Daykahn7317

Multiple sclerosis is a central nervous system autoimmune disease of the white and grey matters. Its pathophysiology is much better well known. It results from the interaction between genetic and environmental susceptibility factors. The role of EBV virus has recently been highlighted. Imaging techniques and neuropathology knowledge allow to distinguish several distinct processes responsible for focal and more diffuse inflammation. Therapeutic advances in recent years have been considerable. Different molecules and treatment sequences can be proposed to the patient with a demonstrated positive impact on the risk of disability secondary progression. Precise follow-up is a key. It requires optimal and early use of various treatments. The therapeutic choice must be guided by obtaining stabilization of the disease, both clinically and in terms of imaging, without exposing the patient to an excessive risk of side effects. Continuous and sequential treatments are available.The therapeutic prospects for patients with moderate to severe atopic dermatitis completely changed in 2017 with the arrival of the first targeted therapy, dupilumab. Achieving important clinical improvement scores are now possible with this monoclonal antibody directed against interleukins 4 and 13. Since that time, other agents such as tralokinumab arrived on the market, but also the small molecules called «JAK inhibitors» (upadacitinib, baricitinib, etc.). This article provides an inventory of the existing or imminent therapeutic options for atopic dermatitis.Endometriosis is the presence of stromal and epithelial cells outside the uterine cavity. This chronic inflammatory disease affects about 10 % of the female population in reproductive age and is responsible for chronic pelvic pain and infertility. Its pathogenesis is complex, and the treatment will rely on medical treatment or/and surgery. Medical treatment consists in alleviating pain thanks to analgesic and hormonal treatment but none can eradicate the disease. Medical treatment often fails and about 10 % will add nonsteroid anti-inflammatory drugs to their hormonal treatment. Major role of immune/inflammatory cells in the disease makes them a promising tool for targeted therapy.A thyroiditis is an inflammatory disease of the thyroid whether autoimmune, infectious or drug-induced. Autoimmune thyroid diseases (including Hashimoto's thyroiditis and Graves' disease) are the most frequent of all autoimmune pathologies. The clinical presentation and history are often revealing of the pathology and its etiology. Complementary examinations allow to confirm the diagnosis and to follow the evolution of the disease. SAdenosylLhomocysteine Sometimes the disease could have a mixed presentation associating two different causes (like a mixed autoimmunity for Graves and Hashimoto diseases). In these cases, the treatment options are not always straightforward and may need to be adapted with the clinical evolution.The relationships between inflammation and cancer are known since the original work by Virchow in the 19th century and have been largely confirmed after-wards. An interesting question is what might be the primum movens. Numerous clinical observations have shown that a chronic inflammatory state, as that observed with some infections, toxic agents or dysimmune diseases, may be associated with the development of cancer later on. Besides, cancer is generally accompanied by an inflammatory microenvironment, with numerous cellular and humoral components, which promotes both tumorigenesis and the invasivity of the tumour. This article aims at defining the pathophysiology of this association, with a description of underlying mechanisms and mediators, and at determining possible therapeutic implications.Acute and/or chronic graft-versus-host disease (GVHD) is a serious complication after allogeneic hematopoietic stem cell transplantation (alloHSCT). It is a multisystemic inflammatory and/or fibrotic disease that occurs when the immune cells derived from the graft (and therefore originating from the donor) recognize recipient's healthy tissues as foreign and react against them. Acute GVHD is one of the main causes of non-relapse mortality after alloHSCT. Chronic GVHD can be very disabling in its severe form and can also be responsible for late mortality, mainly due to long-term immune deficiency and opportunistic infections. In contrast, GVHD can be associated with certain beneficial effects in patients transplanted for hematological malignancies, through simultaneous «graft versus tumour» positive effects. Therefore, one of the challenges of alloHSCT is the prevention and treatment of severe forms of GVHD without losing the beneficial anti-tumour effects of the graft.Renal allograft rejection involves many mechanisms of innate and adaptive immunity, responsible for parenchymal inflammatory lesions that negatively impact the long-term outcomes of the renal allograft. The heterogeneous presentations of rejections in terms of clinical, biological and histological aspects make them difficult to manage in daily clinical practice. Indeed, current therapeutic strategies are disappointing in term of long-term outcomes, including graft survival. In this article, we will discuss the main effector mechanisms of rejection and their histological classification, as well as the existing treatments and those currently under evaluation.Glomerulonephritis are the result of an inflammatory hit to the glomerulus. They are rare and heterogeneous renal diseases. Each glomerular compartment can be affected. The clinical manifestations present with hematuria, proteinuria and/or impaired renal function, either isolated or combined. Two main clinico-biological syndromes are described nephrotic syndrome and nephritic syndrome. The latter can present in a more severe form i.e. rapidly progressive glomerulonephritis with the worst prognosis. These different clinical pictures are related to specific glomerular lesions. Thus, podocytic damage is mainly responsible for nephrotic syndromes, mesangial damage is responsible for proteinuria and hematuria and, finally, endothelial damage is responsible for nephritic syndrome and rapidly progressive glomerulonephritis. Therapeutic approaches include non-specific measures, combining both life-style and pharmacological interventions with the aim to reduce risk factors, and specific measures with the use of different immunosuppressive agents.New therapeutic strategies and new molecules have been recently developed for the management of inflammatory bowel diseases. The treat-to-target strategy aims to define specific objectives based on the patient and the disease characteristics. A regular monitoring using biomarkers and imaging is required to assess the objectives' achievement. Better outcomes have been demonstrated with this approach compared to the standard of care guided by symptoms only. On top of anti-TNF, new biologics have been available for the last few years. Vedolizumab, an anti-integrine, and ustekinumab, an interleukine 12/23 inhibitor, have demonstrated their efficacy in ulcerative colitis and Crohn's disease with an excellent safety profile and a sustained efficacy over time. Small molecules like tofacitinib are available in ulcerative colitis. The delay of action of these oral molecules is short. The risk of infection is similar compared to anti-TNF. Thromboembolic events have been reported with a prolonged double dose in predisposed patients. Preferential JAK inhibitors will be shortly available with an expected better safety profile. The growing number of available molecules allows a more effective management of inflammatory bowel diseases by choosing the right treatment for the right patient.Diseases related to fatty liver, independently of alcohol consumption («non-alcoholic fatty liver disease» or NAFLD), are increasing because of the epidemics of obesity and type 2 diabetes. These disorders reflect a continuum that comprises isolated steatosis, steatohepatitis (NASH) and fibrosis, with, at the end, an increased risk of cirrhosis and hepatocarcinoma. It has been recently proposed to replace the term NAFLD by MAFLD, i.e. «Metabolic (dysfunction) Associated Fatty Liver Disease», which better reflects the pathogenesis of the disease. Inflammation plays a crucial role in the aggravation of the disorder and profoundly influences the prognostic evolution. This article illustrates the natural history of this underestimated metabolic disorder, recall the diagnostic criteria used in clinical practice, emphasizes the deleterious role of inflammation and discusses some therapeutic perspectives.Type 2 diabetes is characterized by chronic hyperglycaemia in a context of insulin resistance and ?-cell dysfunction. A chronic low-grade inflammation is observed in obesity and has been associated with the development of metabolic disorders. The molecular mechanisms underlying this inflammation are not fully understood. Production of interleukin-1? by macrophages infiltrating insulin-sensitive tissues and pancreatic islets plays a major role in the pathogenesis of type 2 diabetes. This pro-inflammatory cytokine is produced through the activation of the NLRP3 inflammasome in response to danger signals that accumulate during obesity, including saturated fatty acids. The composition of the intestinal microbiota differs in obese subjects compared with lean individuals, particularly in response to high saturated fat diet. These modifications could trigger a chronic low-grade inflammation and promote the emergence of type 2 diabetes. The microbiota could therefore constitutes a therapeutic target in the prevention and management of metabolic abnormalities associated with obesity.Chronic inflammation is recognized as a contributing factor to the development, progression and complications of atherosclerosis. The inflammatory nature of atherosclerosis has been proven by the presence of inflammatory cells, cytokines and chemokines at all stages of the disease. There is a widely accepted association between cardiovascular events and serum inflammatory markers, such as CRP, IL-6 and IL-1? produced via the inflammasome pathway. The involvement of inflammatory processes in atherosclerosis and progress in the therapeutic strategy are detailed in the article.Chronic Obstructive Pulmonary Disease (COPD) is a disease caused by a chronic inflammatory response induced by the inhalation of cigarette smoke or toxic particles/gases in the airways. However, we actually know that COPD is a disease that does not only induce inflammation in lung parenchyma and bronchi, but also provokes systemic inflammation which plays a role in multiple comorbidities. Thereby, treatment of COPD should not only focus on the bronchi to relieve symptoms, improve respiratory function and reduce the rate of exacerbations, but must also be extended to the systemic effects of the disease.Asthma is a chronic inflammatory disease of the airways. Classification of asthma in different phenotypes has therapeutic implications and may lead to personalized medicine. Induced sputum is the gold standard for asthma phenotyping but is complex, time-consuming and not widely available. The combination of different biomarkers such as exhaled nitric oxide, blood eosinophils and total serum IgE levels allows the prediction of inflammatory phenotype in 58% of asthmatic patients when sputum is not available. We recently demonstrated the interest of measuring volatile organic compounds in exhaled breath to phenotype asthma. These compounds could play an important role in the future to predict the response to expensive biologicals available in severe asthma to reduce exacerbations and the use of systemic corticosteroids.