Aug 2026· Neurology, neuropsychiatry, Psychosomatics· Vol 18, pp. 111-116· 0 citations· 48 references
TL;DR
This review examines the co-occurrence of multiple sclerosis and neuromyelitis optica spectrum disorders with anti-aquaporin-4 antibodies (AQP4) with the most common associated ADs, and summarises the evidence regarding the preferred therapeutic approaches in each specific case.
Abstract
Autoimmune diseases (ADs) are a broad group of phenotypically heterogeneous conditions characterized by both unique and common clinical and immunological manifestations, with varying rates of progression and responses to pathogenetic therapy. More than 10 per cent of the global population suffers from at least one of ADs, and in recent decades there has been a worldwide trend towards an increase in the number of cooccurring autoimmune conditions, particularly in regions and countries with a high level of socio-demographic development. Given their shared risk factors and immunopathological mechanisms, demyelinating diseases of the central nervous system are associated with an increased likelihood of developing a concomitant ADs, which may unpredictably influence the course of the demyelinating process and the choice of optimal treatment. This review examines the co-occurrence of multiple sclerosis and neuromyelitis optica spectrum disorders (NMOSD) with anti-aquaporin-4 antibodies (AQP4) with the most common associated ADs, and summarises the evidence regarding the preferred therapeutic approaches in each specific case.
Current evidence on advances in clinical research and immunotherapy across the major autoimmune CNS disease groups is synthesized, with a particular focus on trial designs, endpoints, and the evolution from observational cohorts to randomized controlled trials.
Immune thrombocytopenia (idiopathic thrombocytopenic purpura, ITP) and multiple sclerosis (MS) are two autoimmune diseases (AIDs), and their co-occurrence in a single patient is a rare combination. In recent years, there has been an increase in the prevalence of MS, as well as other AIDs; consequently, comorbid autoimmune conditions in individuals with MS are being observed with increasing frequency and are taking on significant scientific and clinical importance. Managing such patients is particularly challenging, as there is currently no established treatment strategy for patients with MS and concomitant ITP. The scientific literature describes isolated cases of the combination of MS and autoimmune thrombocytopenia, which may indicate shared pathogenetic mechanisms underlying these diseases. This article presents clinical cases illustrating two types of relationship between ITP and MS: primary autoimmune comorbidity of the conditions and secondary druginduced ITP. The widespread use in recent years of disease-modifying drugs (DMDs) and the planned expansion of their spectrum necessitate the stratification of the risks associated with this therapy.
K. Bakhtiyarova, T. D. Yunusov, O. V. Lyutov et al.· Neurology, neuropsychiatry,...· 0 citations
Autoimmune diseases comprise a broad group of conditions that affect virtually any organ or tissue and share mechanisms of chronic, autoimmune-based inflammation. Once rare or unknown, they have become increasingly common in recent years, affecting individuals of all ages, including the elderly, due to the growing number of older people. According to evolutionary medicine, if the frequency of a disease, or group of diseases, increases sharply over a few decades, the primary cause cannot be the effect of genetic alterations but rather the consequence of one or more alterations in the living conditions of the species. For autoimmune diseases, there is no environmental, dietary, or infectious factor that appears to correlate with their strong increased frequency. On the contrary, the epidemic of autoimmune diseases is likely correlated with serious alterations of our holobiont (i.e., our organism, the host species, plus the myriad of species coexisting with us). In particular, the critical factor appears to be the decreasing incidence of macroparasite (i.e., parasitic worm) infestations, without, however, excluding the effects of profound alterations in the bacterial ecosystems that are also part of our holobiont. The macroparasites modulate and curb the intensity of immune responses in order to survive in our bodies. In the coevolution of host organism and other species of the holobiont, a delicate balance has developed that is severely altered by the eradication of parasitic worms. Therefore, it is necessary to move beyond the concept of macroparasites as harmful species by definition and therefore to be eliminated without hesitation. Alternatively, it is essential to study our holobiont as a whole and consider the balances of its ecosystems before modern alterations. Furthermore, the evaluation of the effects of reintroducing macroparasite species with which we have coevolved into our holobiont would be enlightening or helpful to understanding autoimmune diseases and implementing effective prevention and treatment.
G. Libertini, G. Corbi, Valeria Conti et al.· Journal of Gerontology and G...· 0 citations
Inborn errors of immunity (IEIs) frequently present with rheumatologic and autoimmune manifestations that closely mimic common polygenic conditions, including systemic lupus erythematosus, juvenile idiopathic arthritis, and vasculitis, posing significant challenges to early recognition and diagnosis. Current data indicate that autoimmunity represents the first clinical manifestation in approximately 18% of IEI cases and the sole presentation in nearly 9%. The majority of affected patients belong to the categories of predominantly antibody deficiencies, combined immunodeficiencies with syndromic features, or disorders of immune dysregulation. In contrast to autoimmunity in the general population, IEI-associated autoimmunity characteristically presents at an earlier age, lacks a marked female predominance, and more frequently involves multiple organ systems, particularly hematopoietic, endocrine, and barrier tissues. Concurrently, the conceptual framework of autoimmunity is undergoing a fundamental shift: the classical model centered on central and peripheral tolerance is increasingly giving way to a pathway-oriented paradigm that foregrounds dominant immunologic mechanisms, including disturbances in T cell development, interferon signaling, and complement regulation. In line with this, a novel multilayer model of autoimmunity has recently been proposed, which integrates causative genes, the functional consequence of allelic variants (loss-of-function, gain-of-function, hypomorphic, haploinsufficient, or dominant-negative), disrupted molecular mechanisms, and their humoral and cellular immune effectors. A deeper understanding of these pathways is essential for enhancing diagnostic precision and for developing targeted, mechanism-based therapeutic strategies.
Rada Mišković· Journal of Human Immunity· 0 citations
According to current concepts, immuno-inflammatory rheumatic diseases are similar to COVID-19 in terms of clinical manifestations, immune responses and pathogenetic mechanisms, which is due to the systemic nature of the lesion. In patients with genetic prerequisites, both infection and vaccination against COVID-19 can trigger the immune-inflammatory process. The article presents a clinical observation demonstrating the diagnostic difficulties encountered in the diagnosis of systemic scleroderma and polymyositis that developed after COVID-19. Оnly timely diagnosis and adequate therapy can significantly improve the condition and, consequently, the prognosis of this category of patients. A special feature of this case is the absence of autoimmune markers – immunoblots confirming the diagnosis of systemic scleroderma and polymyositis in the presence of vivid clinical symptoms of each of these diseases. The addition of rituximab to the standard basic therapy increases its effectiveness.
S. A. Turdialieva, E. A. Mozharovskaya, O. Kudrina et al.· New St. Petersburg Medical R...· 0 citations
: Systematic Lupus Erythematosus, a standard autoimmune disease that has many unpredictable flares and involves multiple organs. SLE’s complexity has made it a central focus in the autoimmune research field. This paper examines the clinical heterogeneity of SLE whilst finding out the pathogenesis that causes immunological disorders. This paper has summarised some of the most crucial and commonly seen complications of SLE in different organ systems, along with heterogeneity involving gender and race. SLE is a clinically diverse disease caused by many mechanisms. The analysis revealed underlying triggers, including environmental (UV light, pollution, stress) and genetic (HLA, IRF5, CLq) factors. This essay also summarises how the complication of SLE has developed and shown up through the theory and the principle, such as loss tolerance of self-antigens and the role of apoptotic cell debris. It also includes a section which focuses on the limitations in current understanding, and identifies the challenges we encounter and possible future direction on SLE. The purpose of this study is to provide a conclusive overview that shows both clinical presentation and immunopathogenesis. Aiming to enhance the diagnostic precision and inform more effective treatment strategies.
Xin-Yan Xie· Proceedings of the 1st Inter...· 0 citations
