Abstract
Treatment with antineoplastic agents can result in both neutropenia and lymphopenia with resulting deficiencies in wound healing. Additionally, many of these agents
target rapidly proliferating malignant cells and as a consequence may also affect proliferating cells in the wound bed. A priori one would expect these agents to result in
impaired wound healing and a number of animal studies support this assumption.
Evaluations in mice of single injections of vincristine, methotrexate, actinomycin
D, bleomycin, and carmustine (BCNU) revealed that all reduced wound breaking
strength (58). Other animal studies have demonstrated impaired wound healing from
cyclophosphamide and 5-FU (58,59). It is surprising then that studies of patients
undergoing pre and=or peri-operative chemotherapy fail to demonstrate clinically
impaired wound healing as measured by length of hospital stay, number of outpatient dressings, seroma formation, and post-operative infections (60,61). Similarly several studies of methotrexate for the treatment of rheumatoid arthritis have failed to
demonstrate impaired wound healing (62-64). Thus, even though these agents may
theoretically affect wound healing as evidenced by animal models, they do not
appear to cause clinically significant impaired wound healing.