The autoimmune tautology

Although autoimmune diseases exhibit contrasting epidemiological features, pathology, and clinical manifestations, three lines of evidence demonstrate that these diseases share similar immunogenetic mechanisms (that is, autoimmune tautology). First, clinical evidence highlights the co-occurrence of distinct autoimmune diseases within an individual (that is, polyautoimmunity) and within members of a nuclear family (that is, familial autoimmunity). Second, physiopathologic evidence indicates that the pathologic mechanisms may be similar among autoimmune diseases. Lastly, genetic evidence shows that autoimmune phenotypes might represent pleiotropic outcomes of the interaction of non-specific disease genes

The Autoimmune Tautology: An In Silico Approach

There is genetic evidence of similarities and differences among autoimmune diseases (AIDs) that warrants looking at a general panorama of what has been published. Thus, our aim was to determine the main shared genes and to what extent they contribute to building clusters of AIDs. We combined a text-mining approach to build clusters of genetic concept profiles (GCPs) from the literature in MedLine with knowledge of protein-protein interactions to confirm if genes in GCP encode proteins that truly interact. We found three clusters in which the genes with the highest contribution encoded proteins that showed strong and specific interactions. After projecting the AIDs on a plane, two clusters could be discerned: Sjögren's syndrome—systemic lupus erythematosus, and autoimmune thyroid disease—type1 diabetes—rheumatoid arthritis. Our results support the common origin of AIDs and the role of genes involved in apoptosis such as CTLA4, FASLG, and IL10

The Autoimmune Tautology: From Polyautoimmunity and Familial Autoimmunity to the Autoimmune Genes

Autoimmune diseases (ADs) are chronic conditions initiated\ud by the loss of immunological tolerance to self-antigens and\ud represent a heterogeneous group of disorders that afflict specific\ud target organs ormultiple organ systems [1]. The chronic\ud nature of these diseases places a significant burden on the utilization\ud of medical care, direct and indirect economic costs,\ud and quality of life. The fact that ADs share several clinical\ud signs and symptoms (i.e., subphenotypes), physiopathological\ud mechanisms, and genetic factors has been called\ud autoimmune tautology and indicates that they have common\ud mechanism

Autoimmune rheumatic diseases

"The term autoimmune rheumatic diseases (ARDs) encompasses a heterogeneous group of conditions characterized by joint involvement along with a wide spectrum of systemic manifestations. The most common ARDs are rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Nevertheless, all these conditions share similar pathophysiological mechanisms [1, 2] and a common risk of developing a process of accelerated atherosclerosis [3]. In this regard, in this special issue J. Amaya-Amaya and colleagues discussed the mechanisms associated with the increased risk of cardiovascular disease (CVD) in patients with autoimmune diseases. These authors emphasize the relevance of the CVD in rheumatic conditions and its connection with inflammation and autoimmunity. They also highlight the need of a more aggressive management of these conditions, both of disease activity and classic cardiovascular risk factors. A good example of accelerated atherosclerosis in the setting of an ARD is SLE, in which endothelial dysfunction, an early step in the atherogenesis process, is observed before cardiovascular events can occur. With respect to this, A. Mak and N. Y. Kow performed a comprehensive review of the mechanisms that are involved in endothelial damage.These authors focused on the factors involved in endothelial damage and repair and, therefore, in the development of CVD in patients with SLE. They discussed the relevant role of factors such as type 1 interferon, proinflammatory cytokines, inflammatory cells, immune complexes, costimulatory molecules, neutrophils extracellular traps, lupus-related autoantibodies, oxidative stress, and dyslipidemia that along with the aberrant function of the endothelial progenitor cells lead to endothelial dysfunction and increased susceptibility to develop CVD in patients with SLE. Based on these lines of evidence, the authors’ claim is in favor of early intervention at the preclinical stage of atherogenesis in these patients

The Autoimmune Tautology: An In Silico Approach

There is genetic evidence of similarities and differences among autoimmune diseases (AIDs) that warrants looking at a general panorama of what has been published. Thus, our aim was to determine the main shared genes and to what extent they contribute to building clusters of AIDs. We combined a text-mining approach to build clusters of genetic concept profiles (GCPs) from the literature in MedLine with knowledge of protein-protein interactions to confirm if genes in GCP encode proteins that truly interact. We found three clusters in which the genes with the highest contribution encoded proteins that showed strong and specific interactions. After projecting the AIDs on a plane, two clusters could be discerned: Sjögren’s syndrome—systemic lupus erythematosus, and autoimmune thyroid disease—type1 diabetes—rheumatoid arthritis. Our results support the common origin of AIDs and the role of genes involved in apoptosis such as CTLA4, FASLG, and IL10

Is there a common genetic basis for autoimmune diseases?

Autoimmune diseases (ADs) represent a diverse collection of diseases in terms of their demographic profile and primary clinical manifestations. The commonality between them however, is the damage to tissues and organs that arises from the response to self-antigens. The presence of shared pathophysiological mechanisms within ADs has stimulated searches for common genetic roots to these diseases. Two approaches have been undertaken to sustain the “common genetic origin” theory of ADs. Firstly, a clinical genetic analysis showed that autoimmunity aggregates within families of probands diagnosed with primary Sjögren's (pSS) syndrome or type 1 diabetes mellitus (T1D). A literature review supported the establishment of a familiar cluster of ADs depending upon the proband's disease phenotype. Secondly, in a same and well-defined population, a large genetic association study indicated that a number of polymorphic genes (i.e. HLA-DRB1, TNF and PTPN22) influence the susceptibility for acquiring different ADs. Likewise, association and linkage studies in different populations have revealed that several susceptibility loci overlap in ADs, and clinical studies have shown that frequent clustering of several ADs occurs. Thus, the genetic factors for ADs consist of two types: those which are common to many ADs (acting in epistatic pleitropy) and those that are specific to a given disorder. Their identification and functional characterization will allow us to predict their effect as well as to indicate potential new therapeutic interventions. Both autoimmunity family history and the co-occurrence of ADs in affected probands should be considered when performing genetic association and linkage studies

Factors associated with mental health outcomes after COVID-19: a 24-month longitudinal follow-up study

Objetivo: Investigar la proporción de resultados de salud mental (MHO) y los factores asociados en los supervivientes del COVID-19 durante un periodo de seguimiento de 24 meses. Método: Se realizó un estudio observacional, prospectivo en un hospital universitario de Barranquilla, Colombia, desde el 1 de abril de 2020 hasta el 30 de agosto de 2022. Se reclutó una cohorte de 1565 sobrevivientes de COVID-19 después del alta de los servicios de urgencias (SU), piso de hospitalización (FI) y unidad de cuidados intensivos (UCI) y se les hizo seguimiento durante 24 -meses. La evaluación clínica incluyó escalas de detección de síntomas de ansiedad, depresión, trastorno de estrés postraumático (TEPT) e insomnio. También se recogieron factores sociodemográficos y clínicos para identificar posibles factores asociados. Se realizaron modelos descriptivos, bivariantes y lineales mixtos de efectos aleatorios. Resultados: Se incluyeron un total de 1565 pacientes, de los cuales 785 (50,35%) eran hombres. Se identificó una gran proporción de pacientes con síntomas mentales. Después de 24 meses, las proporciones de síntomas de ansiedad, depresión, TEPT e insomnio seguían siendo elevadas: 16,55%, 21,79%, 35,27% y 23,86%, respectivamente. Los factores sociales, la localización de las estancias hospitalarias, las comorbilidades físicas y la gravedad del COVID-19 se asociaron significativamente con los síntomas de ansiedad, depresión, TEPT e insomnio. Conclusiones: Se han documentado los efectos nocivos de la COVID-19 sobre la salud mental durante 2 años, así como las variables que influyen en estos resultados. Estos resultados deberían ayudar en el desarrollo de iniciativas de salud pública para reducir las tasas de morbilidad en pacientes post-COVID-19. 2023 Los autores.Objective: Investigate the proportion of mental health outcomes (MHOs) and associated factors in COVID-19 survivors during a 24-month follow-up period. Method: An observational, prospective study was performed in a teaching hospital in Barranquilla, Colombia, from April 1, 2020, to August 30, 2022. A cohort of 1565 COVID-19 survivors was recruited after discharge from the emergency room (ER), inpatient floor (IF), and intensive care unit (ICU) services and followed for 24 -months. The clinical assessment included screening scales for symptoms of anxiety, depressive, post-traumatic stress disorder (PTSD), and insomnia. Sociodemographic and clinical factors were also collected to identify possible associated factors. Descriptive, bivariate and mixed random-effect linear models were performed. Results: A total of 1565 patients were included, of whom 785 (50.35%) were men. A large proportion of patients with mental symptoms were identified. After 24-months, the proportions of anxiety, depression, PTSD, and insomnia symptoms remained high at 16.55%, 21.79%, 35.27%, and 23.86%, respectively. Social factors, location of hospital stays, physical comorbidities, and the severity of COVID-19 were significantly associated with anxiety, depression, PTSD, and insomnia symptoms. Conclusions: COVID-19's 2-year deleterious impacts on mental health, as well as the variables influencing these findings, have been documented. These results should aid in the development of public health initiatives to reduce morbidity rates in post-COVID-19 patients. © 2023 The Authors

Autoimmune neurological conditions associated with Zika virus infection

Zika virus (ZIKV) is an emerging flavivirus rapidly spreading throughout the tropical Americas. mosquitoes is the principal way of transmission of the virus to humans. ZIKV can be spread by transplacental, perinatal, and body fluids. ZIKV infection is often asymptomatic and those with symptoms present minor illness after 3 to 12 days of incubation, characterized by a mild and self-limiting disease with low-grade fever, conjunctivitis, widespread pruritic maculopapular rash, arthralgia and myalgia. ZIKV has been linked to a number of central and peripheral nervous system injuries such as Guillain-Barré syndrome (GBS), transverse myelitis (TM), meningoencephalitis, ophthalmological manifestations, and other neurological complications. Nevertheless, mechanisms of host-pathogen neuro-immune interactions remain incompletely elucidated. This review provides a critical discussion about the possible mechanisms underlying the development of autoimmune neurological conditions associated with Zika virus infection

Introducing Polyautoimmunity: Secondary Autoimmune Diseases No Longer Exist

Similar pathophysiological mechanisms within autoimmune diseases have stimulated searches for common genetic roots. Polyautoimmunity is defined as the presence of more than one autoimmune disease in a single patient. When three or more autoimmune diseases coexist, this condition is called multiple autoimmune syndrome (MAS). We analyzed the presence of polyautoimmunity in 1,083 patients belonging to four autoimmune disease cohorts. Polyautoimmunity was observed in 373 patients (34.4%). Autoimmune thyroid disease (AITD) and Sjögren's syndrome (SS) were the most frequent diseases encountered. Factors significantly associated with polyautoimmunity were female gender and familial autoimmunity. Through a systematic literature review, an updated search was done for all MAS cases (January 2006–September 2011). There were 142 articles retrieved corresponding to 226 cases. Next, we performed a clustering analysis in which AITD followed by systemic lupus erythematosus and SS were the most hierarchical diseases encountered. Our results indicate that coexistence of autoimmune diseases is not uncommon and follows a grouping pattern. Polyautoimmunity is the term proposed for this association of disorders, which encompasses the concept of a common origin for these diseases

The Autoimmune Tautology: From Polyautoimmunity and Familial Autoimmunity to the Autoimmune Genes

Autoimmune diseases (ADs) are chronic conditions initiated by the loss of immunological tolerance to self-antigens and represent a heterogeneous group of disorders that afflict specific target organs ormultiple organ systems [1]. The chronic nature of these diseases places a significant burden on the utilization of medical care, direct and indirect economic costs, and quality of life. The fact that ADs share several clinical signs and symptoms (i.e., subphenotypes), physiopathological mechanisms, and genetic factors has been called autoimmune tautology and indicates that they have common mechanism