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Resume La prevention de la pre-eclampsie, pathologie vasculo-placentaire a l’origine d’une part importante de la morbi-mortalite maternelle et fœtale, constitue un enjeu majeur de sante publique. L’aspirine a prouve son efficacite en prevention primaire et secondaire de la pre-eclampsie, en particulier lorsqu’elle est donnee a la dose de 150 mg/jour au coucher avant 15 SA chez une population de patientes a haut risque. Dans l’etude anglaise ASPRE, les femmes a haut risque de pre-eclampsie ont ete identifiees par le biais d’un algorithme prenant en compte le dosage des biomarqueurs angiogeniques a la fin du premier trimestre de grossesse. Cette mise au point rappelle les mecanismes physiopathologiques, les facteurs de risque de pre-eclampsie et l’interet du dosage sanguin precoce des biomarqueurs angiogeniques sFlt1 et PLGF au cours de la grossesse dans l’evaluation du risque de pre-eclampsie. Contrairement a l’Angleterre ou a Israel, l’application de cet algorithme en population generale n’a pas encore ete evaluee en France et il semblerait important de determiner si ce depistage y serait cout-efficace. Enfin, le lupus erythemateux systemique est associe a un sur-risque de pathologies vasculo-placentaires. Bien que peu nombreuses, les etudes sur l’interet du dosage des biomarqueurs angiogeniques au cours des grossesses lupiques identifient une correlation entre des taux eleves de sFlt1 a la fin du premier trimestre et la survenue ulterieure d’une pathologie vasculo-placentaire grave, avec une tres bonne valeur predictive negative de sFlt1. L’utilisation des biomarqueurs angiogeniques en depistage des pathologies vasculo-placentaires chez les femmes lupiques enceintes pourrait permettre de mieux cibler la population des femmes relevant d’un traitement par aspirine et d’une surveillance plus etroite.

International audience; : Primary Sgögren's syndrome (SSP) is one of the most common connective tissue disorder with an estimated prevalence between 0.6 and 1.7% of the general population. Lymphocytic infiltration of salivary gland is easily accessible favoring the diagnosis, and clinical and fundamental research. However, while many advances have been obtained in the recent decades, the pathophysiology of SSP remains unclear combining environmental factors with genetic predisposition. A central role tends to be attributed to salivary gland epithelial cells, originally designated as "innocent bystanders" and to B cells through the intervention of survey factors like BAFF. New T cells subsets are also carefully studied, particularly natural T regulatory and Th17 cells. They could indeed represent new therapeutic targets.

International audience; PURPOSE: About forty percent of the patients with primary Sjögren's syndrome (pSS) experience chronic neuropathic pain with normal electrodiagnostic studies. Two previous studies suggest that chronic neuropathic pain in pSS is due to small fiber neuropathy (SFN). Quantification of epidermal nerve fiber density after skin biopsy has been validated to diagnose small fiber neuropathy. METHODS: Skin biopsy was performed in 14 consecutive pSS patients (satisfying the american-european classification criteria) with chronic neuropathic pain and normal electrodiagnostic studies suggesting SFN. RéSULTS: Fourteen female pSS patients exhibited chronic neuropathic pain [burning sensation (n=14), prickling (n=4), dysesthesia (n=8)] with paroxystic exacerbations (n=10) and allodynia (n=13), for a mean period of 18.4±12.4 months. Neuropathic pain involved mostly hands and feet (n=13), with a distal (n=9) and leg (n=4) predominant distribution. Neurological examination disclosed normal deep tendon responses and absence of motor weakness (n=14). Small fiber neuropathy was confirmed by skin biopsy in 13 cases. Epidermal nerve fiber density was decreased in distal [(n=12), mean 3.5±1.7 fibers/mm (N>6.9)] and proximal site of biopsy [(n=9), mean 7.04±2.63 fibers/mm (N>9.3)]. CONCLUSION: Small fiber neuropathy is commonly responsible of chronic neuropathic pain in pSS. Prevalence, physiopathology and neurological evolution of such neuropathies still remain unknown.

International audience; OBJECTIVE: To study evolution of pSS immunological profile, impact on pSS activity and the long-term evolution of patients with atypical auto-antibodies in a bicentric cohort of patients with pSS (n=445, mean age 53.6+/-14years, mean follow-up 76.1+/-51months). RESULTS: 212 patients were SSA positive and 131 were both SSA and SSB positive. During follow-up, SSA antibodies disappear in 8 patients; 2 of them exhibit new systemic complications of pSS. 68 patients had cryoglobulinemia. 52 patients had other anti-nuclear antibodies (ANA) specificities: anti-RNP (n=12), anti-centromere (n=14), anti-DNA native (n=19), anti-Scl70 (n=3), anti-JO1 (n=3), anti-Sm (n=3) and anti-histone (n=1). Fourteen patients developed ANA-associated auto-immune disease during the follow-up: 5 polymyositis (mean apparition delay 78months), 6 systemic lupus erythematosus (mean occurrence delay 77months) and 2 systemic sclerosis (mean occurrence delay 133+/-64months). Among these 14 patients, only three presented atypical-ANA at pSS diagnosis. Cryoglobulinemia and anti-SSA and SSB antibodies at diagnosis were associated with new systemic involvements. IN CONCLUSION: Cryoglobulinemia and SSA/SSB positivity are associated with systemic activity after diagnosis in pSS. Although atypical ANA are found in 12% of the cases, long-term evolution to ANA associated auto-immune diseases concerned patients with active immunological profile and extra-glandular manifestations.