Melasma is an acquired hypermelanosis of sun-exposed skin, typically manifesting as symmetrical brown macules over the face. It disproportionately affects women and is influenced by genetic, hormonal, and ultraviolet radiation (UVR) factors.1,2

While external triggers are well-known, systemic contributors, particularly endocrine and autoimmune factors, are increasingly recognized.5

Among these, thyroid dysfunction—especially subclinical hypothyroidism—has garnered interest. Thyroid hormones regulate skin homeostasis, and elevated thyroid-stimulating hormone (TSH) may influence melanogenesis through the melanocortin system or indirectly via inflammatory and oxidative stress pathways.6,7 However, published data on the correlation between TSH levels and melasma remain inconsistent.

This study aimed to explore TSH levels in melasma patients and examine their relationship with clinical patterns and severity.

Study Design and Duration:

Prospective descriptive cross-sectional study conducted over 1 year.

Study Setting:

Department of Dermatology, MVJ Medical College and Research Hospital, Bangalore.

Sample Size:

50 patients clinically diagnosed with melasma.

Inclusion Criteria:

1.Age >18 years

2.Clinical diagnosis of melasma

3.No prior thyroid disorders or systemic conditions affecting thyroid function

Exclusion Criteria:

a.Pregnancy or lactation

b.History of thyroid disease or use of thyroid-altering medications (e.g., lithium, amiodarone)

c.Use of oral contraceptives, HRT, or iron supplements

d.Chronic liver disease or systemic autoimmune illness

Methodology:

1. Detailed demographic and clinical data were collected.
2. Wood’s lamp was used to classify melasma into epidermal, dermal, or mixed types.
3. Modified MASI score was calculated using 0.3 x (Darkness of forehead x Area involved of forehead) + 0.3 x (Darkness of right malar  x Area involved of right malar) + 0.3 x ( (Darkness of left malar  x Area involved of left  malar)+0.1 x (Darkness of chin  x Area involved of chin)10

Intensity and Homogeneity of pigmentation categories:

0 = None, 1 = Mild, 2 = Moderate, 3 = Marked, 4 = Maximal

Affected area categories:

0 = Normal skin; 1 = ≤10%; 2 = 10–29%; 3 = 30–49%; 4 = 50–69%; 5 = 70–89%; 6 = 90–100%

5. TSH levels were measured using a standardized chemiluminescent immunoassay.
6. Statistical tests included ANOVA and Pearson correlation; p < 0.05 was considered significant.

Demographic Characteristics:

37. Mean age: 37.4 years (range 22–54)
38. Female predominance: 83% women

Clinical Distribution:

• Mixed Melasma:39%
• Epidermal Melasma:32%
• Dermal Melasma:29%

Mean TSH Levels by Melasma Type:

3. Dermal: 3.39 ± 1.57 mIU/L
4. Epidermal: 2.80 ± 1.56 mIU/L
5. Mixed: 3.02 ± 1.44 mIU/L
6. ANOVA p-value: 0.313 (not significant)

Correlation Analysis:

TSH vs. mMASI score: r = -0.025, p = 0.807 (non-significant)

Thyroid hormones play a critical role in skin physiology, including melanogenesis, through direct effects on melanocyte metabolism and indirect modulation via the hypothalamic-pituitary-thyroid (HPT) axis. Elevated TSH levels, particularly in subclinical hypothyroidism, have been proposed as potential contributors to hyperpigmentation. However, our study, despite documenting a mildly elevated mean TSH level, did not establish a statistically

Trivedi et al. (2015) demonstrated elevated TSH and thyroid antibodies in melasma patients, highlighting a potential role of thyroid autoimmunity2. Achar and Rathi (2011) presented epidemiological evidence supporting hormonal influences in melasma, particularly in women.3

Kheradmand et al. (2019) conducted a systematic review and meta-analysis that confirmed a statistically significant association between thyroid dysfunction—especially hypothyroidism—and melasma, thereby supporting the theory of endocrine contribution.4

Kim et al. (2020) examined the interplay of thyroid autoimmunity and oxidative stress, suggesting that autoantibodies may amplify melanogenesis through inflammatory cascades. 5

Babu et al. (2015) observed a higher frequency of thyroid dysfunction in melasma patients, although without statistically significant differences in mean TSH levels.6

Shah and Desai (2016) found elevated anti-TPO antibodies and subclinical hypothyroidism, supporting an autoimmune pathogenesis.7

Mehmood et al. (2020) identified that 60% of melasma patients exhibited clinical or subclinical hypothyroidism, reinforcing the recommendation for thyroid function screening in affected individuals.8

Chandrakanth and Shilpa (2022) provided additional insight by linking iron deficiency with thyroid dysfunction in female melasma patients, emphasizing the need to assess both hormonal and nutritional status when managing chronic pigmentary disorders.9

Together, these studies build a compelling narrative that melasma is not merely a result of cutaneous photodamage but may reflect underlying systemic disturbances. Although our study did not reveal statistically significant findings, the trends observed support broader screening protocols. Limitations such as absence of a control group, modest sample size, and lack of anti-TPO and ferritin testing must be addressed in future research.

Comprehensive studies incorporating thyroid profiles, autoantibodies, micronutrient levels, and environmental factors will help clarify the multifactorial pathogenesis of melasma. Such efforts could eventually guide holistic, multidisciplinary therapeutic approaches.

Figure 1                                       Figure 2                                     

Figure 1 melasma noted over the bilateral malar and upper lip

Figure 2melasma noted over the nasal bridge

Figure 3 & 4 melasma noted over the temple and b/l malar area

This study found no significant association between TSH levels and clinical variants or severity of melasma in 50 patients. While thyroid dysfunction remains a plausible systemic contributor to pigmentary disorders, TSH alone may not serve as a reliable biomarker for melasma.

Future studies should focus on thyroid autoantibodies, free T3/T4, and comparative analysis with healthy controls to elucidate the role of thyroid function in melasma more comprehensively.

Conflicts of Interest:None declared.

Funding: Self-funded.

Acknowledgments:We acknowledge the support of our faculty, technical staff, and patients who participated in this study.

Ethical Clearance: Obtained from the Institutional Ethics Committee, MVJ Medical College and Research Hospital, Bangalore.

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