Chemical Leukoderma or Vitiligo – Where Do We Draw the Line? A Case Report

Vitiligo is a depigmenting disorder influenced by genetic and environmental factors. Chemical leukoderma (CL) can be considered as a subtype of vitiligo due to its complicated pathogenesis. In literature, many chemical products were reported to have induced vitiligo [1]. Along with the rise of online platforms, there is a palpable corresponding increase in topical agents’ misuse, usually endorsed by non-licensed advisors [2].

A 26-year-old female, with a family history of vitiligo, presented to our clinic complaining of uneven skin tone. The skin changes began 1 year prior to her visit as generalized macular hypopigmented lesions involving her entire body (shown in Fig. 1a). Within 6 months, the hands became significantly affected, sparing the fingertips (shown in Fig. 1b). Associated symptoms were peeling, burning sensation of the skin, and photosensitivity.

Upon examination, the dyspigmentation involved approximately 60% of her body surface area. Various tones of skin color were appreciated on the neck, trunk, and extremities. Some lesions were discrete macules (confetti) (shown in Fig. 1c), while others were confluent into larger patches with defined geographic borders (shown in Fig. 1d). Areas of hyperpigmentation were also seen (shown in Fig. 1e, f). Under Wood’s lamp, lesions displayed variable accentuation of borders, indicating different degrees of depigmentations.

The patient disclosed that she had been applying multiple “lightening creams” daily over the past year, purchased online from unauthorized suppliers. These creams were used before any lesions appeared.

After investigation, we found that one of these products contained 40% Monobenzyl Ether Hydroquinone (MBEH). The patient’s history of exposure to MBEH with subsequent depigmentation in the form of confetti macules, favors the diagnosis of CL.

Vitiligo is a skin depigmenting disorder, influenced by a variety of genetic and environmental factors. When combined, these factors lower melanocytes’ tolerance threshold to oxidative stress, triggering an auto-immune response that ultimately leads to melanocyte destruction [3]. The ensuing clinical manifestation is a complete loss of pigment in affected skin areas.

On the other hand, CL is another form of acquired depigmentation induced by repeated exposure to specific chemical compounds. MBEH, in particular, inhibits melanogenesis by competitively inhibiting the rate-limiting enzyme; tyrosinase, thus blocking the conversion of DOPA to DOPA-Quinine [4].

Data also suggest that MBEH can indirectly cause melanocytes’ death by oxidative stress and by inducing the secretion of proapoptotic inflammatory cytokines, such as interleukins 6 and 8 [5]. The growing evidence of a similar pathogenesis in both entities, such as involvement of IFNγ-STAT1-CXCL10 signaling axis and production of cytotoxic factors, suggests autoimmunity in MBEH-induced CL [6]. This is supported by the observation that chemical exposure depigments even skin areas remote to application site [6]. Genetically susceptible patients who are exposed to toxic chemicals/phenols stand a higher risk of developing idiopathic vitiligo, compared to the general population [1].

In our patient, the presence of “confetti macules” was highly suggestive of CL; however, this change can also be appreciated in early vitiligo. The diagnostic criteria for chemical-associated vitiligo include the presence of 3 out of 4 specific indicators: acquired vitiligo-like depigmented lesion(s), history of repeated exposure to specific chemical compounds, patterned vitiligo-like macules at site of exposure, and confetti macules. [7] This particular case meets all 4 criteria.

However, widespread loss of skin pigment may suggest an evolution of CL into vitiligo or an overlap of both entities. In the light of reviewed nuanced data, we believe the line between vitiligo and CL remains blurry.

In the context of dyschromatosis, one should always keep in mind other entities such as idiopathic guttate hypomelanosis, which appears mostly on sun exposed areas on extremities, in a slowly progressive manner. In progressive macular hypomelanosis and hypopigmented mycosis fungoides, hypopigmentation is more patchy, faint, and occasionally scaly, with trunk and proximal extremities being the main areas of involvement.

Finally, authorities should take measures to increase awareness about commercially distributed products, particularly given the rising popularity of online vendors. Additionally, legislations should be emphasized to ensure that all ingredients in skin care products are listed on their packaging. The CARE Checklist has been completed by the authors for this case report, attached as online supplementary material (for all online suppl. material, see https://doi.org/10.1159/000539907).

Ethical approval is not required for this study in accordance with local or national guidelines. Written informed consent was obtained from the patient for publication of this case report and any accompanying images.

The authors have no conflicts of interest to declare.

This study was not supported by any sponsor or funder.

Mariam AlAfeefi and Shaden Abdelhadi: contributions to the design of the work, validation, writing – original draft, and writing – review and editing.

All data used in this article are included under the references section. Further inquiries can be directed to the corresponding author.