Abstract
Kligman first coined the term telogen effluvium (TE) in 1961 to describe the state of increased shedding of otherwise normal telogen hairs. TE may be primary or secondary to a wide variety of potential triggers including febrile illness, drugs, thyroid disorders, and child birth. The diagnosis of secondary TE can be made by identifying known triggers from the history in the 3–4 months preceding the onset of increased hair shedding and by investigating to exclude endocrine, nutritional, or auto immune aetiologies. Scalp biopsy to identify the earliest stages of androgenetic alopecia may be required in some cases. Primary TE may be acute or chronic. In acute TE, the shedding resolves within 3–6 months and the hair density recovers completely. In chronic TE, the shedding can continue with minor fluctuations in severity for decades. In this review, possible causative factors, pathogenesis, clinical presentations and treatment options are discussed.
Highlights
Telogen effluvium is a delayed consequence of a shift in the hair cycle phase away from anagen.Termination of anagen results in the onset of catagen and subsequently telogen
Hair cycle is regulated by signalling molecules of the Wnt correct family, Fibroblast Growth Factor (FGF), transforming growth factor β (TGF-β), and Hedgehog pathways
Short anagen syndrome is due to an idiopathic shortening of the duration of anagen and can cause cause a persistent telogen hair shedding in some individuals
Summary
Telogen effluvium is a delayed consequence of a shift in the hair cycle phase away from anagen. Termination of anagen results in the onset of catagen and subsequently telogen. Telogen hair bulbs may remain anchored in the hair follicle until the onset of the anagen phase at the end of telogen or be shed prematurely. While some degree of telogen hair shedding is normal, excessive loss of telogen hairs will manifest as increased hair shedding or diffuse loss of hair volume [1]. Increased hair shedding can be scored using validated visual analogue scales [2]. Important differential diagnoses include female pattern hair loss, anagen effluvium, loose anagen hair syndrome, diffuse alopecia areata, congenital atrichia, congenital hypotrichosis, and hair shaft fragility [1,3]
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