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Bleeding after gynecological surgery remains an infrequent life-threatening complication, demanding appropriate medical and surgical management. Classified as early/“reactionary” and delayed/secondary, unexpected postoperative hemorrhage may arise regardless of the route or subtype of hysterectomy. Timely recognition and prompt intervention to arrest bleeding are essential strategies for the suitable outcome of the patient. The present chapter presents an overview on different aspects of bleeding after hysterectomy such as incidence rate, risk factors, mechanisms, and management techniques aiming to expand knowledge and skills in recognizing and treating this unpredicted potentially serious problem. Furthermore, we intend to offer a guide toward standardizing treatment practice across bleeding issues following hysterectomy considering clear recommendations and algorithms.

Resume Objectif Malgre le lien pathobiologique bidirectionnel largement reconnu entre la polyarthrite rhumatoide (PR) et la maladie parodontale (MP), l’impact des nouveaux traitements antirhumatismaux sur la modulation non seulement des atteintes articulaires inflammatoires et immunitaires mais aussi du microenvironnement parodontal reste sujet a debat. Nous avions pour objectif d’evaluer le status parodontal dans la PR, avec et sans administration de baricitinib, un inhibiteur des Janus kinases (JAK), et de preciser l’association entre ces deux entites. Methodes Nous avons mene une etude prospective longitudinale de 24 semaines chez 21 patients atteints de PR active et debutant un traitement par baricitinib. Les analyses standard comprenaient une double evaluation rhumatologique (activite de la PR, invalidite, serologie, profil inflammatoire) et dentaire (indice de plaque, indice gingival, indice de saignement au sondage, profondeur de sondage et niveau d’attache clinique). Resultats Dans plus de la moitie des cas, les patients PR presentaient une parodontite chronique au depart, comme indique par la prevalence accrue de sites avec accumulation de plaque, saignements au sondage, poches profondes et perte d’attache. Une parodontite agressive a ete rapportee notamment dans les sous-groupes cliniques ayant une inflammation excessive (taux serique de proteine C-reactive) et la presence de biomarqueurs serologiques (anticorps antipeptides citrullines). Par ailleurs, des correlations significatives ont egalement ete rapportees entre la pathologie dentaire, l’activite de la maladie et le taux des ACPA (p Conclusion La PR, en particulier lorsqu’elle est de forme severe, active et ACPA+, est associee a une degradation de la sante parodontale. Le blocage des JAK utilisant le baricitinib par voie orale semble avoir un effet benefique dans la PR active et pourrait moduler le processus inflammatoire au sein du tissu parodontal.

Background. Systemic sclerosis (SSc) is a chronic multisystem autoimmune condition defined by a complex pathobiology, comprising excessive fibrosis of skin and internal organs, peripheral vasculopathy with endothelial cell dysfunction, inadequate vascular repair and neovascularization, and aberrant immunity. Vitamin D is a steroid hormone with pleiotropic effects beyond its traditional role in calcium and bone homeostasis. Since vitamin D has immunomodulatory, cardioprotective, and antifibrotic properties, it could potentially interfere with SSc pathogenesis. Suboptimal vitamin D levels are classically recognized in scleroderma, irrespective of clinical and serological phenotype. Aim. This systematic review is aimed at investigating and clarifying the role of vitamin D in SSc and emphasizing the association of vitamin D status with different clinical settings. Methods and Results. A systematic online search was performed, using PubMed databases to collect articles on the topic of vitamin D in SSc. The final analysis included 40 eligible articles. Conclusions. Hypovitaminosis D is common in SSc patients and could be associated with clinical and serologic patterns of the disease. Intervention for low serum vitamin D levels in SSc pathogenesis remains controversial, as well as the significance of vitamin D supplementation in such patients.

Axial spondyloarthritis (axSpA) is a chronic inflammatory disease that can lead to ankylosis by secondary ossification of inflammatory lesions, with progressive disability and a significant impact on quality of life. It is also a risk factor for the occurrence of comorbidities, especially cardiovascular diseases (CVDs), mood disorders, osteoporosis, and malignancies. Early diagnosis and treatment are needed to prevent or decrease functional decline and to improve the patient’s prognosis. In respect of axSpA, there is an unmet need for biomarkers that can help to diagnose the disease, define disease activity and prognosis, and establish personalized treatment approaches. The aim of this review was to summarize the available information regarding the most promising biomarkers for axSpA. We classified and identified six core categories of biomarkers: (i) systemic markers of inflammation; (ii) molecules involved in bone homeostasis; (iii) HLA-B27 and newer genetic biomarkers; (iv) antibody-based biomarkers; (v) microbiome biomarkers; and (vi) miscellaneous biomarkers. Unfortunately, despite efforts to validate new biomarkers, few of them are used in clinical practice; however, we believe that these studies provide useful data that could aid in better disease management.

Background: The aim of our study was to explore the influence of weekly subcutaneous administration of interleukin-6 (IL-6) receptor inhibitor tocilizumab (TCZ) on periodontal status in a local longitudinal study of patients with rheumatoid arthritis (RA) and periodontal disease (PD). Methods: We performed a 6-month prospective study in 51 patients with chronic periodontitis and moderate-to-severe RA starting TCZ in accordance with local recommendations. Extensive rheumatologic (clinical activity, inflammatory, serological biomarkers) and periodontal (visible plaque index, gingival index, bleeding on probing, probing pocket depth, clinical attachment loss) assessments were done. Changes in RA activity and periodontal status were reassessed after 3 and 6 months. Results: We demonstrated significant correlations between periodontal status, disease activity, and serologic biomarkers (p &lt, 0.05). Tocilizumab significantly improved the gingival index scores and decreased the number of sites with bleeding on probing after only 3 months (p &lt, 0.05), while the probing pocket depth significantly decreased after 6 months, overall, clinical attachment loss presented only slight changes without any statistical significance as well as teeth count and plaque levels (p &gt, 0.05). Conclusion: IL-6 inhibition is able to improve periodontal outcomes in patients with RA and concomitant PD, which is essentially related to a dramatic decrease in serum inflammatory mediators.

Successful pregnancy requires an immunological shift with T helper CD4+ bias based on disbalance Th1/Th17 versus Th2/T regulatory (Tregs) required to induce tolerance against the semi-allogeneic fetus and placenta and to support fetal growth. Considered a pregnancy-specific hypertensive disorder, pre-eclampsia is characterized by multifaceted organ involvement related to impaired maternal immune tolerance to paternal antigens triggered by hypoxic placental injury as well as excessive local and systemic anti-angiogenic and inflammatory factor synthesis. Both systemic and local Th1/Th2 shift further expands to Th17 cells and their cytokines (IL-17) complemented by suppressive Treg and Th2 cytokines (IL-10, IL-4); alterations in Th17 and Tregs cause hypertension during pregnancy throughout vasoactive factors and endothelial dysfunction, providing an explanatory link between immunological and vascular events in the pathobiology of pre-eclamptic pregnancy. Apart from immunological changes representative of normotensive pregnancy, lupus pregnancy is generally defined by higher serum pro-inflammatory cytokines, lower Th2 polarization, defective and lower number of Tregs, potential blockade of complement inhibitors by anti-phospholipid antibodies, and similar immune alterations to those seen in pre-eclampsia. The current review underpins the immune mechanisms of pre-eclampsia focusing on local (placental) and systemic (maternal) aberrant adaptive and innate immune response versus normotensive pregnancy and pregnancy in systemic autoimmune conditions, particularly lupus.

Despite a widely recognized bidirectional pathobiologic relationship between rheumatoid arthritis (RA) and periodontal disease, the impact of innovative anti-rheumatic drugs in modulating not only inflammatory and immune articular damage, but also periodontal microenvironment remains debatable. We aimed to evaluate the periodontal status in RA with and without baricitinib, a Janus kinase (JAK) inhibitor, and to better describe association between these entities.We performed a prospective longitudinal 24-weeks study in 21 active RA initiating baricitinib. Standard assessments included a dual rheumatologic (RA activity, disability, serological, inflammatory profile) and dental evaluation comprising plaque index, gingival index, bleeding on probing, probing depth, clinical attachment level.More than half of RA presented at baseline with chronic periodontitis, as suggested by high prevalence of sites with dental plaque, abnormal bleeding on probing, probing depth and clinical attachment level. Aggressive periodontal disease was reported particularly in disease subsets with excessive inflammatory (serumC reactive protein level) and serologic biomarkers (anti-citrullinated peptide antibodies). Furthermore, significant correlations between dental pathology, disease activity and ACPA levels were also reported (P0.05). Consistent improvement was noticed in both rheumatoid arthritis characteristics and periodontal status after 24 weeks of baricitinib (P0.05).RA, particularly severe active ACPA-positive disease, is basically associated with altered periodontal health. JAK blockade through oral baricitinib may be efficient in patients with active RA and potentially able to modulate the inflammatory process in the periodontal tissue.