ArticleCureus2026
Type II Minocycline-Induced Hyperpigmentation During Long-Term Management of an Epidermal Growth Factor Receptor (EGFR) Inhibitor-Associated Acneiform Eruption.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
3 authors.
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Abstract
Epidermal growth factor receptor (EGFR) inhibitors commonly cause papulopustular eruptions that may significantly impair quality of life and interfere with continuation of effective oncologic therapy. Oral tetracyclines remain the cornerstone of treatment because of their anti-inflammatory properties; however, prolonged therapy, particularly with minocycline, carries a risk of cumulative adverse effects, including drug-induced hyperpigmentation. We report the case of a 40-year-old man with hereditary leiomyomatosis and renal cell carcinoma (HLRCC) who developed an EGFR inhibitor-associated papulopustular eruption shortly after initiating erlotinib and bevacizumab. Persistent disease despite doxycycline therapy and concern for doxycycline-associated photosensitivity prompted a transition to long-term minocycline. After approximately 29 months of treatment, the patient developed symmetric slate-blue macules on the bilateral shins consistent with type II minocycline-induced hyperpigmentation. Reduction of the minocycline dose resulted in gradual improvement of the pigmentation while maintaining adequate control of the eruption. This case highlights the importance of longitudinal dermatologic follow-up in patients receiving prolonged tetracycline therapy for EGFR inhibitor-associated cutaneous toxicities. Periodic reassessment of treatment necessity, dose optimization, and early recognition of delayed medication-related adverse effects may minimize cumulative toxicity while preserving effective oncologic therapy.
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