Pathologic Dynamics of Human Hair Loss

Kligman, Albert M.

doi:10.1001/archderm.1961.01580080005001

Cited by 378 publications

(208 citation statements)

References 19 publications

Supporting

Mentioning

190

Contrasting

Unclassified

Order By: Relevance

“…Increased hair shedding (or telogen effluvium) is thought to occur due to post-partum hormonal changes (Lynfield 1960;Schiff and Kern 1963;Gizlenti and Ekmekci 2013) or stress (Kligman 1961). Our findings that Prl promotes HF quiescence by directly regulating bulge SC activity support a previously hypothesized role for Prl during post-partum hair shedding (Randall 2007).…”

Section: Prl and Hair Cycling In Humanssupporting

confidence: 80%

Calcineurin/Nfatc1 signaling links skin stem cell quiescence to hormonal signaling during pregnancy and lactation

et al. 2014

View full text Add to dashboard Cite

In most tissues, the prevailing view is that stem cell (SC) niches are generated by signals from within the nearby tissue environment. Here, we define genetic changes altered in hair follicle (HF) SCs in mice treated with a potent SC activator, cyclosporine A (CSA), which inhibits the phosphatase calcineurin (CN) and the activity of the transcription factor nuclear factor of activated T cells c1 (Nfatc1). We show that CN/Nfatc1 regulates expression of prolactin receptor (Prlr) and that canonical activation of Prlr and its downstream signaling via Jak/Stat5 drives quiescence of HF SCs during pregnancy and lactation, when serum prolactin (Prl) levels are highly elevated. Using Prl injections and genetic/pharmacological loss-of-function experiments in mice, we show that Prl signaling stalls follicular SC activation through its activity in the skin epithelium. Our findings define a unique CN-Nfatc1-PrlrStat5 molecular circuitry that promotes persistent SC quiescence in the skin.

show abstract

Section: Prl and Hair Cycling In Humanssupporting

confidence: 80%

Calcineurin/Nfatc1 signaling links skin stem cell quiescence to hormonal signaling during pregnancy and lactation

et al. 2014

View full text Add to dashboard Cite

show abstract

“…Telogen effluvium was first described as excessive scalp hair shedding disorder commencing 2-3 months after a triggering event such as high fever, surgical trauma, sudden starvation, haemorrhage, or initiation of a new drug treatment [9]. In about 33% of cases of telogen effluvium, no trigger could be identified [8].…”

Section: Acute Telogen Effluviummentioning

confidence: 99%

Telogen Effluvium

Liyanage

Sinclair

2016

Cosmetics

View full text Add to dashboard Cite

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.

show abstract

“…The longest hairs are produced by follicles with long growing periods, e.g. in the scalp anagen may last for over 3 years (Kligman, 1959;1961) …”

Section: The Hair Growth Cyclementioning

confidence: 99%