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| CASE REPORT |
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| Year : 2014 | Volume
: 6
| Issue : 2 | Page : 67-68 |
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Co-existent presence of alopecia areata in siblings: A rare presentation
Sandip Mohanty, Pallavi C Rohatgi, Kajal Manchanda
Department of Dermatology, Swami Dayanand Hospital, New Delhi, India
| Date of Web Publication | 13-Aug-2014 |
Correspondence Address:
Kajal Manchanda
Department of Dermatology, Swami Dayanand Hospital, New Delhi - 110 093
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0974-7753.138591
 Abstract | | |
Alopecia areata (AA) is a T cell mediated autoimmune disease with multifactorial etiology resulting in partial and total nonscarring alopecia. We hereby report a case of two brothers (aged 7 and 5 years) presenting with coincidental AA over scalp which is a rare presentation. Keywords: Alopecia areata, brothers, co-incidental
How to cite this article:
Mohanty S, Rohatgi PC, Manchanda K. Co-existent presence of alopecia areata in siblings: A rare presentation. Int J Trichol 2014;6:67-8 |
| Introduction | |  |
Alopecia areata (AA) is a chronic inflammatory disease of the hair follicles and nails, its etiology is unknown, probably multifactorial with evident autoimmune and genetic components. [1] The first clinical description of AA is attributed to Celsus (14-37 B.C.) and the designation AA was given by Sauvages. [2] The importance of genetic factors in AA is underlined by the high frequency of a positive family history in affected individuals. In most reports, these range from 10% to 20% of cases. [1] There are several case reports of AA in twins. A study in monozygotic and dizygotic pairs found a concordance rate of 55% for alopecia amongst monozygotic twins with no concordance among the dizygotic pairs. [3] Though it can affect any age group, demographical data on AA is still lacking. We hereby report a case study of coincidental occurrence of AA in two siblings.
| Case report | | |
Two brothers aged 5 and 7 years presented to the outpatient department with complaints of asymptomatic patchy loss of scalp hair for the past 2 and 4 months respectively. There was no similar complaint in any other family member, siblings and no history suggestive of systemic involvement, drug intake, trauma, pus filled lesions or any other skin eruptions. Systemic examination of both the children was normal. Mucocutaneous examination revealed multiple smooth patches of alopecia ranging from 2 cm × 2 cm to 4 cm × 6 cm over occipital and vertex area of elder child and multiple patches over occipital and temporal region measuring 2 cm × 2 cm to 2 cm × 4 cm of the younger one [Figure 1]a and b]. | Figure 1: (a) Multiple areas of nonscarring alopecia involving the occipital and vertex area in a 7-year-old child (b) Multiple areas of nonscarring alopecia involving the occipital and temporal area in sibling 5-year-old
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Surface of the patches was smooth with no apparent changes. Nail examination was normal. There was no loss of hair from any other site of the body.
A provisional diagnosis of AA was made. Routine hematological and biochemical investigations were normal. Potassium hydroxide examination of hair follicle was negative. Histopathological examination of the biopsy sample from the alopecia patch from the scalp confirmed the diagnosis, which showed inflammatory infiltrate in and around the bulbar region of hair follicle. Thus, the final diagnosis of AA was made.
| Discussion | | |
Alopecia areata is T cell mediated autoimmune disease with genetic predisposition resulting in partial and total nonscarring alopecia. [4] Scalp is the predominant site of involvement with the most common clinical pattern involving multiple areas of patchy hair loss. [5] Most patients develop AA before the age 40 years with 11-20% of all cases occurring in children. The ratio of male:female in AA in pediatric age group is 1:1 where as in adolescent and adult it is more common in female. [4]
Familial aggregation has been described in various studies. Human leukocyte antigen (HLA)-DQ3 and HLA-DQB1*03 alleles appear to be marker for genetic susceptibility to AA with the latter serving as a special genetic marker for more severe variants. [6] The diagnostic pathologic feature is peribulbar lymphocytic inflammation (swarm of bees) predominately CD4+ cells along with CD8+ T cells affecting anagen follicles or follicles in early catagen. [7] The characteristic initial lesion is a circumscribed, totally bald, smooth patch. Short, easily extractable broken hairs, known as exclamation mark hairs, are often seen at the margins of the bald patches during active phases of the disease. [1] The scalp is the first affected site in most cases, but any hair-bearing skin can be affected. The term alopecia totalis is applied to total or almost total loss of scalp hair, and alopecia universalis is the loss of all body hair. The extension of alopecia along the scalp margin is known as ophiasis. [1]
Children with AA demonstrate an increased levels of activated T cells leading to various autoimmune diseases like vitiligo, thyroiditis, connective tissue disorders, lichen planus, Type 1 diabetes, and pemphigus foliaceous. [4] AA causes fine stippled pitting of the nails. [1]
Geometric and superficial pits are typical of AA whereas deep and irregularly distributed pits are seen in psoriasis and atopic dermatitis. Familial aggregation of AA has been studied and it has been found that estimated lifetime risk has been 7.1% in siblings, 7.8% in parents, 5.7% in offspring. [8] Concomitant presentation of AA in siblings has been reported very rarely in the literature. AA has been also reported after allogenic bone marrow transplantation from an affected, HLA matched sibling. [9] Menon and Kiran reported a case of concomitant occurrence of AA in the sibling with emphasis on environmental precipitating factors. [10]
Evidence based management of AA in children is limited due to the lack of well controlled randomized studies. Treatment should be determined according to the patient's age and extent of alopecia. Reassurance should be given to patients with limited disease as spontaneous remission occurs in 80% of patients. [4]
Various treatment options tried in AA are topical, intralesional, and systemic corticosteroids, topical immunomodulators, and topical irritants like dithranol, psoralen plus ultraviolet A therapy, excimer laser therapy. [10],[11]
| Conclusion | | |
The authors thus conclude that although AA is a common dermatological condition. Its simultaneously occurrence in siblings is very rare. This case has been reported for its rare occurrence in siblings.
| References | | |
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| 3. | Colombe BW, Price VH, Khoury EL, Garovoy MR, Lou CD. HLA class II antigen associations help to define two types of alopecia areata. J Am Acad Dermatol 1995;33:757-64.
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| 5. | Sharma VK, Kumar B, Dawn G. A clinical study of childhood alopecia areata in Chandigarh, India. Pediatr Dermatol 1996;13:372-7.
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| 6. | Colombe BW, Lou CD, Price VH. The genetic basis of alopecia areata: HLA associations with patchy alopecia areata versus alopecia totalis and alopecia universalis. J Investig Dermatol Symp Proc 1999;4:216-9.
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| 7. | Ioffreda MD. Inflammatory diseases of hair follicles, sweat glands and cartilage. In: Elder DE, Elenitsas R, Johnson BL, Murphy GF, editors. Lever's Histopathology of the Skin. 10 th ed. Philadelphia: Lippincott Williams and Williams; 2009. p. 459-501.
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| 8. | Blaumeiser B, van der Goot I, Fimmers R, Hanneken S, Ritzmann S, Seymons K, et al. Familial aggregation of alopecia areata. J Am Acad Dermatol 2006;54:627-32.
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| 9. | Barahmani N, Whaley K, Duvic M. Alopecia areata after allogeneic bone marrow transplantation from an affected, human leukocyte antigen-matched sibling. J Am Acad Dermatol 2003;49:1192.
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| 10. | Menon R, Kiran C. Concomitant presentation of alopecia areata in siblings: A rare occurrence. Int J Trichology 2012;4:86-8.
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| 11. | Haynes JW, Persons R, Jamieson B. Clinical inquiries: Childhood alopecia areata: What treatment works best? J Fam Pract 2011;60:45-52.
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