A 42-year-old Italian patient with a 20-year history of plaque psoriasis and psoriasis arthropathica presented to our hospital with numerous ulcerations or nodules within his psoriatic lesions that had appeared 6 months earlier. He had been treated with subcutaneous methotrexate (25 mg per week) for the past 9 years and adalimumab (40 mg every other week) for the past 7 years. Topical treatment included halometasone 0.05% plus triclosan 1% cream and calcipotriol plus betamethasone dipropionate foam in the weeks before hospitalization.
The obese patient (BMI 39 kg/m2) showed multiple psoriatic lesions characterized by erythemato-squamous plaques disseminated over the integument (PASI 16.6). Moreover, the patient showed erosive and partly ulcerating plaques and nodules, some of them covered by distinct brown crusts, at the right forearm, right knee, left flank and the abdomen (Figures 1A,B). Physical examination showed no pathological findings. There was no lymphadenopathy.
The histopathology of an externally performed lesion biopsy reported dermal T-cell infiltrates without evidence repeated of malignancy. Two repeat biopsies and histologies from morphologically different lesions on the right forearm and right flank revealed an interface dermatitis with pseudolymphomatous infiltrates, thickening of the epidermis, follicular hyperparakeratosis, and perivascular, periadnexal, superficially accentuated lymphocytic infiltrates with a preponderance of T cells (Figures 2A,B). Tissue clonality analyses demonstrated polyclonal IgH and TCR gamma chain gene expression, thus excluding lymphoma. Direct immunofluorescence did not detect any IgG, IgM, IgA, or C3 depositions. Syphilis serology, carried out due to numerous plasma cells in the tissue, yielded negative results. Moreover, an HIV infection, borreliosis and tuberculosis were ruled out by negative antibody or PCR tests. A serum sample was negative for antibodies against (extractable) nuclear antigens. Complement factors were within normal ranges. In hematoxylin-eosin (Figure 1C), Giemsa (Figure 1D) and Feulgen stains, intracellular Leishmania amastigotes with kinetoplasts were seen, which were identified by culture, miniexon PCR and restriction fragment length polymorphism-analysis as L. infantum. The patient also had a positive anti-Leishmania serology (maximum titer detected by indirect immunofluorescence using viable L. major promastigotes was 1:1,600). Since the patient originated from and repeatedly visited southern Italy, it is likely that he acquired the infection during his temporary stays.
The therapy with adalimumab was stopped, while treatment with methotrexate was continued (Figure 2). Interestingly, the ulcerations already started to heal under intensive topical treatment with salicylic acid, dithranol, and clobetasol propionate 0.05% ointment. Visceral involvement was excluded based on clinical parameters and sonography of liver and spleen. Therefore, we pursued a watch-and-wait strategy without specific therapy for leishmaniasis. The ulcerative skin lesions, which were clinically compatible with cutaneous leishmaniasis, completely regressed. After switching the systemic treatment to secukinumab (anti-IL-17A) or apremilast, the psoriatic lesions remained unaltered, but finally improved with ixekizumab (anti-IL-17A). During regular medical follow-up for almost 5 years the clinical condition of the patient remained stable (Figure 3).