronic telogen effluvium, postulated to be a result of a reduction in the variance of anagen duration.[1]



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.[2]

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.[3] 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.



Anagen effluvium is entirely reversible, with hair regrowth typically occurring after a delay of 3-6 months.[2] Upon the cessation of drug therapy, the follicle resumes its normal activity within a few weeks. Mitotic inhibition apparently stops the reproduction of matrix cells, but it does not permanently destroy the hair. In some cases, hair regrows despite continued or maintenance therapy. On occasion, the color and texture of the hair that regrows after chemotherapy-induced alopecia is different from those of the original hair.


Patient Education

Drug-induced alopecia can be psychologically devastating to a patient. Patients have even refused possibly palliative or life-saving treatments because they could not accept the temporary or prolonged baldness.

Patients must be warned of the potential for hair loss when they undergo treatment with any of the medications responsible for anagen effluvium (see Causes).

Patients should also be reassured that the hair loss is temporary. Normal hair growth resumes a few weeks after the termination of treatment, although the color or texture of the regrowing hair may differ from those of the original hair.

Contributor Information and Disclosures

Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, Rutgers New Jersey Medical School; Visiting Professor, Rutgers University School of Public Affairs and Administration

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, New York Academy of Medicine, American Academy of Dermatology, American College of Physicians, Sigma Xi

Disclosure: Nothing to disclose.


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

Pere Gascon, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, New York Academy of Medicine, New York Academy of Sciences, Sigma Xi

Disclosure: Nothing to disclose.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

David F Butler, MD is a member of the following medical societies: American Medical Association, Alpha Omega Alpha, Association of Military Dermatologists, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Phi Beta Kappa

Disclosure: Nothing to disclose.

Rosalie Elenitsas, MD Herman Beerman Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System

Rosalie Elenitsas, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society of Dermatopathology, Pennsylvania Academy of Dermatology

Disclosure: Received royalty from Lippincott Williams Wilkins for textbook editor.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.


Günter Burg, MD Professor and Chairman Emeritus, Department of Dermatology, University of Zürich School of Medicine; Delegate of The Foundation for Modern Teaching and Learning in Medicine Faculty of Medicine, University of Zürich, Switzerland

Günter Burg, MD is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, International Society for Dermatologic Surgery, North American Clinical Dermatologic Society, and Pacific Dermatologic Association

Disclosure: Nothing to disclose.

Bryan D Seiff, MD Staff Physician, Department of Ophthalmology, NY Presbyterian Hospital-Cornell

Bryan D Seiff, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

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