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It most commonly affects young girls. The pathogenesis of LAHS is thought to involve a sporadic, autosomal dominant mutation that leads to a defect between the hair cuticle and the inner root sheath.1 This defect results in the hair being poorly anchored to the scalp, and therefore easily and painlessly plucked or lost during normal hair care.
The classic presentation of LAHS is that of hair thinning and hair that may be unruly and/or lackluster; the hair rarely, if ever, requires cutting.2 The key feature is the ability to easily and painlessly pluck hairs from the patient’s scalp. The affected area is limited to the scalp, and loss of eyebrows, eyelashes, and body hair should not be seen.
Diagnosis and consideration of the differential
The diagnosis of LAHS can in some cases be made on history and physical exam alone. Patients with LAHS typically will show hair thinning with or without dullness or unruliness. They lack evidence of scalp inflammation, such as erythema, scale, pruritus, and pain. Areas of hair thinning or aberration are typically not well demarcated, and there are typically not areas of complete hair loss. There is no scarring or atrophy of the scalp itself.
Diagnostic tests include the “hair pull test,” as well as trichogram testing. In the “hair pull test” a provider grasps a set of hair at the proximal shaft near the scalp. The traction applied should result in the painless and easy extraction of more than 10% of grasped hairs in a patient with LAHS. Removal of less than 10% of hair is a normal finding, as patients without LAHS typically have about 10% of their scalp hair in the telogen phase at any given time, which would result in removal during the hair pull test.3 In trichography, plucked hairs are examined under magnification, with or without the use of selective dyes. Cinnamaldehyde is a dye that stains citrulline, which is abundant in the inner root sheath, and can be a tool in identifying its presence and/or aberrations.4 A trichogram of the pulled hairs in a patient with LAHS may classically show ruffled appearance of the cuticle, misshapen anagen hair bulbs, and absence of the inner root sheath.5 Examination under magnification also allows providers to better identify telogen versus anagen hairs, which aids in the diagnosis. By carefully considering the patient history, physical exam, and results of additional hair tests, providers can make the diagnosis of LAHS and avoid unnecessary blood work and invasive procedures like scalp biopsies.
The differential diagnosis of hair loss frequently includes alopecia areata. However, in alopecia areata, patients typically have sharply demarcated areas of hair loss, which may involve the eyebrows, eyelids, and body hairs. In alopecia areata, providers may be able to identify the “exclamation point sign” in which the hair shaft thins proximally, leading to the appearance of more pigmented, thicker hairs floating above the scalp.
Telogen effluvium is a condition in which a medical illness or stress, such as systemic illness, surgery, severe emotional distress, childbirth, dietary changes, or another traumatic event, causes a disruption in the natural cycle of hair growth such that the percentage of hairs in the telogen phase increases from about 10% to up to 70%.6 Unlike in LAHS, in which shed hairs are in the anagen phase, the hair that is shed in telogen effluvium is in the telogen phase and will have a different appearance when magnified.
Anagen effluvium, loss of hairs in their growing phase, is typically associated with chemotherapy. The hairs become broken and fractured at the shaft leading to breakage at different points throughout the scalp. Affected areas can include the eyebrows, eyelashes, and body hair. In the absence of a history of administration of a chemotherapy agent (or other drug known to trigger hair loss), the diagnosis of anagen effluvium should not be made.
Patients with trichotillosis (also known as trichotillomania) present with areas of hair loss caused by intentional or subconscious hair pulling. It is considered a psychological condition that can be associated with obsessive compulsive disorder, although the presence of a secondary psychological diagnosis is not required. Providers may see irregular geometric shapes of hair loss, and on close inspection see broken hair shafts of different lengths. Patients most often pull hair from their scalps (over 70% of patients), but also can pull eyelashes, eyebrow hairs, and pubic hairs.7
Treatment
LAHS is self-limited and does not necessitate treatment. However, if patients or parents feel there is significant disease burden, perhaps with poor effects on quality of life or with psychosocial impairment, treatment with minoxidil 5% solution has been studied with some success reported in the literature.1,8,9
Ms. Natsis is a medical student at the University of California, San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital-San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. Ms. Natsis and Dr. Eichenfield had no relevant financial disclosures. Email them at pdnews@mdedge.com.
References
1. Arch Dermatol. 2002;138(4):501-6.
2. Int J Trichology. 2010;2(2):96-100.
3. Pediatric Dermatol. 2016:33(50):507-10.
4. Dermatol Clin. 1986;14:745-51.
5. Arch Dermatol. 2009;145(10):1123-8.
6. J Clin Diagn Res. 2015;9(9):WE01-3.
7. Am J Psychiatry. 2016;173(9):868-74.
8. Australas J Dermatol. 2018;59:e286-e287.
9. Pediatr Dermatol. 2014;31:389-90.
It most commonly affects young girls. The pathogenesis of LAHS is thought to involve a sporadic, autosomal dominant mutation that leads to a defect between the hair cuticle and the inner root sheath.1 This defect results in the hair being poorly anchored to the scalp, and therefore easily and painlessly plucked or lost during normal hair care.
The classic presentation of LAHS is that of hair thinning and hair that may be unruly and/or lackluster; the hair rarely, if ever, requires cutting.2 The key feature is the ability to easily and painlessly pluck hairs from the patient’s scalp. The affected area is limited to the scalp, and loss of eyebrows, eyelashes, and body hair should not be seen.
Diagnosis and consideration of the differential
The diagnosis of LAHS can in some cases be made on history and physical exam alone. Patients with LAHS typically will show hair thinning with or without dullness or unruliness. They lack evidence of scalp inflammation, such as erythema, scale, pruritus, and pain. Areas of hair thinning or aberration are typically not well demarcated, and there are typically not areas of complete hair loss. There is no scarring or atrophy of the scalp itself.
Diagnostic tests include the “hair pull test,” as well as trichogram testing. In the “hair pull test” a provider grasps a set of hair at the proximal shaft near the scalp. The traction applied should result in the painless and easy extraction of more than 10% of grasped hairs in a patient with LAHS. Removal of less than 10% of hair is a normal finding, as patients without LAHS typically have about 10% of their scalp hair in the telogen phase at any given time, which would result in removal during the hair pull test.3 In trichography, plucked hairs are examined under magnification, with or without the use of selective dyes. Cinnamaldehyde is a dye that stains citrulline, which is abundant in the inner root sheath, and can be a tool in identifying its presence and/or aberrations.4 A trichogram of the pulled hairs in a patient with LAHS may classically show ruffled appearance of the cuticle, misshapen anagen hair bulbs, and absence of the inner root sheath.5 Examination under magnification also allows providers to better identify telogen versus anagen hairs, which aids in the diagnosis. By carefully considering the patient history, physical exam, and results of additional hair tests, providers can make the diagnosis of LAHS and avoid unnecessary blood work and invasive procedures like scalp biopsies.
The differential diagnosis of hair loss frequently includes alopecia areata. However, in alopecia areata, patients typically have sharply demarcated areas of hair loss, which may involve the eyebrows, eyelids, and body hairs. In alopecia areata, providers may be able to identify the “exclamation point sign” in which the hair shaft thins proximally, leading to the appearance of more pigmented, thicker hairs floating above the scalp.
Telogen effluvium is a condition in which a medical illness or stress, such as systemic illness, surgery, severe emotional distress, childbirth, dietary changes, or another traumatic event, causes a disruption in the natural cycle of hair growth such that the percentage of hairs in the telogen phase increases from about 10% to up to 70%.6 Unlike in LAHS, in which shed hairs are in the anagen phase, the hair that is shed in telogen effluvium is in the telogen phase and will have a different appearance when magnified.
Anagen effluvium, loss of hairs in their growing phase, is typically associated with chemotherapy. The hairs become broken and fractured at the shaft leading to breakage at different points throughout the scalp. Affected areas can include the eyebrows, eyelashes, and body hair. In the absence of a history of administration of a chemotherapy agent (or other drug known to trigger hair loss), the diagnosis of anagen effluvium should not be made.
Patients with trichotillosis (also known as trichotillomania) present with areas of hair loss caused by intentional or subconscious hair pulling. It is considered a psychological condition that can be associated with obsessive compulsive disorder, although the presence of a secondary psychological diagnosis is not required. Providers may see irregular geometric shapes of hair loss, and on close inspection see broken hair shafts of different lengths. Patients most often pull hair from their scalps (over 70% of patients), but also can pull eyelashes, eyebrow hairs, and pubic hairs.7
Treatment
LAHS is self-limited and does not necessitate treatment. However, if patients or parents feel there is significant disease burden, perhaps with poor effects on quality of life or with psychosocial impairment, treatment with minoxidil 5% solution has been studied with some success reported in the literature.1,8,9
Ms. Natsis is a medical student at the University of California, San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital-San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. Ms. Natsis and Dr. Eichenfield had no relevant financial disclosures. Email them at pdnews@mdedge.com.
References
1. Arch Dermatol. 2002;138(4):501-6.
2. Int J Trichology. 2010;2(2):96-100.
3. Pediatric Dermatol. 2016:33(50):507-10.
4. Dermatol Clin. 1986;14:745-51.
5. Arch Dermatol. 2009;145(10):1123-8.
6. J Clin Diagn Res. 2015;9(9):WE01-3.
7. Am J Psychiatry. 2016;173(9):868-74.
8. Australas J Dermatol. 2018;59:e286-e287.
9. Pediatr Dermatol. 2014;31:389-90.
It most commonly affects young girls. The pathogenesis of LAHS is thought to involve a sporadic, autosomal dominant mutation that leads to a defect between the hair cuticle and the inner root sheath.1 This defect results in the hair being poorly anchored to the scalp, and therefore easily and painlessly plucked or lost during normal hair care.
The classic presentation of LAHS is that of hair thinning and hair that may be unruly and/or lackluster; the hair rarely, if ever, requires cutting.2 The key feature is the ability to easily and painlessly pluck hairs from the patient’s scalp. The affected area is limited to the scalp, and loss of eyebrows, eyelashes, and body hair should not be seen.
Diagnosis and consideration of the differential
The diagnosis of LAHS can in some cases be made on history and physical exam alone. Patients with LAHS typically will show hair thinning with or without dullness or unruliness. They lack evidence of scalp inflammation, such as erythema, scale, pruritus, and pain. Areas of hair thinning or aberration are typically not well demarcated, and there are typically not areas of complete hair loss. There is no scarring or atrophy of the scalp itself.
Diagnostic tests include the “hair pull test,” as well as trichogram testing. In the “hair pull test” a provider grasps a set of hair at the proximal shaft near the scalp. The traction applied should result in the painless and easy extraction of more than 10% of grasped hairs in a patient with LAHS. Removal of less than 10% of hair is a normal finding, as patients without LAHS typically have about 10% of their scalp hair in the telogen phase at any given time, which would result in removal during the hair pull test.3 In trichography, plucked hairs are examined under magnification, with or without the use of selective dyes. Cinnamaldehyde is a dye that stains citrulline, which is abundant in the inner root sheath, and can be a tool in identifying its presence and/or aberrations.4 A trichogram of the pulled hairs in a patient with LAHS may classically show ruffled appearance of the cuticle, misshapen anagen hair bulbs, and absence of the inner root sheath.5 Examination under magnification also allows providers to better identify telogen versus anagen hairs, which aids in the diagnosis. By carefully considering the patient history, physical exam, and results of additional hair tests, providers can make the diagnosis of LAHS and avoid unnecessary blood work and invasive procedures like scalp biopsies.
The differential diagnosis of hair loss frequently includes alopecia areata. However, in alopecia areata, patients typically have sharply demarcated areas of hair loss, which may involve the eyebrows, eyelids, and body hairs. In alopecia areata, providers may be able to identify the “exclamation point sign” in which the hair shaft thins proximally, leading to the appearance of more pigmented, thicker hairs floating above the scalp.
Telogen effluvium is a condition in which a medical illness or stress, such as systemic illness, surgery, severe emotional distress, childbirth, dietary changes, or another traumatic event, causes a disruption in the natural cycle of hair growth such that the percentage of hairs in the telogen phase increases from about 10% to up to 70%.6 Unlike in LAHS, in which shed hairs are in the anagen phase, the hair that is shed in telogen effluvium is in the telogen phase and will have a different appearance when magnified.
Anagen effluvium, loss of hairs in their growing phase, is typically associated with chemotherapy. The hairs become broken and fractured at the shaft leading to breakage at different points throughout the scalp. Affected areas can include the eyebrows, eyelashes, and body hair. In the absence of a history of administration of a chemotherapy agent (or other drug known to trigger hair loss), the diagnosis of anagen effluvium should not be made.
Patients with trichotillosis (also known as trichotillomania) present with areas of hair loss caused by intentional or subconscious hair pulling. It is considered a psychological condition that can be associated with obsessive compulsive disorder, although the presence of a secondary psychological diagnosis is not required. Providers may see irregular geometric shapes of hair loss, and on close inspection see broken hair shafts of different lengths. Patients most often pull hair from their scalps (over 70% of patients), but also can pull eyelashes, eyebrow hairs, and pubic hairs.7
Treatment
LAHS is self-limited and does not necessitate treatment. However, if patients or parents feel there is significant disease burden, perhaps with poor effects on quality of life or with psychosocial impairment, treatment with minoxidil 5% solution has been studied with some success reported in the literature.1,8,9
Ms. Natsis is a medical student at the University of California, San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital-San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. Ms. Natsis and Dr. Eichenfield had no relevant financial disclosures. Email them at pdnews@mdedge.com.
References
1. Arch Dermatol. 2002;138(4):501-6.
2. Int J Trichology. 2010;2(2):96-100.
3. Pediatric Dermatol. 2016:33(50):507-10.
4. Dermatol Clin. 1986;14:745-51.
5. Arch Dermatol. 2009;145(10):1123-8.
6. J Clin Diagn Res. 2015;9(9):WE01-3.
7. Am J Psychiatry. 2016;173(9):868-74.
8. Australas J Dermatol. 2018;59:e286-e287.
9. Pediatr Dermatol. 2014;31:389-90.
A 5-year-old female is brought to clinic for hair loss. The mother reports that when styling her daughter's hair, she has noticed areas of hair thinning, especially at the temples and at the occiput. The mother denies scale, pruritus, and erythema. The patient reports that her scalp does not hurt. She has never had a haircut because her hair hasn't grown long enough to cut. There is no history of specific bald spots. The patient has no personal history of psoriasis, seborrheic dermatitis, or autoimmune disease. No picking has been noted, and there is no history of compulsive behaviors or anxiety. The patient's mother has a history of Graves disease. The mother reports that the patient's older sister may have had hair thinning when she was younger as well, but no longer has thin hair.
The patient was previously seen by another provider who prescribed hydrocortisone 2.5% ointment, which the mother has been applying nightly without improvement.
The child is otherwise medically well and thriving, with no recent change in activity level and with growth parameters consistently around the 75th percentile for height and weight. On physical exam, the patient has blondish, fine hair with areas of poorly demarcated hair thinning at the left temple and at the occiput. The hair remaining at the occiput is normal in texture. There are no areas of complete hair loss. There is no scale, erythema, or abnormal pigmentation, and no cervical or occipital adenopathy. The patient has intact eyebrows and eyelashes.