Mechanism of gallium-67 accumulation in inflammatory lesions.

Multiple factors contribute to the accumulation and retention of gallium-67 in inflammatory lesions. Adequate blood supply is essential. Gallium-67, mainly in the form of transferrin-Ga-67 complex, is delivered to the inflammatory lesions through capillaries with increased permeability. At the site of inflammation, some Ga-67 is taken up by leukocytes and bacteria when they are present. In addition, Ga-67 may also bind to lactoferrin and bacterial siderophores. Multiple contributing factors often coexist at any given inflammatory lesion. The nature and intensity of the inflammation affects the relative contribution of these factors. Thus, there may be situations in which all the contributing factors are present, but in such a low intensity that they escape clinical detection by Ga-67 scans. On the other hand, there may be situations in which one or more contributing factors are missing, such as in patients with agranulocytosis, while they are readily detected by Ga-67 scans.