Abstract
AbstractBackground: In-vitro studies showed that Leucine-rich glioma inactivated 3 (LGI3) is a keratinocyte-derived cytokine that stimulates melanin synthesis and is increased after ultra violet B (UVB) irradiation. So, we postulated that LGI3 may be involved in vitiligo aetiopathogenesis and may participate in narrow band ultra violet B (NB-UVB) induced pigmentation in vitiligo.Objectives: To assess this hypothesis, lesional LGI3 immunohistochemical expression of vitiligo patients before and after NB-UVB phototherapy was studied, and its correlation with repigmentation was evaluated.Methods: Forty vitiligo patients and 20 age, sex, and skin phenotype-matched controls were enrolled. Patients were treated with NB-UVB thrice weekly for 12 weeks. VASI score was evaluated before and after NB-UVB sessions. For vitiligo patients, baseline LGI3 immunohistochemical staining was estimated, and compared to that of controls and to its post-treatment data in those patients. Results: Baseline LGI3 immunohistochemical studied parameters (expression, intensity, percentage and H score) were significantly lower in vitiligo cases than controls (p=0.003, 0.013, 0.001 and 0.001 respectively). After 12 weeks of NB-UVB phototherapy, these LGI3 immunohistochemical parameters were up-regulated and became comparable to that of controls (p >0.05 for all). There was a significant positive correlation between the improvement of both VASI score and LGI3 H score mean values (r=-0.349 , p=0.027).Study limitations: Small number of investigated subjects.Conclusion: Decreased LGI3 protein may play an active role in vitiligo pathogenesis and its up-regulation after NB-UVB phototherapy, may actively participate in NB-UVB photo-induced melanogenesis.
Highlights
Vitiligo, the most common acquired variety of leukoderma, affects nearly 0.5% - 2% of the population worldwide, irrespective of ethnic origin or race, and causes significant social and psychological complications in all affected patients.[1]Due to its multifactorial nature, the pathogenesis of vitiligo is poorly well-known.[2]
In vitiligo patients, Leucine-rich glioma inactivated 3 (LGI3) immunohistochemistry before phototherapy showed that LGI3 expression was positive in 27 patients (67.5%), most of which were of cytoplasmic localization (24, 88.9%), and revealed mild intensity (22, 81.5%) (Figure 1B)
The observed up-regulated LGI3 immunohistochemical staining parameters in vitiligo patients after phototherapy matched that of controls (p > 0.05 for all) (Table 2)
Summary
The most common acquired variety of leukoderma, affects nearly 0.5% - 2% of the population worldwide, irrespective of ethnic origin or race, and causes significant social and psychological complications in all affected patients.[1]Due to its multifactorial nature, the pathogenesis of vitiligo is poorly well-known.[2]. In segmental vitiligo, a neural hypothesis was proposed. We postulated that LGI3 may be involved in vitiligo aetiopathogenesis and may participate in narrow band ultra violet B (NB-UVB) induced pigmentation in vitiligo. Objectives: To assess this hypothesis, lesional LGI3 immunohistochemical expression of vitiligo patients before and after NBUVB phototherapy was studied, and its correlation with repigmentation was evaluated. Results: Baseline LGI3 immunohistochemical studied parameters (expression, intensity, percentage and H score) were significantly lower in vitiligo cases than controls (p=0.003, 0.013, 0.001 and 0.001 respectively). After 12 weeks of NB-UVB phototherapy, these LGI3 immunohistochemical parameters were up-regulated and became comparable to that of controls (p >0.05 for all). Conclusions: Decreased LGI3 protein may play an active role in vitiligo pathogenesis and its up-regulation after NB-UVB phototherapy, may actively participate in NB-UVB photo-induced melanogenesis.
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