[Can we prevent the occurrence of Rheumatoid Arthritis in 2023?] / Peut-on prévenir la survenue de la polyarthrite rhumatoïde en 2023 ?

The improvement of our knowledge about the pathogenic mechanisms, the identification of the risks factors and the development of new antirheumatic drugs have enabled significant progress in the management of patients suffering of Rheumatoid Arthritis (RA). We know now that the disease develops long before the first clinical signs appear (immunological onset of the disease or asymptomatic period). One of the current lines of research is the prevention of the disease using early interventions during the asymptomatic stage. In this article, we will summarize the current knowledge concerning the risk factors, the identification of asymptomatic patients at high risk developing rheumatoid arthritis, as well as potential interventions that would allow prevention of the disease.

L'amélioration de nos connaissances sur les mécanismes pathogéniques, l'identification des facteurs de risque, ainsi que le développement de nouveaux traitements antirhumatismaux, ont permis un progrès significatif dans la prise en charge des patients souffrant d'une polyarthrite rhumatoïde (PR). On sait maintenant que la maladie se développe bien avant l'apparition des premiers signes de la maladie (début immunologique de la maladie ou période asymptomatique). Un des axes de recherche actuel est de prévenir la maladie par une intervention précoce, au stade asymptomatique. Dans cet article, nous allons résumer les connaissances actuelles sur les facteurs de risque, l'identification des patients asymptomatiques à haut risque de développer une PR, ainsi que sur les mesures étudiées qui permettraient la prévention de cette maladie.

[Mastcell activation syndrome]. / Syndrome d'activation mastocytaire.

Mast cell activation syndrome (MCAS) encompasses a heterogeneous group of pathologies, which are characterized by the existence of clinical symptoms secondary to the systemic effects of mediators released by activated mast cells. MCAS-related symptoms may be mild, moderate, severe, or even life-threatening. Detailed knowledge of the pathogenesis and complexity of MCAS can help in the management and treatment of these patients.

Le syndrome d'activation mastocytaire (MCAS) englobe un groupe hétérogène de pathologies qui sont caractérisées par la présentation des symptômes cliniques secondaires aux effets systémiques des médiateurs libérés par les mastocytes activés. Les symptômes liés au MCAS peuvent être légers, modérés, graves ou même mortels. Une connaissance détaillée de la pathogenèse et de la complexité du MCAS peut aider dans la prise en charge et le traitement de ces patients.

[Spinal injection : risks and side effects]. / Complications des infiltrations rachidiennes.

The efficacy of spinal injection for chronic spinal pain is dubious for most conditions. They are however frequently prescribed. Side effects are poorly reported in the literature. In addition to benign and transient problems, serious and lethal side effects have been reported due to infection, hematoma or central and spinal cord infarctions which could be related to intravascular injection of corticoids. Although their frequency is excessively low, they should be discussed with every patient before prescription and should be mentioned in the consent form.

Malgré leur efficacité hautement contestée dans la plupart des situations, les infiltrations épidurales sont fréquemment utilisées dans le traitement des rachialgies chroniques. Les effets secondaires sont rarement considérés et la littérature à leur sujet est pauvre. Il apparaît qu'en plus des effets secondaires bénins, des complications graves et parfois létales doivent être connues des praticiens. Il s'agit principalement de complications infectieuses, hémorragiques mais aussi d'infarctus centraux ou médullaires qui pourraient être secondaires à des injections intravasculaires de corticostéroïdes. Bien qu'extrêmement rares, ils doivent être évoqués avec le patient au moment de la proposition de l'acte thérapeutique et apparaître dans le formulaire de consentement.

Using Baseline and Peak Serum Tryptase Levels to Diagnose Anaphylaxis: a Review.

The diagnosis of anaphylaxis relies on a suggestive clinical history after exposure to a potential triggering factor. Serum tryptase concentrations increase on degranulation of mast cells and therefore serum tryptase levels are measured to diagnose anaphylaxis. There is no standardized method for assessing total serum mast cell tryptase (MCT) in anaphylaxis. The Working Conference in 2010 proposed a consensus equation (peak MCT should be > 1.2x baseline tryptase + 2 ng/L) to diagnose acute mast cell activation (aMCA). Our objective was to narratively review the literature since the Working Conference in 2010, examining the use of the consensus equation and other equations comparing baseline and peak serum tryptase during anaphylaxis. Computerized bibliographic searches of PUBMED and EMBASE were supplemented with a manual search of reference lists. English-language studies were included. Eleven studies met our inclusion criteria with a total of 4551 participants. However, only four studies with 653 participants used the consensus equation. The other seven studies used other methods to compare peak and baseline serum tryptase concentrations. Measuring serum tryptase levels is valuable in the diagnosis of anaphylaxis but is unable to detect all anaphylactic reactions. Based on our current literature review, the consensus equation is underused in the diagnosis of anaphylaxis. There is also a need for exploration of other biomarkers which could be used in parallel to peak and baseline serum tryptase measurements for further diagnostic certainty. Serum tryptase is the most studied biomarker in anaphylaxis but is still far from being the ideal biomarker for this. There is a need to identify new potential useful biomarkers. Serum tryptase levels are valuable in the diagnosis of anaphylaxis, but are unable to detect all anaphylactic reactions. Additionally serial tryptase measurements are laborious in daily clinical practice.

"Late" Withdrawal Syndrome after Carbamazepine In Utero Exposure in a CYP2C9 Slow Metabolizer Newborn.

We report a case of carbamazepine withdrawal syndrome following in utero exposure to carbamazepine related to a pharmacogenetic predisposition factor. The infant was born at 37 1/7 weeks' gestation by cesarean section to a mother treated for epilepsy with carbamazepine. One hour and thirty minutes after birth, the infant presented a respiratory distress with severe oxygen desaturation requiring intubation 5 h after birth. On the third day of life the infant developed clinical signs of a withdrawal syndrome which resolved progressively after 16 days and symptomatic treatment. The infant genotype analysis showed two low activity CYP2C9 allelic variants (∗2/∗3 heterozygote) predicting a CYP2C9 slow metabolizer phenotype which could explain reduced carbamazepine elimination and a late and long-lasting withdrawal symptoms observed 3 days after birth. The association of a withdrawal syndrome with carbamazepine exposure has not been previously reported and pharmacogenetic tests might therefore be useful in identifying patients at risk.