Inflammatory Rheumatism

Pseudo-rheumatoid arthritis (PRA) is a common inflammatory rheumatic disease of the elderly, characterized by inflammatory shoulder and/or hip pain. Its routine diagnosis is based on a number of clinical criteria, the presence of a biological inflammatory syndrome and the elimination of the main differential diagnoses. It is sometimes referred to as PPR syndrome, since around 25% of initial diagnoses are not confirmed at one year's follow-up (PPR syndrome revealing rheumatoid arthritis, microcrystalline rheumatism, etc.). Diagnosis may be facilitated by ultrasound scans of the shoulders and hips, which may show characteristic inflammatory lesions, or by PET scans when there is a marked deterioration in general condition or other clinical atypia. PPR may be associated at the outset, or it may evolve into the rarer vasculitis of the elderly, giant cell arteritis (GCA), a condition that can lead to severe and irreversible neurological vascular damage if not treated early. Prolonged, moderate-dose corticosteroid therapy is the cornerstone of PPR treatment, although new treatments are in the process of obtaining marketing authorization to enable cortisone sparing. Anti-IL-6 agents, and in particular Tocilizumab, have demonstrated their efficacy in recent cortico-dependent PPR, Sarilumab has obtained marketing authorization for cortico-dependent PPR in the USA in 2023, and other therapeutic classes are currently being evaluated in this situation. Recommendations, including those of ACR/EULAR in 2015, advise a strategy of initiating corticosteroid therapy at a moderate dose, with a dosage of between 12.5 and 25 mg prednisone equivalent per day, and gradually tapering off with the aim of reaching a dosage of 10 mg prednisone equivalent per day at week 8, to achieve complete weaning at 12 months. However, on the one hand, these recommendations are not based on clinical trials and, on the other, the main comorbidities associated with PPR are related to this long-term corticosteroid therapy. Lastly, we know that around 50% of patients do not follow this tapering-off protocol, with either relapses (estimated at 50% during tapering) or the impossibility for around 25% of patients to stop corticosteroid therapy. However, there are currently no predictive factors for the evolution of PPR. PPR activity can be measured either using a validated score, the DAS-PPR, or according to the opinion of the rheumatologist. Good progression of rheumatoid arthritis is characterized by a low activity score (DAS-PPR\<10) and, wherever possible, discontinuation of treatment within one year, as recommended by international experts. The main objective of this cohort is therefore to evaluate the percentage of patients with low-activity PPR (DAS-PPR\<10) and no treatment at 12 months. Secondary objectives will concern the initial phenotypic and evolutionary description of PPR (complete initial phenotypic characteristics, including some exploratory ones (imaging, biology, immunology, genetics, microbiota, avatars). The evolution of the disease, with the percentage of relapses during the decline or distant relapses, percentage of association with ACG, mortality rate, as well as the prognostic factors of these different evolutionary forms. A description of the disease-modifying treatments used (corticosteroid therapy and its decline, other immunomodulators), as well as a record of the complications presented by patients (development of ACG, corticosteroid toxicity, sarcopenia, osteoporosis fractures, diverticular perforation). Finally, many pathologies can clinically and biologically mimic PPR, leading to erroneous prescriptions of glucocorticoids for prolonged periods, and sometimes a delay in the diagnosis of serious conditions. These classic differential diagnoses will be investigated according to the clinical context and the clinician's judgement, and the diagnostic value of tests such as joint ultrasound, PET scans and biomarkers can be assessed. With regard to patient follow-up, if an alternative diagnosis is identified immediately after the completion of additional examinations, the patient is no longer followed up in the study, and the alternative diagnosis is noted by the investigator. For patients for whom the investigator's conviction concerning the diagnosis of PPR remains above 50%, as at inclusion, follow-up in the study is continued. At one year's follow-up, if an alternative diagnosis has been made, this is collected and the patient is no longer followed up in the cohort. Follow-up for other patients then continues for 5 years. Deterministic matching to the SNDS will be performed for each patient included. To date, there is no French prospective cohort dedicated to the follow-up of patients with a recent form of PPR, as has been done for rheumatoid arthritis, spondyloarthritis and psoriatic arthritis. The creation of such a cohort will improve our knowledge of this pathology, in terms of both pathophysiology and routine management.

Bone turnover markers (BTMs) are recommended as an important tool in follow-up of osteoporosis treatment. However, there is a lack of knowledge in the reliability of BTMs during and after glucocorticoid treatment. Glucocorticoids suppresses BTMs during treatment with at least 30% and, moreover, glucocorticoids increase the risk of fractures. Patients with an inflammatory joint disease are at increased risk of osteoporosis, and disease flares are often treated with glucocorticoids, which in turn can lead to loss in reliability of the BTMs in patients who also are on osteoporosis treatment. There is a need of more knowledge on BTM changes during and after glucocorticoid treatment for optimized patientcare, reduced risk of side effects and reduced health economic costs.

Glucocorticoids remain to be among the most important and most frequently used anti-inflammatory and immunosuppressive or immune-modulatory acting drugs to treat rheumatic (and other) diseases. Unfortunately, glucocorticoids also exert undesired effects, especially if higher dosages have to be given over longer periods of time. The available data describing frequency and severity of these adverse effects are fragmentary. This statement is especially true for glucocorticoid-induced osteoporosis (GIOP) in the context of chronic inflammatory rheumatic diseases or (in part) psoriasis(arthritis). The state of knowledge and scientific data, being sparse, is partly conflicting and often derived from over-aged projects or studies. Therefore, there are urgent needs to work on various current questions systematically and at the highest scientific level possible. In order to address these needs, we aim at collecting and analyzing disease- and bone-related data from patients with chronic inflammatory rheumatic diseases or psoriasis and therapy with glucocorticoids, and to build a respective GIOP-Databank. Patients will attend for diagnostics, and where necessary therapy and follow-up of GIOP, according to current guidelines. Clinical, laboratory and instrumental examination results from more than 1000 patients in the first three years of the project are planned to be documented in a prospective database.

Study of the diagnostic performance of 18-FDG PET scores in Polymyalgia rheumatica and comparaison with others inflammatories diseases.