A rapidly emerging clinical application of positron emission tomography (PET) is the detection and staging of cancer with the glucose analogue tracer 2-[fluorine-18]fluoro-2-deoxy-D-glucose (FDG). Proper interpretation of FDG PET images requires knowledge of the normal physiologic distribution of the tracer, frequently encountered physiologic variants, and benign pathologic causes of FDG uptake that can be confused with a malignant neoplasm. One hour after intravenous administration, high FDG activity is present in the brain, the myocardium, and--due to the excretory route--the urinary tract. Elsewhere, tracer activity is typically low, a fact that allows sensitive demonstration of tracer accumulation in many malignant neoplasms. Interpretive pitfalls commonly encountered on FDG PET images of the body obtained 1 hour after tracer administration can be mistaken for cancer. Such pitfalls include variable physiologic FDG uptake in the digestive tract, thyroid gland, skeletal muscle, myocardium, bone marrow, and genitourinary tract and benign pathologic FDG uptake in healing bone, lymph nodes, joints, sites of infection, and cases of regional response to infection and aseptic inflammatory response. In many instances, these physiologic variants and benign pathologic causes of FDG uptake can be specifically recognized and properly categorized; in other instances, such as the lymph node response to inflammation or infection, focal FDG uptake is nonspecific.

SUV-Lean is a weight-independent index for blood FDG accumulation at PET and may be more appropriate than SUV for quantifying F-18 activity in tumors.

Background. Breast cancers have higher than normal glucose metabolism, but the mechanism of glucose entry into these tumors is not well understood. Methods. The expression of five facilitative glucose transporters, Glut‐1 (erythrocyte type), Glut‐2 (liver type), Glut‐3 (brain type), Glut‐4 (muscle/fat type), and Glut‐5 (small intestine type), was studied by immunohistochemistry of paraffin sections from 12 primary human breast cancers and 8 lymph node metastases from 2 patients. Rat tissues known to express these glucose transporters were used as controls. Results. All the primary breast cancers and the lymph node metastases were positive for Glut‐1. This transporter was expressed on the cell membrane and in the cytoplasm of the tumor cells, but exhibited marked intratumoral and intertumoral variability in the proportions of positive cells and the intensity of staining. Staining of the normal mammary epithelium, if present, was much lower than observed in tumor cells from the same patient. Glut‐2 was expressed in all of the tumors, but the intensity of staining was not consistently stronger than that seen in healthy breast. Clusters of Glut‐4‐positive granule were observed in cells in six of the tumors. None of the tumors or the healthy breast in the tissues studied expressed Glut‐3 or Glut‐5. Conclusions. Higher expression of the glucose transporter Glut‐1 by breast cancer cells compared with the healthy breast tissue is common. Increased glucose transporter protein expression may contribute to the increased uptake of 2‐[18F]‐fluoro‐2‐deoxy‐D‐glucose (FDG) by these tumors observed by positron emission tomography (PET) imaging.

Autoimmune diseases have a high prevalence in the population, and autoimmune thyroid disease (AITD) is one of the most common representatives. Thyroid autoantibodies are not only frequently detected in patients with AITD but also in subjects without manifest thyroid dysfunction. The high prevalence raises questions regarding a potential role in extra-thyroidal diseases. This review summarizes the etiology and mechanism of AITD and addresses prevalence of antibodies against thyroid peroxidase, thyroid-stimulating hormone receptor (TSHR), and anti-thyroglobulin and their action outside the thyroid. The main issues limiting the reliability of the conclusions drawn here include problems with different specificities and sensitivities of the antibody detection assays employed, as well as potential confounding effects of altered thyroid hormone levels, and lack of prospective studies. In addition to the well-known effects of TSHR antibodies on fibroblasts in Graves’ disease (GD), studies speculate on a role of anti-thyroid antibodies in cancer. All antibodies may have a tumor-promoting role in breast cancer carcinogenesis despite anti-thyroid peroxidase antibodies having a positive prognostic effect in patients with overt disease. Cross-reactivity with lactoperoxidase leading to induction of chronic inflammation might promote breast cancer, while anti-thyroid antibodies in manifest breast cancer might be an indication for a more active immune system. A better general health condition in older women with anti-thyroid peroxidase antibodies might support this hypothesis. The different actions of the anti-thyroid antibodies correspond to differences in cellular location of the antigens, titers of the circulating antibodies, duration of antibody exposure, and immunological mechanisms in GD and Hashimoto’s thyroiditis.

PET is superior to CT for mediastinal staging of non-small cell lung cancer, independent of performance index or clinical context of PET imaging.