Vitiligo is a condition of the skin distinguished by hypo-pigmentation. Etiology of this disorder is unknown, and several theories and mechanisms have been hypothesized. The inflammatory response in vitiligo is thought to be mediated by polymorphism in genes such as FOXP3, ACE, APE, GSTP1, TLR, SOD, CTLA-4, TAP/LMP gene cluster, etc. Theories including reactive oxygen species model, Nrf2-antioxidant response element (ARE) pathway, WNT pathway, tyrosinase activity, biochemical, molecular, and cellular alterations have been hypothesized to explain vitiligo pathogenesis. Melanosomal proteins are involved in antigen processing. The antigens are expressed to the T-cells in the form of peptides with HLA class II molecules. T-cells are activated in response to the discharge of co-stimulatory molecules such as LFA-3 as well as ICAM-1. An adaptive immune response is thus elicited, and the melanocytes eventually die or start malfunctioning and the skin undergoes hypo-pigmentation. IFN-γ is known to be a melanocyte inhibitor of paracrine origin; it is clearly involved in the early onset of symptoms of vitiligo disease. The surge in the IFN-γ levels mediates augmented expression of ICAM-1 molecule on the melanocytes, thereby establishing cytokine-mediated destruction of melanocytes. Mainly, mediators released by melanocytes and the functionality of keratinocytes decrease the disease activity. Such mediators include ET-1 as well as SCF, increase the pigmentation particularly when a patient is given with the UVB treatment. By scavenging ROS and screening UV radiation, melanin limits the damage caused to the cutaneous cells by UV radiation. Various immune responses play important roles in vitiligo.

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Vitiligo is a hypopigmentation disorder that is caused by the loss of melanocyte activity for melanin pigment generation. Vitiligo is distinguished by the existence of white macules. Vitiligo affects 0.1%-2% of individuals of different populations, irrespective of skin color, ethnic origin, race, or age. Although the actual mechanism behind this disease is not yet known, it is thought to be caused by a cumulative effect of various mechanisms (e.g., neurohormonal, genetic, cytotoxic, oxidative stress, autoimmune, and biochemical). This article reviews the published literature on various treatment modalities that might be effective in successfully treating patients with vitiligo, including phototherapies or some photochemotherapies, vitamin D analogs, topical and systemic corticosteroids, zinc treatment, anti-tumor necrosis factor agents, calcineurin inhibitors (tacrolimus, pimecrolimus), and surgical methods. This critical review also discusses a few herbal medications that may be worthy of future investigation because they have no significant side effects.

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The present investigation was planned to evaluate the nephroprotective activity of jaggery against acetaminophen (APAP)-induced renal damage in rats. The protective activity of jaggery at different doses (250, 500, and 750 mg/kg, orally) was evaluated against oxidative damage induced by APAP administration (2 g/kg, once orally in acute exposure; 20 mg/kg, orally for 21 days in subchronic exposure) in rats. APAP administration significantly increased the levels of serum urea, creatinine, and renal lipid peroxidation (LPO), whereas substantial decreases were observed in levels of glutathione (GSH), adenosine triphosphatase (ATPase), superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), and glutathione peroxidase (GPx) enzymatic activities after APAP administration. Administration of jaggery significantly moved the studied parameters toward normal levels and also reversed the histopathologic alterations. Thus, jaggery can be used to reduce renal damage and may serve as an alternative medicine in the treatment of renal etiologies.