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Relevant bibliographies by topics / Autoimmune disorder

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Academic literature on the topic 'Autoimmune disorder'

Author: Grafiati

Published: 4 June 2021

Last updated: 17 June 2025

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Journal articles on the topic "Autoimmune disorder"

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Dale, Russell C., and Fabienne Brilot. "Autoimmune Basal Ganglia Disorders." Journal of Child Neurology 27, no. 11 (2012): 1470–81. http://dx.doi.org/10.1177/0883073812451327.

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The basal ganglia are deep nuclei in the brain that include the caudate, putamen, globus pallidus, and substantia nigra. Pathological processes involving the basal ganglia often result in disorders of movement and behavior. A number of different autoimmune disorders predominantly involve the basal ganglia and can result in movement and psychiatric disorders. The classic basal ganglia autoimmune disorder is Sydenham chorea, a poststreptococcal neuropsychiatric disorder. Resurgence in the interest in Sydenham chorea is the result of the descriptions of other poststreptococcal neuropsychiatric disorders including tics and obsessive-compulsive disorder, broadly termed pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection. Encephalitic processes affecting the basal ganglia are also described including the syndromes basal ganglia encephalitis, encephalitis lethargica, and bilateral striatal necrosis. Last, systemic autoimmune disorders such as systemic lupus erythematosus and antiphospholipid syndrome can result in chorea or parkinsonism. Using paradigms learned from other autoantibody associated disorders, the authors discuss the autoantibody hypothesis and the role of systemic inflammation in autoimmune basal ganglia disorders. Identification of these entities is important as the clinician has an increasing therapeutic repertoire to modulate or suppress the aberrant immune system.

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Oliveira, S. G., S. M. Pereira, and J. C. Mendes. "Psychosis and autoimmune disorders." European Psychiatry 26, S2 (2011): 1186. http://dx.doi.org/10.1016/s0924-9338(11)72891-7.

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IntroductionPsoriasis is a common, chronic, erythematous dermatosis with prevalence estimates ranging from 0, 3% to 2, 5%. This recurring disorder is associated with significant psychological distress, a decrease in health-related quality of life and psychiatric morbidity. The most common psychiatric comorbidities are mental retardation, personality disorder and affective disorders.ObjectivesThe authors’ aim is to present a clinical vignette of a 27-year-old male suffering from psoriasis who was admitted to the psychiatric yard exhibiting psychotic symptoms. A literature's review about the association between psychosis and autoimmune disorders, particularly with psoriasis vulgaris, was also made.Case reportThe patient is a 27-year-old single male with normal IQ. He had no physical ilnesses during childhood and adolescence. There was no history of psychiatric or developmental disorders in the patient and his family. In early adulthood he was diagnosed with psoriasis vulgaris. The patient's father also suffered from the same skin disorder. At the age of 27 he began to hear voices commenting on his behaviour and he exhibited psychomotor agitation, delusions of persecution, and sexual disinhibition. Admission in psychiatric yard was necessary to treat psychotic symptoms.ConclusionsThe skin and the brain are embryologically related. Consequently, a relationship between psychological factors and skin diseases has long been hypothesized. Schizophrenia has been associated with nearly 50% higher lifetime prevalence of one or more autoimmune disorders but further studies are necessary to elucidate the possible association between psoriasis vulgaris and psychosis.

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Tripathi, Purnima, and Peeyush Bhardwaj. "Psoriasis: An autoimmune disorder." Journal of Drug Delivery and Therapeutics 10, no. 5 (2020): 316–24. http://dx.doi.org/10.22270/jddt.v10i5.4327.

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Psoriasis is an auto-immune disorder of the skin. It is characterized by the hyperproliferation of keratinocytes. Severity of the disease depends on the body area affected. Both genetic as well as environmental factors are responsible for it. It affects around 2-3% of world’s population. Psoriasis not only causes physical problems, it also affects mental and social well being of the patient. It may also lead to some Comorbidities like heart problems, diabetes, psychological problems, Crohn’s disease , etc. Keeping in view the impact it creats in the patient’s life, steps should be taken to create awareness of psoriasis. This article attempts to provide a comprehensive view on the psoriasis. It includes the various forms of psoriasis with their specific features, causes of psoriasis, diagnosis and assessment tools used, treatments available for its management including topical as well as systemic therapy and associated problems. Keywords: Plaque, Psoriasis, Pustules

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Endres, Dominique. "Autoimmune obsessive-compulsive disorder." Journal of Affective Disorders Reports 12 (April 2023): 100539. http://dx.doi.org/10.1016/j.jadr.2023.100539.

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Abhinav Ankur, Dimple Gupta, and Bushra Zahoor. "Prevalence, Severity and Predictors of Psychiatric Disorders in Patients with Autoimmune Disorder." Indian Journal of Public Health Research & Development 15, no. 3 (2024): 12–19. http://dx.doi.org/10.37506/18g8hq58.

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In recent years, there has been growing attention to the idea that immunological pathways may play a role in some types of psychotic disorders. Researchers have become particularly interested in the connection between autoimmune diseases and psychotic disorders. Genetic studies have linked immune-related genetic markers with schizophrenia, and clinical studies have found elevated levels of inflammatory markers in individuals with psychosis. Additionally, several large-scale epidemiologic studies have found a positive association between autoimmune diseases and psychosis. Specifically, autoimmune diseases like multiple sclerosis and lupus are known to have a higher incidence of neuropsychiatric symptoms, including psychosis, compared to healthy individuals. Research has shown a link between autoimmune conditions and greater chances of experiencing mental health problems. There is a proposed connection between autoimmune diseases and schizophrenia that works both ways. Previous findings underlined an association between autoimmune disorders and schizophrenia, with evidence of a reciprocal relationship. In addition, having a family history of autoimmune diseases may elevate the likelihood of developing psychotic disorders. This review will examine the epidemiological evidence that supports the association between autoimmune diseases and psychosis. Possible explanations for this link will be explored, including shared genetic risk factors, the impact of infections on autoimmunity and psychotic disorders, and the role of the microbiome. The review will also discuss the effects of autoantibodies and T- and B-cell dysregulation on both disease categories and the need for further research. Examining the connection between autoimmune diseases and psychosis is essential in understanding the etiological mechanisms of psychotic disorders and highlighting the significance of somatic comorbidity in patients with these disorders.

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LOISELLE, CHRISTOPHER R., and HARVEY S. SINGER. "Genetics of Childhood Disorders: XXXI. Autoimmune Disorders, Part 4: Is Sydenham Chorea an Autoimmune Disorder?" Journal of the American Academy of Child & Adolescent Psychiatry 40, no. 10 (2001): 1234–36. http://dx.doi.org/10.1097/00004583-200110000-00019.

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Molnár, Emese, Gábor Kovács, Lívia Varga, et al. "Nem malignus, nem infectiosus lymphoproliferatio: kihívások az autoimmun lymphoproliferativ szindróma diagnosztikájában és kezelésében." Orvosi Hetilap 163, no. 4 (2022): 123–31. http://dx.doi.org/10.1556/650.2022.32353.

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Összefoglaló. Az autoimmun lymphoproliferativ szindróma egy ritka, immundeficientiával járó genetikai betegség. Hátterében az extrinszik apoptotikus útvonal génjeinek örökletes vagy szerzett mutációi és a következményesen kialakuló, aktivált lymphocyták negatív szelekciójának a defektusa áll. Az autoimmun lymphoproliferativ szindróma klinikai megjelenésére jellemző a jóindulatú lymphocytaburjánzás következtében kialakuló lymphadenopathia és lépmegnagyobbodás. Gyakran társul olyan autoimmun kórképekkel, mint az autoimmun haemolyticus anaemia vagy az autoimmun thrombocytopenia. A betegségben jellemző laboratóriumi eltérések a következők: az αβ+ CD4–/CD8– kettős negatív T-sejtek szaporulata, a szolúbilis Fas-ligand, az interleukin-10 és interleukin-18, valamint a B12-vitamin szérumszintjének emelkedése. A kórkép diagnózisához hozzátartozik az in vitro Fas-mediált apoptózis funkciójának vizsgálata, valamint a genetikai vizsgálat. Differenciáldiagnosztikai szempontból fontos elkülöníteni a lymphomáktól, valamint az autoimmun lymphoproliferativ szindrómaszerű betegségektől. A kezelés alapja a társuló autoimmun kórképek tüneteinek csökkentése immunszuppresszív terápiával. Orv Hetil. 2022; 163(4): 123–131. Summary. The autoimmune lymphoproliferative syndrome is a rare genetic disorder causing immunodeficiency. In the background of the disease, germline or somatic mutations of genes participating in the extrinsic apoptotic pathway and the consequential defect in the negative selection of activated lymphocytes were discovered. The clinical appearance of autoimmune lymphoproliferative syndrome consists of non-malignant lymphoproliferation, lymphadenopathy and splenomegaly, it is frequently accompanied by autoimmune disorders such as autoimmune haemolytic anaemia or autoimmune thrombocytopenia. The main diagnostic laboratory findings of this disease are the following: an elevation in αβ+, CD4–/CD8– double-negative T cell count, elevated serum levels of soluble Fas-ligand, interleukin-10, interleukin-18 and vitamin B12. Other useful laboratory tests are the in vitro Fas-mediated apoptotic functional assay and the genetic screening for gene mutations. Differential diagnosis should exclude malignant lymphoproliferation in lymphomas and non-malignant autoimmune lymphoprolipherative syndrome-like diseases. The main aim of the treatment is the amelioration of the accompanying autoimmune disease with immunosuppressive therapy. Orv Hetil. 2022; 163(4): 123–131.

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Villarreal, Veronica R., Maja Z. Katusic, Scott M. Myers, Amy L. Weaver, James J. Nocton, and Robert G. Voigt. "Risk of Autoimmune Disease in Research-Identified Cases of Autism Spectrum Disorder: A Longitudinal, Population-Based Birth Cohort Study." Journal of Developmental & Behavioral Pediatrics 45, no. 1 (2024): e46-e53. http://dx.doi.org/10.1097/dbp.0000000000001232.

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ABSTRACT: Objective: Determine the risk of autoimmune disease in research-identified cases of autism spectrum disorder (ASD) compared with referents using a longitudinal, population-based birth cohort. Methods: ASD incident cases were identified from a population-based birth cohort of 31,220 individuals. Inclusive ASD definition based on DSM-IV-TR autistic disorder, Asperger syndrome, and pervasive developmental disorder, not otherwise specified, was used to determine ASD cases. For each ASD case, 2 age- and sex-matched referents without ASD were identified. Diagnosis codes assigned between birth and December 2017 were electronically obtained. Individuals were classified as having an autoimmune disorder if they had at least 2 diagnosis codes more than 30 days apart. Cox proportional hazards models were fit to estimate the hazard ratio (HR) between ASD status and autoimmune disorder. Results: Of 1014 ASD cases, 747 (73.7%) were male. Fifty ASD cases and 59 of the 1:2 matched referents were diagnosed with first autoimmune disorder at the median age of 14 and 17.1 years, respectively. ASD cases had increased risk of autoimmune disease compared with matched referents (HR 1.74; 95% confidence interval [CI], 1.21–2.52). The increased risk was statistically significant among male patients (HR 2.01; 95% CI, 1.26–3.21) but not among the smaller number of female subjects (HR 1.38; 95% CI, 0.76–2.50). Conclusion: This study provides evidence from a longitudinal, population-based birth cohort for co-occurrence of ASD and autoimmune disorders. Thus, children with ASD should be monitored for symptoms of autoimmune disease and appropriate workup initiated.

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Keshari, Adarsh, Kriti Jain, Roshan Pandey, et al. "Review on Bullous Pemphigoid: Fixed Drug Eruption or Autoimmune Disorder." Journal of Pharmaceutical Technology, Research and Management 12, no. 2 (2024): 15–24. https://doi.org/10.15415/jptrm.2024.122002.

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Background: Bullous pemphigoid is a blistering disease of autoimmune nature predominantly affecting the geriatric population. It is characterized by blister formation at the subepidermal level, due to autoantibodies at the dermo-epidermal junction targeting proteins BP180XV11 and BP230. Mainly an autoimmune condition, diagnosis and treatment get complicated as it overlaps with drug-induced hypersensitivity reactions, including fixed drug eruption. Unlike Bullous Pemphigoid, it is a condition of localized hypersensitivity mediated by T cells. Purpose: The review tries to establish Bullous Pemphigoid as an autoimmune condition separate from fixed drug eruption. It is centered on the causative role of medications, which include diuretics, antibiotics, and dipeptidyl peptidase-4 inhibitors, in drug-induced bullous pemphigoid. Besides, it examines genetic, immunological, and environmental etiologies of the disease and delineates clinical and diagnostic characteristics of Bullous Pemphigoid and fixed drug eruptions. Method: A systematic analysis of current literature was performed, focusing on the pathophysiology, immunological mechanisms, and histopathological differences between Bullous Pemphigoid and fixed drug eruptions. The review also examines the role of medications, genetic predispositions such as specific human leukocyte antigen haplotypes, and the diagnostic utility of histopathological and immunological methods like direct immunofluorescence. Results: Autoantibodies against BP180 and BP230 in bullous pemphigoid initiate inflammatory cascades, causing subepidermal blistering and eosinophilic infiltration. Fixed drug eruption involves basal cell necrosis and localized lymphocytic infiltration. Drugs like dipeptidyl peptidase-4 inhibitors exacerbate bullous pemphigoid through immune modulation and oxidative stress. Genetic susceptibility plays a significant role, and immunological tests such as direct immunofluorescence help distinguish the two conditions. Conclusion: Bullous pemphigoid is a distinct autoimmune disease with unique immunopathological mechanisms compared to fixed drug eruption. Understanding its pathogenesis, drug interactions, and diagnostic methods enhances accurate diagnosis and management of both spontaneous and drug-induced bullous pemphigoid.

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Das, Kiron M., and Livia Biancone. "Is IBD an autoimmune disorder?" Inflammatory Bowel Diseases 14, Supplement (2008): S97—S101. http://dx.doi.org/10.1097/00054725-200810001-00049.

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Dissertations / Theses on the topic "Autoimmune disorder"

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Padmos, R. C. "Inflammatory monocyte in bipolar disorder and related endocrine autoimmune deseases." [S.l.] : [The Author], 2009. http://hdl.handle.net/1765/14920.

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Stöckl, Andrea. "Social performances of an autoimmune disorder (SLE) : shifting knowledge and practices." Thesis, University of Cambridge, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620492.

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Ryan, James Joseph. "Characterisation of the Goodpasture antigen." Thesis, Imperial College London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286355.

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Jones, Hannah. "Maternal Autoimmunity and Inflammation are associated with Childhood Tics and Obsessive-Compulsive Disorder." Thesis, The University of Sydney, 2021. https://hdl.handle.net/2123/26281.

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Although genetic variation is a major risk factor of neurodevelopmental disorders (NDDs) such as tics and childhood obsessive-compulsive disorder (OCD), environmental factors during pregnancy and early life are important in disease expression. Epidemiological studies and animal models indicate maternal inflammation is one potential environmental factor. In my thesis, I compared the frequency of proinflammatory states in mothers of 200 children with tics/OCD with 100 autoimmune neurological controls and 100 age- and sex-matched healthy controls. I prospectively recruited children with tics/OCD aged ≤16 years sequentially referred to the Children’s Hospital at Westmead, and used a structured interview to capture data, focusing on maternal autoimmunity. Children with tics/OCD were phenotyped to identify associations with maternal autoimmunity, and exploratory biomarker testing and transcriptome analysis were performed in a subgroup of mothers to identify immune pathways potentially relevant to neurodevelopment in offspring. A total of 61 (30.5%) mothers of children with tics/OCD had autoimmune disease compared with 20 (20%) mothers of children with autoimmune neurological conditions (p=0.054) and 12 (12%) mothers of healthy controls (p=0.0004, adj OR 2.7 (95th CI 1.28-5.68)). Other proinflammatory states were also more common in mothers of children with tics/OCD than mothers of healthy controls (p<0.0001). Maternal autoimmunity was not associated with a distinct clinical phenotype in the child. Maternal blood and published Tourette brain transcriptomes showed common enrichment of differentially expressed genes in innate immune pathways. Our results indicate dysregulation of innate immune pathways may be pivotal in the expression of NDDs and should be a focus of further research. Understanding immune mechanisms in neurodevelopment could unveil opportunities to mitigate risk to children by reducing exposure to inflammation and open new avenues for treatment.

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Kling, Lovisa, and Alva Karlsson. "Barriärer till fysisk aktivitet hos individer med typ 1 diabetes : En enkätstudie." Thesis, Linnéuniversitetet, Institutionen för idrottsvetenskap (ID), 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-104597.

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Bakgrund: Typ 1 diabetes är en obotlig autoimmun sjukdom där immunförsvaret angriper och förstör de insulinproducerande ß-cellerna i bukspottkörteln. Detta leder tillslut till total insulinbrist vilket är ett dödligt tillstånd. Genom att öka mängden fysisk aktivitet hos individer med typ 1 diabetes minskar risken för följdsjukdomar. Syfte: Syftet med studien var att undersöka de barriärer som finns till fysisk aktivitet hos individer med typ 1 diabetes. Metod: Den metod som valdes var kvantitativ metod där enkäten “Barriers to Physical Activity in Diabetes type 1” (BAPAD1) valdes ut. Totalt svarade 66 individer med typ 1 diabetes på enkäten. Resultatet analyserades sedan med hjälp av Excel. Resultat: Den vanligaste barriären till fysisk aktivitet var “rädslan för hypoglykemi” följt av “Att du tappar kontrollen över din diabetes under fysisk aktivitet” och “att du tappar kontrollen över din diabetes efter fysisk aktivitet”. Konklusion: Sammanfattningsvis fick vi vår frågeställning besvarad. Tidigare studier visar att rädsla för hypoglykemi är den vanligaste barriären till fysisk aktivitet och det bekräftades även i denna studie.<br>Background: Type 1 diabetes is an autoimmune disorder where the immune system destroys the insulin-producing pancreatic-ß cells. This eventually leads to total insulin deficiency which is a fatal condition. By increasing the amount of physical activity in individuals with type 1 diabetes the risk of sequelae reduces. Objective: The aim of this study was to investigate the barriers to physical activity in individuals with type 1 diabetes. Method: The chosen method to this study was the questionnaire “Barriers to Physical Activity in Diabetes type 1” (BAPAD1). A total of 66 individuals with type 1 diabetes filled the questionnaire according to their own barriers to physical activity. The answers were later analysed in Excel. Result: The most common barrier to physical activity was “the fear of hypoglycemia” followed by “The loss of control over your diabetes during physical activity” and “The loss of control over your diabetes after physical activity”. Conclusion: Over all the result of the study got our question answered. Previous studies show that fear of hypoglycemia is the most common barrier to physical activity, and this was also confirmed in this study

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Bukhari, Wajih u. "Epidemiology and Clinical Features of NMOSD in Australia and New Zealand." Thesis, Griffith University, 2022. http://hdl.handle.net/10072/411539.

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Neuromyelitis optica (NMO) is a rare autoimmune disorder, distinct from multiple sclerosis, causing inflammatory lesions predominantly in the optic nerves and spinal cord. An autoantibody (NMO IgG) against aquaporin-4 (AQP4), a water channel expressed on astrocytes, is thought to be causative. A clinic and laboratory-based survey of neuromyelitis optica spectrum disorders (NMOSDs) in Australia and New Zealand was undertaken to establish incidence and prevalence across the region and in populations of differing ancestry. Patients with clinical and laboratory features that were suspicious for NMOSD were referred to me. Testing for NMO antibodies was undertaken in all suspected cases. From this group, cases were identified who fulfilled the 2015 Wingerchuk diagnostic criteria for NMOSD. A capture-recapture methodology was used to estimate incidence and prevalence based on additional laboratory identified cases. The capture-recapture analysis gave an adjusted incidence estimate of 0.37 (95% CI 0.35 to 0.39) per million per year and a prevalence estimate for NMOSD of 0.70 (95% CI 0.61 to 0.78) per 100,000. NMOSD was three times more common in the Asian population (1.57 (95% CI 1.15 to 1.98) per 100,000) compared with the remainder of the population (0.57 (95% CI 0.50 to 0.65) per 100,000). The latitudinal gradient evident in multiple sclerosis was not seen in NMOSD. These figures are comparable with figures from other populations of largely European ancestry. I found NMOSD to be more common in the population with Asian ancestry.Frequencies of self-determined ethnic ancestry were calculated for confirmed NMOSD, suspected NMOSD, and MS. Prevalence rates for NMOSD and MS according to ancestry were compared. NMOSD cases were more likely to have Asian, Indigenous, or Other ancestry compared to suspected NMOSD or MS. There were no differences in the clinical phenotype of NMOSD seen in Indigenous compared to European ancestry populations. Per 100,000, the prevalence estimate for NMOSD in people with Māori ancestry was 1.50 (95% CI 0.52–2.49), which was similar to those with Asian ancestry 1.57 (95% CI 1.15–1.98). NMOSD prevalence in Australian Aboriginal and Torres Strait Islander populations was 0.38 (95% CI 0.00–0.80) per 100,000. I found the prevalence of NMOSD in the Māori population was similar to South East Asian countries, reflecting their historical origins. The prevalence of MS in this group is intermediate between those with South East Asian and European ancestry living in New Zealand. Both NMOSD and particularly MS appear to be uncommon in the Indigenous populations of Australia. In collaboration with laboratory scientists, I compared five different assays for antibodies to aquaporin-4 in cases of NMOSD and controls to assess their relative utility. All aquaporin-4 antibody assays proved to be highly specific. Sensitivities ranged from 60 to 94%, with cell-based assays having the highest sensitivity. Antibodies to MOG were detected in 8/79 (10%) of the residual suspected cases of NMOSD. Under the 2015 IPND diagnostic criteria for NMOSD, cell-based assays for aquaporin-4 are sensitive and highly specific, performing better than tissue-based and ELISA assays. A fixed cell-based assay showed near-identical results to a live-cell based assay. Antibodies to MOG account for only a small number of suspected NMOSD cases (8/177 [5%]).When compared to multiple sclerosis (MS), age at onset, relapse rates and disability levels (EDSS) were significantly higher in NMOSD than in MS. Lesions and symptoms referable to the optic nerve were more common in NMOSD, whereas brainstem, cerebellar and cerebral lesions were more common in MS. Longitudinally extensive spinal cord lesions were seen in two thirds of cases with NMOSD. Elevations of CSF, white cell count and protein were more common in NMOSD. I have confirmed a clinical pattern of NMOSD that has been seen in several geographical regions. I have demonstrated the clinical utility of the current diagnostic criteria. Distinct patterns of disease are evident in NMOSD and MS, but there remains a large number of patients with NMOSD-like features who do not meet the current diagnostic criteria for NMOSD. This group remain a diagnostic challenge<br>Thesis (PhD Doctorate)<br>Doctor of Philosophy (PhD)<br>School of Medicine & Dentistry<br>Griffith Health<br>Full Text

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Vaidya, Bijayeswar. "Genetics of autoimmune endocrine disorders." Thesis, University of Newcastle Upon Tyne, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341439.

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Indugula, Reshmi. "Fungal Exposure and Development of Autoimmune Disorders." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1505124409594398.

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Ekström, Smedby Karin. "Ultraviolet light, autoimmune disorders and the etiology of malignant lymphomas /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-313-2/.

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Spillane, J. "Clinical and functional studies of autoimmune disorders of neuromuscular transmission." Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1461232/.

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Inherited and acquired disorders of the neuromuscular junction are an important cause of muscle weakness and fatigability. In this thesis I focus on the autoimmune disorders of neuromuscular transmission. Myasthenia Gravis (MG) is the most common of these diseases and is typically caused by antibodies against the post-synaptic acetylcholine receptor. Lambert Eaton Myasthenic Syndrome (LEMS) is a pre-synaptic disorder typically caused by antibodies against voltage gated calcium channels (VGCC). With regard to LEMS, my main aim was to gain a more complete understanding of the pathomechanisms of the disease. To date, the direct effect of LEMS IgG on presynaptic neurotransmitter release had not been investigated in detail. I examined how LEMS IgG affects neurotransmitter release by imaging action potential dependent vesicle exocytosis using a fluorescent dye. I found that LEMS IgG significantly inhibited the rate of synaptic vesicle release but this effect was lost in synapses from a Cacna1a knockout mouse. These data provide direct evidence that LEMS is caused by impaired neurotransmitter release due to an effect on P/Q-type VGCCs. With regard to MG, I studied the long-term outcome of patients with thymomatous and non-thymomatous MG after thymectomy and found that in general the outcome was favourable in the majority of patients with 34% of patients achieving complete stable remission. I also reviewed the long-term outcome of patients after a severe exacerbation of MG requiring ITU admission. Despite the significant mortality associated with severe exacerbations of MG, it was found that specialised neuro-intensive care was associated with a good long-term prognosis in the majority of patients. There were no significant differences in outcome in those with early or late onset MG. Overall the data presented in this thesis provide new insights into the pathomechanisms of LEMS IgG and provide new information regarding the long-term outcome of patients with MG.

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Books on the topic "Autoimmune disorder"

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Sticherling, Michael, and Enno Christophers, eds. Treatment of Autoimmune Disorders. Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-6016-9.

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Michael, Sticherling, and Christophers Enno, eds. Treatment of autoimmune disorders. Springer, 2003.

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L, Vogel Fynn, and Zimmermann Lucas F, eds. Autoimmunity: Role, regulation, and disorders. Nova Science Publishers, 2008.

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Pokorski, Mieczyslaw, ed. Lung Cancer and Autoimmune Disorders. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-09752-7.

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E, Silberstein Leslie, ed. Autoimmune disorders of the blood. American Association of Blood Banks, 1996.

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Petrov, Maria E. Autoimmune disorders: Symptoms, diagnosis, and treatment. Nova Science Publishers, 2010.

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Alois, Gratwohl, and Tyndall Alan, eds. Stem cell transplantation for autoimmune disorders. Baillière Tindall, 2004.

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S, Scott J., and Bird H. A. 1945-, eds. Pregnancy, autoimmunity, and connective tissue disorders. Oxford University Press, 1990.

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Autoimmune Diet: The Autoimmune Cookbook, Recipe Collection for Autoimmune Disorder. WebNetworks Inc, 2013.

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Autoimmune Diet: The Autoimmune Cookbook, Recipe Collection for Autoimmune Disorder. Speedy Publishing LLC, 2013.

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Book chapters on the topic "Autoimmune disorder"

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Gooch, Jan W. "Autoimmune Disorder." In Encyclopedic Dictionary of Polymers. Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13200.

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Champion, Howard R., Nova L. Panebianco, Jan J. De Waele, et al. "Autoimmune Disorder of the Neuromuscular Junction." In Encyclopedia of Intensive Care Medicine. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_1186.

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Heckenlively, John R., and Steven K. Lundy. "Autoimmune Retinopathy: An Immunologic Cellular-Driven Disorder." In Retinal Degenerative Diseases. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-75402-4_24.

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Panzer, Jessica, and Josep Dalmau. "Anti-NMDA Receptor Encephalitis and Other Autoimmune and Paraneoplastic Movement Disorders." In Movement Disorder Emergencies. Humana Press, 2012. http://dx.doi.org/10.1007/978-1-60761-835-5_22.

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Panzer, Jessica, Josep Dalmau, and Russell C. Dale. "Anti-NMDA Receptor Encephalitis and Other Autoimmune and Paraneoplastic Movement Disorders." In Movement Disorder Emergencies. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-75898-1_16.

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Noris-García, Elena, Mercedes Adalys Rodríguez-Ravelo, Yamila Adams Villalón, Gustavo Sierra, and Maria de los Angeles Robinson-Agramonte. "Antibody Mediating Autoimmune Reaction in Autism Spectrum Disorder." In Translational Approaches to Autism Spectrum Disorder. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-16321-5_10.

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Karwasra, Ritu, Sneha Sharma, Isha Sharma, and Shiv Kant Sharma. "Autoimmune Autonomic Disorder: AI-Based Diagnosis and Prognosis." In Studies in Computational Intelligence. Springer Nature Singapore, 2024. http://dx.doi.org/10.1007/978-981-99-9029-0_4.

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Sahu, Satya Narayan, Biswajit Mishra, Rojalin Sahu, and Subrat Kumar Pattanayak. "Current Strategies and Future Perspectives of Autoimmune Disorder." In Digital Future of Healthcare. CRC Press, 2021. http://dx.doi.org/10.1201/9781003198796-9.

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Iranzo, Alex. "RBD Associated with Paraneoplastic Neurological Syndromes and Autoimmune Disorders." In Rapid-Eye-Movement Sleep Behavior Disorder. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-90152-7_8.

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de Latour, Régis Peffault, Antonio Risitano, Austin Kulasekararaj, and Carlo Dufour. "Acquired Bone Marrow Failure: Severe Aplastic Anemia and Paroxysmal Nocturnal Hemoglobinuria." In The EBMT Handbook. Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-44080-9_78.

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AbstractSevere aplastic anemia (SAA) is an autoimmune disorder due to the attack of autoreactive cytotoxic T lymphocytes to the hematopoietic component of the bone marrow. SAA might be associated with PNH, resulting from the clonal expansion of hematopoietic stem cells that have somatic mutations in the X-linked gene PIG-A. This review is summarizing the management of SAA from the diagnosis, where inherited disorders need to be excluded, to the overall treatment algorithm of this disease, including immunosuppression and bone marrow transplantation.

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Conference papers on the topic "Autoimmune disorder"

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Cui, Jie, Andrea Duque Lopez, Gabriella Brinkmann, et al. "Automatic Monitoring of High-Frequency Autoimmune Disorder Related Seizures with Wearable Devices." In 2024 46th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2024. https://doi.org/10.1109/embc53108.2024.10782939.

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Bhuvaneshwari, V., R. Sadaieswaran, P. Malathi, N. Legapriyadharshini, T. Thirumalaikumari, and S. R. Raja. "IoT-Enhanced Innovations in Drug Delivery Systems for Targeted Therapy in Autoimmune Disorders." In 2024 10th International Conference on Advanced Computing and Communication Systems (ICACCS). IEEE, 2024. http://dx.doi.org/10.1109/icaccs60874.2024.10716958.

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Teschner, M., A. Fuchs, N. Baerlecken, T. Lenarz, and T. Witte. "Autoimmune pathogenesis in chronic obstructive tube ventilation disorder." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1640643.

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Wiech, Kasia, Shreya Godishala, Dan Phan, Shivani Garg, and Melissa Skala. "Autofluorescence Lifetime Imaging Resolves Metabolic Abnormalities in T cells from Lupus Patients." In Clinical and Translational Biophotonics. Optica Publishing Group, 2024. http://dx.doi.org/10.1364/translational.2024.ttu3b.3.

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Optical metabolic imaging of T cells from patients with Systemic Lupus Erythematosus (SLE), a chronic autoimmune disorder, shows metabolic differences compared to healthy donors and reveals a moderate correlation to disease severity.

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Pinto, Icaro França Navarro, Wladimir Bocca Vieira de Rezende Pinto, Igor Braga Farias, et al. "Lambert-Eaton Myasthenic Syndrome in Brazil: a single center experience." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.120.

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Introduction: Lambert-Eaton Myasthenic Syndrome (LEMS) is an ultrarare autoimmune disorder of neuromuscular junction characterized by proximal muscle weakness, arreflexia and autonomic dysfunction due to presynaptic dysfunction caused by autoantibodies against the P/Q-type voltagegated calcium channel with diminished release of acetylcholine. LEMS can occurs as a primary autoimmune disorder or as paraneoplastic disorder with more than half of LEMS cases associated with small cell lung cancer. Objectives: The main objective of this study is described clinical, epidemiological, serological, and neurophysiological findings of a Brazilian cohort with definitive diagnosis of Lambert-Eaton Myasthenic Syndrome (LEMS). Results We identified eight patients with definitive LEMS with a 2:1 male/ female prevalence, all present with proximal muscle weakness with lower limb predominance and the most common autonomic dysfunction were xeropthalmia in 100% of patients, orthostatic hypotension presented in 6 of 9 patients and erectile dysfunction in all male patients. Conclusions: LEMS should always be suspected in patients with proximal muscle weakness associated with autonomic dysfunction and in this Brazilian cohort most cases were seronegative and do not have correlation with small-cell lung cancer in contrast with the current knowledge of disease.

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de Vries, Heike, Dietlind Klaus, Katrin Leister, Ulrich Brandl, and Peter Huppke. "Panic Attacks and Anxiety Disorder in a Child with Autism Spectrum Disorder and ADHD Triggered by GAD65 Autoimmune Encephalitis." In Abstracts of the 46th Annual Meeting of the Society for Neuropediatrics. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1739596.

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Tsuzuki, Sayaka, Hideyuki Takahashi, Fangyi Chen, and Keigo Setoguchi. "AB0354 CAN CANCER TRIGGER AUTOIMMUNITY DISEASE? FEATURES OF AUTOIMMUNE DISORDER OF CANCER PATIENTS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.5277.

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Manca, E., A. Petraccaro, S. Gorgoglione, et al. "P107 Autoimmune lymphoproliferative syndrome (ALPS) in a child: a new disorder to ‘climb’." In 8th Europaediatrics Congress jointly held with, The 13th National Congress of Romanian Pediatrics Society, 7–10 June 2017, Palace of Parliament, Romania, Paediatrics building bridges across Europe. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313273.195.

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Khaled, Salma Mawfek, Catalina Gabriela Petcu, Maryam Ali Al-Thani, Aisha Mohammed Al-Hamadi, and Peter Woodruff. "Prevalence and Potential Determinants of Insomnia Disorder in the General Population of Qatar." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0130.

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Aims: To estimate the prevalence of Insomnia Disorder in the household population of Qatar and explore potential associations with depressive and anxiety symptoms in addition to sociodemographic variables. Methods: Probability-based sampling was used to select a representative sample (N= 1,611) of Qatar’s household population. Face-to-face household interviews were conducted by trained staff using computer-assisted technology with consenting participants who were 18 years or older living in Qatar by the Social and Economic Research Institute (SESRI) at Qatar University as part of the Annual Omnibus survey in February/ March, 2019. The Sleep Condition Indicator (Epsie, 2014), a brief screening tool for DSM-5 criteria, was used to estimate the prevalence of insomnia in Qatar’s general population. Depressive and anxiety symptoms were ascertained using the PHQ-9 and GAD-2. Sociodemographic and health information including personal and family history of autoimmune disease were also collected. Univariate, bivariate, and multivariate statistics were conducted. Results: The prevalence of insomnia was 5.5% (95%CI: 4.3-6.7) and was higher in females (6.3%) than males (4.6%), though these differences were not statistically significant (P = 0.216). Insomnia was strongly associated with depressive (OR=5.4, P<0.01) and anxiety symptoms (OR=3.0, P<0.05). Having one or more autoimmune diseases were strongly associated with insomnia (OR=3.9, P<0.001) in Qatar’s general population. Insomnia was positively associated with younger age (P<0.01) and negatively associated with higher (post-secondary) education (OR=0.4, P<0.05). Conclusion: There is a significant association between mental illness and insomnia in Qatar with interesting findings in context of Qatar for role of age, education, and ethnicity. These findings need to be taken into account in provision of mental health services. Future studies should delineate the role of cultural attitudes towards sleep as potential mechanism linking insomnia to mental illness.

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Martin Nares, E., G. Hernández Molina, and H. Fragoso Loyo. "THU0347 Aquaporin-4 immunoglobulin g antibody positive neuromyelitis optica spectrum disorder and systemic autoimmune diseases overlap syndrome: a single centreexperience." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.6173.

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Reports on the topic "Autoimmune disorder"

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Blanken, Annelies, Bafrin Abdulmajid, Eva van Geel, Joost Daams, Martin van der Esch, and Michael Nurmohamed. Effect of tumor necrosis factor inhibiting treatment on arterial stiffness and arterial wall thickness in rheumatoid arthritis patients: protocol for a systematic review and planned meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.1.0131.

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Review question / Objective: The aim of this systematic review is to evaluate the effect of TNF inhibiting treatment on arterial stiffness (as measured with pulse wave velocity and augmentation index) and arterial wall thickness (as measured with carotid intima media thickness) in rheumatoid arthritis patients. Condition being studied: Rheumatoid arthritis is a chronic autoimmune disorder, which affects approximately 1% of the population worldwide. Information sources: The following electronic databases will be searched for potentially eligible studies: EMBASE, MEDLINE, ClinicalTrials.gov and WHO International Clinical Trials Registry Platform. For the studies identified as eligible for inclusion, similarity tracking will be used to identify more potentially relevant articles with the ‘related article’ feature in PubMed. In addition, a citation search will be performed for included studies to identify articles that have cited them. Reference lists of the included studies and previous reviews on the subject will be searched for potentially relevant studies. ResearchGate profiles of top authors on the subject will be investigated to identify potentially relevant data points. For ongoing or finished studies that are potentially eligible, but without a publication, study authors will be contacted for information. When additional information is needed, study authors will be contacted as well.

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Tedla, Jaya Shanker, Devika Rani Sangadala, Debjani Mukherjee, et al. Quality of life among children with special needs in the Kingdom of Saudi Arabia. A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2023. http://dx.doi.org/10.37766/inplasy2023.3.0016.

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Review question / Objective: The purpose of this systematic review is to find the details of the quality of life among children with disabilities in the Kingdom of Saudi Arabia. Condition being studied: Quality of life is a holistic concept that goes beyond the health dimension. Quality of life is not affected by disability alone but also by the person's experiences. Different disorders affect neurological, sensory, respiratory, metabolic, cardiac, musculoskeletal, hematological, and autoimmune disorders, either prenatal, perinatal, post-natal or during the development of the children. These disorders affect any of the physical, emotional, social, and spiritual domains of the life of children. If any one aspect of domains of life is affected, which in turn influences the quality of life in these children. There is a prevalence of disability in children due to different disorders in the Kingdom of Saudi Arabia. In the current systematic review, we intended to review the quality of life of children with different disorders in Saudi Arabia.

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Gupta, Kshitij. Evaluating Rituximab’s Role in Reducing Relapse Rates: Insights Into Long-Term Efficacy and Predictive Factors in Autoimmune Disorders. ResearchHub Technologies, Inc., 2025. https://doi.org/10.55277/researchhub.i37iua79.

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King, Ebony. Plain Language Summary: Naltrexone Utilization Along its Dosing Spectrum - a Literature Review. WritePharma, 2025. https://doi.org/10.70390/cwc0auh7n.

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Naltrexone, a widely recognized opioid receptor antagonist, has been primarily used at standard doses of 50–100 mg daily to treat opioid and alcohol use disorders. Recent studies, however, reveal its versatility across a broader dosing spectrum. This review examines the therapeutic effects and safety profiles of naltrexone across three dosing strategies: standard doses for substance use disorders, low-dose naltrexone (LDN, 1–5 mg/day) for chronic pain and autoimmune diseases, and ultra-low-dose naltrexone (ULDN, microgram levels) as a complement to opioid therapy. However, naltrexone’s role in reducing opioid misuse among those with a history of dependency remains limited. Our results serve to highlight naltrexone’s expanding clinical applications and highlights the need for further research to optimize its use across diverse dosing regimens and conditions.

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Zeng, Qingxiang, Junjiang Liu, Fanglong Wu, and Hongmei Zhou. The optimal oral biopsy site in the diagnosis of oral mucosal autoimmune bullous disorders: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2020. http://dx.doi.org/10.37766/inplasy2020.8.0024.

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Timm, Eliane, Julia Vieregg, and Ursula Wolf. Movement based mindfulness therapies in patients with multiple sclerosis – a systematic review protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.2.0102.

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Review question / Objective: The aim is to review the clinical benefits of mindful moving techniques for persons with multiple sclerosis. Condition being studied: Multiple sclerosis. Multiple sclerosis (MS) is a chronic autoimmune disease affecting the central nervous system (Gholamzad et al., 2019; Oh, Vidal-Jordana, & Montalban, 2018). It has shown to be increasing since 2013, and as of 2020 the estimated number of people with MS is 2.8 million worldwide (Walton et al., 2020). Due accumulation of relapses or gradual progression, disability from MS is worsening over time (Cameron & Nilsagard, 2018), which results in common symptoms like pain, imbalance, weakness, motor disorders, fatigue, depression, and more (Cameron & Nilsagard, 2018; Guicciardi et al., 2019).

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C. Uy, Genevieve, Raymond L. Rosales, and Satish Khadilkar. Myopathies in Clinical Care: A Focus on Treatable Causes. Progress in Neurobiology, 2024. http://dx.doi.org/10.60124/j.pneuro.2024.10.01.

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Myopathies present a wide range of clinical symptoms that affect the skeletal muscles, including weakness, fatigue, and pain. While acquired myopathies receive significant attention due to the availability of treatment options, it is important to note that some inherited myopathies can also be effectively managed. These myopathies can be classified based on their underlying causes, such as infectious agents, autoimmune disorders leading to muscle inflammation, granulomatous inflammation, metabolic abnormalities within the muscle cells, skeletal muscle channel dysfunctions, prolonged ICU stay, and inherited conditions such as Duchenne muscular dystrophy. In this review, we initially present a clinical approach to neuromuscular diseases and subsequently place specific emphasis on myopathies, particularly to those that have treatment options available.

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Hirankarn, Nattiya, Tanapat Palaga, Yingyos Avihingsanon, and Pimpayao Sodsai. The characterization of the two new genes, PTGS2 and PSN2 involving in the T lymphocyte apoptosis of lupus patients: Role of genetic polymorphism and epigenetic alteration. Chulalongkorn University, 2006. https://doi.org/10.58837/chula.res.2006.28.

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Systemic lupus erthematosus (SLE) is a prototype of autoimmune disease characterized by tissue deposition of autoantibody immune complex formation. However, etiology of disease remains unclarified. Defects of T lymphocytes lead to loss of immunological tolerance and support autoantibody production suggested that they may consistently have a central role in pathogenesis of SLE. Notch signaling is an evolutionarily conserved pathway responsible for thymocyte development, activation, proliferation, differentiation and T cell functions. Several evidences suggest Notch signaling involvement in autoimmune disorders. The aim of this study was to investigate the correlation of Notch1 receptor expression in T lymphocytes with disease progression. Twenty-two Thai SLE patients and eleven healthy controls were recruited for the study. Notch1 expression in PHA-stimulated T lymphocytes of SLE patients that indicated significantly defective regulation of Notch1 in activated T lymphocytes of SLE patients with active stage (p=0.025) while stimulated T lymphocytes of SLE patients with inactive stage were indifferent expression of Notch1 compared with healthy controls that quantified by real-time RT-PCR. It was confirmed by conventional RT-PCR that showed deceleration of Notch1 expression in SLE (p=0.015). As well as Notch1 protein expression, it was downregulated in active SLE compared to controls and inactive SLE (p=0.001 and 0.037, respectively). However, Hes1 that was target of Notch signaling did not reduce expression in SLE T lymphocytes. Moreover, proliferation capacity in SLE patients did not defect. These results showed converse correlation of Notch1 expression with severity of SLE. The data reveal the defective Notch1 in T cells that is possibly uncovered new factor of pathogenesis in SLE.

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Palaga, Tanapat, Nattiya Hirankarn, and Hathaipat Phuwapirom. Level of IL-17 in Thai SLE patients. Chulalongkorn University, 2009. https://doi.org/10.58837/chula.res.2009.30.

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Systemic Lupus Erythematosus (SLE) is an autoimmune disorder which affects various systems. Currently, the etiology of this disease has not been fully elucidated. One of potential causes which may play an important role is the defects in cytokine network and the functions of T lymphocytes. Previously, it was reported that SLE patients showed elevated elevated level of various cytokines such as IL-1β IL-6 IL-23. The aim of this study was to investigate the level of cytokine IL-17 which could be produced by various cell types including T lymphocytes CD4+ T lymphocytes mainly producing IL-17 form a distinct lineage called Th17. Differentiation of Th17 is under the influence IL-1β/IL-6 and IL-23. Furthermore, IL-23 also plays an important role in maintaining the phenotype of Th17. In this study, 29 SLE patients at King Chulalongkorn Memorial Hospital were recruited and were divided based on SLEDAI score which is an indicator of the severity of disease. There were 13 patients in active stages and 16 patients in inactive stages and 10 normal subjects were used as control group. First, the frequency of T lymphocytes expressing IL-23R in PBMC was analyzed. The frequency of CD4+IL-23R+ and CD8+IL-23R+T lymphocytes in PBMC from SLE patients were found to be significantly higher than those of controls, both in freshly isolated PBMC (day 0) (p=0.0025, p=0.0201 and p=0.0021 for CD4+ and p=0.0021, p=0.0032 and p=0.0008 for CD8+ for the inactive, the active and the total SLE groups in comparison with normal subjects, respectively) and PBMC receiving ex vivo stimulation by anti-CD3 and CD28 antibodies (day 3) (p=0.0057, p=0.0011 and p=0.0007 for CD4+ and p=0.0041, p=0.0101 and p=0.0019 for CD8+ for the inactive, the active and the total SLE groups in comparison with normal subjects, respectively). When the frequency of T cells which could produce IL-17 was measured, PBMC from SLE patients showed significantly lower percentages of CD4+IL-17+ T lymphocytes than those from the control group in samples from day 0 (p=0.0219 and p = 0.0197 for the inactive and the total SLE in comparison with normal subjects, respectively) but the trend reversed on day 3 when SLE patients exhibited a tendency to have higher percentage of CD4+IL-17+ T cells. In contrast, the frequency of CD8+IL-17+T cells in SLE patients was significantly higher on day 3 (p=0.0007, p=0.0007, p=0.0120 and p=0.0007 for the inactive, the active and the total SLE in comparison with normal subjects, respectively), while there was no difference on day 0. When the level of IL-17 in serum and plasma were measured by ELISA, only two samples were found to show detectable IL-17 at 5.12-6.78 pg/ml, while the level in the rest of the samples was below detectable. When IL-23 was measured in sera by ELISA, all samples showed negative results. Therefore, the expression of IL-17A was analyzed by Realtime RT-PCR and it was found that PBMC from patients showed increased, but not statistically significant, level of IL-17A, when compared with the controls. Analysis of all results obtained in this study, the correlation was found to be significant between percentages of CD4+IL-23R+, CD8+IL-23R+T lymphocytes and CD4+IL-17+, CD8+IL-17+ T lymphocytes in SLE patients. Furthermore, the percentages of CD4+IL-23R+T cells at day 3 were found to have a correlation with IL-17A expression in SLE patients. When the active patients were compared against the inactive patients for all indicators investigated in this study, no statistically significant difference was detected. Taken together, these results suggest that T lymphocytes in SLE patients increase IL-23R and IL-17 expression, which may play an important role in pathology of SLE.

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Wang, Xinrun, Tianye Li, Xuechai Bai, Yun Zhu, and Meiliang Zhang. Therapeutic prospect on umbilical cord mesenchymal stem cells in animal model with primary ovarian insufficiency: A meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2023. http://dx.doi.org/10.37766/inplasy2023.5.0075.

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Review question / Objective: Participants: experiment POI animal models; Interventions: human umbilical cord mesenchymal stem cells; Comparisons: POI animal models without hUCMSC therapy; Outcomes: estrous cycle situation, serum sex hormone level and ovarian follicle count; Studies: randomized controlled animal study; The aim of the review is to figure out whether hUCMSC can recover ovarian function in POI animal models. Condition being studied: Primary ovarian insufficiency (POI) is a syndrome characterized by reduced or absent ovarian function (hypogonadism) and elevated levels of gonadotropins, specifically luteinising hormone (LH) and follicle-stimulating hormone (FSH). Etiologies of POI are various. Genetic disorders, autoimmune diseases, iatrogenic injuries like chemotherapy and radiotherapy, and infectious diseases all contribute to the development of POI. Main manifestation of POI includes decreased ovarian function and infertility. Patients may suffer from menopausal symptoms, such as increased cardiovascular disease, decreased bone mineral density, vulvovaginal atrophy, psychological distress and so on. Current treatment of POI is limited. HRT mainly ameliorates symptoms while ART can achieve fertility in some patients but faces many challenges in clinical practice because it's hard to get satisfied oocytes. Stem cell therapy is proved to be efficient in recovering organ functions and hUCMSC is one of the easiest cell to obtain. So we think hUCMSC is promising in treating POI.

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