Article Sidebar
Main Article Content
Abstract
Background: Inflammatory dermatoses, such as seborrheic dermatitis (SD) and atopic dermatitis (AD), affect a significant portion of the population, yet their precise etiology often remains debated. Nicotine, a ubiquitous alkaloid primarily associated with tobacco but also present in certain plants and therapeutic products, has been proposed as a potential hapten capable of triggering hypersensitivity reactions manifesting as inflammatory skin conditions. This systematic review aimed to evaluate the existing evidence supporting the role of nicotine as a cutaneous hapten involved in the pathophysiology of inflammatory dermatoses.
Methods: A systematic literature search was conducted using PubMed, Embase, and Google Scholar databases for studies published between January 2014 and December 2024. Keywords included "nicotine," "hapten," "allergy," "hypersensitivity," "contact dermatitis," "seborrheic dermatitis," "atopic dermatitis," "urticaria," and "skin reaction." Inclusion criteria encompassed original research (in vivo human studies, case reports/series, in vitro mechanistic studies) investigating nicotine's potential to elicit immune-mediated skin reactions consistent with a hapten mechanism. Data extraction focused on study design, population, nicotine source/exposure, diagnostic methods (patch test, prick test), and key findings related to hypersensitivity. Quality assessment was performed using appropriate tools (CARE guidelines for case reports, Joanna Briggs Institute checklists for other study types).
Results: Following title/abstract screening and full-text review, six studies met the inclusion criteria. These included one cross-sectional prick-test study, two case reports detailing reactions to electronic cigarettes, one patch-test study, and two in vitro studies investigating mast cell responses. The prick-test study (N=30) reported positive reactions to nicotine in 20% of non-smokers and 7% of smokers, including one patient with SD. Case reports described eczematous reactions (perioral, hand dermatitis) associated with e-cigarette use. The patch test study indicated positive reactions in a subset of individuals exposed to nicotine patches. In vitro studies demonstrated nicotine-induced mast cell degranulation and mediator release (histamine), potentially inhibited by mast cell stabilizers.
Conclusion: Consistent evidence from the included studies published between 2014-2024 suggests nicotine possesses the potential to act as a cutaneous hapten, capable of eliciting hypersensitivity reactions in susceptible individuals. Findings include positive diagnostic tests (prick/patch), clinical correlations (e-cigarette dermatitis), and plausible biological mechanisms involving mast cell activation. These reactions may contribute to or mimic inflammatory dermatoses like SD or contact dermatitis. Further robust clinical and mechanistic research is warranted to confirm these findings and clarify the prevalence and clinical significance of nicotine hypersensitivity in various dermatological conditions.
Keywords
Article Details
As our aim is to disseminate original research article, hence the publishing right is a necessary one. The publishing right is needed in order to reach the agreement between the author and publisher. As the journal is fully open access, the authors will sign an exclusive license agreement.
The authors have the right to:
- Share their article in the same ways permitted to third parties under the relevant user license.
- Retain copyright, patent, trademark and other intellectual property rights including research data.
- Proper attribution and credit for the published work.
For the open access article, the publisher is granted to the following right.
- The non-exclusive right to publish the article and grant right to others.
- For the published article, the publisher applied for the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.
