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* Male pattern: The frontal hairline is thinner, hair loss occurs at the crown of the scalp, hair recession is seen at the temporal aspects of the scalp; Female pattern: Hair loss occurs at the crown of the scalp, however the frontal hair line remains preserved. <ref name="pmid24591533">{{cite journal| author=Qi J, Garza LA| title=An overview of alopecias. | journal=Cold Spring Harb Perspect Med | year= 2014 | volume= 4 | issue= 3 | pages=  | pmid=24591533 | doi=10.1101/cshperspect.a013615 | pmc=3935391 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24591533  }} </ref>
* Male pattern: The frontal hairline is thinner, hair loss occurs at the crown of the scalp, hair recession is seen at the temporal aspects of the scalp; Female pattern: Hair loss occurs at the crown of the scalp, however the frontal hair line remains preserved. <ref name="pmid24591533">{{cite journal| author=Qi J, Garza LA| title=An overview of alopecias. | journal=Cold Spring Harb Perspect Med | year= 2014 | volume= 4 | issue= 3 | pages=  | pmid=24591533 | doi=10.1101/cshperspect.a013615 | pmc=3935391 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24591533  }} </ref>
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* It is the most common cause of hair loss.<ref name="pmid24591533">{{cite journal| author=Qi J, Garza LA| title=An overview of alopecias. | journal=Cold Spring Harb Perspect Med | year= 2014 | volume= 4 | issue= 3 | pages=  | pmid=24591533 | doi=10.1101/cshperspect.a013615 | pmc=3935391 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24591533  }} </ref> Unlike in telogen effluvium, hair pull test is negative.<ref name="pmid26455063">{{cite journal| author=Vidal CI| title=Overview of Alopecia: A Dermatopathologist's Perspective. | journal=Mo Med | year= 2015 | volume= 112 | issue= 4 | pages= 308-12 | pmid=26455063 | doi= | pmc=6170065 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26455063  }} </ref>
* It is the most common cause of hair loss.<ref name="pmid24591533">{{cite journal| author=Qi J, Garza LA| title=An overview of alopecias. | journal=Cold Spring Harb Perspect Med | year= 2014 | volume= 4 | issue= 3 | pages=  | pmid=24591533 | doi=10.1101/cshperspect.a013615 | pmc=3935391 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24591533  }} </ref> Unlike in telogen effluvium, hair pull test shows a less than 20% telogen count .<ref name="pmid26455063">{{cite journal| author=Vidal CI| title=Overview of Alopecia: A Dermatopathologist's Perspective. | journal=Mo Med | year= 2015 | volume= 112 | issue= 4 | pages= 308-12 | pmid=26455063 | doi= | pmc=6170065 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26455063  }} </ref>
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| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |Alopecia Areata
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |Alopecia Areata

Revision as of 08:13, 4 January 2021

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Ogechukwu Hannah Nnabude, MD

Overview

There is a very wide list of diseases and conditions that can lead to alopecia. Proper history taking and physical examination, along with laboratory, microbiology, and in some cases, imaging studies, are helpful in narrowing down the diagnosis. Alopecia can be caused by many different diseases. Some of the most well known and common causes are: androgenetic alopecia, alopecia areata, telogen effluvium, anagen effluvium, traction alopecia, and trichotillomania. Endocrine disorders such as hypothyroidism, hypoparathyroidism and Cushing's syndrome as well as malnutrition and medications are also possible causes of alopecia.

Differentiating Alopecia from Other diseases
Differential Diagnosis Findings Unique Information
Androgenetic Alopecia
  • Male pattern: The frontal hairline is thinner, hair loss occurs at the crown of the scalp, hair recession is seen at the temporal aspects of the scalp; Female pattern: Hair loss occurs at the crown of the scalp, however the frontal hair line remains preserved. [1]
  • It is the most common cause of hair loss.[1] Unlike in telogen effluvium, hair pull test shows a less than 20% telogen count .[2]
Alopecia Areata
  • It presents with round patches of total hair loss with retained follicular ostia with the beard and scalp being the most frequently affected areas.[1] It occurs most often before the age of 30 and is evenly distributed between the sexes[1].
  • Close observation reveals the characteristic exclamation mark hairs.[1] A hair pull test followed by trichogram shows telogen and pencil point shafts [2]. It is associated with several autoimmune diseases including thyroid disease, rheumatoid arthritis, inflammatory bowel disease, and vitiligo. [3] [4] [5]
Telogen Effluvium
  • There is a massive amount of hair shedding which could be an acute self-limiting form triggered by stressors such as crash diets, childbirth, febrile illness or psychological stress or it could be chronic and present in association with female pattern hair loss. [6]
  • Hair pull test followed by trichogram reveals numerous clubbed-shaped hairs; telogen count must exceed 20% for diagnosis. [2]
Anagen Effluvium
  • Associated with exposure to radiation, as in radiotherapy and cancer chemotherapy. There is diffuse hair loss and it is characterized by hair breakage that takes place in the anagen phase. [1]
  • Trichoscopy would reveal the characteristic narrowing, fractured hair shafts with an absence of bulbs. [1]
Trichotillomania
  • It occurs as a result of a lack of impulse control in which an individual pulls on hair. Scalp inspection reveals uneven patches of hair loss with broken hairs that remain well attached to the skin. [7] The most frequently selected areas are scalp, eyebrows, eyelashes, body hair, facial hair, and pubic hair. It usually starts around the age of 12–13 years [8] and is more common in males during the childhood years while it is more common in females in the adult years. [1]
  • Scalp inspection reveals uneven patches of hair loss with broken hairs that remain well attached to the skin. [9]. A characteristic finding that distinguishes trichotillomania from alopecia areata is that the affected are not totally devoid of hair shafts. [10] [11]
Traction Alopecia
  • It is due to from tension on hair follicles for a prolonged period of time caused from tight hairstyles including braids and ponytails. Black populations are more prone due to widespread use of tight hairstyles. [12] [1] [13]
  • Black populations are most at risk. [14] With early detection and switching to more loose hairstyles, it is reversible but with prolonged tension on the scalp destruction of the hair follicles will occur making the condition irreversible. [13]
Chronic Cutaneous Lupus Erythematosus
  • Presents with an area with hair loss that gradually converts into a scaly, thickened papules then into poorly-defined, variably-shaped plaques with atrophy, follicular plugging, telangiectasia and depigmentation. [15] Black populations tend to have more serious disease. [1]
  • Histological analysis after a hair pull test reveals a higher anagen count during active disease. Direct immunofluorescence may reveal granular C3 and IgG at the dermo-epidermal boundary which is found in greater than 70% of cases. [16]
Tinea Capitis
  • Presents in diverse ways such as ordinary scaling without any obvious hair loss which is considered to be a seborrheic form, a crusted or pustular form that may be localized or diffuse, a ‘black dot’ type that is characterized by tiny black dots within regions of alopecia, an inflammatory mass called kerion, [17] and a round, bald, scaly patch where the follicular ostia are filled with keratinous debris. [18]
  • It is more common in the pediatric population. [2] A unique feature of tinea capitis is the presence of post-auricular and cervical lymphadenopathy. [19] Potassium hydroxide preparation can be added to skin scrapings of affected areas in order to diagnose the condition. [1] Wood's light can also be used in diagnosis as majority of Microsporum spp will appear bluish-green, occasionally dull yellow (Microsporum gypseum) and dull blue (Trichophyton schoenleinii). However, in the U.S., under 5% of cases will show fluorescence. [20]


The following lists the complete differential diagnosis of Alopecia:

Non-Scarring Alopecia

Scarring Alopecia

Miscellaneous

References

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 Qi J, Garza LA (2014). "An overview of alopecias". Cold Spring Harb Perspect Med. 4 (3). doi:10.1101/cshperspect.a013615. PMC 3935391. PMID 24591533.
  2. ↑ 2.0 2.1 2.2 2.3 Vidal CI (2015). "Overview of Alopecia: A Dermatopathologist's Perspective". Mo Med. 112 (4): 308–12. PMC 6170065. PMID 26455063.
  3. ↑ Villasante Fricke AC, Miteva M (2015). "Epidemiology and burden of alopecia areata: a systematic review". Clin Cosmet Investig Dermatol. 8: 397–403. doi:10.2147/CCID.S53985. PMC 4521674. PMID 26244028.
  4. ↑ Chu SY, Chen YJ, Tseng WC, Lin MW, Chen TJ, Hwang CY; et al. (2011). "Comorbidity profiles among patients with alopecia areata: the importance of onset age, a nationwide population-based study". J Am Acad Dermatol. 65 (5): 949–56. doi:10.1016/j.jaad.2010.08.032. PMID 21616562.
  5. ↑ Chen CH, Wang KH, Lin HC, Chung SD (2016) Follow-up study on the relationship between alopecia areata and risk of autoimmune diseases. J Dermatol 43 (2):228-9. DOI:10.1111/1346-8138.13165 PMID: 26499292
  6. ↑ Sperling LC, Cowper SE, Knopp EA. An atlas of hair pathology with clinical correlations. 2. Informa Healthcare; 2014. [Google Scholar]
  7. ↑ Sperling LC, Cowper SE, Knopp EA. An atlas of hair pathology with clinical correlations. 2. Informa Healthcare; 2014. [Google Scholar]
  8. ↑ Quercetani R, Rebora AE, Fedi MC, Carelli G, Mei S, Chelli A; et al. (2011). "Patients with profuse hair shedding may reveal anagen hair dystrophy: a diagnostic clue of alopecia areata incognita". J Eur Acad Dermatol Venereol. 25 (7): 808–10. doi:10.1111/j.1468-3083.2010.03869.x. PMID 20946585.
  9. ↑ Sperling LC, Cowper SE, Knopp EA. An atlas of hair pathology with clinical correlations. 2. Informa Healthcare; 2014. [Google Scholar]
  10. ↑ Habif TP 2010. Hair diseases. In Clinical dermatology, 5th ed Mosby, Maryland Heights, MO [Google Scholar]
  11. ↑ Otberg N, Shapiro J 2012. Hair growth disorders. In Fitzpatrick’s dermatology in general medicine, 8th ed (ed. Goldsmith LA, et al.). McGraw-Hill, New York [Google Scholar]
  12. ↑ Otberg N, Shapiro J 2012. Hair growth disorders. In Fitzpatrick’s dermatology in general medicine, 8th ed (ed. Goldsmith LA, et al.). McGraw-Hill, New York [Google Scholar]
  13. ↑ 13.0 13.1 Callender VD, McMichael AJ, Cohen GF (2004). "Medical and surgical therapies for alopecias in black women". Dermatol Ther. 17 (2): 164–76. doi:10.1111/j.1396-0296.2004.04017.x. PMID 15113284.
  14. ↑ Habif TP 2010. Hair diseases. In Clinical dermatology, 5th ed Mosby, Maryland Heights, MO [Google Scholar]
  15. ↑ Sperling LC, Cowper SE, Knopp EA. An atlas of hair pathology with clinical correlations. 2. Informa Healthcare; 2014. [Google Scholar]
  16. ↑ Sperling LC, Cowper SE, Knopp EA. An atlas of hair pathology with clinical correlations. 2. Informa Healthcare; 2014. [Google Scholar]
  17. ↑ Pomeranz AJ, Sabnis SS (2002). "Tinea capitis: epidemiology, diagnosis and management strategies". Paediatr Drugs. 4 (12): 779–83. doi:10.2165/00128072-200204120-00002. PMID 12431130.
  18. ↑ Kos L, Conlon J (2009). "An update on alopecia areata". Curr Opin Pediatr. 21 (4): 475–80. doi:10.1097/MOP.0b013e32832db986. PMID 19502982.
  19. ↑ Sperling LC, Cowper SE, Knopp EA. An atlas of hair pathology with clinical correlations. 2. Informa Healthcare; 2014. [Google Scholar]
  20. ↑ Ponka D, Baddar F (2012). "Wood lamp examination". Can Fam Physician. 58 (9): 976. PMC 3440273. PMID 22972730.
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