Dermoscopic Features of Acutely Exacerbated Plaque Psoriasis Induced by Anti-Programmed Death-1 for Lung Cancer
Programmed death-1 (PD-1) inhibitors represent a significant advancement in cancer therapy, offering new hope for patients with various malignancies, including lung cancer. However, these immunotherapies are not without their risks. Among the immune-related adverse events associated with PD-1 inhibitors, skin reactions such as toxic epidermal necrolysis and psoriasis exacerbation have been reported. This article delves into a case study of a patient who experienced acutely exacerbated plaque psoriasis following treatment with the anti-PD-1 monoclonal antibody, Sintilimab, highlighting the dermoscopic features and clinical management of this condition.
Case Presentation
The patient, a 56-year-old man, had a 25-year history of psoriasis, which had been relatively mild and localized to the scalp and limbs. He was diagnosed with lung adenocarcinoma with multiple metastases and underwent video-assisted thoracoscopic surgery followed by regular chemotherapy. Three months prior to the onset of skin symptoms, he developed chest tightness, dyspnea, and restricted left-arm movement. Imaging studies revealed metastases in the lymph nodes, pleura, and liver. As part of his treatment regimen, the patient received his first dose of Sintilimab (200 mg) one month before the skin exacerbation.
Two weeks after the Sintilimab injection, the patient developed generalized red and swollen plaques accompanied by severe itching. Dermatological examination revealed numerous plaques, scales, scratches, crusts, and areas of pigmentation on the scalp, trunk, and limbs. The patient was hospitalized in the thoracic surgery department, where dermoscopic and histopathological examinations were conducted on a lesion located on his left leg.
Dermoscopic and Histopathological Findings
Dermoscopic examination revealed regular scales under a 50x lens and dotted blood vessels under a 200x lens. These findings are characteristic of plaque psoriasis and helped differentiate the condition from other dermatoses such as pityriasis rubra pilaris and eczematous drug eruption. Pityriasis rubra pilaris typically presents with round-to-oval yellowish areas surrounding a central hair, with or without follicular plugs, and lacks the dotted blood vessels seen in psoriasis. Eczematous drug eruption, on the other hand, does not exhibit regular white scales or dotted blood vessels.
Histopathological analysis of the lesion showed hyperkeratosis with hypokeratosis, acanthosis, epidermal ridge extension, and mild infiltration of lymphocytes surrounding the blood vessels in the superficial dermis. These features are consistent with plaque psoriasis but with some variations, such as less hypokeratosis and denser hyperkeratosis compared to typical cases.
Management and Clinical Course
Upon hospitalization, Sintilimab was discontinued, and the patient was treated with intravenous methylprednisolone (40 mg per day) for three days. Following consultation with a dermatologist, the treatment regimen was adjusted to include oral prednisone (30 mg per day), antihistamines, and tripterygium glycoside tablets. The use of glucocorticoids was continued to prevent further progression of the psoriasis. The patient’s condition improved rapidly, and he was discharged with instructions to continue the oral medications and follow up in two weeks.
However, the patient discontinued the oral medications on his own accord two weeks later, leading to a rapid recurrence of scaly plaques covering most of his body and severe itching. He was readmitted to the hospital, where he was treated with oral antihistamines and topical hydrocortisone mixed with Vaseline applied twice daily. This regimen provided slight relief from pruritus, and the patient’s condition gradually improved. He was discharged after a few days of observation without further exacerbation.
Discussion
The exacerbation of psoriasis in this patient following treatment with Sintilimab is consistent with previous reports of immune-related adverse events associated with PD-1 inhibitors. The mechanism underlying this reaction is thought to involve the downregulation of PD-1 on the surface of T cells, leading to the indirect activation of downstream cytokines such as interleukin (IL)-1, IL-17, and IL-22. These cytokines play a crucial role in the pathogenesis of psoriasis, contributing to the development and exacerbation of the disease.
The management of psoriasis exacerbated by PD-1 inhibitors presents a clinical challenge. While the general approach is similar to that for common psoriasis, the decision to continue or discontinue the use of PD-1 inhibitors remains controversial. In this case, the patient was advised to discontinue Sintilimab due to the severity of the skin reaction. Further research is needed to establish standardized treatment protocols for such cases.
Conclusion
This case highlights the importance of recognizing and managing immune-related adverse events associated with PD-1 inhibitors, particularly in patients with a history of psoriasis. Dermoscopy serves as a valuable tool for the rapid and accurate diagnosis of psoriasis exacerbation, aiding in the differentiation from other dermatoses. Collaboration between oncologists, thoracic surgeons, and dermatologists is essential for the early diagnosis and effective management of these adverse reactions. As the use of PD-1 inhibitors continues to expand, increased attention to their potential skin-related side effects is warranted.
doi.org/10.1097/CM9.0000000000000958
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