Topical Micronutrient Products by Darlene McCord
PART II

David E. Davenport, M.D., FACR
Darlene McCord, Ph.D., FAPWCA
Brenda Bull R.T. (R)(T)

Introduction

Skin is the largest organ of the human body and provides protection against the external environment. In addition, skin restores itself every 28 days and is the body’s largest producer of enzymes and hormones. Skin consists of three layers; the dermis, epidermis and the protective, semi-permeable stratum corneum that permits terrestrial life1. The stratum corneum is metabolically active and protects against excessive transepidermal water loss (e-TEWL), mechanical trauma, microbial infection, temperature variation and percutaneous toxin absorption2. However, ionizing radiation commonly disturbs or damages several of the skin’s protective functions. Studies have shown that 36-100% of patients receiving radiotherapy experience some degree of skin reaction 7-14 days into treatment. During treatment, patients may experience pruritus, erythema, edema, desquamation, necrosis, ulceration and/or hemorrhage5. The whole of possible skin reactions associated with radiotherapy are collectively known as radiation dermatitis.

In the past 20 years radiotherapy has experienced tremendous advances, allowing for increased tissue sparing techniques. Nevertheless, radiotherapy routinely causes severe acute and chronic damage of the skin6. In fact, skin injury may be the dose-limiting factor for radiotherapy. Once a threshold dose has been exceeded, the severity of the radiation effect at any point on the skin increases with increasing dose. The most currently available fluoroscopic measuring systems do not provide the operator with sufficient information to perfectly minimize skin dose.

During radiotherapy, vascular injury occurs, followed by leukocyte infiltration and barrier breakdown. Leukocyte infiltration is frequently observed in irradiated skin and plays a significant role in tissue damage. Cell adhesion molecules (CAMs) expressed on leukocytes and endothelial cells control the transmigration of leukocytes out of the blood vessel lumen. CAMs including platelet-, leukocyte-, and endothelial-selectins, vascular cell adhesion molecule-1, as well as β1 and β2 integrins are involved in the trafficking of leukocytes through the inflamed endothelium.

Leukocyte transmigration is also accompanied by monocyte and macrophage infiltration, causing inflammation, pruritus other symptoms associated with radiation dermatitis10. Furthermore, radiation deposition results in DNA damage manifested by single- and double-strand breaks in the sugar phosphate backbone of epidermal and dermal skin cells11. Most cell types do not show morphologic evidence of radiation damage until they attempt to divide. Since skin cells have extraordinarily high rates of division, symptoms associated with sub-lethal and potentially lethal damage may appear almost immediately.