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Metabolites Sep 2023Autoimmune diseases, characterized by the immune system's loss of self-tolerance, lack definitive diagnostic tests, necessitating the search for reliable biomarkers.... (Review)
Review
Autoimmune diseases, characterized by the immune system's loss of self-tolerance, lack definitive diagnostic tests, necessitating the search for reliable biomarkers. This systematic review aims to identify common metabolite changes across multiple autoimmune diseases. Following PRISMA guidelines, we conducted a systematic literature review by searching MEDLINE, ScienceDirect, Google Scholar, PubMed, and Scopus (Elsevier) using keywords "Metabolomics", "Autoimmune diseases", and "Metabolic changes". Articles published in English up to March 2023 were included without a specific start date filter. Among 257 studies searched, 88 full-text articles met the inclusion criteria. The included articles were categorized based on analyzed biological fluids: 33 on serum, 21 on plasma, 15 on feces, 7 on urine, and 12 on other biological fluids. Each study presented different metabolites with indications of up-regulation or down-regulation when available. The current study's findings suggest that amino acid metabolism may serve as a diagnostic biomarker for autoimmune diseases, particularly in systemic lupus erythematosus (SLE), multiple sclerosis (MS), and Crohn's disease (CD). While other metabolic alterations were reported, it implies that autoimmune disorders trigger multi-metabolite changes rather than singular alterations. These shifts could be consequential outcomes of autoimmune disorders, representing a more complex interplay. Further studies are needed to validate the metabolomics findings associated with autoimmune diseases.
PubMed: 37755267
DOI: 10.3390/metabo13090987 -
Frontiers in Immunology 2023Parkinson's disease (PD) is a neurodegenerative disorder that frequently occurs in the older population. Previous epidemiological studies have suggested an association... (Meta-Analysis)
Meta-Analysis
UNLABELLED
Parkinson's disease (PD) is a neurodegenerative disorder that frequently occurs in the older population. Previous epidemiological studies have suggested an association between PD and autoimmune diseases (AIDs). However, some studies have shown conflicting results. This study aimed to summarize existing epidemiological studies on the association between PD with AIDs and to conduct a meta-analysis of combinable results. Four electronic databases (PubMed, Embase, Web of Science Core Collection, and MEDLINE) were searched from each database's inception date until December 12, 2022. All studies that explored the relationship between PD and AIDs were included for quantitative analysis and qualitative review. The pooled relative risk with 95% confidence intervals (CIs) was calculated using a random or fixed effects model. A total of 46 observational studies involving 873,643 patients and 13,402,821 controls were included; ultimately, 38 studies were included in the meta-analysis. The risk of PD combined with AIDs was significantly higher (odds ratio [OR]=1.55, 95% CI: 1.33-1.81), and subgroup analysis found no significant differences in risk by study type, gender, age, and race. Regarding the AID types, the results showed an increased risk of PD combined with bullous pemphigoid (OR=2.67, 95% CI: 2.15-3.31), inflammatory bowel disease (OR=1.30, 95% CI: 1.18-1.45), Crohn's disease (OR=1.30, 95% CI: 1.20-1.42), ulcerative colitis (OR=1.31, 95% CI: 1.14-1.50), Sjögren's syndrome (OR=1.61, 95% CI: 1.24-2.09), and Graves' disease (OR=1.45, 95% CI: 1.24-1.70) than controls. However, there appeared to be no significant association between PD and systemic lupus erythematosus (OR=0.82, 95% CI: 0.66-1.03), multiple sclerosis (OR=2.02, 95% CI: 0.87-4.70), rheumatoid arthritis (OR=0.79, 95% CI: 0.61-1.03), or celiac disease (OR=1.16, 95% CI: 0.79-1.69). This study supports the existence of a strong link between AIDs and PD. When PD and AIDs are identified, clinicians need to be aware of the possibility of coexistence. However, there are some limitations of this study, such as the apparent heterogeneity of some of the results and the fact that most of the included study types were retrospective. Therefore, future larger prospective cohort studies are needed to further explore the interaction between PD and AIDs.
SYSTEMATIC REVIEW REGISTRATION
INPLASY, identifier INPLASY202280088.
Topics: Humans; Parkinson Disease; Prospective Studies; Retrospective Studies; Autoimmune Diseases; Sjogren's Syndrome
PubMed: 36761731
DOI: 10.3389/fimmu.2023.1103053 -
Frontiers in Immunology 2023Bullous pemphigoid is the most common autoimmune blistering disease in industrialized countries and particularly affects the elderly. In this patient population,...
Bullous pemphigoid is the most common autoimmune blistering disease in industrialized countries and particularly affects the elderly. In this patient population, comorbid diseases are frequent and may complicate management and treatment of bullous pemphigoid. A better understanding why distinct diseases are more frequent in bullous pemphigoid patients may lead to new pathophysiological insights and - as a consequence - result in better patient care. The association of bullous pemphigoid with neurological and psychiatric diseases is well known and confirmed by several case-control studies. Association with further diseases such as malignancy and metabolic diseases are still discussed controversially. In recent years new relationships between bullous pemphigoid and autoimmune as well as inflammatory skin diseases have been reported. This review provides a systematic overview on studies addressing comorbidity in bullous pemphigoid patients. Increasing the awareness of both, common and rare comorbid diseases, may enable clinicians to optimize patient support and individualized treatment of bullous pemphigoid.
Topics: Humans; Aged; Pemphigoid, Bullous; Autoimmune Diseases; Blister; Comorbidity; Case-Control Studies
PubMed: 37457698
DOI: 10.3389/fimmu.2023.1196999 -
Particle and Fibre Toxicology Jan 2022Autoimmunity can result from the interplay between genetic background and effects of environmental and/or occupational exposure to hazardous materials. Several... (Review)
Review
BACKGROUND
Autoimmunity can result from the interplay between genetic background and effects of environmental and/or occupational exposure to hazardous materials. Several compounds, including silica dust, have been linked with systemic autoimmunity and systemic autoimmune diseases, based on epidemiological evidence. For asbestos, a strong link with systemic autoimmune diseases does not yet exist, however, several studies have documented features of autoimmunity following asbestos exposure. Even so, human studies are limited in their ability to identify and examine isolated exposures, making it difficult to demonstrate causation or to assess pathogenic mechanisms. Therefore, this systematic review examines the existing animal evidence regarding autoimmunity and exposure to silicates (silica and asbestos).
METHODS
PubMed and EMBASE were systematically searched for peer-reviewed studies examining systemic autoimmune disease-related outcomes after silicate exposure in rodents. Literature databases were searched up to September 2021 for studies written in English and where the full text was available. Search strings were established based on a PECO (Population, Exposure, Comparator, Outcome) format. After title, abstract, and full-text screening, thirty-four studies were identified for further analysis. Quality assessment through ToxR tool and qualitative analysis of the results was performed.
RESULTS
Although there was significant heterogeneity in the included studies in terms of exposure protocol and genetic background of the rodent models used, it was noted that both genetic background and exposure to silicates [(crystalline) silica and asbestos] are highly relevant to the development of (sub-) clinical systemic autoimmune disease.
CONCLUSION
Parallels were observed between the findings from the animal (this review) and human (epidemiological) studies, arguing that experimental animal models are valuable tools for examining exacerbation or development of autoimmune disease after silicate exposure. However, genetic background and synergism between exposures should be considered in future studies.
Topics: Animals; Autoimmunity; Dust; Occupational Exposure; Rodentia; Silicates
PubMed: 34996462
DOI: 10.1186/s12989-021-00439-6 -
Alimentary Pharmacology & Therapeutics Jun 2022Inflammatory bowel disease (IBD) is a chronic inflammatory immune-mediated disorder of the gut with frequent extra-intestinal complications. Pancreatic involvement in... (Review)
Review
BACKGROUND
Inflammatory bowel disease (IBD) is a chronic inflammatory immune-mediated disorder of the gut with frequent extra-intestinal complications. Pancreatic involvement in IBD is not uncommon and comprises a heterogeneous group of conditions, including acute pancreatitis (AP), chronic pancreatitis (CP), autoimmune pancreatitis (AIP) and pancreatic exocrine insufficiency (PEI); however, data on such an association remain sparse and heterogeneous.
METHOD
PubMed/MEDLINE and EMBASE databases were searched for studies investigating pancreatic involvement in patients with IBD.
RESULTS
Four thousand one hundred and twenty-one records were identified and 547 screened; finally, 124 studies were included in the review. AP is the most frequent pancreatic manifestation in IBD; the majority of AP cases in IBD are due to gallstones and drugs but cases of idiopathic AP are increasingly reported. AIP is a rare disease, but a strong association with IBD has been demonstrated, especially for type 2 and ulcerative colitis. The pathogenetic link between IBD and AIP remains unclear, but an immune-mediated pathway seems plausible. An association between CP and PEI with IBD has also been suggested, but data are to date scarce and conflicting.
CONCLUSION
This is the first systematic review of the association between IBD and pancreatic diseases. Gallstones and drugs should be considered the most probable causes of AP in IBD, with type 2 AIP also being possible.
Topics: Acute Disease; Autoimmune Diseases; Chronic Disease; Colitis, Ulcerative; Exocrine Pancreatic Insufficiency; Gallstones; Humans; Inflammatory Bowel Diseases; Pancreatitis, Chronic
PubMed: 35505465
DOI: 10.1111/apt.16949 -
Autoimmunity Reviews Mar 2021Regulatory T cells (Tregs) are a subset of T cells responsible for the regulation of immune responses, thereby maintaining immune homeostasis and providing immune... (Review)
Review
Regulatory T cells (Tregs) are a subset of T cells responsible for the regulation of immune responses, thereby maintaining immune homeostasis and providing immune tolerance to both self and non-self-antigens. An increasing number of studies revealed Treg numbers and functions in a variety of autoimmune diseases. Treg deficiency can cause the development of several autoimmune skin diseases including vitiligo, alopecia areata, pemphigoid and pemphigus, psoriasis, and systemic sclerosis. Many clinical trials have been performed for autoimmune conditions using polyclonal Tregs, but efficiency can be significantly improved using antigen-specific Tregs engineered using T cell receptor (TCR) or chimeric antigen receptor (CAR) constructs. In this review, we systematically reviewed altered frequencies, impaired functions, and phenotypic features of Tregs in autoimmune skin conditions. We also summarized new advances in TCR and CAR based antigen-specific Tregs tested both in animal models and in clinics. The advantages and limitations of each approach were carefully discussed emphasizing possible clinical relevance to patients with autoimmune skin diseases. Moreover, we have reviewed potential approaches for engineering antigen-specific Tregs, and strategies for overcoming possible hurdles in clinical applications. Thereby, antigen-specific Tregs can be infused using autologous adoptive cell transfer to restore Treg numbers and to provide local immune tolerance for autoimmune skin disorders.
Topics: Animals; Autoimmune Diseases; Humans; Immune Tolerance; Receptors, Antigen, T-Cell; Skin Diseases; T-Lymphocytes, Regulatory
PubMed: 33476816
DOI: 10.1016/j.autrev.2021.102761 -
Frontiers in Immunology 2019Despite the large number of performed studies, the etiology and pathogenesis of sarcoidosis still remain unknown. Most researchers allude to the possible autoimmune or...
Despite the large number of performed studies, the etiology and pathogenesis of sarcoidosis still remain unknown. Most researchers allude to the possible autoimmune or immune-mediated genesis of the disease. This review attempts an integral analysis of currently available information suggesting an autoimmune genesis of sarcoidosis and is divided into four categories: the evaluation of clinical signs described both in patients with sarcoidosis and "classic" autoimmune diseases, the role of triggering factors in the development of sarcoidosis, the presence of immunogenic susceptibility in the development of the disease, and the analysis of cellular and humoral immune responses in sarcoidosis. Studying the etiology and pathogenesis of sarcoidosis will improve diagnostic procedures as well as the prognosis and patients' quality of life.
Topics: Animals; Autoimmune Diseases; Humans; Immunity, Cellular; Immunity, Humoral; Sarcoidosis
PubMed: 31969879
DOI: 10.3389/fimmu.2019.02933 -
Frontiers in Neurology 2023Juvenile myasthenia gravis (JMG) is a rare autoimmune disease that has so far only been described in small cohort studies. We defined the clinical characteristics,...
BACKGROUND
Juvenile myasthenia gravis (JMG) is a rare autoimmune disease that has so far only been described in small cohort studies. We defined the clinical characteristics, management, and outcomes of JMG patients over the past 22 years.
METHODS
A search of PubMed, EMBASE, and web of science (1/2000-2/2022) identified all English language and human studies of JMG. The population was patients diagnosed with JMG. Outcomes included the history of myasthenic crisis, autoimmune comorbidity, mortality, and treatment outcome. Data extraction was performed by independent reviewers. And we performed a pooled reanalysis of all published data in the included studies and compared with other studies of adult cohorts.
RESULTS
We identified 11 articles describing 1,109 patients diagnosed between 2006 and 2021. JMG occurred in 60.4% of female patients. The mean age at presentation was 7.38 years old, and 60.6% of the patients had ocular symptoms as the first clinical manifestation. The most common initial presentation was ptosis, which occurred in 77.7% patients. AchR-Ab positive accounted for 78.7%. 641 patients received thymus examination, found to have thymic hyperplasia in 64.9% and thymoma in 2.2%. Autoimmune comorbidity was found in 13.6% and the most common one is thyroid disease (61.5%). First-line therapy, including pyridostigmine and steroids, was initiated in 97.8 and 68.6%, respectively. Six patients resolved spontaneously without treatment. Thymectomy was performed in 45.6%. 10.6% of patients had a history of myasthenic crisis. Completely stable remission was achieved in 23.7% and mortality was reported in 2 studies, which reported 8 deaths.
CONCLUSION
JMG is a rare disease with a relatively benign course, and differs from adult MG in some clinical features. The treatment regimen guideline for children is still not well-established. There is a need for prospective studies to properly evaluate treatment regimes.
PubMed: 36970540
DOI: 10.3389/fneur.2023.1119294 -
Allergy, Asthma, and Clinical... Aug 2023Immunoglobulin A deficiency (IgAD) is a common disease with an unknown genetic defect, characterized by the decreased or absent IgA with other isotypes normal, normal... (Review)
Review
OBJECTIVES
Immunoglobulin A deficiency (IgAD) is a common disease with an unknown genetic defect, characterized by the decreased or absent IgA with other isotypes normal, normal subclasses, and specific antibodies. Patients with this disorder represent a spectrum of clinical manifestations including infections, autoimmune disorders, malignancy, and allergic diseases. The current study aimed to evaluate their prevalence and categorized them.
METHODS
We searched PubMed, Web of Science, and Scopus databases to find eligible studies from the earliest available date to January 2022 with standard keywords. Pooled estimates of clinical manifestations prevalence and the corresponding 95% confidence intervals were calculated using random-effects models.
RESULTS
The most prevalent clinical manifestations belonged to infection (64.8%) followed by allergic diseases (26.16%) and autoimmunity (22.0%), respectively. In selective IgA deficiency patients as the largest group of IgAD in current study, celiac disease (6.57%), Inflammatory bowel disease (4.01%), and rheumatoid arthritis (3.80%) were the most prevalent autoimmunity. Meanwhile, the most frequent infection was respiratory tract infection, fungal infection, and gastrointestinal infection at 50.74%, 18.48%, and 15.79%, respectively. In addition, the pooled prevalence of asthma, allergic rhinitis, and allergic conjunctivitis were 19.06%, 15.46%, and 11.68%, respectively which were reported as the most widespread allergic diseases.
CONCLUSIONS
Our results showed that apart from undiagnosed IgAD patients, IgAD patients represent a wide range of clinical manifestations. Infection, allergy, and autoimmunity are the most common clinical manifestations. The concurrent presence of IgA and IgG subtypes deficiency could be associated with increased susceptibility to infection. Considering the probability of developing new clinical complications during follow-up, periodic assessments of IgAD patients should be inspected.
PubMed: 37641141
DOI: 10.1186/s13223-023-00826-y -
Antibiotic-induced gut dysbiosis and autoimmune disease: A systematic review of preclinical studies.Autoimmunity Reviews Sep 2022Antibiotic-induced gut dysbiosis is believed to be associated with the onset and development of autoimmune diseases. To evaluate microbiota's variations triggered by... (Review)
Review
Antibiotic-induced gut dysbiosis is believed to be associated with the onset and development of autoimmune diseases. To evaluate microbiota's variations triggered by antibiotic therapy and its outcomes on autoimmune diseases, preclinical studies regarding these subjects were included in this review. The studies were selected on PubMed, Scopus and Web of Science from 2011 to 2021 by three researchers that extracted study data and risk of bias, which were verified by a further 3 independent researchers. The team assessed the strength of evidence across studies. Of the eligible studies, 17 showed an improvement of the studied disease after antibiotic therapy and 10 had a negative effect on the course of the condition. The ameliorating factors of the studied diseases were mostly seen when using an antibiotic cocktail. Male animals had a good outcome after therapy and, for all genders, the increase in IL-10 and Treg cells was often shown to ameliorate disease after the antibiotic intervention. Firmicutes, Proteobacteria and Bacteroidetes appeared altered after the antibiotic intervention, leading to amelioration or worsening of the condition depending on the autoimmune disease. We identified that the number of autoimmune conditions approached leads to specific conclusions regarding the interventions, making it difficult to achieve an overall conclusion. Overall, even though pre-clinical studies must be translated to the human model, the studied aspects of gender, age, lineage and disease model substantially impact the outcomes that make for many intricacies that were not-established in the study of antibiotic-induced gut dysbiosis and autoimmunity.
Topics: Animals; Anti-Bacterial Agents; Autoimmune Diseases; Bacteroidetes; Dysbiosis; Female; Gastrointestinal Microbiome; Humans; Male
PubMed: 35830954
DOI: 10.1016/j.autrev.2022.103140