Hair Growth and Alopecia in Hypothyroidism

Freinkel, Ruth K.; Freinkel, Norbert

doi:10.1001/archderm.1972.01620120037007

Cited by 96 publications

(23 citation statements)

References 9 publications

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“…Thyroid disorders, for example, lead to changes in hair quality and growth, androgen excess causes sebaceous hyperplasia and alopecia, and adrenocorticotropic hormone (ACTH) overproduction leads to hyperpigmentation and hypertrichosis. (3)(4)(5) In addition, in monilethrix, a keratinrelated hair disorder characterized by beading and fragility of the hair shaft, there is a substantial, although temporary, improvement in hair growth during pregnancy (Fig. 1).…”

Section: Introductionmentioning

confidence: 99%

Endocrine controls of keratin expression

et al. 2009

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Keratins are a family of intermediate filaments that serve various crucial roles in skin physiology. For mammalian skin to function properly, and to produce epidermal and hair keratins that are optimally adapted for their environment, it is critical that keratin gene and protein expression are stringently controlled. Given that the skin is not only targeted by multiple hormones, but also constitutes a veritable peripheral endocrine organ, it is not surprizing that intracutaneous keratin expression is underlined by tight endocrine controls. These controls encompass thyroid hormones, steroid hormones such as glucocorticoids (GCs), retinoic acid (RA) and vitamin D, and several neuroendocrine mediators. Here, we review why a better understanding of the endocrine controls of keratin expression is not only required for an improved insight into normal human skin and hair function, but may also open new therapeutic avenues in a wide range of skin and hair diseases.

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Section: Introductionmentioning

confidence: 99%

Endocrine controls of keratin expression

et al. 2009

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“…In humans, thyroid hormone (TH) deficiency frequently causes thickening of the skin and hair loss (Bernhard et al, 1996;Freinkel and Freinkel, 1972). Like mutations in Hr, some mutations in the gene encoding VDR result in congenital hair loss in mice and humans (Malloy et al, 1999;Miller et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

The co-repressor hairless has a role in epithelial cell differentiation in the skin

et al. 2004

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Although mutations in the mammalian hairless (Hr) gene result in congenital hair loss disorders in both mice and humans, the precise role of Hr in skin biology remains unknown. We have shown that the protein encoded by Hr (HR) functions as a nuclear receptor co-repressor. To address the role of HR in vivo, we generated a loss-of-function (Hr-/-) mouse model. The Hr-/- phenotype includes both hair loss and severe wrinkling of the skin. Wrinkling is correlated with increased cell proliferation in the epidermis and the presence of dermal cysts. In addition,a normally undifferentiated region, the infundibulum, is transformed into a morphologically distinct structure (utricle) that maintains epidermal function. Analysis of gene expression revealed upregulation of keratinocyte terminal differentiation markers and a novel caspase in Hr-/- skin, substantiating HR action as a co-repressor in vivo. Differences in gene expression occur prior to morphological changes in vivo, as well as in cultured keratinocytes, indicating that aberrant transcriptional regulation contributes to the Hr-/-phenotype. The properties of the cell types present in Hr-/- skin suggest that the normal balance of cell proliferation and differentiation is disrupted, supporting a model in which HR regulates the timing of epithelial cell differentiation in both the epidermis and hair follicle.

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“…Although these hair effects may well reflect a direct modulatory influence of TH on human hair follicle (HF) cycling (2,4) and/or on hair keratin expression (14), this remains to be documented. Also, it remains to be conclusively shown that TH affects human HF pigmentation.…”

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confidence: 99%

Thyroid Hormones Directly Alter Human Hair Follicle Functions: Anagen Prolongation and Stimulation of Both Hair Matrix Keratinocyte Proliferation and Hair Pigmentation

Beek

Bodó

Kromminga³

et al. 2008

The Journal of Clinical Endocrinology &Amp; Metabolism

134

138

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Context: Both insufficient and excess levels of thyroid hormones (T 3 and T 4 ) can result in altered hair/skin structure and function (e.g. effluvium). However, it is still unclear whether T 3 and T 4 exert any direct effects on human hair follicles (HFs), and if so, how exactly human HFs respond to T 3 /T 4 stimulation.Objective: Our objective was to asses the impact of T 3 /T 4 on human HF in vitro. Methods:Human anagen HFs were isolated from skin obtained from females undergoing facelift surgery. HFs from euthyroid females between 40 and 69 yr (average, 56 yr) were cultured and treated with T 3 /T 4 . Results:Studying microdissected, organ-cultured normal human scalp HFs, we show here that T 4 up-regulates the proliferation of hair matrix keratinocytes, whereas their apoptosis is down-regulated by T 3 and T 4 . T 4 also prolongs the duration of the hair growth phase (anagen) in vitro, possibly due to the down-regulation of TGF-␤2, the key anagen-inhibitory growth factor. Because we show here that human HFs transcribe deiodinase genes (D2 and D3), they may be capable of converting T 4 to T 3 . Intrafollicular immunoreactivity for the recognized thyroid hormone-responsive keratins cytokeratin (CK) 6 and CK14 is significantly modulated by T 3 and T 4 (CK6 is enhanced, CK14 down-regulated). Both T 3 and T 4 also significantly stimulate intrafollicular melanin synthesis. Conclusions:Thus, we present the first evidence that human HFs are direct targets of thyroid hormones and demonstrate that T 3 and/or T 4 modulate multiple hair biology parameters, ranging from HF cycling to pigmentation. (J Clin Endocrinol Metab 93: 4381-4388, 2008) C linically, it has long been observed that patients with thyroid dysfunction may show prominent hair abnormalities (1-4) and several in vivo studies have demonstrated (partially conflicting) hair growth-modulatory effects of thyroid hormone (TH) in sheep, rats, and mice (5-8). In humans, hypothyroidism can be associated with telogen effluvium, along with the presentation of dry, brittle, and dull hair shafts (2-4). Confusingly, hyperthyroid states can also lead to effluvium, together with thinned hair shaft diameter and brittle, greasy hair (1, 9 -11), despite an apparently increased hair matrix proliferation (3). Hair shafts of patients with hyperthyroidism also show substantially reduced tensile strength (10). Early graying has been claimed to be related to autoimmune thyroid disease, hypothyroidism, and hyperthyroidism (11, 12), whereas darkening of

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Hair Growth and Alopecia in Hypothyroidism

Cited by 96 publications

References 9 publications

Endocrine controls of keratin expression

Endocrine controls of keratin expression

The co-repressor hairless has a role in epithelial cell differentiation in the skin

Thyroid Hormones Directly Alter Human Hair Follicle Functions: Anagen Prolongation and Stimulation of Both Hair Matrix Keratinocyte Proliferation and Hair Pigmentation

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