Anagen Effluvium
No Results
No Results
processing….
Normal human hairs can be classified according to the three 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.
Chemotherapeutics used to treat cancer are the most common causes of anagen effluvium. [4, 5, 6, 7] A study of 384 patients with chemotherapy reactions showed the most common overwhelmingly was anagen effluvium (78.6%). [8] The most severe alopecia is caused by doxorubicin, the nitrosoureas, and cyclophosphamide. Other causative agents include bleomycin, dactinomycin, daunorubicin, fluorouracil, methotrexate, and azathioprine. [9] Anagen effluvium was also linked with a Ganoderma lucidum–induced aplastic crisis.
Other medications that can cause anagen effluvium include bismuth, levodopa, colchicine, cyclosporine, and, possibly, strontium ranelate and pegylated interferon alfa-2a/ribavirin therapy. [10, 11, 12] Anagen effluvium with permanent alopecia has been described in patients treated with taxanes. [13]
Exposure to chemicals such as thallium, boron, and arsenic can precipitate anagen effluvium. [14]
Causes of anagen arrest also include radiation therapy, endocrine diseases, alopecia areata, cicatrizing disease, and trauma or pressure. [15]
Pemphigus vulgaris is reported to be a cause of anagen effluvium.
Acute vesiculobullous hand dermatitis and anagen effluvium can occur in Ganoderma lucidum –induced aplastic crisis. [16]
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.
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.
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.
Gilmore S, Sinclair R. Chronic telogen effluvium is due to a reduction in the variance of anagen duration. Australas J Dermatol. 2010 Aug. 51(3):163-7. [Medline].
Trueb RM. Chemotherapy-induced alopecia. Semin Cutan Med Surg. 2009 Mar. 28(1):11-4. [Medline].
Delmonte S, Semino MT, Parodi A, Rebora A. Normal anagen effluvium: a sign of pemphigus vulgaris. Br J Dermatol. 2000 Jun. 142(6):1244-5. [Medline].
Bronner AK, Hood AF. Cutaneous complications of chemotherapeutic agents. J Am Acad Dermatol. 1983 Nov. 9(5):645-63. [Medline].
Tosi A, Misciali C, Piraccini BM, Peluso AM, Bardazzi F. Drug-induced hair loss and hair growth. Incidence, management and avoidance. Drug Saf. 1994 Apr. 10(4):310-7. [Medline].
Tosti A, Pazzaglia M. Drug reactions affecting hair: diagnosis. Dermatol Clin. 2007 Apr. 25(2):223-31. [Medline].
Cardoza-Torres MA, Liy-Wong C, Welsh O, Gómez-Flores M, Ocampo-Candiani J, González-Llano O, et al. Skin Manifestations Associated with Chemotherapy in Children with Hematologic Malignancies. Pediatr Dermatol. 2011 Nov 2. [Medline].
Biswal SG, Mehta RD. Cutaneous Adverse Reactions of Chemotherapy in Cancer Patients: A Clinicoepidemiological Study. Indian J Dermatol. 2018 Jan-Feb. 63 (1):41-46. [Medline].
Sonthalia S, Daulatabad D. Azathioprine-associated anagen effluvium. Indian J Dermatol Venereol Leprol. 2016 May-Jun. 82 (3):322-4. [Medline].
Lee YY, Yang CH, Chen CH, Hwang JS. Alopecia associated with strontium ranelate use in a 62-year-old woman. Osteoporos Int. 2013 Mar. 24(3):1127-9. [Medline].
Turker K, Tas B, Ozkaya M, Tas E, Caglar A, Tetikkurt US. Dystrophic-Anagen Effluvium Occurring During Pegylated Interferon-a-2a/Ribavirin Therapy. Hepat Mon. 2015 Mar. 15(3):e24804. [Medline]. [Full Text].
Combalia A, Baliu-Piqué C, Fortea A, Ferrando J. Anagen Effluvium Following Acute Colchicine Poisoning. Int J Trichology. 2016 Oct-Dec. 8 (4):171-172. [Medline].
Fonia A, Cota C, Setterfield JF, Goldberg LJ, Fenton DA, Stefanato CM. Permanent alopecia in patients with breast cancer after taxane chemotherapy and adjuvant hormonal therapy: Clinicopathologic findings in a cohort of 10 patients. J Am Acad Dermatol. 2017 May. 76 (5):948-957. [Medline].
Campbell C, Bahrami S, Owen C. Anagen Effluvium Caused by Thallium Poisoning. JAMA Dermatol. 2016 Jun 1. 152 (6):724-6. [Medline].
Irune E, Bast F, Williams G, Kirkpatrick N. Recovery of Transplanted Eyebrow From Radiation-Induced Anagen Effluvium. J Cutan Med Surg. 2015 Mar 16. [Medline].
Choi MJ, Kim DY, Kim JS, Kim H, Cho SB. Acute vesiculobullous hand dermatitis and anagen effluvium in Ganoderma lucidum-induced aplastic crisis. Ann Hematol. 2013 Mar 10. [Medline].
Patel M, Harrison S, Sinclair R. Drugs and hair loss. Dermatol Clin. 2013 Jan. 31(1):67-73. [Medline].
Kanti V, Nuwayhid R, Lindner J, Hillmann K, Stroux A, Bangemann N, et al. Analysis of quantitative changes in hair growth during treatment with chemotherapy or tamoxifen in patients with breast cancer: a cohort study. Br J Dermatol. 2014 Mar. 170(3):643-50. [Medline].
Tallon B, Blanchard E, Goldberg LJ. Permanent chemotherapy-induced alopecia: Case report and review of the literature. J Am Acad Dermatol. 2010 May 12. [Medline].
Miteva M, Misciali C, Fanti PA, Vincenzi C, Romanelli P, Tosti A. Permanent Alopecia After Systemic Chemotherapy: A Clinicopathological Study of 10 Cases. Am J Dermatopathol. 2011 Mar 11. [Medline].
Quercetani R, Rebora AE, Fedi MC, Carelli G, Mei S, Chelli A, et al. Patients with profuse hair shedding may reveal anagen hair dystrophy: a diagnostic clue of alopecia areata incognita. J Eur Acad Dermatol Venereol. 2011 Jul. 25(7):808-10. [Medline].
Cassano N, Amerio P, D’Ovidio R, Vena GA. Hair disorders associated with autoimmune connective tissue diseases. G Ital Dermatol Venereol. 2014 Oct. 149(5):555-65. [Medline].
van Beek N, Bodo E, Kromminga A, et al. Thyroid hormones directly alter human hair follicle functions: anagen prolongation and stimulation of both hair matrix keratinocyte proliferation and hair pigmentation. J Clin Endocrinol Metab. 2008 Nov. 93(11):4381-8. [Medline].
Trovato MJ, Schwartz RA, Janniger CK. Tinea capitis: current concepts in clinical practice. Cutis. 2006 Feb. 77(2):93-9. [Medline].
Olszewska M, Warszawik O, Rakowska A, Slowinska M, Rudnicka L. [Methods of hair loss evaluation in patients with endocrine disorders]. Endokrynol Pol. 2011. 62 Suppl 1:29-34. [Medline].
Uce Özkol H, Çalka Ö, Akdeniz N. Is TrichoScan a new diagnostic method for diffuse hair loss?. Turk J Med Sci. 2014. 44(3):432-8. [Medline].
Duvic M, Lemak NA, Valero V, Hymes SR, et al. A randomized trial of minoxidil in chemotherapy-induced alopecia. J Am Acad Dermatol. 1996 Jul. 35(1):74-8. [Medline].
Merial-Kieny C, Nocera T, Mery S. [Medical corrective make-up in post- chemotherapy]. Ann Dermatol Venereol. 2008 Jan. Spec No 1:25-8. [Medline].
Bleiker TO, Nicolaou N, Traulsen J, Hutchinson PE. ‘Atrophic telogen effluvium’ from cytotoxic drugs and a randomized controlled trial to investigate the possible protective effect of pretreatment with a topical vitamin D analogue in humans. Br J Dermatol. 2005 Jul. 153 (1):103-12. [Medline].
Jimenez JJ, Roberts SM, Mejia J, et al. Prevention of chemotherapy-induced alopecia in rodent models. Cell Stress Chaperones. 2008 Spring. 13(1):31-8. [Medline]. [Full Text].
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.
David F Butler, MD Former 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: Alpha Omega Alpha, American Academy of Dermatology, American Society for MOHS Surgery, Association of Military Dermatologists, 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.
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.
Anagen Effluvium
Research & References of Anagen Effluvium|A&C Accounting And Tax Services
Source
0 Comments