Alopecia Areata Has Low Plasma Levels of the Vasodilator/Immunomodulator Calcitonin Gene-Related Peptide

Daly, Theodore J.

doi:10.1001/archderm.134.9.1164

Cited by 23 publications

(16 citation statements)

References 4 publications

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“…A previous study indicated that CGRP immunoreactivity is high in nerves around the eccrine glands of people with AA 28 . Additional studies have found low amounts of CGRP in the blood of people with AA 29 . Together, these studies suggest that CGRP is involved in the pathophysiology of AA, with a vascular hyperreactivity to vasodilatory substances such as neuropeptides, including CGRP, probably because of the lack of these substances, hypothesized 5 .…”

Section: Discussionmentioning

confidence: 89%

“…28 Additional studies have found low amounts of CGRP in the blood of people with AA. 29 Together, these studies suggest that CGRP is involved in the pathophysiology of AA, with a vascular hyperreactivity to vasodilatory substances such as neuropeptides, including CGRP, probably because of the lack of these substances, hypothesized. 5 Another hypothesis for the pathophysiology of AA is that CGRP deficiency might annihilate a CGRP-promoted tolerance to a hapten or antigen responsible for the autoimmune destruction of hair.…”

Section: Discussionmentioning

confidence: 89%

See 1 more Smart Citation

Treatment Effects of Intradermal Botulinum Toxin Type A Injection on Alopecia Areata

Cho

Lew

et al. 2010

Dermatologic Surgery

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Section: Discussionmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 89%

Treatment Effects of Intradermal Botulinum Toxin Type A Injection on Alopecia Areata

Cho

Lew

et al. 2010

Dermatologic Surgery

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“…The peripheral nervous system is now recognized for its ability to modulate a variety of proliferative and inflammatory processes (6). Abnormalities in circulating levels of the neuropeptide calcitonin gene‐related peptide (CGRP) have been found in patients with AA, as have exaggerated vasodilatory responses to local injection of CGRP (16–18). Using immunocytochemical techniques and laser scanning confocal microscopy to analyze the peripheral nervous system in AA scalp biopsy specimens, we found perifollicular innervation to be condensed and arranged in a basket‐weave pattern around the small miniaturized scalp hair follicle (Fig.…”

Section: Alterations In the Peripheral Nervous Systemmentioning

confidence: 96%

Clinical presentations of alopecia areata

Hordinsky

2001

Dermatol Ther

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Alopecia areata (AA) may can occur on any hair‐bearing region. Patients can develop patchy nonscarring hair loss or extensive loss of all body hair. Hair loss may fluctuate. Some patients experience recurrent hair loss followed by hair regrowth, whereas others may only develop a single patch of hair loss, never to see the disease again. Still others experience extensive loss of body hair. The heterogeneity of clinical presentations has led investigators conducting clinical therapeutic trials to typically group patients into three major groups, those with extensive scalp hair loss [alopecia totalis (AT)], extensive body hair loss [alopecia universalis (AU)], or patchy disease (AA). Treatment outcomes have been correlated with disease duration and extent. Recently, guidelines were established for selecting and assessing subjects for both clinical and laboratory studies of AA, thereby facilitating collaboration, comparison of data, and the sharing of patient‐derived tissue. For reporting purposes the terms AT and AU, though still used are defined very narrowly. AT is 100% terminal scalp hair loss without any body hair loss and AU is 100% terminal scalp hair and body loss. AT/AU is the term now recommended to define the presence of AT with variable amounts of body hair loss. In this report the term AA will be used broadly to encompass the many presentations of this disease. Development of AA may occur with changes in other ectodermal‐derived structures such as fingernails and toenails. Some investigators have also suggested that other ectodermal‐derived appendages as sebaceous glands and sweat glands may be affected in patients experiencing AA. Whether or not function of these glands is truly impaired remains to be confirmed. Many patients who develop patchy or extensive AA complain of changes in cutaneous sensation, that is, burning, itching, tingling, with the development of their disease. Similar symptoms may occur with hair regrowth. The potential involvement of the nervous system in AA has led to morphologic investigations of the peripheral nervous system as well as analysis of circulating neuropeptide levels. In this article the clinical presentations of AA are reviewed. The guidelines for conducting treatment studies of AA are presented and observations on changes in cutaneous innervation are introduced. Throughout the text, unless otherwise noted, AA will be used in a general way to denote the spectrum of this disease.

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“…CGRP expression in epidermal innervation also stimulates keratinocyte proliferation and thickening of epidermis (Takahashi et al 1993;Huang et al 1999). Paradoxically, in the related human autoimmune skin disease, alopecia areata, CGRP content in the skin and in the plasma is significantly lower than in normal individuals (Rossi et al 1997;Daly 1998;Meyronet et al 2003). This difference might indicate differences in the mechanisms of genetic hair loss in Hr and autoimmune hair loss in alopecia areata (National Alopecia Areata Foundation, www.naaf.org).…”

Section: Ectopic Innervation and Epidermal Thickeningmentioning

confidence: 99%

Immunohistochemical comparison of whisker pad cutaneous innervation in Swiss Webster andhairlessmice

Mosconi

Gruber

2010

Somatosensory & Motor Research

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To establish the mouse mutant, hairless (Hr), as a useful model for future analyses of target-ending interactions, we assessed the cutaneous innervation in the whisker pad after loss of primary hair targets. Postnatal (P) development of fur in Hr begins similarly to that of "normal" Swiss Webster (SW) mice. Around P10, hairs are shed and the follicles rendered permanently incompetent. Hair loss progresses rostrocaudally until the entire skin is denuded. Substantial alterations in the distribution and density of sensory and autonomic endings in the mystacial pad vibrissal and intervibrissal fur innervation were discovered. Pilo-neural complexes innervating fur hairs were dismantled in Hr. Epidermal innervation in SW was rich; only a few endings expressed growth-associated protein-43 kdal (GAP), suggesting limited changes in axonal elongation. Innervation in Hr formed a dense layer passing upward through the thickened epidermis, with substantial increases among all types of endings. Vibrissal follicle-sinus complexes were also hyperinnervated. Endings in Hr vibrissae and fur were strongly GAP-positive, suggesting reorganization of innervation. Dermal and vascular autonomic innervation in both strains co-localized tyrosine hydroxylase and neuropeptide Y, but only in Hr did neuropeptide Y co-localize calcitonin gene-related peptide (CGRP) and express GAP immunolabeling. Stereological quantitation of trigeminal ganglia revealed no differences in neuron number between Hr and SW, although there were small increases in cell volume in Hr trigeminal ganglion cells. These results suggested that a form of collateral sprouting was active in Hr mystacial pads, not in response to local injury, but as a result of loss of primary target tissues.

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Alopecia Areata Has Low Plasma Levels of the Vasodilator/Immunomodulator Calcitonin Gene-Related Peptide

Cited by 23 publications

References 4 publications

Treatment Effects of Intradermal Botulinum Toxin Type A Injection on Alopecia Areata

Treatment Effects of Intradermal Botulinum Toxin Type A Injection on Alopecia Areata

Clinical presentations of alopecia areata

Immunohistochemical comparison of whisker pad cutaneous innervation in Swiss Webster andhairlessmice

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