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Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly prescribed to alleviate pain and inflammation in conditions like arthritis, migraines, and post-operative recovery. Their mechanism involves inhibiting prostaglandins that contribute to inflammation. NSAIDs are categorized based on their structure, selectivity for COX-1 and COX-2 enzymes, and plasma half-life. They are effective in treating osteoarthritis, spondyloarthritis, and rheumatoid arthritis but might carry an elevated risk of adverse events. Despite their effectiveness, NSAIDs have limitations and risks that warrant cautious consideration. Extensive research has investigated their side effects, and this review aims to examine the current limitations of oral NSAID therapy, including safety profiles, specific scenarios where their use may not be appropriate, and gaps in knowledge. By critically evaluating these aspects, healthcare practitioners can make informed decisions about prescribing NSAIDs, optimizing patient outcomes while minimizing potential risks. This narrative review summarizes existing knowledge and underscores the importance of risk-benefit assessments in NSAID prescribing. Ultimately, the goal is to enhance the rational use of NSAIDs, maximizing benefits while mitigating adverse effects., (Copyright © 2023 Société française de rhumatologie. Published by Elsevier Masson SAS. All rights reserved.)

Objective: The prevalence of the musculoskeletal immune-related adverse events (irAEs) is probably underestimated, as most studies report only severe side effects. Our aim was to describe and characterize all musculoskeletal irAEs in a large cohort of patients treated with immune checkpoint inhibitors (ICI)., Methods: We conducted a retrospective study among patients who received ICI from 07/27/2014 to 05/08/2020 at the medical oncology department of the Institut Paoli-Calmettes, Marseille, France. All medical files were systemically reviewed by a rheumatologist who collected clinical features, time of occurrence, treatment regimen, irAEs management, course and outcomes. We also assessed tumor response 3 months after introduction of ICI, according to severity and treatments used to manage musculoskeletal irAEs., Results: Among 927 patients treated with ICI for a solid tumor, 118 patients (12.7%) presented a musculoskeletal irAE. Their median age was 66.5, 61% were male, and they mainly had a lung (57.6%) or urological cancer (27.1%). The most frequently involved ICI was an anti PD-1. Arthralgias and myalgias were the most frequent musculoskeletal irAEs (9.8%) and inflammatory rheumatic features were reported in 36 patients (3.9%) with elevated acute phase reactants and negative immunological markers. The median time of onset was 2 months (IC 95% 1.8; 2.7). Tumor response at 3 months did not differ according to musculoskeletal irAE severity, type of manifestation (arthralgias/myalgias versus inflammatory rheumatic features), pain patterns (mechanical versus inflammatory) or irAE treatments., Conclusion: Musculoskeletal irAEs in this large cohort of patients treated with ICI were frequent (12.7%), mostly mild and well tolerated., (Copyright © 2022 Société française de rhumatologie. Published by Elsevier Masson SAS. All rights reserved.)

There is agreement to label as bone infarcts avascular necrosis (AVN) occurring in the metaphyses or diaphyses of long bones, the terms AVN or osteonecrosis being used at the epiphyses. One might expect bone infarction to hold no mysteries. Oddly enough, however, scientific evidence about bone infarcts is extraordinarily scant. The prevalence of bone infarcts is unknown. The main sites of involvement are the distal femur, proximal tibia, and distal tibia. In patients without sickle cell disease or Gaucher's disease, involvement of the upper limbs and lesions confined to the diaphysis are so rare as to warrant a reappraisal of the diagnosis. Although widely viewed as a generally silent event, bone infarcts causes symptoms in half the cases. Standard radiographs are normal initially then show typical high-density lesions in the center of the marrow cavity. A periosteal reaction is common and may be the first and only radiographic change. Magnetic resonance imaging consistently shows typical features and therefore, in principle, obviates the need for other investigations. Bone infarcts are multifocal in over half the cases and, when multifocal, are usually accompanied with multiple foci of epiphyseal avascular necrosis. Thus, bone infarcts, whose prognosis is good per se (with the exception of the very low risk of malignant transformation), are usually a marker for systemic avascular necrosis. Consequently, patients with bone infarcts must be investigated both for known risk factors and for other foci of avascular necrosis, which may, in contrast, have function-threatening effects., (Copyright © 2016 Société française de rhumatologie. Published by Elsevier SAS. All rights reserved.)

Brucellosis is uncommon in humans and only rarely manifests as osteomyelitis. We report the case of a 57-year-old patient with chronic Brucella osteomyelitis of both humeri. The diagnosis was established upon evaluation of a spontaneous fracture of the right humerus. The organism was recovered in fluid draining to the skin from an abscess located in the bone and soft tissues.

Background: Pregnancy-related hip diseases epidemiology has been poorly evaluated. We report our experience of gestational and postpartum hip diseases and evaluate their incidence., Methods: (1) Prospective survey: all pregnant or early postpartum women suspected to have hip involvement during their follow-up in an Obstetric unit were referred to a rheumatologist. If clinically confirmed, magnetic resonance imaging (MRI) and additional investigations as needed were performed. This survey had 2 years duration. (2) Retrospective study: all cases of definite (with MRI confirmation) pregnancy-related hip disease referred to our Rheumatology unit during the past 15 years were analyzed., Results: During the 2-year prospective survey, 3 patients (4 hips) of pregnancy-related hip disease were observed over 4900 pregnancies (1 case of transient osteoporosis of the hip (TOH) and 2 cases of occult fracture of the femoral head). During the 15-year retrospective study, 12 patients (17 hips) with hip diseases during pregnancy or early postpartum were identified. There were 6 patients (9 hips) with TOH, 4 patients (6 hips) with occult fracture of the femoral head, 1 patient with osteonecrosis of the femoral head, and 1 coxitis in a patient with ankylosing spondylitis. Differentiating diagnosis between TOH and occult fractures could only be made by MRI. Five of the 6 women with TOH had osteopenia at the lumbar spine at dual energy X-ray absorptiometry (DEXA). The 4 women with occult fractures had either osteopenia or osteoporosis at the lumbar spine., Conclusion: Hip diseases are infrequent during pregnancy and early postpartum. Transient osteoporosis of the hip and occult stress fractures of the femoral head appear the main causes and those diagnoses justify evaluation for an underlying bone fragility. Osteonecrosis is very rare in this setting.

Avascular necrosis of bone (AVN) occurs as two main variants, local and systemic. Local AVN is usually caused by trauma or microtrauma; examples include primary osteonecrosis of the medial condyle, vertebral osteonecrosis, necrosis after meniscectomy, and osteonecrosis of the mandible or small bones. Systemic AVN manifests as epiphyseal necrosis or bone infarction, which is often multifocal. Little is known about the factors that trigger AVN. One possible mechanism is intraluminal obliteration of blood vessels by microscopic fat emboli, sickle cells, nitrogen bubbles (caisson disease), or focal clotting due to procoagulant abnormalities. Extraluminal obliteration may result from elevated marrow pressure or increased marrow fat. Cytotoxicity and genetic factors may be involved also. Many factors are probably capable of inducing AVN, and combinations of factors may be required, although the final mechanism is always critical ischemia. The natural history of AVN is better understood than the early triggering factors. AVN becomes detectable 1-6 months after exposure to an easily identifiable risk factor such as high-dose glucocorticoid therapy or femoral neck fracture. Later on, AVN is uncommon even when the patient remains exposed to the risk factor. The turning point in the natural history of AVN is subchondral plate fracture, which leads to collapse of the necrotic segment of the epiphysis, usually within the first 2 years. The risk of collapse depends chiefly on the initial size and location of the necrotic segment, which can be determined accurately by magnetic resonance imaging (MRI). This natural history has obvious clinical implications.

Introduction: The pathophysiology of intravertebral vacuum (IVV) remains unclear, although vertebral osteonecrosis is often incriminated. Gas may migrate from the disk to the vertebral body. The objective of this study was to investigate the relations between IVV and intradiscal vacuum (IDV)., Methods: We prospectively evaluated the presence of radiological findings suggestive of IVV in patients admitted to a rheumatology department for vertebral fracture, over a 6-year period. Suggestive radiological findings were defined as a radiolucent collection within a vertebral body, an increase in the anteroposterior diameter of the vertebral body, and/or evidence of horizontal dissection of a vertebral body. Patients with any of these findings underwent computed tomography; when this investigation showed IVV, the adjacent disks were examined for IDV, and when this was found a communication between the two cavities was looked for., Results: Of 278 patients admitted for vertebral fracture during the study period, 15 had IVV. IDV adjacent to the fractured endplate was visible in 13 of these 15 patients. All 15 patients had severe fractures (Genant semi-quantitative classification, grade 3 in 10 patients and grade 2 in five patients). A communication between the intradiscal and intravertebral collections was seen in five patients. Only two patients had evidence of IVV on plain radiographs., Conclusion: Our findings support migration of gas from the disk to a fracture in the adjacent vertebral body. The term "vertebral osteonecrosis" used to designate IVV may be inappropriate. IVV is rarely shown by plain radiographs, indicating a need for other morphological criteria.

Thromboangiitis obliterans (or Buerger disease) is a rare vascular disease that selectively affects young males who are inveterate smokers. We report a case in a young female smoker who presented with recurrent episodes of polyarthralgia and distal extremity ischemia. The initial diagnosis was connective tissue disease, and the correct diagnosis was established only 7 years after symptom onset. Joint manifestations are common in thromboangiitis obliterans and usually antedate the diagnosis, which should be considered in patients with superficial venous thrombosis, upper limb ischemia, or Raynaud's phenomenon. This is true even in females, as shown by the case described here.

Objective: The purpose was to analyze magnetic resonance imaging (MRI) abnormalities in reflex sympathetic dystrophy syndrome (RSDS) of the foot, with the goal of helping to meet the difficult diagnostic challenges raised by this condition., Methods: Retrospective study of 20 patients with RSDS of the foot, 15 at the warm phase and five at the dystrophic phase., Results: Of the 15 patients at the warm phase, seven had evidence of bone edema (low signal on T1-weighted images and high signal on T2, T2 STIR, and fat saturation images) and five had occult fractures (linear band of low signal on T1 and T2 weighted images with no enhancement after contrast injection). Other abnormalities included soft tissue changes in three patients, joint effusion in five, and synovial hypertrophy in one. Of the five patients at the dystrophic phase, one had a fracture with a joint effusion, one had isolated joint edema, and three had normal MRI findings., Conclusion: Bone marrow edema is inconsistent at the warm phase of RSDS and is never present at the dystrophic phase. Thus, absence of bone edema does not rule out RSDS. Fractures may be visible by MRI in one-third of patients with RSDS and no clinical or plain radiography evidence of fracturing.

Concepts related to the pathophysiology of reflex sympathetic dystrophy syndrome (RSDS) are changing. Although sympathetic influences are still viewed as the most likely mechanism underlying the development and/or perpetuation of RSDS, these influences are no longer ascribed to an increase in sympathetic tone. Rather, the most likely mechanism may be increased sensitivity to catecholamines due to sympathetic denervation with an increase in the number and/or sensitivity of peripheral axonal adrenoceptors. Several other pathophysiological mechanisms have been suggested, including neurogenic inflammation with the release of neuropeptides by primary nociceptive afferents and sympathetic efferents. These neuromediators, particularly substance P, calcitonin gene-related peptide, and neuropeptide Y (NPY), may play a pivotal role in the genesis of pain in RSDS. They induce an inflammatory response (cutaneous erythema and edema) and lower the pain threshold. Neurogenic inflammation at the site of the lesion with neuromediator accumulation or depletion probably contributes to the pathophysiology of RSDS. However, no single neuromediator has been proved responsible, and other hypotheses continue to arouse interest.

We report the case of a 45-year-old woman who presented with a six-year history of diffuse polyarthralgia responsible for major disability. She reported bilateral symmetric arthralgia in nearly every joint, as well as back pain. Muscle wasting predominating in the roots of the limbs was found. Laboratory tests showed hypocalcemia, severe hypophosphatemia, hypokalemia, alkaline phosphatase elevation, aminoaciduria, and hyperphosphaturia, with no glycosuria. Radiographs disclosed osteolysis of the pubic symphysis, multiple pelvic fractures, vertebral compression fractures, and diffuse demineralization. A bone scan visualized symmetric foci of hyperactivity in nearly all joints and fracture sites. Dramatic improvements in clinical and radiographic abnormalities were noted after six months of treatment with phosphate and calcitriol. This is a case of incomplete Fanconi syndrome, with no glycosuria. The clinical presentation of Fanconi syndrome can be misleading. Fanconi syndrome should be borne in mind as a possible cause of polyarthralgia to avoid diagnostic delay, which in our patient led to a picture of pseudomyopathy with multiple fractures.

Ophthalmologic adverse effects of bisphosphonate therapy are infrequent and of unclear pathogenesis. The most common has been anterior uveitis, of which 18 cases have been reported. Onset was within 24 to 48 hours after infusion initiation, and both eyes were affected in most patients. The outcome was favorable within a few days after bisphosphonate discontinuation and topical glucocorticoid therapy, although rechallenge was frequently followed by a recurrence. Bisphosphonates are being used successfully in an increasingly broad range of disorders. We report a case of pamidronate-induced anterior uveitis and present a review of the relevant literature.