Abstract
Drug-induced lupus erythematosus (dile) syndromes are documented complications of chemotherapeutic agents, including paclitaxel. Subacute cutaneous lupus erythematosus (scle) is a distinct dile syndrome presenting with characteristic annular or papulosquamous skin lesions in a photosensitive distribution with associated high anti-ssa titres. Previously, dile syndromes complicating paclitaxel therapy have been attributed to polyethoxylated castor oil (Kolliphor EL: BASF, Ludwigshafen, Germany), the biologic solvent included in the drug's original formulation (Taxol: Bristol-Myers Squibb, Montreal, QC), rather than the parent chemotherapy molecule. Here, we report a characteristic case of drug-induced scle complicating treatment with nanoparticle albumin bound (nab)-paclitaxel (Abraxane: Celgene, Summit, NJ, U.S.A.), a solvent-free taxane formulation. The pertinent English-language literature is also discussed. This case report is the first to link solvent-free paclitaxel with scle, and it suggests that the parent molecule is responsible for the reaction.
Highlights
Drug-induced lupus erythematosus syndromes are documented complications of chemotherapeutic agents, including paclitaxel
A previously healthy 62-year-old woman was seen in the outpatient medical oncology clinic after presenting with right-sided inflammatory breast cancer
The patient was started on first-line systemic therapy for metastatic breast cancer, using nanoparticle albumin bound–paclitaxel 260 mg/m2 intravenously every 21 days
Summary
A previously healthy 62-year-old woman was seen in the outpatient medical oncology clinic after presenting with right-sided inflammatory breast cancer. The patient was started on first-line systemic therapy for metastatic breast cancer, using nanoparticle albumin bound (nab)–paclitaxel 260 mg/m2 intravenously every 21 days. She initially tolerated the nab-paclitaxel well, with toxicities limited to alopecia and mild fatigue. The patient was referred to a consultant dermatologist who confirmed the diagnosis of scle, papulosquamous-type, and prescribed topical glucocorticoid therapy together with sun protection Before her 6th cycle of systemic therapy, the patient developed locoregional cancer progression, and nab-paclitaxel was discontinued. Her eruption began to regress 4 weeks after her final nab-paclitaxel infusion, with initial decreased erythema and scaling. Ten weeks after discontinuing nab-paclitaxel, the patient’s eruption had resolved without scarring, though her anti-ssa activity index remained elevated at more than 8.0
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