DISCUSSION
Familial vitiligo is frequently reported in the literature [4], and this has lent credence to the genetic theory of the pathogenesis of vitiligo. Transmissibility is thought to be polygenic with variable expressivity. The genes involved in the pathogenesis of vitiligo includes those associated with biosynthesis of melanin, response to oxidative stress and autoimmunity [5]. Genetically primed reduction in pro-opiomelanocortin peptides and α-MSH, as well as reduced expression of other genes involved in the melanocortin system (POMC, ASIP, MC1R, MC2R, MC3R, MC4R, MC5R) and melanogenesis (TRPI, DCT) has been described in association with vitiligo [6].
Bradley et al, in their work, suggested an association between catalase gene (CAT) and vitiligo [7]. Association between HLA system and vitiligo has been described with variable and inconsistent findings. Additionally, IFN-γ, TNF-α and IL-10 and their receptors have been shown to be associated with vitiligo [8].
A number of factors have been described in associated with the onset of vitiligo. These factors as shown by Behl et al include malnutrition, emotional trauma such as loss of Job, a death of a close relative, etc, and recurrent infections. Systemic antibiotic, topical chemical agent such as adhesive binds and wearing of rubber footwears were also associated with the onset of vitiligo. These factors were probably thought to be associated with vitiligo, by disturbing the immune balance and initiating autoimmune response [4].
The occurrence of vitiligo in the mother and her daughter as shown in our case strongly suggest familial predisposition. This may not be uncommon as it has been frequently reported in the literature [2]. However, the onset of vitiligo in the child at a younger age of 3 years in contrast to the mother in whom the onset was 34 years, and the increasing severity of the lesions in the child suggests a phenomenon akin to genetic anticipation. Genetic anticipation is a phenomenon whereby genetic diseases present earlier and with increased severity in succeeding generation. These are commonly reported in association with neurological diseases such as Huntington’s disease, myotonic dystrophy, spinocerebellar ataxia and Friedreich ataxia. It has also been demonstrated in association with Behçet’s disease by Fresko et al [9].
The occurrence of vitiligo lesions on the similar site (dorsum of the foot) was noted in the mother as well as the child. The similar location in both mother and child may actually be coincidental but it’s a food for thought. Environmental factors, as well as shared traits may have played a role.
While we consider the possibility of genetic anticipation, in these patients, we also gave consideration to the concurrent onset of the lesions in both the mother and the daughter. Since the onset of disease in both parent and offspring may not necessarily occur concurrently in genetic anticipation, we thought of the likelihood of two genetically predisposed individuals (mother and daughter) being exposed to triggers since they share the same environment. Although suspected, we did not identify any triggers in these patients. Several factors including malnutrition, emotional trauma, infections, antibiotics and topical chemical agents have described in association with the onset of vitiligo [4].