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Although it appeared that the hair loss was preceded by some dry skin, the patch of hair loss was smooth and nonscarring, consistent with a diagnosis of alopecia areata (AA).
AA typically is found on the scalp in solitary areas but can affect the whole body, including the eyelashes and eyebrows. Affected hair typically is narrower at the proximal end, resembling an exclamation point, as the hair fails to grow and falls out. Sometimes, patches of alopecia may coalesce into a larger area. Nail changes may be noted, as well. Nails may become brittle, with pitting and/or longitudinal ridges. Patients are usually asymptomatic but may complain of pruritus.
AA is believed to be an autoimmune disorder. It affects males and females of all ages but is more common in children and young adults. AA is believed to result from a T-cell–mediated immune response that transitions the hair follicles from the growth phase to the resting phase. This leads to sudden hair loss and inhibition of regrowth of the hair. However, the hair follicle is not permanently destroyed as in other processes of alopecia. There is also an association between AA and other autoimmune disorders such as vitiligo, thyroid disease, and lupus.
The diagnosis usually is made clinically, as in this patient, but a definitive diagnosis can be made by biopsy and pathology. Other differential diagnoses to consider are trichotillomania, tinea, traumatic alopecia, and lupus.
In almost half of cases, AA is self-resolving; therefore, in first episodes of localized disease, watchful waiting is appropriate. Treatment is tailored to the individual patient and may be difficult. Intralesional corticosteroids often are used for mild cases. Typically, 10 mg/mL of a glucocorticoid is injected into the mid-dermis every 4 to 6 weeks; however, this treatment carries a risk of transient or even permanent atrophy of the injection site. Potent topical corticosteroids often are used, especially in children who do not tolerate intralesional injections, and success can be variable. Other topical treatments to consider are photochemotherapy (psoralen plus UVA), or an irritant agent such as anthralin and a vasodilator such as minoxidil. Regrowth can be expected in a few months to a year, but recurrence is common.
Image courtesy of Stacy Nguy, MD, and text courtesy of Stacy Nguy, MD, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.
Papadopoulos AJ, Schwartz RA, Janniger C. Alopecia areata: pathogenesis, diagnosis, and therapy. Am J Clin Dermatol. 2000;1:101-105
Although it appeared that the hair loss was preceded by some dry skin, the patch of hair loss was smooth and nonscarring, consistent with a diagnosis of alopecia areata (AA).
AA typically is found on the scalp in solitary areas but can affect the whole body, including the eyelashes and eyebrows. Affected hair typically is narrower at the proximal end, resembling an exclamation point, as the hair fails to grow and falls out. Sometimes, patches of alopecia may coalesce into a larger area. Nail changes may be noted, as well. Nails may become brittle, with pitting and/or longitudinal ridges. Patients are usually asymptomatic but may complain of pruritus.
AA is believed to be an autoimmune disorder. It affects males and females of all ages but is more common in children and young adults. AA is believed to result from a T-cell–mediated immune response that transitions the hair follicles from the growth phase to the resting phase. This leads to sudden hair loss and inhibition of regrowth of the hair. However, the hair follicle is not permanently destroyed as in other processes of alopecia. There is also an association between AA and other autoimmune disorders such as vitiligo, thyroid disease, and lupus.
The diagnosis usually is made clinically, as in this patient, but a definitive diagnosis can be made by biopsy and pathology. Other differential diagnoses to consider are trichotillomania, tinea, traumatic alopecia, and lupus.
In almost half of cases, AA is self-resolving; therefore, in first episodes of localized disease, watchful waiting is appropriate. Treatment is tailored to the individual patient and may be difficult. Intralesional corticosteroids often are used for mild cases. Typically, 10 mg/mL of a glucocorticoid is injected into the mid-dermis every 4 to 6 weeks; however, this treatment carries a risk of transient or even permanent atrophy of the injection site. Potent topical corticosteroids often are used, especially in children who do not tolerate intralesional injections, and success can be variable. Other topical treatments to consider are photochemotherapy (psoralen plus UVA), or an irritant agent such as anthralin and a vasodilator such as minoxidil. Regrowth can be expected in a few months to a year, but recurrence is common.
Image courtesy of Stacy Nguy, MD, and text courtesy of Stacy Nguy, MD, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.
Although it appeared that the hair loss was preceded by some dry skin, the patch of hair loss was smooth and nonscarring, consistent with a diagnosis of alopecia areata (AA).
AA typically is found on the scalp in solitary areas but can affect the whole body, including the eyelashes and eyebrows. Affected hair typically is narrower at the proximal end, resembling an exclamation point, as the hair fails to grow and falls out. Sometimes, patches of alopecia may coalesce into a larger area. Nail changes may be noted, as well. Nails may become brittle, with pitting and/or longitudinal ridges. Patients are usually asymptomatic but may complain of pruritus.
AA is believed to be an autoimmune disorder. It affects males and females of all ages but is more common in children and young adults. AA is believed to result from a T-cell–mediated immune response that transitions the hair follicles from the growth phase to the resting phase. This leads to sudden hair loss and inhibition of regrowth of the hair. However, the hair follicle is not permanently destroyed as in other processes of alopecia. There is also an association between AA and other autoimmune disorders such as vitiligo, thyroid disease, and lupus.
The diagnosis usually is made clinically, as in this patient, but a definitive diagnosis can be made by biopsy and pathology. Other differential diagnoses to consider are trichotillomania, tinea, traumatic alopecia, and lupus.
In almost half of cases, AA is self-resolving; therefore, in first episodes of localized disease, watchful waiting is appropriate. Treatment is tailored to the individual patient and may be difficult. Intralesional corticosteroids often are used for mild cases. Typically, 10 mg/mL of a glucocorticoid is injected into the mid-dermis every 4 to 6 weeks; however, this treatment carries a risk of transient or even permanent atrophy of the injection site. Potent topical corticosteroids often are used, especially in children who do not tolerate intralesional injections, and success can be variable. Other topical treatments to consider are photochemotherapy (psoralen plus UVA), or an irritant agent such as anthralin and a vasodilator such as minoxidil. Regrowth can be expected in a few months to a year, but recurrence is common.
Image courtesy of Stacy Nguy, MD, and text courtesy of Stacy Nguy, MD, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.
Papadopoulos AJ, Schwartz RA, Janniger C. Alopecia areata: pathogenesis, diagnosis, and therapy. Am J Clin Dermatol. 2000;1:101-105
Papadopoulos AJ, Schwartz RA, Janniger C. Alopecia areata: pathogenesis, diagnosis, and therapy. Am J Clin Dermatol. 2000;1:101-105