Palmate Erythema With Pruritus Following Contact With Lime Juice, a Variant of “Margarita Photodermatitis”

Phototoxic dermatitis, often referred to as phytophotodermatitis, is a skin reaction resulting from the interaction of certain plant-derived substances with ultraviolet (UV) light, leading to inflammation and erythema. This condition commonly occurs following contact with photosensitizing agents, such as psoralens found in citrus fruits like limes, combined with subsequent sun exposure. The clinical presentation typically includes well-defined erythematous lesions, blisters, and in some cases, pruritus, which can significantly impact a patient's quality of life [1]. Understanding the underlying mechanisms and preventive measures is crucial, as increased awareness of such conditions can help mitigate risks, particularly with outdoor activities during the summer months [2]. This case report details a patient who developed phototoxic dermatitis after handling lime juice, illustrating the importance of recognising and addressing this often-overlooked dermatological complication. A 32-year-old female patient presented to our university outpatient clinic for a routine examination of her psoriasis vulgaris under systemic therapy with tildrakizumab. The patient reported that she had been on vacation in Brazil 2 weeks earlier. While there, she had pressed limes for cocktail preparation and had come into contact with lime juice on her hands. She wiped this juice on her bare thighs and then sunbathed. Two days later, she developed a pronounced solar dermatitis with multiple bullae and intense burning pain. Currently, she is experiencing pruritus. Upon presentation, the patient exhibited a sharply defined, palm-sized erythema on both thighs with partially accentuated brown pigmentation at the edges. Scattered, approximately 0.5 cm round erythemas could be observed (Figure 1). Phototoxic dermatitis due to external photosensitization (phytophotodermatitis). Given the clear findings, a diagnosis of phototoxic dermatitis due to external photosensitization was established. This is attributed to psoralens found in limes and other citrus fruits. This secondary plant substance sensitises the skin to sunlight and UV radiation [3]. The same active ingredient is used in dermatology for the treatment of psoriasis with UV light (PUVA). The patient was informed about the aetiology of the condition. She was also advised to maintain consistent sun protection, particularly through clothing and sunscreen, to reduce the risk of secondary hyperpigmentation. For the existing pruritus, a 0.1% methylprednisolone aceponate cream was prescribed for external application once daily for a period of 14 days. Following the initial diagnosis and treatment of the phototoxic dermatitis, the patient was scheduled for a follow-up appointment 2 weeks later to assess the effectiveness of the prescribed therapy and patient adherence to the recommended sun protection measures. During the follow-up visit, the patient reported a significant reduction in pruritus and an overall improvement in her skin condition. The application of the 0.1% methylprednisolone aceponate cream resulted in decreased inflammation, and the erythema on her thighs showed signs of healing. The patient expressed satisfaction with the treatment and reported consistent use of sun protection measures, including applying sunscreen and wearing protective clothing. Additionally, the patient reported no adverse effects or complications from the prescribed medication or preventive strategies. However, 6 months later, the patient presented with residual hyperpigmentation in the affected areas. We initiated a topical therapy with Mela B3 Intense Anti-Dark Spot Serum by La Roche-Posay (Mela B3 Intense Anti-Dark Spot Serum contains Niancinamide [INCI; CAS 98-92-0] and Hyaluronic Acid [INCI; 900-4-61-9] and beta-lipohydroxy acid). The patient was informed about the mechanism of action of the cream and the timeline for expected outcomes. In cases of suspected phototoxic dermatitis, a careful anamnesis, particularly regarding exposure to photosensitizers at home, in the workplace, and during leisure time, is essential. An eruption caused by contact with photosensitizing compounds found in various plants is also referred to as phytophotodermatitis. Major triggers include fruits and vegetables (limes, lemons, bitter oranges, figs, celery, and parsnips), essential oils (cosmetics, insect repellents), and summer crops [4]. While literature highlights that UVA-induced binding of psoralens to DNA can inhibit cell proliferation and partially elucidate the therapeutic effects of PUVA therapy, it is crucial to recognise that the photo irritant response may primarily involve psoralens that do not bind to DNA [5, 6]. These unbound psoralens can transfer their UVA-induced energy to molecular oxygen, leading to the formation of singlet oxygen, a highly reactive species. This singlet oxygen can interact with ascorbate—our key aqueous antioxidant—resulting in the production of hydrogen peroxide, an oxidising agent that contributes to oxidative stress and fosters a state of inflammation. The clinical diagnosis of phytophotodermatitis is generally straightforward, as well-defined, sometimes painful, erythematous lesions form, which may develop into blisters. These lesions occur on areas that have come into contact with a phototoxic agent and were exposed to sunlight 6–12 h earlier. Secondary hyperpigmentation is a common phenomenon and can help differentiate this diagnosis from differential diagnoses such as chemical burns or bullous impetigo. Typically, reactions are mild, requiring no additional therapeutic measures. In cases of severe reactions, as-needed analgesia should be initiated, potentially in combination with topical steroids in cases of significant inflammatory activity. In differentiating between phototoxic dermatitis and photoallergic dermatitis, it is important to note that phototoxic dermatitis generally occurs upon direct skin exposure to a photosensitizing agent and ultraviolet light, leading to immediate and dose-dependent reactions. In contrast, photoallergic dermatitis is characterised by a delayed hypersensitivity reaction that develops after sensitization to a photosensitizer, resulting in eczema-like lesions that may appear several hours to days after sun exposure [1]. This case impressively illustrates the importance of phytophotodermatitis as a potential diagnosis for well-defined lesions in contact with photosensitizing externals. In terms of primary prevention, broad public awareness is desirable. Jan Nicolai Wagner: conceptualization, methodology, data curation, writing – original draft, resources. Franziska Zirkenbach: conceptualization, methodology, data curation, writing – original draft, resources. Matthias Augustin: writing – review and editing, conceptualization, methodology. We would like to thank the patient for her consent to the publication of the image and the entire team at the Institute for Health Services Research in Dermatology for their support. The authors also thank the Scientific Communication Team of the IVDP, in particular Julia Zechlin for copy editing. Open Access funding enabled and organized by Projekt DEAL. The patient has signed written formal consent to publication of medical history and clinical picture. The authors declare no conflicts of interest.