CTRI

Need of the study:- Hyperpigmented lesions on the face have always been a distressing symptom to the patient. In the present era, people have been showing a growing interest in physical appearance. Hence, the number of patients seeking dermatologist care for facial hypermelanosis has been increasing day by day¹.

Melasma is a common acquired disorder characterized by symmetric, hyperpigmented patches with an irregular outline, occurring most commonly on the face².

In Unani books it is termed “kalaf” or “Jhayian” [IUMT-5.13.13] and has been described by ancient Unani physicians as the accumulation of blood under the skin due to the rupture of minute capillaries, this accumulated blood is the reason for hyperpigmentation³.

Hence, the present study was planned to clinically evaluate the efficacy of topical unani formulation Ghaza Husne Afza in the management of Epidermal Melasma (Kalaf).

Review of Literature:

The term MELASMA (Kalaf) comes from the Greek word “melas”, which means black. In 1923, Dr. W.G Spencer proposed a theory for the origin of melanin. In 1929, Dr. Gupta used the term “Melanoderma” to describe a butterfly distribution of facial pigmentation with varying intensity⁹.

Melasma is the most common cause of facial melanosis and is manifested by hyperpigmented macules on the face that become more pronounced after sun exposure⁵. Light to dark brown or brown-gray patches with irregular borders appear primarily on the face. The areas of hypermelanosis are distributed symmetrically in three classic patterns: [1] centrofacial (most common), involving the forehead, cheeks, nose, upper lip (sparing the philtrum and nasolabial folds), chin; [2] malar, affecting the cheeks and nose; and [3] mandibular, along the jawline². The etiology is multifactorial. Ultraviolet radiation is thought to be the most significant trigger. It activates inducible nitric oxide and reactive oxygen species (ROS), thereby promoting melanogenesis. Genetic predisposition is thought to be an important factor in the development of melasma. Increased prevalence of melasma in pregnancy, OCP use, and other hormonal therapies suggest a possible hormonal etiology as well. Besides, melasma has been found to coexist with lentigines, nevi, and thyroid disease. Histology shows increased melanin deposition in the epidermis (basal and suprabasal keratinocytes) and/or dermis (superficial and mid, maybe perivascular)⁶.

Melasma has classically been subdivided into four types: -²

1. Epidermal

2. Dermal

3. Mixed

4. Indeterminate

In theory, lesions with increased epidermal melanin are accentuated and those with increased dermal melanin becomes less obvious (i.e. blend with uninvolved skin) with Wood’s lamp examination². Treatment options include photoprotection and topical medications [hydroquinone(HQ), corticosteroids, retinoids, 4-n-butyl resorcinol, tranexamic acid, niacinamide, ascorbic acid, azelaic acid, kojic acid, arbutin, N-acetyl-4-S-cysteaminylphenol, mequinol, alpha-tocopheryl ferulate, licorice, flavonoids, beta-carotene, rucinol, dioic acid, methimazole, silymarin, etc.] Systemic medications include tranexamic acid, glutathione, L-cysteine peptide, polypodium leucotomos extract, oral antioxidants (vitamins A, C, and E), pycnogenol/procyanidin, melatonin, herbal extracts (Rhus vernciflua), etc. Procedural therapies include chemical peeling (glycolic, mandelic, trichloroacetic acid, tretinoin, obagi blue peel, combination peels, etc.), micro-needling, lasers (low-frequency Q-switched Nd: YAG laser), nonpolar radiofrequency, and a newer technique (laser toning or laser facial). Other physical modalities like microneedling are also used for recalcitrant melasma⁶.