Psoriasis is one of the most common skin diseases. It can be triggered or exacerbated by various external stimuli.1 Psoriatic skin lesions are well-known to be provoked by stress, alcohol, infections, and different medications.1 Among them, best documented are antimalarial drugs, beta-adrenolytics, lithium, or interferons (IFNs).1

On the other hand, there are drugs that are not typically considered antipsoriatic, and yet are proven to improve psoriatic skin lesions. These are, for example, statins, glitazones, metformin, and glucagon-like peptide-1 agonists.2 The last group includes liraglutide, administered in subcutaneous injections for treating diabetes mellitus, insulin resistance, and obesity.3 There are many reports on the beneficial influence of this drug on psoriasis.4,5 However, this report presents a case of a patient in whom liraglutide exacerbated skin lesions.

A 34-year-old woman, with a history of mild psoriasis, was admitted to the Department of Dermatology. The patient had suffered from psoriasis for many years, albeit her lesions were very discreet and left without any treatment. The patient started taking liraglutide due to insulin resistance, and after 2 weeks new psoriatic lesions appeared. At first, the patient did not notice the association, so she continued taking the drug for further 2 months and the lesions still exacerbated. Finally, she discontinued the medication and sought ambulatory dermatology care. She received topical agents but they were insufficient, hence she was referred to a hospital. At the Department of Dermatology, the patient presented numerous erythematous-scaly lesions on her face (Figure 1A) and scalp (Figure 1B) and in the intertriginous areas (Figure 1C and 1D). Cyclosporin A was introduced because of the patient’s reproductive plans. After 2 months of treatment, partial improvement was visible, and the lesions slowly resolved. The patient is still not taking liraglutide.

Figure 1. Erythematous-scaly lesions appearing after the introduction of liraglutide on the face (A) and scalp (B), on the genital area (C) and submammary region (D)

The majority of cases involving liraglutide introduction in psoriatic patients present a positive impact and improvement of skin lesions. The case in question requires special attention because, to the best of our knowledge, it is the only one where administration of this drug caused exacerbation of the skin lesions.

The suspected positive influence of liraglutide on psoriatic lesions is probably associated with the inhibition of inflammatory cytokines, including interleukin 23 (IL-23), IL-17, and tumor necrosis factor α (TNF-α).4 A study by Lin et al4 showed reduced degree of dermal inflammatory cell infiltration and relative expression levels of IL-23, IL-17, and TNF-α in the skin tissue after 12 weeks of treatment with liraglutide. Moreover, liraglutide efficacy can be indirectly related to weight loss and lowering glycemia,5 which are both known to improve skin lesions in psoriasis due to the reduction of adipokine levels and attenuation of inflammation.2

Our hypothesis, which could explain the mechanism of paradoxical worsening of skin lesions after liraglutide, is based on cytokine imbalance, similarly to what is suspected in the case of exacerbation after administration of antipsoriatic biological treatment, especially anti-TNF-α.1 Perhaps after inhibition of TNF-α, IL-17, and IL-23 by liraglutide, increased release of IFN-α and leukocyte chemotaxis occurred, triggering psoriatic lesions.

However beneficial it may be, liraglutide can also act adversely and exacerbate skin lesions. Diabetologists and dermatologists should be aware of such a possibility and consider changing the drug if adverse effects occur.