A few studies have reported abnormalities along with Becker’s nevus in some patients. There are cases of breast hypoplasia, pectoralis major aplasia, hypoplasia of right leg, defects in the maxilla, and adipose tissue simultaneously with the presence of Becker’s nevus. The observation of these abnormalities, together with Becker’s nevus (which can have an ectodermal origin), suggest that the lesion be a part of an epidermal nevus syndrome called Becker’s nevus syndrome (
4). These cases indicate the importance of the clinical and laboratory investigations and precise follow-up in identifying associated abnormalities in each patient with this lesion. After examining the patient for the presence of the mentioned abnormalities, we found no suspicious findings. Previous studies have not reported an association between RA and this lesion. Besides, although RA and the lesion co-existed in this patient, the development of RA was apparently after the development of the lesion; therefore, it is unlikely that this presentation can be interpreted as Becker’s nevus syndrome. Another remarkable factor is that the patient had been treating with prednisolone, methotrexate, and hydroxychloroquine for a long period for RA. Various reports have described the effects of these drugs on skin pigmentation. A study in 2016 reported that although topical corticosteroids might result in hypopigmentation due to potential melanocyte dysfunction, topical or oral use of corticosteroids, such as prednisolone, was effective in improving the pigmentation of patients with vitiligo (
5). Another study revealed the development of hyperpigmentation in the skin of some patients taking methotrexate (
6). Also, Chloroquine has a high affinity for melanin and potentially could increase the photosensitivity and phototoxicity; therefore, it could impair melanogenesis (
7). A case-control study in 2013 reported the prevalence of hydroxychloroquine-induced hyperpigmentation up to 7% (
8). On the other hand, previous studies have suggested intermittent maintenance laser therapy, due to a high chance of recurrence, especially in the sun-exposed areas (
9). Moreover, transient hyperpigmentation following laser was reported in another study (
10). Notably, the compelling point about this case was that not only she did not develop hyperpigmentation, but also after laser therapy, recovery was evident in the nevus, and recurrence did not occur.
The significant role of these drugs in the effectiveness of treatment cannot be verified by the previous pieces of evidence presented in this report. Nevertheless, given that immune cells, such as dermal melanophage may be present in the lesion, a correlation between the immune system alteration and the exacerbation of this lesion may exist (
11); therefore, the immune deficiency caused by these immunosuppressive drugs can contribute to the healing of the lesion and the favorable response to laser therapy (without any recurrence). Iyidal et al. (
12) described a patient who had both vitiligo and Becker’s nevus at the same time; however, Becker’s nevus had developed ten years after the onset of vitiligo. Although it cannot be justified scientifically, the effects of cytokines released by CD8+ T lymphocytes may have been a possible cause of this observation. According to these observations, as well as considering our patient’s status, it can be concluded that immune system involvement may be useful in the occurrence of such a lesion. If such a connection exists, it may be effective to suppress the immune system for the treatment of these patients. However, this justification for choosing treatment is not yet decisive, and extensive studies with large sample sizes are needed to prove these theories.