The potential adverse effects of aromatase inhibitors on wound healing: in vitro and in vivo evidence.
BACKGROUND
Estrogens and several other endogenous substances are recognised as being important in the process of wound healing. However, the effect of aromatase and aromatase inhibition in the wound healing process has yet to be fully defined.


OBJECTIVE
A review of the in vitro and in vivo evidence on the effect of aromatase inhibition on wound healing.


METHODS
The primary medical search engines used for the study were Ovid MEDLINE (1950 - March 2009) and EMBASE (1980 - March 2009) databases.


CONCLUSIONS
The delayed healing of cutaneous wounds in aged individuals may in part reflect the decline in circulating levels of dehydroepiandrosterone (DHEA) and estrogens. The beneficial response on wound healing that DHEA and estrogen exert may be blocked by aromatase inhibition. Based on animal models, aromatase inhibitors may adversely affect cutaneous wound healing in the acute setting. So far, there have been no clinical trials investigating the adverse affect of aromatase inhibitors on the process of cutaneous wound healing in humans. Postmenopausal patients who take aromatase inhibitors as an adjunct to breast cancer therapy may, therefore, be at increased risk of delayed wound healing. Further studies are necessary to assess the extent of the effects on the wound healing process.
Howgate
Daniel J
DJ
University of Leeds, School of Medicine, Leeds General Infirmary Teaching Hospitals NHS Trust, Academic Department of Trauma and Orthopaedics, Clarendon Wing A, Great George Street, Leeds, LS1 3EX, UK.
Gamie
Zakareya
Z
Panteliadis
Pavlos
P
Bhalla
Amit
A
Mantalaris
Athanasios
A
Tsiridis
Eleftherios
E
D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism; D000368:Aged; D000818:Animals; D018931:Antineoplastic Agents, Hormonal / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D001141:Aromatase / Q000235:genetics / Q000502:physiology; D047072:Aromatase Inhibitors / Q000009:adverse effects* / Q000494:pharmacology / Q000627:therapeutic use; D001943:Breast Neoplasms / Q000188:drug therapy; D002478:Cells, Cultured / Q000187:drug effects / Q000378:metabolism; D016207:Cytokines / Q000494:pharmacology / Q000502:physiology; D003687:Dehydroepiandrosterone / Q000502:physiology; D004353:Drug Evaluation, Preclinical; D004967:Estrogens / Q000096:biosynthesis / Q000502:physiology; D005109:Extracellular Matrix / Q000187:drug effects; D005260:Female; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D009389:Neovascularization, Pathologic / Q000188:drug therapy; D018919:Neovascularization, Physiologic / Q000187:drug effects; D017698:Postmenopause; D012867:Skin / Q000293:injuries; D006377:T-Lymphocytes, Helper-Inducer / Q000378:metabolism; D014945:Wound Healing / Q000187:drug effects* / Q000235:genetics
D018931:Antineoplastic Agents, Hormonal; D047072:Aromatase Inhibitors; D016207:Cytokines; D004967:Estrogens; D003687:Dehydroepiandrosterone; D001141:Aromatase