Secondary Logo

Journal Logo

Metabolic syndrome in Egyptian patients with vitiligo

a case–control study

Sallam, Manara; Gaballah, Mohammad A.a; State, Ahmed F.a; Al-Harrass, Mohammadb

Journal of the Egyptian Women’s Dermatologic Society: May 2017 - Volume 14 - Issue 2 - p 100–105
doi: 10.1097/01.EWX.0000513078.01555.d6
Original articles

Background Metabolic syndrome (MS) is a complex of interrelated risk factors for cardiovascular diseases, diabetes mellitus, and stroke. Vitiligo is an acquired depigmenting skin disease of unknown origin and multifactorial pathogenesis. There is growing evidence that vitiligo can also be related to systemic inflammatory disorders such as obesity and MS.

Objective To clarify the association of vitiligo with chronic vascular and metabolic disorders that constitute MS.

Patients and methods A case–control study was carried out on 102 vitiligo patients and 89 age-matched and sex-matched healthy controls. MS and its individual components (abdominal obesity, hypertension, insulin resistance, and dyslipidemia) were compared between cases and controls.

Results BMI, waist circumference (WC), and serum triglycerides (TGs) were significantly lower in the patient group than the control group, whereas diastolic blood pressure, serum high-density lipoprotein cholesterol, serum fasting insulin, and insulin resistance were significantly higher in the patient group than the control group. There were no significant differences between cases and controls regarding systolic blood pressure, fasting blood glucose, and number of patients having MS. Serum fasting insulin was significantly the highest in patients with acrofacial vitiligo compared with other types of vitiligo. Patients with MS had significantly higher mean age, disease duration, Vitiligo Area Scoring Index (disease severity), and insulin resistance compared with patients without MS. Age, serum TGs, body weight, BMI, WC, and insulin resistance showed significant positive correlations with Vitiligo Area Scoring Index (disease severity).

Conclusion Vitiligo patients showed a better lipid profile, with higher levels of high-density lipoprotein cholesterol and lower TGs and WC values. In patients with vitiligo, increased insulin levels and insulin resistance may be related to other mechanisms than obesity, such as production of cytokines or autoimmune reaction to melanocytes. Further large-scale studies are needed to confirm these findings.

Departments of aDermatology, Andrology and STDs

bClinical Pathology, Faculty of Medicine, Mansoura University, Mansoura, Egypt

Correspondence to Mohammad A. Gaballah, MD, Department of Dermatology, Andrology & STDs, Faculty of Medicine, Mansoura University, El-Gomhoria St., Mansoura 35111, Egypt Tel: +20 111 861 2527; e-mail:

Received December 21, 2016

Accepted January 27, 2017

Back to Top | Article Outline


Metabolic syndrome (MS) is a complex of interrelated risk factors for cardiovascular diseases (CVDs), diabetes mellitus (DM), and stroke. These risk factors include abdominal obesity, dyslipidemia, insulin resistance (IR), hyperinsulinemia, glucose intolerance, hypertension, and a proinflammatory and prothrombotic state 1. It is a well-established condition in some inflammatory diseases including psoriasis 2–4.

Vitiligo is an acquired depigmenting skin disease of unknown origin and multifactorial pathogenesis, with an incidence of 0.5–2% worldwide. The involvement of genetic, autoimmunological, neuronal, and autocytotoxic factors is supported by several studies, and the autoimmune hypothesis remains the most accepted hypothesis 5.

There is still a debate about the relationship between vitiligo and MS. If the existence of metabolic disturbance in vitiligo is proved, the development of atherosclerosis and other CVD can be expected, which will change the future management of vitiligo patients 6.

It is well known that production of autoantibodies in vitiligo results in development of autoimmunological comorbidities such as alopecia areata, thyroiditis Hashimoto), Addison’s disease, pernicious anemia, type 1 DM, rheumatoid arthritis, systemic lupus erythematosus, and myasthenia gravis 7. Furthermore, proinflammatory cytokines such as tumor necrosis factor α (TNFα), interleukin 1 (IL-1), and IL-6 and other inflammatory factors engaged in vitiligo are known to be involved in evoking IR as well as other metabolic complications and atherosclerosis 8.

A few reports have provided information on the metabolic disturbance in vitiligo, with contradicting results – some have shown that IR and lipid profile disturbances may occur in vitiligo patients 6–9, whereas others have shown that patients with vitiligo present fewer CVD risk factors 10.

The aim of the present study was to investigate the association of chronic vascular and metabolic disorders, which constitute MS, and vitiligo in Egyptian patients. We also aimed at determining whether the prevalence of these risk factors is related to the severity of vitiligo or not.

Back to Top | Article Outline

Patients and methods

This case–control study was conducted on vitiligo patients attending the outpatient clinic of the Dermatology Department of Mansoura University Hospital, Egypt. A total of 191 individuals were included – 102 vitiligo patients and 89 individuals as controls. The control group included healthy, age-matched and sex-matched volunteers who had no dermatological or systemic diseases.

This study was approved by the Institutional Research Board of the Faculty of Medicine, Mansoura University (R/16.03.71). Informed consent was obtained from each participant before enrollment.

Exclusion criteria were as follows: age below 16 years, vitiligo lasting for less than 6 months, alcohol consumption, smoking, psoriasis, rheumatoid arthritis, ankylosing spondylitis, chronic obstructive pulmonary diseases, thyroid dysfunction, autoimmune diseases, liver diseases, malignancy, use of oral immunosuppressive or systemic corticosteroids, infections, pregnancy, lactation, and women on hormone replacement therapy.

All participants were subjected to the following:

  • Detailed history taking with regard to age, sex, occupation, marital status, special habits, drug intake, vitiligo history including onset, course, and duration of the disease, progression characteristics, associated psychological disturbances, associated medical or surgical conditions, and family history of vitiligo, DM, and CVD.
  • A general examination was carried out, and height, weight, BMI [calculated as weight (kg)/height2 (m2)], blood pressure, and waist circumference (WC) of the participants were obtained. WC was measured as the smallest trunk circumference midway between the lowest rib margin (12th rib) and the iliac crest at the end of a gentle expiration. The measurements were performed with the patients in a standing position with a relaxed abdomen, arms at sides, and their feet joined together, ensuring that the tape measure was horizontal and did not cause skin compression.
  • Dermatological examination of skin, hair, nails, and oral mucosa was carried out. Patients were diagnosed as having vitiligo through clinical examination. Diagnostic criteria for vitiligo were those of the Vitiligo European Task Force that classifies vitiligo vulgaris, acrofacial vitiligo, and vitiligo universalis as subtypes of generalized vitiligo and segmental and focal vitiligo as subtypes of localized vitiligo 11. The Vitiligo Area Scoring Index (VASI) for each patient was calculated as follows 12:
    • The percentage of vitiligo involvement is calculated in terms of hand units. One hand unit (which encompasses the palm plus the volar surface of all digits) is approximately equivalent to 1% of the total body surface area 13 and is used as a guide to estimate the baseline percentage of vitiligo involvement in each body region. The body is divided into five separate and mutually exclusive regions: hands, upper extremities (excluding hands), trunk, lower extremities (excluding feet), and feet. The axillary and inguinal regions were included with the upper and lower extremities, respectively, whereas the buttocks were included with the lower extremities. The face and neck areas were assessed for vitiligo, but these areas were not included in the overall evaluation. The extent of vitiligo is measured according to the VASI score.
    • The degree of pigmentation is estimated to the nearest of one of the following percentages: 100% – complete depigmentation, no pigment is present; 90% – specks of pigment present; 75% – depigmented area exceeds the pigmented area; 50% – pigmented and depigmented areas are equal; 25% – pigmented area exceeds depigmented area; and 10% – only specks of depigmentation present.
    • The VASI score for each body region is determined by the product of the area of vitiligo in hand units and the extent of depigmentation within each hand unit-measured patch (possible values of 0, 10, 25, 50, 75, 90, or 100%).
    • The total body VASI score is then calculated using the following formula by considering the contributions of all body regions (possible range 0–100):
  • Laboratory investigations:
    • Sampling:
    • All participants were instructed to fast for 12 h. A venous blood sample was collected from all participants. The blood samples (5 ml) were allowed to clot for 15 min and centrifuged at 7000 rpm for 10 min for serum separation into two aliquots – one was used for determining fasting serum glucose, triglycerides (TGs), and high-density lipoprotein cholesterol (HDL-C) concentrations, and the other aliquot was stored at −20°C for insulin assay.
    • Methods of assays:
      • Fasting serum glucose, TGs, and HDL-C concentrations were measured on a Cobas Integra 400 chemistry analyzer (Roche Diagnostics, Basel, Switzerland) using commercially available reagents.
      • Serum insulin was measured by enzyme-linked immunosorbent assay using an insulin quantitative BIOS kit (Chemux BioScience Inc., San Francisco, California, USA) 14.
    • IR:
    • Homeostatic model assessment of IR 15: normal less than or equal to 1.6 and IR at least 2.50:

On the basis of the clinical and laboratory data, diagnosis of MS was made according to the diagnostic criteria outlined by Alberti et al.1. A minimum of three of the following five criteria need to be fulfilled to obtain a diagnosis of MS:

  • Elevated WC: population-specific and country-specific definitions (Middle East, Mediterranean men≥94 cm and women≥80 cm).
  • Systolic blood pressure of at least 130 mmHg and/or diastolic blood pressure of at least 85 mmHg (or use of antihypertensive medication).
  • Fasting TGs of at least 150 mg/dl or use of relevant medication.
  • Fasting HDL-C of less than 40 mg/dl in males and less than 50 mg/dl in females or use of relevant medication.
  • Fasting glucose of at least 100 mg/dl.
Back to Top | Article Outline

Statistical analysis

Data were fed to a computer, and all statistical analyses were performed using statistical package for social sciences, version 20 software (IBM Corporation, Armonk, New York, USA) 16. Qualitative data were described using numbers and percentages. Quantitative data were described using minimum and maximum values, means and their SD, and medians. Comparison between different groups regarding categorical variables was performed using χ2-tests, and for continuous parametric data t-tests and analysis of variance were used. When more than 20% of the cells had expected count less than 5, correction for χ2 was conducted using Fisher’s exact test or the Monte Carlo correction. For abnormally distributed data, comparison between two groups was carried out using the Mann–Whitney U-test. Correlations between two quantitative variables were assessed using Spearman’s coefficient. Significance of the obtained results was judged at the 5% level 17. P is the calculated probability, and it was considered significant if less than 0.05.

Back to Top | Article Outline


Demographic, metabolic, and clinical criteria of vitiligo patients compared with controls are presented in Table 1. There were no significant differences between cases and controls regarding age, sex, systolic blood pressure, fasting blood glucose, and number of participants having MS. The patient group showed significantly lower BMI, WC, and serum TGs than the control group, whereas diastolic blood pressure, serum HDL-C, serum fasting insulin, and IR were significantly higher than the control group. Table 2 shows a comparison between vitiligo patients according to their clinical type regarding demographic, metabolic, and clinical criteria. Serum fasting insulin was significantly higher in patients with acrofacial vitiligo.

Table 1

Table 1

Table 2

Table 2

Comparison between vitiligo patients with and without MS (Table 3) revealed that patients with MS had significantly higher mean age, disease duration, VASI (disease severity), and IR. Table 4 shows that there were nonsignificant differences regarding VASI, serum fasting insulin, and IR between male and female patients. Finally, age, serum TGs, body weight, BMI, WC, and IR showed significant positive correlations with VASI (disease severity) (Table 5).

Table 3

Table 3

Table 4

Table 4

Table 5

Table 5

Back to Top | Article Outline


In the present study, there was no significant difference between patients and controls regarding the number of individuals fulfilling the previously mentioned criteria for diagnosis of MS as well as systolic blood pressure and fasting blood glucose levels. In addition, patients showed significantly lower BMI, WC, and serum TGs compared with the control group, whereas diastolic blood pressure and serum HDL-C were significantly higher than the control group. Diastolic blood pressure was the only characteristic of MS that showed a significant increase in vitiligo patients than in controls.

These results are in agreement with Rodriguez-Martin et al.10, who found that analysis of MS parameters revealed lower significant prevalence of altered WC, TGs, and low HDL-C in vitiligo patients. In addition, no significant differences could be observed in blood glucose levels or BMI. According to these findings, they suggested that patients with vitiligo tended to present lower CVD risk than controls, as vitiligo patients presented a better lipid profile, with higher levels of HDL-C and lower TGs and WC values.

Rodriguez-Martin et al.10 explained that these results were a result of increased levels of superoxide dismutase and glutathione peroxidase in patients with active vitiligo 18,19. This upregulation could be an enzymatic basis that makes vitiligo patients less prone to CVD 10. However, this explanation is doubted, as oxidative stress presents in vitiligo and it is responsible for the cytotoxic effects on melanocytes. Excess reactive oxygen species (ROS) were documented in active vitiligo skin – for example, high H2O2 levels were found throughout the epidermis 20.

We suggested that a relatively short vitiligo history (2–6 years duration) may explain the nonstatistically different values between the studied and control groups as well as absence of lipid abnormalities and metabolic disturbances such as obesity, hypertension, and DM in the studied patients. We found that vitiligo patients with MS had statistically significant higher mean age, disease duration, VASI (disease severity), and IR than patients without MS. In addition, this explanation was suggested by Pietrzak et al.21 but in children with vitiligo (0.5–9 years duration).

Almost similar to our results, Karadag et al.9 reported that no significant differences were present between vitiligo patients and controls regarding BMI, WC, fasting blood glucose, serum TGs, and diastolic blood pressure measurements. Yet, vitiligo patients had significantly lower HDL-C levels than controls, and systolic blood pressure of the patients was significantly higher than controls. These changes could be due to IR and hyperinsulinemia found in vitiligo patients. Hyperinsulinemia may increase the production of very low-density lipoprotein TGs, and IR can raise blood pressure 22.

On the other hand, investigation of lipid disturbances in vitiligo children revealed decreased levels of HDL-C as well as increased TGs concentrations in the studied group of vitiligo girls 6. In another study, HDL-C concentration was significantly lower in the studied vitiligo children in comparison with the healthy control group 7. In addition, in more recent study, it was reported that HDL-C concentration was significantly lower in children with vitiligo compared with healthy controls, whereas no significant differences were observed regarding height, weight, BMI, fasting serum glucose, and serum TGs of children with vitiligo and healthy children 21.

This can be explained as proinflammatory cytokines TNF, IL-1, IL-6 and other inflammatory factors (e.g. C-reactive protein) are involved in evoking IR as well as other metabolic complications and atherosclerosis 8. In addition, higher levels of homocysteine reported in vitiligo patients may be involved in the development of the metabolic disturbances in vitiligo patients and increase CVD risk 23,24. Furthermore, hypovitaminosis D reported in vitiligo patients may increase CVD risk 25.

As oxidative stress plays a vital role in the pathogenesis of both MS and vitiligo, metabolic disturbances in vitiligo seem to be a result of increased production of ROS. Excessive ROS is known to be responsible for lipid peroxidation, protein oxidation, and oxidative DNA damage 26. The processes promoting lipid peroxidation that occur in the epidermis, and perhaps in the adipose tissue as well, may be a plausible explanation for the lipid abnormalities detected 21.

In the present study, serum fasting insulin and IR (homeostatic model assessment of IR) were significantly higher in the patient group compared with the control group. Serum fasting insulin was significantly higher in patients with acrofacial vitiligo. In agreement with this, Karadag et al.9 reported similar results. Additional contributors to IR include abnormalities in insulin secretion and insulin receptor signaling, impaired glucose disposal, and proinflammatory cytokines. The relationship between impaired glucose tolerance and IR is well documented. Reilly et al.27 believe that insulin assays or alternative biomarkers of IR may facilitate CVD risk prediction in individuals with MS. Even without diabetes, IR is a major risk factor for CVD and early mortality.

The association of vitiligo with glucose intolerance, IR, lipid abnormalities, hyperhomocysteinemia also characterizes systemic involvement in the skin disease 6,9,20, and the proinflammatory cytokines TNF, IL-1, and IL-6 and other inflammatory factors involved in vitiligo are known to be involved in evoking IR as well as other metabolic complications and atherosclerosis 8.

There were nonsignificant differences regarding VASI, serum fasting insulin, and IR between male and female patients. Rodriguez-Martin et al.10 also reported that no significant differences could be observed between all studied variables regarding sex in the patient group.

Finally, in the present study, age, serum TGs, body weight, BMI, WC, and IR of the vitiligo patients showed significant positive correlations with VASI (disease severity). This can be expected as proinflammatory cytokines (TNF, IL-1, IL-6), other inflammatory factors, ROS, and lipid peroxidation involved in vitiligo showed increased levels and activity with increased disease severity. These factors also are known to be involved in evoking IR, lipid abnormalities, as well as other metabolic complications and atherosclerosis 8,20,26.

Finally, despite absence of a defined significant association between vitiligo and MS, we expect development of such a relationship with longer duration of the disease and lifetime of the patient as vitiligo and MS have shared etiopathogenic factors – for example, proinflammatory cytokines and oxidative stress. In addition, there is a shared genetic background for both conditions. The angiotensin-converting enzyme gene and catalase gene were reported to be susceptibility genes in vitiligo and MS patients 28–32. In addition, the HLA region, IFIH1, BTNL2, IL2RA, SH2B3, IKZF4, and CASP7 are vitiligo risk loci involved in pathways and are shared with type 1 DM, whereas the ZMIZ1 gene is shared with type 2 DM 33.

Back to Top | Article Outline


Although the present study showed a nonsignificant relationship between vitiligo and MS, further studies are needed to approve or deny our results and to reach a clear conclusion about the pathogenic connection between them that will be of clinical importance.

Back to Top | Article Outline

Conflicts of interest

There are no conflicts of interest.

Back to Top | Article Outline


1. Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, et al. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation 2009; 120:1640–1645.
2. Reich K. The concept of psoriasis as a systemic inflammation: implications for disease management. J Eur Acad Dermatol Venereol 2012; 26 (Suppl 2):3–11.
3. Armstrong AW, Harskamp CT, Armstrong EJ. Psoriasis and metabolic syndrome: a systematic review and meta-analysis of observational studies. J Am Acad Dermatol 2013; 68:654–662.
4. Ahmed EF, Seliem MK, El-kamel MF, Abdelgawad MM, Shady I. Prevalence of metabolic syndrome in Egyptian patients with psoriasis. Egypt J Derm Androl 2009; 29:91–100.
5. Alikhan A, Felsten LM, Daly M, Petronic C, Rosic V. Vitiligo: a comprehensive overview part 1. Introduction, epidemiology, quality of life, diagnosis, differential diagnosis, associations, histopathology, etiology and work up. J Am Acad Dermatol 2011; 65:473–491.
6. Pietrzak A, Lecewicz-Torun B, Urban J. Comparison of serum lipids in girls affected with vitiligo and control group. Ann Univ Mariae Curie Sklodowska Med 2000; 55:269–274.
7. Pietrzak A, Bartosinska J, Hercogova J, Lotti TM, Chodorowska G. Metabolic syndrome in vitiligo. Dermatol Ther 2012; 25:41–43.
8. Page S, Chandhoke V, Baranova A. Melanin & melanogenesis in adipose tissue: possible mechanisms abating oxidative stress and inflammation. Obes Rev 2011; 12:e21–e31.
9. Karadag AS, Tutal E, Ertugrul DT. Insulin resistance is increased in patients with vitiligo. Acta Derm Venereol 2011; 91:541–544.
10. Rodriguez-Martin M, de Paz NM, Mehtani P, Ferrer PC, Eliche MP, Martin BR, et al. Patients with vitiligo present fewer cardiovascular risk factors: results from a case control study. J Eur Acad Dermatol Venereol 2013; 27:124–125.
11. Taieb A, Picardo M. The definition and assessment of Vitiligo: a consensus report of The Vitiligo European Task Force. Pigment Cell Res 2007; 20:27–35.
12. Hamzavi I, Jain H, McLean D, Shapiro J, Zeng H, Lui H. Parametric modeling of narrowband UV-B phototherapy for vitiligo using a novel quantitative tool: the Vitiligo Area Scoring Index. Arch Dermatol 2004; 140:677–683.
13. Rossiter ND, Chapman P, Haywood IA. How big is a hand? Burns 1996; 22:230–231.
14. Turkington RW, Estkowkski A. Secretion of insulin or connecting peptide; a predictor of insulin dependence of obese diabetics. Arch Intern Med 1982; 142:1102–1105.
15. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985; 28:412–419.
16. Ketoz S, Balakrishnan N, Read CB, Vidakovic B. Encyclopedia of statistical sciences, 2nd ed. Hoboken, NJ: Wiley-Interscience; 2006.
17. Leslie E, Geoffrey J, James M. Leslie E, Geoffrey J. Statistical analysis. . Interpretation and uses of medical statistics, 4th ed. Oxford, UK: Scientific Publications; 1991. 411–416.
18. Feily A, Pazyar N. Why vitiligo is associated with fewer risk of skin cancer? Providing a molecular mechanism. Arch Dermatol Res 2011; 303:623–624.
19. Danmak I, Boudaya S, Ben Abdallah F, Turki H, Attia H, Hentati B. Antioxidant enzymes and lipid peroxidation at the tissue level in patients with stale and active vitiligo. Int J Dermatol 2009; 48:476–480.
20. Arunachalam M, Dragoni F, Colucci R, Berti S, Crocetti E, Galeone M, et al. Nonsegmental vitiligo and psoriasis comorbidity – a case–control study in Italian patients. J Eur Acad Dermatol Venereol 2014; 28:433–437.
21. Pietrzak A, Bartosinska J, Dybiec E, Chodorowska G, Krasowska D, Hercogova J, Lotti T. Hepato-splenic and lipid profile abnormalities – do they exist in children affected with vitiligo? Acta Dermatovenerol Croat 2014; 22:19–25.
22. Grundy S. Obesity, metabolic syndrome, and cardiovascular disease. J Clin Endocrinol Metab 2004; 89:2595–2600.
23. Silverberg JI, Silverberg NB. Serum homocysteine as a biomarker of vitiligo vulgaris severity: a pilot study. J Am Acad Dermatol 2011; 64:445–447.
24. Karadag AS, Tutal E, Ertugrul DT, Akin KO, Bilgili SG. Serum holotranscobalamine, vitamin B12, folic acid and homocysteine levels in patients with vitiligo. Clin Exp Dermatol 2012; 37:62–64.
25. Nunes JP, Martins CS. Myocardial infarction, hypovitaminosis D and vitiligo. Rev Port Cardiol 2010; 29:839–840.
26. Zhou SS, Li D, Zhou YM, Cao JM. The skin function: a factor of anti-metabolic syndrome. Diabetol Metab Syndr 2012; 4:15.
27. Reilly M, Wolfe M, Rhodes R, Girman C, Mehta N, Rader D. Measures of insulin resistance add incremental value to the clinical diagnosis of metabolic syndrome in association with coronary atherosclerosis. Circulation 2004; 110:803–809.
28. Abdel Azeem NE, Attallah DA, Hussein AA, Alzzubidi NAS. The angiotensin-converting enzyme insertion/deletion polymorphism of vitiligo in a population in Upper Egypt: a hospital-based study. J Egypt Women Dermatol Soc 2016; 13:129–132.
29. Casp CB, She JX, Mccormack WT. Genetic association of the catalase gene (CAT) with vitiligo susceptibility. Pigment Cell Melanoma Res 2002; 15:62–66.
30. Alvarez-Aguilar C, Enriquez-Ramirez ML, Figueroa-Nunez B, Gomez-Garcia A, Rodriguez-Ayala E, Moran-Moguel C, et al. Association between angiotensin-1 converting enzyme gene polymorphism and the metabolic syndrome in a Mexican population. Expert Mol Med 2007; 39:327–334.
31. Fiatal S, Szigethy E, Szeles G, Toth R, Adany R. Insertion/deletion polymorphism of angiotensin-1 converting enzyme is associated with metabolic syndrome in Hungarian. J Renin Angiotensin Aldosterone Syst 2011; 12:531–538.
32. Hebert-Schuster M, Fabre E, Nivet-Antoine V. Catalase polymorphisms and metabolic diseases. Curr Opin Clin Nutr Metab Care 2012; 15:397–402.
33. Shen C, Gao J, Sheng Y, Dou J, Zhou F, Zheng X, et al. Genetic susceptibility to vitiligo: GWAS approaches for identifying vitiligo susceptibility genes and loci. Front Genet 2016; 7:3.

homeostatic model assessment of insulin resistance; insulin resistance; metabolic syndrome; vitiligo

© 2017 Egyptian Women's Dermatologic Society