Wart responses.
HPVs infecting immunodeficiency, HPV disease, wart, pedunculated gluteal lipoma
REGRESSION, WARTS, WART
At baseline, 69 wart areas were defined for 13 patients with warts (average 5.3/patient; range 1–16/patient), 87% on the upper or lower extremities (The statistical analysis plan limited analysis of wart regression to treatment phase 1 because of the possibility of carryover effects. In this phase, there was detectable wart regression in 3 patients given plerixafor (M03, M06, and M12) and in 3 patients given G-CSF (M04, M07, and M17) (For 4 patients (M05, M09, M10, and M18) wart burden was unaffected by either drug. The other 9 patients (69%) improved on at least one treatment (Of the 69 wart areas identified at baseline in the 13 patients, 26 improved on plerixafor, 13 improved on G-CSF, 1 worsened on plerixafor, and 10 enlarged on G-CSF. Responses were highly heterogeneous in responding patients (A plerixafor dose-response relationship for wart regression was not apparent (The 5 patients with major wart responses on plerixafor represented 71% of the subset of 7 patients with major wart burdens (We previously published a survey of HPVs infecting immunodeficiency patients, including 10 patients from the present study before enrollment (Of 62 HPVs identified, 16 were novel, all gammas, including 13 types and 3 species. HPV diversity correlated poorly with HPV disease burden. As extreme examples, patients M09 and M16 had low wart burdens yet harbored many HPV types, even in areas lacking warts. In particular, M09 had widespread plerixafor-induced psoriasiform lesions with no warts, from which we identified 8 different HPV types, including 5 γ and 3 β types. Likewise, M16 had a large pedunculated gluteal lipoma associated with 6 different HPV types, including 5 γ and one β type.