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| LETTER TO THE EDITOR |
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| Year : 2022 | Volume
: 9
| Issue : 1 | Page : 59-62 |
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Premature graying of hair observed as the commonest cutaneous association in vitiligo in a comparative cross-sectional study: a component to be pondered
Nair Divya1, Priya Prathap2, Neelakandhan Asokan2
1 West Fort Hospital, Thrissur, Kerala, India
2 Government Medical College, Thrissur, Kerala, India
| Date of Submission | 12-Mar-2021 |
| Date of Decision | 03-Oct-2021 |
| Date of Acceptance | 28-Oct-2021 |
| Date of Web Publication | 16-May-2022 |
Correspondence Address:
Dr. Priya Prathap
Gitanjali, Kadavil Lane, Chembukkavu, Thrissur 680020, Kerala
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/pigmentinternational.pigmentinternational_
How to cite this article:
Divya N, Prathap P, Asokan N. Premature graying of hair observed as the commonest cutaneous association in vitiligo in a comparative cross-sectional study: a component to be pondered. Pigment Int 2022;9:59-62 |
How to cite this URL:
Divya N, Prathap P, Asokan N. Premature graying of hair observed as the commonest cutaneous association in vitiligo in a comparative cross-sectional study: a component to be pondered. Pigment Int [serial online] 2022 [cited 2022 Jun 29];9:59-62. Available from: https://www.pigmentinternational.com/text.asp?2022/9/1/59/345296 |
Premature graying of hair (PGH) is an entity of concern. PGH is defined as graying of hair before the age of 20 years in Whites, 25 years in Asians, and 30 years in Africans.[1] PGH was noted as the commonest cutaneous association among patients with vitiligo when we did a comparative cross-sectional analysis. Our observation suggests that PGH could have similar pathogenesis as that of vitiligo. Treatment options for PGH could be expanded by exploring our finding.
One hundred and twenty consecutive patients with vitiligo (cases) and an equal number of age- and gender-matched patients with dermatophytic infections (controls) were examined for coexisting cutaneous illness. Relatives of patients with vitiligo were excluded as controls.
Demographic and clinical characteristics of patients with vitiligo are summarized in [Table 1]. | Table 1 Demographic and clinical characteristics of patients with vitiligo
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Clinical types of vitiligo observed among our patients are shown in [Figure 1]. Coexisting cutaneous illnesses were noted (44/120; 36.6%) among cases and (22/120; 18.3%) controls. The commonest cutaneous association identified was PGH (7/120; 6%) among cases, whereas dermatosis papulosis nigra (10/120; 8%) in controls. PGH was not identified as a cutaneous association among controls. In our study, graying of hair among patients ≤25 years were considered to have PGH. None of our patients with PGH had family history of PGH.
Cutaneous associations observed among cases and controls are summarized in [Table 2].
Statistical significance was noted on comparing occurrence of PGH among cases and controls by Fisher exact test (P = 0.0143) [Table 3]. | Table 3 Comparison of occurrence of premature graying of hair between cases and controls
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The etiopathogenesis of PGH remains obscure. Autosomal dominant inheritance is suggested. PGH has been associated with pernicious anemia, vitamin B12 deficiency, hyper/hypothyroidism, ageing syndromes such as progeria, or can be idiopathic.[2]
Thyroid function test, peripheral smear, and serum vitamin B12 estimation were performed as part of evaluation for all patients with vitiligo. The results were normal among those who had PGH. Hence, those factors as the cause for PGH were ruled out.
Sehgal et al. had mentioned PGH, alopecia areata, halo nevus, and lichen planus as frequently reported associations in vitiligo.[3] Cutaneous associations in patients with vitiligo reported in previous studies are summarized in [Table 4]. | Table 4 Comparison of cutaneous diseases associated with vitiligo reported in previous studies with the present study
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The PGH was observed as the commonest cutaneous association of vitiligo in our study but not in certain other earlier studies. This may be explained by the impact of oxidative stress as an etiologic factor in PGH. Reactive oxygen species (ROS) disrupts tyrosinase activity, melanogenesis, melanosome transfer, and melanocyte survival in hair follicle pigmentary unit.[4] The modern lifestyle associated with environmental stressors (ultra violet rays, ionizing radiations, and pollutants) and xenobiotics has a significant influence in induction of oxidative stress.[5]
On searching the literature to know whether PGH is linked to vitiligo, we came across the concept of follicular vitiligo (FV). Ezzedine et al. in 2012 had initially proposed FV, which has distinct clinical, histopathologic, and dermoscopic features.[6] FV is diagnosed by noting the absence of follicular melanocytes on biopsy from a depigmented hair follicle, with preserved melanocytes in surrounding normal skin and absence of perifollicular inflammation. Molecular studies have suggested that epidermal and follicular melanocyte units are antigenically distinct. Hence, autoantibodies can target follicular melanocyte alone without affecting the normal skin around. Treg cells have been considered to result in loss of immune tolerance of stem cells in hair follicle which in turn results in FV.[7]
The FV has to be differentiated from leukotrichia where vellus hairs are usually affected in contrast to terminal hairs in FV. In leukotrichia, hair involvement is secondary to skin involvement.[8]
To the best of our knowledge, FV is reported only in less than 10 patients. The clinical presentation in them was as generalized white hairs on normal skin. Kamat et al. reported that all these patients developed vitiligo later. Family history of PGH was present among the three of them.[9]
Kumar et al. had tried psoralen + ultra violet A obtained from sunlight (PUVASOL) therapy in PGH when he observed that PGH improved in a patient with psoriasis on PUVA.[10] This treatment response reinforces the link between FV and PGH. However, Nigam and Nigam had observed inconsistent results with PUVASOL in PGH. Agarwal and Khemani had tried narrow band ultraviolet B (NB-UVB) comb phototherapy in 32 patients thrice weekly for 6 months.[11] None of them had repigmentation of hair at sixth month. Hence, they had suggested for a larger study design to assess the role of NB-UVB comb in treatment of PGH.
Jimbow et al. had suggested an association of vitiligo with early graying of hair.[12] Oxidative stress on follicular melanocytes was projected as the reason. So antioxidants could be beneficial in PGH.
Pathogenesis of vitiligo and PGH are multifactorial. Some factors such as oxidative stress, catalase depletion, vitamin B12 deficiency, and hormonal factors such as thyroid are in common to both vitiligo and PGH. Vitamin B12 downregulates homocysteine production. Homocysteine inhibits tyrosinase and leads to release of ROS that can inhibit melanin synthesis and destructs melanocytes. Hence, therapies against oxidative stress, pseudocatalase, phototherapy, and correction of vitamin B12 and thyroid hormone deficiency if any were found to be beneficial for vitiligo and PGH. Topical steroids and calcineurin inhibitors which are used in management of vitiligo are not mentioned in treatment of PGH.
The strength of our study was the comparative cross-sectional study design. However, the temporal association between cutaneous associations and vitiligo could not be ascertained was our limitation.
To conclude, PGH as the commonest cutaneous association observed among patients with vitiligo in our study compared to controls (P = 0.0143) deserves attention. Patients with PGH need to be followed up for the development of vitiligo in the future. FV may also be considered as one among the reasons for PGH which may open up newer armamentarium for treatment options in PGH. NB-UVB comb phototherapy and antioxidants could be beneficial in PGH. Evaluation to rule out other causes of PGH is mandatory as multiple factors often coexist. Future studies with larger cohorts will enable us to establish the link between PGH and FV.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | |  |
| 1. | Pandhi D, Khanna D. Premature greying of hair. Indian J Dermatol Venereol Leprol 2013;79:641-53.  [ PUBMED] [Full text] |
| 2. | Nigam PK, Nigam P. Premature greying of hair (premature canities): a concern for parent and child. J Pigment Disord 2017;4:260. |
| 3. | Sehgal VN, Srivastava G. Vitiligo: Compendium of clinico-epidemiological features. Indian J Dermatol Venereol Leprol 2007;73:149-56. [ PUBMED] [Full text] |
| 4. | O’Sullivan JD, Nicu C, Picard M et al. The biology of human hair greying. Biol Rev Camb Philos Soc 2021;96:107-28. |
| 5. | Pizzino G, Irrera N, Cucinotta M et al. Oxidative stress: harms and benefits for human health. Oxid Med Cell Longev 2017;2017:8416763. |
| 6. | Ezzedine K, Amazan E, Séneschal J, Cario-André M, Léauté-Labrèze C, Vergier B et al. Follicular vitiligo: a new form of vitiligo. Pigment Cell Melanoma Res 2012; 25:527-9. |
| 7. | Gan EY, Cario-André M, Pain C et al. Follicular vitiligo: a report of 8 cases. J Am Acad Dermatol 2016;74:1178-84. |
| 8. | Cabrera R, Reculé F, Hojman L, Lorrando J. Follicular vitiligo: dermatoscopic features of a new subtype of vitiligo. An Bras Dermatol 2019;94:120-1. |
| 9. | Kamat D, Prabhakaran N, Malathi M. Follicular vitiligo: a rare presentation of vitiligo. Indian J Dermatol Venereol Leprol 2019;85:414-5. [ PUBMED] [Full text] |
| 10. | Kumar AB, Shamim H, Nagaraju U. Premature graying of hair: review with updates. Int J Trichol 2018;10:198-203. [Full text] |
| 11. | Agarwal S, Khemani U. Premature canities: a clinical and investigative study with role of phototherapy in treatment. Unpublished data. Downloaded from abstract book of 24th World Congress of Dermatology. Milan; 2019. |
| 12. | Jimbow, Chen H, Park JS, Thomas PD. Increased sensitivity of melanocytes to oxidative stress and abnormal expression of tyrosinase-related protein in vitiligo. Br J Dermatol 2001;144:55-65. |
[Figure 1]
[Table 1], [Table 2], [Table 3], [Table 4]
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