PubMed · 10955186
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J H Kuflik, R A Schwartz. 2000. Acneiform eruptions.. https://pubmed.ncbi.nlm.nih.gov/10955186/
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The biological agent cetuximab specifically inhibits the epidermal growth factor receptor (EGFR) function. Cetuximab is licensed for treatment of metastatic colorectal carcinoma, as it enhances the efficacy of cytostatic therapy. Acneiform drug eruptions are common side effects. We report two patients with metastatic colorectal carcinoma, who developed a severe acneiform drug eruption on the face and upper part of the body during the treatment with cetuximab. Triple therapy consisting of systemic isotretinoin, topical nadifloxacin and topical corticosteroid produced rapid improvement with moderate cheilitis the only side effect. We conclude that triple therapy is an effective treatment for patients with severe acneiform drug eruptions caused by cetuximab.
The growing investigation and use of epidermal growth factor receptor (EGFR) inhibitors in anticancer therapy has been motivated by their specificity for EGFR, which improves their ability to target cancer cells and enhances their safety profile compared with many other conventional chemotherapeutic agents. However, their growing use has been accompanied by an increasing incidence of cutaneous toxicities, which can cause serious discomfort and be disabling. This review illustrates the common cutaneous side effects seen in patients receiving EGFR inhibitors and discusses various options for management. With effective management of these side effects, dermatologists can play an integral role in facilitating compliance with anti-EGFR therapy and aid with effective oncologic management.
Tetrachlorodibenzo-p-dioxin (TCDD) is classified as a human carcinogen and exerts toxic effects on the skin (chloracne). Effects on reproductive, immunological, and endocrine systems have also been observed in animal models. TCDD acts through the aryl hydrocarbon receptor (AhR) pathway influencing largely unknown gene networks. An industrial accident in Seveso, Italy in 1976 exposed thousands of people to substantial quantities of TCDD. Twenty years after the exposure, this study examines global gene expression in the mononuclear cells of 26 Seveso female never smokers, with similar age, alcohol consumption, use of medications, and background plasma levels of 22 dioxin congeners unrelated to the Seveso accident. Plasma dioxin levels were still elevated in the exposed subjects. We performed analyses in two different comparison groups. The first included high-exposed study subjects compared with individuals with background TCDD levels (average plasma levels 99.4 and 6.7ppt, respectively); the second compared subjects who developed chloracne after the accident, and those who did not develop this disease. Overall, we observed a modest alteration of gene expression based on dioxin levels or on chloracne status. In the comparison between high levels and background levels of TCDD, four histone genes were up-regulated and modified expression of HIST1H3H was confirmed by real-time PCR. In the comparison between chloracne case-control subjects, five hemoglobin genes were up-regulated. Pathway analysis revealed two major networks for each comparison, involving cell proliferation, apoptosis, immunological and hematological disease, and other pathways. Further examination of the role of these genes in dioxin induced-toxicity is warranted.