“To be or not to be” for PET in rheumatology. A marriage of love or of convenience?

The mechanisms responsible for the development and course of rheumatic diseases are not yet fully explained. Molecular imaging is one of the tools used to investigate them, with nuclear medicine being its prominent part. Unlike computed tomography (CT), ultrasonography (USG), or magnetic resonance imaging (MRI), which reveal only structural disorders, radioisotope imaging enables us to present the functional changes. Its methods are characterised by high sensitivity – radioisotope examination can reveal changes in substance concentration as small as 10–11 mmol, while MRI, respectively, 10–3–10–4 mol. This means that radioisotope methods can be used to effectively trace the changes in concentrations of chosen chemical compounds while they take place in the course of the disease. Thus the assessment of functional changes becomes possible, which should be essential for the choice of proper therapy. Nuclear medicine methods meet numerous vital requirements determined by the standards for modern medical science, such as: • They enable early diagnosis of the changes caused by the disease and allow us to establish their nature. The diagnosis should precede the emergence of irreversible structural damage. • They can be used for the precise establishment of the state of progress of pathologic neoplastic changes. • The employed imaging methods should enable us to predict the course of the disease and use a personalised treatment to counter the illness. • As the costs of modern therapies increase, it should be possible to use the diagnostic methods to evaluate the effectiveness of ongoing therapy. • Modern medicine requires diagnostic methods that can definitely determine the disease regression and reveal its recurrence as early as possible. Nuclear medicine has proven to be effective in solving all of the above listed clinical issues; moreover, it meets pharmacoeconomic cost-effectiveness criteria. Fluorodeoxyglucose (18FDG) is a radiopharmaceutical most commonly used in PET examinations. It is an analogue of glucose. The areas of the increased marker accumulation are evidence of intensified metabolism associated with raised glucose demand. This can be a result of neoplasmic or of inflammatory processes. The increased 18FDG accumulation is an effect of the increased activity of Glut1 and Glut 3 transport mechanisms, as well as with the elevated activity of hexokinase. These phenomena are typical for cells undergoing rapid proliferation, e.g. the macrophages, neutrophils, and new granulation tissue. 18FDG-PET examination allows for the assessment of the inflammation progress. Matsui et al. [1] demonstrated in their in vitro research that the highest accumulation of 18FDG occurs in the course of the pannus creation and destruction of the bone structure by inflammation. This process is the effect of fibroblast proliferation. The role of the macrophages must also be noticed: the accumulation of 18FDG by unactivated macrophages is minimal, but after their activation by hypoxia or tumour necrosis factor α (TNF-α), their demand for glucose increases significantly. Beckers et al. [2] showed that the sensitivity of the described method in rheumatoid arthritis is 90%. A number of publications indicate that 18FDG-PET is able to reveal pathologic changes in their subclinical stage or during clinical remission. This may play a vital role in the therapeutic proceedings [3]. PET can also be used to evaluate the stage of progress of pathologic changes in spondyloarthritis, polymyalgia rheumatica, Still’s disease, polychondritis, IgG4-related disease, polymyositis, and dermatomyositis [4]. A number of publications point to the fact that 18FDG is a very efficient marker for therapy effectiveness assessment. Elisng et al. [5] demonstrated that the decrease in 18FDG uptake, subsequent to the start of the anti-TNF drug therapy, is an important prognostic factor for the effectiveness of treatment. It is important to stress the additional aspect of PET – the diagnosis of neoplastic illnesses coexisting with lupus erythematosus, systemic sclerosis, dermatomyositis/ polymyositis, or Sjögren’s disease. Epidemiological data