|Year : 2017 | Volume
| Issue : 4 | Page : 149-153
Insignificant correlation between thyroid hormone and antithyroid peroxidase antibodies in alopecia areata patients in Northern Rajasthan
Gagandeep Kaur, CM Kuldeep, Puneet Bhargava, Deepak Kumar Mathur, Sonam Sharda, Pulkit Chaturvedi
Department of Dermatology, STDs and Leprosy, SMS Medical College, Jaipur, Rajasthan, India
|Date of Web Publication||5-Oct-2017|
C M Kuldeep
Department of Dermatology, STDs and Leprosy, SMS Medical College, Jaipur, Rajasthan
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Background: Alopecia areata (AA) is a common, recurrent form of nonscarring alopecia which often presents as circumscribed patches of spontaneous hair loss. The global prevalence of this disease varies from 0.1% to 0.2% in general population and 7–30 cases per 1000 dermatological patients. The etiology of AA still remains uncertain; however, genetic or environmental factor and autoimmunity are claimed responsible for it. Various autoimmune diseases, such as Hashimoto's thyroiditis, diabetes mellitus, vitiligo, and lupus erythematosus, have been reported in association with AA. Aim: The index study was aimed at estimation of serum T3, T4, thyroid-stimulating hormone, and antithyroid peroxidase (TPO) antibodies. Material and Methods: Similar age/sex-matched AA patients and controls (110 in each group). Enhanced chemiluminescence immunoassay for thyroid profile and anti-TPO antibody level estimation in veinous blood sample. Observations: The mean/standard deviation (SD) of T3 was 3.30 ± 0.84 pg/ml in AA while 3.27 ± 0.67 pg/ml in controls (P = 0.302). Serum mean/SD of T4 level was1.23 ± 0.76 ng/dl in AA patients while 1.17 ± 0.34 ng/dl in controls (P = 0.522). The mean/SD of anti-TPO levels in AA patients was 21.52 ± 35.09 while 56.43 ± 140.72 in controls (P = 0.136). Limitation: The limitation of this study was moderate number of AA patients and different genotype of study population. Conclusion: Occurrence of thyroid dysfunction and evidence of anti-TPO antibodies in AA is rare event in this study population.
Keywords: Alopecia areata, thyroid hormone, thyroperoxidase antibody
|How to cite this article:|
Kaur G, Kuldeep C M, Bhargava P, Mathur DK, Sharda S, Chaturvedi P. Insignificant correlation between thyroid hormone and antithyroid peroxidase antibodies in alopecia areata patients in Northern Rajasthan. Int J Trichol 2017;9:149-53
|How to cite this URL:|
Kaur G, Kuldeep C M, Bhargava P, Mathur DK, Sharda S, Chaturvedi P. Insignificant correlation between thyroid hormone and antithyroid peroxidase antibodies in alopecia areata patients in Northern Rajasthan. Int J Trichol [serial online] 2017 [cited 2019 Nov 19];9:149-53. Available from: http://www.ijtrichology.com/text.asp?2017/9/4/149/216024
| Introduction|| |
The word “alopecia areata” (AA) was introduced by Sauvages in his “Nosologica Medica” published in1760, in France. It is a common form of nonscarring, chronic alopecia which often presents as circumscribed patches of hair loss at scalp, beard, moustache, or body. Occasionally, it may lead to diffuse, total, ophiasis or universal baldness. In a population study of AA from Olmsted County, Minnesota, USA, the incidence was 0.1%–0.2% with a projected lifetime risk of 1.7%. Its etiology is multifactoral, where genetic , or environmental  and autoimmune hypotheses are prevailing., Current evidence indicate that AA is caused by a T-cell-mediated autoimmune mechanism., Various autoimmune disorders, such as Hashimoto's thyroiditis,, diabetes mellitus, vitiligo, and systemic lupus erythematosus, have been reported with AA., Hence, the index case–control study was conducted to observe any correlation between AA and serum T3, T4, thyroid-stimulating hormone (TSH), and antithyroid peroxidase (TPO) antibodies in the sera.
| Materials and Methods|| |
This was a hospital-based observational analysis.
This study was conducted from June 2015 to June 2016.
A total of 110 cases of clinically diagnosed AA and 110 persons of other dermatoses (without any known immunological disorders) were subjected to serum T3, T4, TSH, and anti-TPO antibody estimation. Written informed consent from every AA case and control was taken. The college Ethical Committee's permission was also taken before starting the study.
Blood samples from antecubital vein of every selected AA case and control were collected in sterilized vial, taking all aseptic precaution. The blood samples were kept at room temperature for 1 h. Then, sera were separated using test tubes and rotated in a centrifuge machine at 3000 rpm for 30 s. These sera were then subjected to enhanced chemiluminescence immunoassay - chemiluminescence (real-time polymerase chain reaction technique) for estimation of T3, T4, TSH, and anti-TPO antibodies. Important tests, such as hemogram, blood sugar, venereal disease research laboratory, and antinuclear antibody test, were performed to exclude possibility of any other diseases.
Continuous data were summarized in the form of mean and standard deviation. The differences in mean were analyzed using Student's t-test. Count data were expressed in the form of proportion. The difference in proportion was analyzed using “Chi-square test.” The level of significance was kept 95% for all statistical analysis.
| Observations|| |
Statistical analysis was performed with SPSS trial version 20 for Windows statistical software package (SPSS Inc., Chicago, IL, USA). The test normality was done by Kolmogorov–Smirnov test. The categorical data were compared as percentage and were compared among groups using “Chi-square” test. The differences among groups were analyzed using “Student's t-test.” Probability P < 0.05 was considered statistical significant.
The age-wise distribution of AA patients indicated highest percentage among 21–30 years' age group (39, 35.5%), while in controls, it was 48 (43.6%) patients [Figure 1]. The mean age of AA patients and controls was 23.64 ± 11.2 and 24.78 ± 10.51 years, respectively. It showed insignificant age difference among both groups (P = 0.270). However, any age may be affected by AA, with a peak between the second and fourth decades.
The sex distribution indicated male predominance among AA patients (71, 64.5%) and in controls (62, 56.4%) (P = 0.270). The students were predominantly affected in both groups (AA patients were 64, 54.5% while controls were 57, 51.8%, respectively). However, all occupational groups may be affected.
The family history of atopy was evident in 24 (21.8%) AA patients while in 6 (5.4%) controls. Atopic disease, especially atopic eczema, is also a common association with AA. Majority of AA patients (90, 81.8%) evidenced localized patches of alopecia (number 1–5) [Figure 2] while majority of controls (99, 90%) had acne vulgaris. Other variants of AA patients evidenced ophiasis in 6, diffuse hair loss in  alopecia universalis in 2, totalis in 2, subtotalis in 2 and sisaipho in 1 case, respectively [Figure 3] and [Figure 4]. Nail pitting in AA patients was an additional finding in 24 cases (21.8%).
The mean serum T3 level in AA patients was 3.30 ± 0.84 pg/ml with the range of 1.8–4.2 pg/ml, while in controls, it was 3.27 ± 0.67 pg/ml [P = 0.302, [Figure 5]. The mean of serum T4 level in AA group was 1.23 ± 0.76 ng/dl, while in controls, it was 1.17 ± 0.34 ng/dl (P = 0.522) [Figure 6]. The mean anti-TPO level in AA patients was 21.52 ± 35.09 IU/ml, while in control group, it was 56.43 ± 240.72 IU/ml [P = 0.176, [Figure 7].
|Figure 5: Insignificant difference in T3 level in alopecia areata patients and controls (P = 0.302)|
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|Figure 6: Serum T4 level in alopecia areata patients and controls (P = 0.522)|
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|Figure 7: Distribution of antithyroid peroxidase antibody levels in alopecia areata cases and controls (P = 0.139 NS)|
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| Discussion|| |
AA is a common, recurrent form of nonscarring hair loss. The global statistic reports show its incidence 0.1%–0.2% in general population, with lifetime risk 1.7. In the index study, the incidence of AA was 0.07% (110 cases out of 165,708 patients), which is quite less than Sharma et al. (1.3%).,,
The majority of AA patients (56%) and controls (68.2%) in this study were in the age group of 11–30 years. The mean age of AA patients was 23.6 years, while in controls, it was 26 years. It indicates that AA affects predominantly young persons, just other previous studies. It may be because of the fact that AA preferably affects pigmented hair and graying of hair usually starts at 35 years., However, many authors have reported its peak at the third to fourth decade.,,
The sex distribution of AA patients is often equal in both the genders., However, Sharma et al. reported male preponderance. The index study also showed male preponderance.
Besides genetic predisposition , and autoimmunity,,,, psychological stress  may play important role in the pathogenesis of AA. It is also indicated in the index study which showed that majority of AA patients were students. There is a complex correlation of stress and AA. Probably, sympathetic system stimulation and substance P secretion during stress of study and job, the vascular supply to scalp hair may be altered or there is an alteration of hair cycle which ultimately leads to hair loss.
Patch(es) over the scalp is the most common form of involvement in AA,,,, which was also substantiated in the index study also (84, 76% patients). However, certain uncommon forms, such as diffuse alopecia (seven cases), ophiasis/sisaipho (five cases), total/subtotal alopecia (three cases) and universal alopecia (one case), were also reported. Beard and moustache were also involved in some cases. Various authors have also reported uncommon forms of AA., The National Alopecia Areata Foundation Committee has devised “Severity of Alopecia Tool Score.” Occasionally, nails may be affected in AA in the form of fine/coarse pitting and dystrophy of nail plates. Similarly, the index study has also reported nail pitting in 21% AA patients.
The severity of AA may depend on family/personal history ,, of atopy, autoimmune disorders such as Hashimoto's thyroiditis, vitiligo, pernicious anemia, diabetes mellitus, lupus erythematosus, and other diseases.,,,,
Serum T3 and T4 levels were reported to be similar in AA cases and controls in index study (P = 0.302 and 0.136, respectively). However, Ahmed et al. have reported thyroid dysfunction in AA patients (hypothyroidism in 8.9% and hyperthyroidism in 1%). Rahnama Z et al. have also reported insignificant difference of thyroid disorders in AA cases and controls.
Bakry et al. have concluded that most of AA patients screened for thyroid functions may show thyroid autoantibodies in the absence of clinical manifestations of thyroid affection. The anti-TPO antibodies were found to be insignificant in AA patients and controls in index study. It may be because the herd population in this geographical area which may not have high prevalence of autoimmunity. However, Sharma et al. and others have also detected antithyroid antibodies in AA patients.
Seyrafi et al. conducted a retrospective analysis over 123 AA patients. Thyroid function abnormalities were found in 8.9% of patients. Positive autoantibodies were associated in 51.4% patients; however, insignificant correlation was found between severity and duration of AA and the titer of antibodies.
Kasumagic-Halilovic  conducted a study on seventy AA patients and thirty healthy volunteers. He reported thyroid dysfunction in 8 (11.4%) patients. Positive autoantibodies were associated in 18 (25.7%) patients only. The frequency of thyroid autoantibodies was significantly higher than controls (P < 0.05%).
Bakry et al. conducted a study on 55 AA patients and 50 controls regarding TSH, fT3, fT4, thyroglobulin antibody (TgAb), and anti-TPO antibody levels. They found subclinical hypothyroidism in 16% cases. They also found statistically significant difference in the values of thyroid hormones and TgAb and anti-TPO antibodies in AA patients and controls.
Saylam Kurtipek et al. studied 92 patients of AA and 108 vitiligo patients and found elevated TSH level in 7.6% of patients and 1.1% of AA patients. About 5.4% of AA patients had raised fT3 levels, 2.2% had raised anti-Tg, and 14.1% had anti-TPO antibody levels in AA patients.
Wang et al. studied the association between AA and thyroid autoimmunity in 158 Chinese patients. They reported anti-TPO antibody in 22 patients while fT3, fT4, and TSH were comparable in AA patients and controls.
| Conclusion|| |
We found insignificant correlation between thyroid profile and anti-TPO antibody levels in Alopecia Areata patients.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Bolduc C. Alopecia Areata. Medscape web portal: eMedicine 2006. p. 1-33.
Safavi KH, Muller SA, Suman VJ, Moshell AN, Melton LJ 3rd
. Incidence of alopecia areata in Olmsted County, Minnesota, 1975 through 1989. Mayo Clin Proc 1995;70:628-33.
Yang S, Yang J, Liu JB, Wang HY, Yang Q, Gao M, et al.
The genetic epidemiology of alopecia areata in China. Br J Dermatol 2004;151:16-23.
Dogra D, Sood A, Khaitan BK. Alopecia areata in identical twins. Indian J Dermatol Venereol Leprol 1996;62:199.
] [Full text]
Friedmann PS. Alopecia areata and auto-immunity. Br J Dermatol 1981;105:153-7.
Gilhar A, Kalish RS. Alopecia areata: A tissue specific autoimmune disease of the hair follicle. Autoimmun Rev 2006;5:64-9.
Friedmann PS. Decreased lymphocyte reactivity and autoimmunity in alopecia areata. B J D 1981;105:145-52.
Madani S, Shapiro J. Alopecia areata update. J Am Acad Dermatol 2000;42:549-66.
Hordinsky MK, Hallgren H, Nelson D, Filipovich AH. Suppressor cell number and function in alopecia areata. Arch Dermatol 1984;120:188-94.
Puavilai S, Puavilai G, Charuwichitratana S, Sakuntabhai A, Sriprachya-Anunt S. Prevalence of thyroid diseases in patients with alopecia areata. Int J Dermatol 1994;33:632-3.
Lewinski A, Broniarczyk-Dyla G, Sewerynek E, Zerek-Melen G, Szkudlinski M. Abnormalities in structure and function of the thyroid gland in patients with alopecia areata. J Am Acad Dermatol 1990;23(4 Pt 1):768-9.
Thomas EA, Kadyan RS. Alopecia areata and autoimmunity: A clinical study. Indian J Dermatol 2008;53:70-4.
] [Full text]
Sharma VK, Sialy R, Kumar B, Gupta S. Evaluation of thyroid function in north Indians with alopecia areata: Response to intravenous injection of 100 micrograms thyrotropin releasing hormone (TRH). J Dermatol 1999;26:339-42.
Ahmed I, Nasreen S, Jaehangir U and Wahid Z. Clinical spectrum of alopecia areata and its association with thyroid dysfunction. J Pak Assoc Dermatol 2012;22:207-12.
Messenger AG, Bleehen SS. Expression of HLA-DR by anagen hair follicles in alopecia areata. J Invest Dermatol 1985;85:569-72.
McDonagh AJ, Tazi-Ahnini R. Epidemiology and genetics of alopecia areata. Clin Exp Dermatol 2002;27:405-9.
Tobin DJ, Orentreich N, Fenton DA, Bystryn JC. Antibodies to hair follicles in alopecia areata. J Invest Dermatol 1994;102:721-4.
Baker GH. Psychological factors and immunity. J Psychosom Res 1987;31:1-10.
Price VH. Alopecia areata: Clinical aspects. J Invest Dermatol 1991;96:68S.
Muller SA, Winkelmann RK. Alopecia areata. An evaluation OF 736 patients. Arch Dermatol 1963;88:290-7.
Tan E, Tay YK, Goh CL, Chin Giam Y. The pattern and profile of alopecia areata in Singapore – A study of 219 Asians. Int J Dermatol 2002;41:748-53.
Sharma VK, Dawn G, Kumar B. Profile of alopecia areata in Northern India. Int J Dermatol 1996;35:22-7.
Manzoor S, Masood C. Aeopecia areata in Kashmir: A study of 200 patients. Indian J Dermatol Venereol Leprol 2001;67:324-5.
] [Full text]
Finner AM. Alopecia areata: Clinical presentation, diagnosis, and unusual cases. Dermatol Ther 2011;24:348-54.
Ikeda T. A new classification of alopecia areata. Dermatologica 1965;131:421-45.
Jain S, Marfatia YS. Alopecia areata – Pattern in industrial city of Baroda. Indian J Dermatol Venereol Leprol 2003;69:81-2.
] [Full text]
Kaur S, Sharma VK, Kumar L, Kumar B. Atopy and alopecia areata in North Indians. Indian J Dermatol Venereol Leprol 2002;68:267-9.
] [Full text]
Cline DJ. Changes in hair color. Dermatol Clin 1988;6:295-303.
Werth VP, White WL, Sanchez MR, Franks AG. Incidence of alopecia areata in lupus erythematosus. Arch Dermatol 1992;128:368-71.
Gandhi V, Baruah MC, Bhattacharaya SN. Nail changes in alopecia areata: Incidence and pattern. Indian J Dermatol Venereol Leprol 2003;69:114-5.
] [Full text]
Brenner W, Diem E, Gschnait F. Coincidence of vitiligo, alopecia areata, onychodystrophy, localized scleroderma and lichen planus. Dermatologica 1979;159:356-60.
Rahnama Z, Farajzadeh S, Mohmamdi S, Masaudi MA. Prevalence of thyroid disorders in patients with alopecia areata. J Pak Assoc Dermatol 2014;24:246-50.
Seyrafi H, Akhiani M, Abbasi H, Mirpour S, Gholamrezanezhad A. Evaluation of the profile of alopecia areata and the prevalence of thyroid function test abnormalities and serum autoantibodies in Iranian patients. BMC Dermatol 2005;5:11.
Kasumagic-Halilovic E. Thyroid autoimmunity in patients with alopecia areata. Acta Dermatovenerol Croat 2008;16:123-5.
Bakry OA, Basha MA, El Shafiee MK, Shehata WA. Thyroid disorders associated with alopecia areata in Egyptian patients. Indian J Dermatol 2014;59:49-55.
] [Full text]
Saylam Kurtipek G, Cihan FG, Erayman Demirbas S, Ataseven A. The frequency of autoimmune thyroid disease in alopecia areata and vitiligo patients. Biomed Res Int 2015;2015:435947.
Wang H, Gan M, Mei L, Yang G, Fang F. The association between AA and thyroid auto immunity in Chinese adult patients: A controlled study. Biomed Res 2016.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]