#00066008

The presented image depicts the characteristic cyanotic phase of Raynaud's phenomenon in the finger of an adult male patient with established fluoroquinolone toxicity syndrome following exposure to a fluoroquinolone antibiotic. The sharply demarcated, intense livedo of the distal phalanx, with relative sparing of adjacent digits, reflects profound digital vasospasm leading to tissue hypoxia, while preservation of the epidermal ridge pattern indicates absence of ulceration distinguish this reversible ischemic episode from fixed occlusive vasculopathy. Fluoroquinolone-associated delayed multisystem toxicity is mediated by mitochondrial dysfunction, excessive reactive oxygen species generation, topoisomerase interference, and collagen/matrix degradation that may involve vascular endothelium and smooth muscle. Although peripheral neuropathy and tendinopathy predominate, vasospastic manifestations resembling secondary Raynaud’s phenomenon can occur, likely through magnesium chelation–induced impairment of endothelial nitric oxide synthesis and enhanced cold-sensitive α2C-adrenoceptor translocation and vasoconstriction—mechanisms shared with connective tissue disease–associated Raynaud’s phenomenon. This observation extends the recognized vasculopathic spectrum of severe fluoroquinolone adverse reactions to include reversible episodic digital ischemia.