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Loose Anagen Syndrome Workup

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

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The normal scalp cycle is divided into 3 phases: the active growth anagen phase, followed by a brief catagen phase, and finally the resting telogen phase. Typically, 85-95% of hairs are in the anagen phase, which lasts about 3 years. Less than 1% of hairs are in catagen, the transitional phase, which lasts from a few days to weeks. The telogen phase, which accounts for 5-15% of hairs and lasts about 3 months, ends when the new anagen hair emerges from the follicle. A telogen count of 20% is considered the upper limit of normal. In healthy individuals, removing hair with light traction yields few hairs, almost all of which are in the telogen phase. These hairs are readily identified by their dry, nonpigmented, clublike roots and the absence of an inner and outer root sheath.

The diagnosis of loose anagen syndrome is confirmed by firmly pulling locks of hair (the gentle hair pull) and by microscopically examining those extracted hairs. A gentle hair pull normally yields only 0-2 hairs per pull, but, in loose anagen syndrome, the number extracted may be much higher. Patients with loose anagen syndrome feel no discomfort as hairs are extracted. In normal individuals, only telogen hairs are extracted during a gentle hair pull. The presence of anagen hairs on a gentle pull test, as found in loose anagen syndrome, is pathologic. Easily extractable hairs may be seen in active lesions of lupus erythematosus or lichen planopilaris. They differ from the hairs of loose anagen syndrome in that they lack the characteristic "rumpled sock" cuticle. Forcible plucking with a hemostat in patients with loose anagen syndrome also results in easy and painless hair extraction. The hair is not fragile, and plucking does not cause breaks within the hair shaft.

Under light microscopy,[19] the epilated hairs are predominantly in anagen phase. The proximal end demonstrates a distorted hair bulb that is often bent at an acute angle to the hair shaft. The hair bulb may also appear long and tapered or twisted in relation to the long axis of the hair shaft. The hairs lack an inner and outer root sheath, and the cuticle has a characteristic rippled or ruffled, sawtooth, baggy-stocking appearance (rumpled sock appearance) (see following image).

Microscopic view of easily plucked hair demonstrat Microscopic view of easily plucked hair demonstrating a distorted anagen bulb lacking inner and outer root sheaths, and a ruffled, sawtooth, baggy-stocking appearance of the cuticle (original magnification X100).

On scanning electron microscopy, loose anagen hairs may demonstrate abnormal ridging and fluting of the hair shaft.

Trichograms (forcible hair plucks) reveal an abnormally large percentage of anagen hairs lacking inner and outer sheaths. Few or no telogen hairs are present.

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Histologic Findings

Although a scalp biopsy is not indicated to diagnose loose anagen syndrome, a few investigators have reported histologic findings. However, the histologic features of loose anagen syndrome have not yet been critically studied.

Cleft formations between hair shafts and inner root sheaths and fragmentation of the inner root sheaths may be visualized. Regressive changes of the inner root sheath, including homogenization and crumbly degeneration, may be seen, particularly on transversely cut biopsy specimens. Loose anagen hairs may demonstrate abnormal configurations on cross-section rather than the typical round or oval shape seen in normal hair shafts.

Anagen follicles showing premature keratinization in the cells of Henle and Huxley layers have been reported in hairs from patients with loose anagen syndrome. Although keratinization occurs at more distal areas of the follicle in normal anagen hairs, it may be seen at the lower bulbar level in loose anagen hairs.

Notably, no inflammatory infiltrates are present in loose anagen syndrome.

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Contributor Information and Disclosures
Author

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.

Coauthor(s)

Supriya Goyal, MD Consulting Dermatologist

Supriya Goyal, MD is a member of the following medical societies: Alpha Omega Alpha

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.

Paul Krusinski, MD Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine

Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

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.

Additional Contributors

Leonard Sperling, MD Chair, Professor, Department of Dermatology, Uniformed Services University of the Health Sciences

Leonard Sperling, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

References
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  17. Price VH. What looks like alopecia areata is not always alopecia areata. J Investig Dermatol Symp Proc. 2013 Dec. 16(1):S63-4. [Medline].

  18. Zmolikova M, Puchmajerova A, Hecht P, Lebl J, Trkova M, Krepelova A. Coarctation of the aorta in Noonan-like syndrome with loose anagen hair. Am J Med Genet A. 2014 May. 164A(5):1218-21. [Medline].

  19. Smith VV, Anderson G, Malone M, Sebire NJ. Light microscopic examination of scalp hair samples as an aid in the diagnosis of paediatric disorders: retrospective review of more than 300 cases from a single centre. J Clin Pathol. 2005 Dec. 58(12):1294-8. [Medline].

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Thinning, dull, lackluster blonde hair with matting over the occipital region.
Microscopic view of easily plucked hair demonstrating a distorted anagen bulb lacking inner and outer root sheaths, and a ruffled, sawtooth, baggy-stocking appearance of the cuticle (original magnification X100).
 
 
 
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