Failed Treatment of Classic Kaposi’s Sarcoma with Topical Timolol: Case Report and Review of the Literature

Abstract

Classic Kaposi’s sarcoma (CKS) is an angioproliferative cutaneous neoplasm which currently lacks a well-defined treatment regimen. Because the disease is often localized, topical therapies offer therapeutic potential without the morbidity of systemic or surgical treatment. Timolol, a topical β-adrenergic receptor antagonist, has shown promise in the treatment of CKS in individual cases. Here we report a patient with classic Kaposi’s sarcoma who failed treatment with 0.5% topical timolol three times daily for 12 weeks. Topical timolol use has been previously reported in eight patients with CKS who all responded to treatment with no adverse effects. Our divergent experience from the literature implies that while topical timolol may be an effective and safe treatment alternative to traditional therapies for patients with CKS, further prospective studies are needed.

The role of topical timolol in wound healing and the treatment of vascular lesions: A narrative review

“…The duration of the treatment varied from 4 to 24 weeks and the patients ranged from 52 to 94 years in age. Except for one case where treatment failed and two cases where the lesion remained macular, all the patients recovered fully 45 …”

“…Except for one case where treatment failed and two cases where the lesion remained macular, all the patients recovered fully. 45…”

Topicalbeta‐blockersin dermatologic therapy

“…In fact, some topical agents have been used, including retinoids, imiquimod, rapamycin, and recently timolol maleate solution, with varying results. 33 , 34 …”

“…To date, 12 patients with KS treated with topical timolol have been described in the literature 33–35 . All the patients (except one) 33 responded rapidly to treatment in a time period between 5 and 24 weeks; different timing responses can be possibly related to lesions size.…”

“…In fact, some topical agents have been used, including retinoids, imiquimod, rapamycin, and recently timolol maleate solution, with varying results. 33,34 Molecular studies have shown that KS lesions are dependent on beta-adrenergic signaling for the reactivation of human herpes virus-8, which could explain why beta-blockers can reduce KS proliferation by suppressing cAMP and protein kinase A signaling pathways.…”