Stasis Dermatitis: Pathophysiology, Current Treatment Paradigms, and the Use of the Flavonoid Diosmin.

Objective: We sought to examine the role of flavonoids, particularly diosmin, as a therapeutic agent for stasis dermatitis (SD) through discussion of pathophysiology, current treatment paradigms, potential mechanisms of action, and a systematic review of evidence on clinical efficacy. Methods: In addition to articles on pathophysiology and standard treatment, a search of PubMed was conducted using the following query: ("Diosmin" OR "MPFF" OR "Micronized Purified Flavonoid Fraction" OR "Flavonoid") AND ("Stasis Dermatitis" OR "Venous Ulcer" OR "Lipodermatosclerosis"). Emphasis was placed on studies that were randomized controlled trials examining an oral flavonoid against a placebo or standard of care. Results: Diosmin is effective at improving stasis changes, increasing ulcer healing frequency, decreasing the time to ulcer healing, and reducing tissue edema. They also cause significant improvement in patient quality of life and reduction of venous symptoms. Diosmin has been shown to have a favorable safety profile with very few mild adverse events which did not differ significantly from placebo. Flavonoids also appear to be effective for other dermatologic conditions, including rosacea and senile purpura. Conclusion: There is a growing body of evidence indicating that diosmin has therapeutic efficacy in managing stasis dermatitis. Data from studies in diseases with pathogenic similarities suggests the potential for even broader dermatologic applications.

Postherpetic granulomatous dermatitis occurring in the setting of immune checkpoint inhibitor therapy: A case report.

We report a case of a 72-year-old man presenting with a 2-month history of a persistent, painful rash of the chest, axilla, and back. He had a history of recently resolved varicella zoster virus reactivation in the same distribution of the current rash and metastatic malignant melanoma treated with nivolumab and ipilimumab. The histopathology was consistent with granulomatous dermatitis (GD), and a diagnosis of postherpetic isotopic response manifesting as GD was made. Given the paucity of reported cases of postherpetic GD in the setting of treatment with immune checkpoint inhibitors (ICIs), we discuss the clinicopathologic features of this case and potential mechanisms by which ICIs may contribute to the development of granulomatous disease.