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Telogen Effluvium
Quratulanne H. Jan, MD
Arham K. Barakzai, MD
image BASICS
Diffuse hair loss or hair thinning; most often an acute self-limited process
Telogen effluvium (TE) is a transient condition in which there is a premature conversion of a significant proportion of anagen (growth phase) hairs into telogen (resting phase) hairs resulting in increased shedding of these resting hair follicles and the clinical appearance of moderate to severe hair thinning.
  • Five proposed types of TE (1)
    • Immediate anagen release: a highly common form, lasting 3 to 4 weeks, in which follicles meant to remain in anagen phase enter telogen prematurely due to a signal, including high fever, drug induced, or stress
    • Delayed anagen release: occurs most often postpartum, in which a large group of hair follicles that have remained in the anagen phase for an extended period all together enter the telogen phase, resulting in hair loss
    • Short anagen: a somewhat speculative type, in which at least 50% of the hair follicles have an idiopathic shortening of the anagen phase, resulting in a corresponding doubling of the follicles in the telogen phase
    • Immediate telogen release: Normal resting club hairs remain within the hair follicle until an unknown signal causes their release, initiating the anagen stage to begin. In this type, the resting club hairs are prematurely released, ending the telogen phase abruptly and causing diffuse shedding.
    • Delayed telogen release: in this type, the presence of increased visible light, whether it be a seasonal or environmental change, is thought to end a prolonged telogen phase and initiate the anagen phase, resulting in diffuse shedding of hair follicles.
Second most common cause of alopecia
  • The hair cycle consists of two predominant phases. The anagen (growth phase) and the telogen (resting phase), lasting ˜ 3 years and 3 months, respectively. On the scalp, ˜ 10-15% of hairs are in the telogen phase normally. Due to the presence of some types of external/internal stress, there may be an increase in the percentage of telogen hairs. As new anagen hairs emerge, these telogen hair follicles are forced out. The preceding event usually occurs 2 to 3 months prior to the appearance of hair loss.
  • It is hypothesized that substance P plays a key role in the pathogenesis of TE through various mechanisms (2,3). Studies have been conducted on human hair follicles in vitro and mice hair follicles in vivo, which support this theory.
  • Role of substance P includes the following (4):
    • Upregulation of substance P receptor, NK1, at the gene and protein level, leading to premature catagen development and hair growth inhibition
    • Upregulation of nerve growth factor (NGF) and subsequently its hair apoptosis-producing receptor, p75NTR
    • Downregulation of hair growth-promoting receptor, TrkA
    • Upregulation of major histocompatibility class (MHC) I and &bgr;2-microglobulin resulting in loss of hair follicle immune-privilege
    • Increase in tumor necrosis factor-&agr; release by mast cells resulting in hair keratinocyte apoptosis
  • Decreased cortisol levels in chronic stress states may also enhance the effects of substance P (5).
  • Infection
  • Trauma
  • Major surgery
  • Thyroid disorder
  • Febrile illness
  • Malignancy
  • Allergic contact dermatitis (6)
  • Iron deficiency anemia (7,8)
  • Excess vitamin A (1)
  • Protein-calorie restriction (1)
  • End-stage liver or renal disease
  • Hormonal changes (including pregnancy, delivery, and estrogen-containing medications) (1)
  • Chronic stress
  • Drug induced (&bgr;-blockers, anticonvulsants, antidepressants, anticoagulants, retinoids, ACE-inhibitors, etc.) (1)
  • Immunizations
  • Decreased density of hair on the scalp, most commonly involving the crown
  • In rare cases of chronic TE, there is hair loss of eyebrows and pubic region.
  • May be able to demonstrate diffuse shedding of hair when running fingers through scalp
  • Shed hairs are telogen hairs, which have a small bulb of unpigmented or pigmented keratin on the root end.
  • May affect nail growth, resulting in the appearance of Beau lines, which are transverse grooves on the nails of the hands and feet
  • Hypothyroidism
  • Hyperthyroidism
  • Alopecia areata (diffuse pattern)
  • Androgenetic alopecia
  • Drug-induced alopecia
  • Systemic lupus erythematosus
  • Secondary syphilis
  • Trichotillomania

Most often, TE is a clinical diagnosis of exclusion. Blood work may be collected primarily to rule out other possible causes of hair loss and/or to identify a possible cause for TE.
Initial Tests (lab, imaging)
If indicated:
  • CBC, ferritin
  • TSH
  • Creatinine
  • Consider hepatic enzymes.
  • Consider RPR/VDRL.
Diagnostic Procedures/Other
  • Hair pull test: unreliable; performed by gently pulling 25 to 30 hairs from various sites on a patient's scalp. Each pull should elicit <5 normal club hairs; increased quantity may indicate possibility of TE (1).
  • Hair clip test: Performed by cutting 25 to 30 hairs from the patient's scalp and examining them under a microscope. A negative test (not indicative of TE) will demonstrate <10% of hair shafts of small diameter. A positive test will demonstrate >10% of hair shafts of small diameter (1).
  • Trichogram: ˜ 50 hairs are plucked from the patient's scalp, and the number of telogen and anagen hairs present are counted. In TE, there will be >10% of hairs in the telogen phase.
  • Scalp biopsy: rarely needed; it is recommended that several 4-mm punch biopsies be obtained, all horizontally embedded to determine an accurate anagen-to-telogen ratio. Histologically, catagen-totelogen hairs have numerous apoptotic cells in the outer sheath epithelium. > 12-15% of hair follicles in telogen phase is consistent with TE (1,9).
TE is a benign, self-limited process. Identify and correct underlying cause. Patient should be reassured that full hair growth will occur in ˜ 6 months to 1 year. No treatment is required.
  • Minoxidil stimulates hair regrowth via arteriolar smooth muscle vasodilation; not effective in TE
  • Oral zinc therapy: New medication that may have benefits for patients with TE through various mechanisms all essential to hair growth, including the following (10)[C]:
    • Cofactor for enzymes needed in nucleic acid and protein synthesis and cell division
    • Inhibition of the catagen phase by blocking certain enzymes involved in hair apoptosis
    • Involved in hair growth regulation via hedgehog signaling
Nigella Sativa (black cumin) essential oil has also been studied and may be beneficial (11).
1. Headington JT. Telogen effluvium. New concepts and review. Arch Dermatol. 1993;129(3):356-563.
2. Grover C, Khurana A. Telogen effluvium. Indian J Dermatol Venereol Leprol. 2013;79(5):591-603.
3. Hadshiew IM, Foitzik K, Arck PC, et al. Burden of hair loss: stress and the underestimated psychosocial impact of telogen effluvium and androgenetic alopecia. J Invest Dermatol. 2004;123(3):455-457.
4. Peters EMJ, Liotiri S, Bodó E, et al. Probing the effects of stress mediators on the human hair follicle: substance P holds central position. Am J Pathol. 2007;171(6):1872-1886.
5. Katayama I, Bae SJ, Hamasaki Y, et al. Stress response, tachykinin, and cutaneous inflammation. J Investig Dermatol Symp Proc. 2001;6(1):81-86.
6. Tosti A, Piraccini BM, van Neste DJ. Telogen effluvium after allergic contact dermatitis of the scalp. Arch Dermatol. 2001;137(2):187-190.
7. Trost LB, Bergfeld WF, Calogeras E. The diagnosis and treatment of iron deficiency and its potential relationship to hair loss. J Am Acad Dermatol. 2006;54(5):824-844.
8. Karadag AS, Ertugrel DT, Tutal E, et al. The role of anemia and vitamin D levels in acute and chronic telogen effluvium. Turk J Med Sci. 2011;41(5):827-833.
9. Sinclair R, Jolley D, Mallari R, et al. The reliability of horizontally sectioned scalp biopsies in the diagnosis of chronic diffuse telogen hair loss in women. J Am Acad Dermatol. 2004;51(2): 189-199.
10. Karashima T, Tsuruta D, Hamada T, et al. Oral zinc therapy for zinc deficiency-related telogen effluvium. Dermatol Ther. 2012;25(2):210-213.
11. Rossi A, Priolo L, Iorio A, et al. Evaluation of a therapeutic alternative for telogen effluvium: a pilot study. J Cosmet Dermatol Sci Appl. 2013;3(3-A):9-16.
Additional Reading
Mounsey AL, Reed SW. Diagnosing and treating hair loss. Am Fam Physician. 2009;80(4):356-362.
L65.0 Telogen effluvium
Clinical Pearls
  • TE is a self-limited form of nonscarring alopecia; most often acute.
  • TE is due to a premature conversion of a significant proportion of anagen (growth phase) hairs into telogen (resting phase) hairs, resulting in increased shedding of these resting hair follicles and the clinical appearance of moderate to severe hair thinning and loss when growth resumes.
  • There are many potential causes of TE, both emotional and physiologic. Often it is hard to determine the etiology, but eliminating the stressor often is the key to resolving TE and stimulating new hair growth.
  • No treatment is needed. Patient should be reassured that complete hair regrowth will occur in 6 months to 1 year.