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Статті в журналах з теми "Autoimmune and idiopathic organic disease"
1
Keda, YM, IV Krjukova, IA Ilovaiskaia, et al. "Antibodies to pituitary surface antigens during various pituitary disease states." Journal of Endocrinology 175, no. 2 (2002): 417–23. http://dx.doi.org/10.1677/joe.0.1750417.
Повний текст джерелаАнотація:
Autoantibodies to cell surface antigens of human somatotropinoma (ASAS), human prolactinoma (ASAP) and rat adenohypophysis (ASARA) were assayed in the serum of patients with pituitary diseases associated with GH deficiency (GHD), such as pituitary dwarfism and primary empty sella syndrome (ESS), and in the serum of patients with hyperprolactinaemia of different etiologies: idiopathic hyperprolactinaemia, prolactinoma and ESS. The investigation was carried out with a cellular variant of an ELISA. Among children with GHD, the highest percentage of antibody-positive patients was found in the group with idiopathic isolated GHD (89% of ASAS(+) patients and 30% of ASARA(+) patients vs 33.3% and 0% respectively in the group with idiopathic combined pituitary hormone deficiency, and 33.3% and 9% in patients with pituitary hypoplasia associated with isolated GHD or combined pituitary hormone deficiency). Among hyperprolactinaemic patients, the highest ASAP and ASARA frequency was observed in patients with idiopathic hyperprolactinaemia (67.7% and 41.9% respectively) where it was twice as high as in the group of patients with prolactinoma. The proportion of ASAS(+) and ASARA(+) did not differ significantly between the groups of patients with ess with or without GHD. Similarly, there was no significant difference between the number of ESS ASAP(+) and ASARA(+) patients with or without hyperprolactinaemia. The data obtained suggested that autoimmune disorders may be primary, and responsible, at least in part, for pituitary dysfunction in the cases of idiopathic isolated GHD and idiopathic hyperprolactinaemia. At the same time, the autoimmune disorders in the patients with prolactinoma or ESS are probably secondary to the organic pituitary lesion and their significance in the development of the pituitary dysfunction is obscure.
2
Krug, Susanne M. "Solving the Puzzle: Molecular Research in Inflammatory Bowel Diseases." International Journal of Molecular Sciences 24, no. 17 (2023): 13389. http://dx.doi.org/10.3390/ijms241713389.
Повний текст джерелаАнотація:
Inflammatory bowel disease (IBD) encompasses chronic idiopathic relapsing and remitting gastrointestinal autoimmune diseases characterized by chronic inflammatory disorders of complex etiology, posing clinical challenges due to their often therapy-refractory nature [...]
3
Meunier, Lucy, and Dominique Larrey. "Hepatotoxicity of Drugs Used in Multiple Sclerosis, Diagnostic Challenge, and the Role of HLA Genotype Susceptibility." International Journal of Molecular Sciences 24, no. 1 (2023): 852. http://dx.doi.org/10.3390/ijms24010852.
Повний текст джерелаАнотація:
Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system and the association with other autoimmune diseases is well-documented. There are many therapeutic options for the treatment of MS. Most of the available drugs cause drug-induced liver injury (DILI) to variable extents with heterogeneous clinical and biological manifestations, including liver injury with or without signs of hypersensitivity and autoimmunity. The diagnosis of DILI may be particularly difficult because MS is frequently associated with idiopathic autoimmune hepatitis. Recent advances suggest that MS and immune-mediated DILI could be promoted by genetic factors, including HLA genotype. In addition, some of these drugs may promote hepatitis B virus reactivation. This review explores the potential hepatotoxicity of drugs used to treat MS and the criteria to distinguish DILI from idiopathic autoimmune hepatitis associated with MS. The role of susceptible genes both promoting MS and causing the hepatotoxicity of the drug used for MS treatment is also discussed.
4
Fukushima, Kiyoharu, Kazuyuki Tsujino, Shinji Futami, and Hiroshi Kida. "Natural Autoantibodies in Chronic Pulmonary Diseases." International Journal of Molecular Sciences 21, no. 3 (2020): 1138. http://dx.doi.org/10.3390/ijms21031138.
Повний текст джерелаАнотація:
In autoantibody-mediated autoimmune diseases, pathogenic autoantibodies generated by a failure of central or peripheral tolerance, have different effects mediated by a variety of mechanisms. Interestingly, even non-autoimmune chronic diseases have a set of disease-specific natural autoantibodies that are maintained for a long time. Because most of these natural autoantibodies target intracellular proteins or long non-coding RNAs, they are speculated to be non-pathological and have some important as yet unrecognized physiological functions such as debris clearance. Recently, we revealed a set of disease-specific natural autoantibodies of chronic pulmonary diseases with unknown etiology by protein arrays that enable detection of specific autoantibodies against >8000 targets. Surprisingly, some of the targeted antigens of disease-specific autoantibodies were subsequently reported by other laboratories as strongly associated with the disease, suggesting that these antigens reflect the pathology of each disease. Furthermore, some of these autoantibodies that target extracellular antigens might modify the original course of each disease. Here, we review the disease-specific natural autoantibodies of chronic pulmonary diseases, including chronic fibrosing idiopathic interstitial pneumonias, sarcoidosis, and autoimmune pulmonary alveolar proteinosis, and discuss their utility and effects.
5
Pulito-Cueto, Verónica, Fernanda Genre, Raquel López-Mejías, et al. "Endothelin-1 as a Biomarker of Idiopathic Pulmonary Fibrosis and Interstitial Lung Disease Associated with Autoimmune Diseases." International Journal of Molecular Sciences 24, no. 2 (2023): 1275. http://dx.doi.org/10.3390/ijms24021275.
Повний текст джерелаАнотація:
The aim of this study was to determine the role of endothelin-1 (ET-1), a molecule involved in multiple vascular and fibrosing abnormalities, as a biomarker of interstitial lung disease (ILD), as well as its use for the differential diagnosis between idiopathic pulmonary fibrosis (IPF) and ILD associated with autoimmune diseases (AD-ILD), using a large and well-defined cohort of patients with ILD. A total of 112 patients with IPF, 91 patients with AD-ILD (28 rheumatoid arthritis (RA), 26 systemic sclerosis, 20 idiopathic inflammatory myositis and 17 interstitial pneumonia with autoimmune features) and 44 healthy controls were included. ET-1 serum levels were determined by enzyme-linked immunosorbent assay. A significant increase in ET-1 levels was found in patients with IPF compared to controls. Likewise, AD-ILD patients also showed higher ET-1 levels than controls when the whole cohort was stratified by the type of AD. Similar ET-1 levels were found in IPF and AD-ILD patients, regardless of the underlying AD. Interestingly, increased ET-1 levels were correlated with worse lung function in IPF and RA-ILD patients. Our study supports that serum ET-1 may be useful as a biomarker of ILD, although it could not help in the differential diagnosis between IPF and AD-ILD. Moreover, ET-1 levels may be associated with ILD severity.
6
Kageyama, Reiko, Tetsuya Honda, and Yoshiki Tokura. "Acquired Idiopathic Generalized Anhidrosis (AIGA) and Its Complications: Implications for AIGA as an Autoimmune Disease." International Journal of Molecular Sciences 22, no. 16 (2021): 8389. http://dx.doi.org/10.3390/ijms22168389.
Повний текст джерелаАнотація:
Acquired idiopathic generalized anhidrosis (AIGA) is a rare disorder in which systemic anhidrosis/hypohidrosis occurs without causative dermatological, metabolic or neurological disorder. Most cases of AIGA have been reported in Asia, especially in Japan, but there have been only a few reports in Europe and the United States. Severe AIGA may result in heatstroke and can reduce quality of life due to restriction of exercise and outdoor works. AIGA is often accompanied by cholinergic urticaria (CholU), and it is thought that AIGA and CholU with anhidrosis/hypohidrosis belong to the same spectrum of the disease. However, the pathophysiology of AIGA has not yet been clarified. Decreased expression of cholinergic receptor M3 on the epithelial cells of eccrine sweat glands is often accompanied by T cell infiltration around eccrine apparatus, suggesting an immunological mechanism of disordered perspiration. AIGA is occasionally associated with various complications indicative of autoimmune disorders. The association of autoimmune complications further suggests that AIGA is an autoimmune disorder. Studies on complications may lead to a better understanding of the pathophysiology of AIGA.
7
Löfdahl, Anna, Göran Tornling, Jenny Wigén, Anna-Karin Larsson-Callerfelt, Christina Wenglén, and Gunilla Westergren-Thorsson. "Pathological Insight into 5-HT2B Receptor Activation in Fibrosing Interstitial Lung Diseases." International Journal of Molecular Sciences 22, no. 1 (2020): 225. http://dx.doi.org/10.3390/ijms22010225.
Повний текст джерелаАнотація:
Interstitial lung disease (ILD) encompasses a heterogeneous group of more than 200 conditions, of which primarily idiopathic pulmonary fibrosis (IPF), idiopathic nonspecific interstitial pneumonia, hypersensitivity pneumonitis, ILD associated with autoimmune diseases and sarcoidosis may present a progressive fibrosing (PF) phenotype. Despite different aetiology and histopathological patterns, the PF-ILDs have similarities regarding disease mechanisms with self-sustaining fibrosis, which suggests that the diseases may share common pathogenetic pathways. Previous studies show an enhanced activation of serotonergic signaling in pulmonary fibrosis, and the serotonin (5-HT)2 receptors have been implicated to have important roles in observed profibrotic actions. Our research findings in support by others, demonstrate antifibrotic effects with 5-HT2B receptor antagonists, alleviating several key events common for the fibrotic diseases such as myofibroblast differentiation and connective tissue deposition. In this review, we will address the potential role of 5-HT and in particular the 5-HT2B receptors in three PF-ILDs: ILD associated with systemic sclerosis (SSc-ILD), ILD associated with rheumatoid arthritis (RA-ILD) and IPF. Highlighting the converging pathways in these diseases discloses the 5-HT2B receptor as a potential disease target for PF-ILDs, which today have an urgent unmet need for therapeutic strategies.
8
Kim, Ji-Won, Mi-Hyun Ahn, Ju-Yang Jung, Chang-Hee Suh, and Hyoun-Ah Kim. "An Update on the Pathogenic Role of Neutrophils in Systemic Juvenile Idiopathic Arthritis and Adult-Onset Still’s Disease." International Journal of Molecular Sciences 22, no. 23 (2021): 13038. http://dx.doi.org/10.3390/ijms222313038.
Повний текст джерелаАнотація:
Neutrophils are innate immune phagocytes that play a key role in immune defense against invading pathogens. The main offensive mechanisms of neutrophils are the phagocytosis of pathogens, release of granules, and production of cytokines. The formation of neutrophil extracellular traps (NETs) has been described as a novel defense mechanism in the literature. NETs are a network of fibers assembled from chromatin deoxyribonucleic acid, histones, and neutrophil granule proteins that have the ability to kill pathogens, while they can also cause toxic effects in hosts. Activated neutrophils with NET formation stimulate autoimmune responses related to a wide range of inflammatory autoimmune diseases by exposing autoantigens in susceptible individuals. The association between increased NET formation and autoimmunity was first reported in antineutrophil cytoplasmic antibody-related vasculitis, and the role of NETs in various diseases, including systemic lupus erythematosus, rheumatoid arthritis, and psoriasis, has since been elucidated in research. Herein, we discuss the mechanistic role of neutrophils, including NETs, in the pathogenesis of systemic juvenile idiopathic arthritis (SJIA) and adult-onset Still’s disease (AOSD), and provide their clinical values as biomarkers for monitoring and prognosis.
9
Rawanduzy, Cameron A., Alexander Winkler-Schwartz, and William T. Couldwell. "Hypophysitis: Defining Histopathologic Variants and a Review of Emerging Clinical Causative Entities." International Journal of Molecular Sciences 24, no. 6 (2023): 5917. http://dx.doi.org/10.3390/ijms24065917.
Повний текст джерелаАнотація:
Inflammatory disease of the pituitary gland is known as hypophysitis. There are multiple histological subtypes, the most common being lymphocytic, and the pathogenesis is variable and diverse. Hypophysitis can be primary and idiopathic or autoimmune related, or secondary to local lesions, systemic disease, medications, and more. Although hypophysitis was previously accepted as an exceedingly rare diagnosis, a greater understanding of the disease process and new insights into possible etiologic sources have contributed to an increased frequency of recognition. This review provides an overview of hypophysitis, its causes, and detection strategies and management.
10
Engin, Muhammet Mesut Nezir, and Öner Özdemir. "Current mechanisms in the pathogenesis of lung fibrosis." Trends in Immunotherapy 7, no. 1 (2023): 2028. http://dx.doi.org/10.24294/ti.v7.i1.2028.
Повний текст джерелаАнотація:
Pulmonary fibrosis is a diverse group of lung disorders defined by varying degrees of fibrosis and inflammation in the pulmonary parenchyma. While it may be caused by a known disease, e.g., autoimmune or connective tissue disorder, drugs, hypersensitivity to inhaled organic antigens, or sarcoidosis, it also occurs to be idiopathic. When we examine the pathogenesis of lung fibrosis, we see that cellular aging plays a major role. Lung fibroblasts play an active role in the regeneration process. However, despite all the information, the pathogenesis of lung fibrosis is not clearly understood. It is not yet clear how senescent cells in the lung mingle and cause fibrosis. The pathogenesis of lung fibrosis will be understood more clearly following future studies.
Дисертації з теми "Autoimmune and idiopathic organic disease"
1
Malichin, Aikaterini. "Jouissance, écriture et nombre dans les maladies auto-immune et idiopathique : l'assomption de la métaphore subjective par l'organisme." Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCC317.
Повний текст джерелаАнотація:
La recherche clinique et bibliographique présente s’articule sur trois points et constitue l’entreprise tripartite de cette thèse doctorale. Le premier concerne l’étude proche de la théorie freudienne et de l'enseignement lacanien et du concept de phénomène psychosomatique, afin d’aborder la maladie organique auto-immune et idiopathique, la Sclérose par Plaques et la maladie de Crohn, sur deux sujets souffrants au sein d'une cure analytique. Le deuxième concerne l’investigation des objets de construction dans leur discours et de leur place occasionnée, et le troisième l’investigation de savoir s’il y a eu pause du symptôme et ratage de l’induction signifiante, c’est-à-dire échec de la métaphore subjective, ainsi que de savoir si la maladie des sujets souffrants remplit les critères du phénomène psychosomatique et si la métaphore subjective est prise en charge par l’organisme. L’analyse qualitative de l’énoncé et de l’énonciation des sujets à travers les séances se réalise avec une analyse de discours structurelle critique et une analyse de leur parole durant une période de cure dépassant les quatre ans, en faisant une comparaison avec des recherches antérieures. Nous en concluons que la maladie remplit les critères du phénomène psychosomatique et que la prise en charge de la métaphore subjective a fonctionné, confirmant ainsi nos hypothèses. Nous aboutissons également à des conclusions qui sont principalement en accord avec des recherches préalables. Enfin, nous notons l'amélioration de l'état de la santé des sujets et la stabilisation ou la disparition des récidives durant leur analyse, en parallèle avec leur traitement médical, ce qui n’avait pas été le cas auparavant, et l'appropriation ses points de la douleur et la souffrance de leur histoire de façon qu'il ne conduise pas à la voie des pathologiques pulsionnelles actes et à la décharge par l’organisme<br>The present clinical and bibliographical research is articulated on three points and constitutes the tripartite undertaking of this doctoral thesis. The first relates to the study closely the Freudian theory and the Lacanian teaching and the concept of phenomenon psychosomatic, in order to approach the auto-immune and idiopathic organic disease, the Multiple Sclerosis and the disease of Crohn, on two suffering subjects within an analytical cure. The second relates to the investigation of the objects of construction in their discourses and their caused positions, and the third the investigation of knowing if exists pause of symptom and failure of signifying induction, i. E. Failure of the subjective metaphor, as to know if the disease of the suffering subjects fills the criteria of the phenomenon psychosomatic and if is held assumption of subjective metaphor by the organism. The qualitative analysis of the enunciate and the enunciation of the subjects through the sessions is carried out with an analysis of discourses structural criticism and an analysis of their speech during one period of cure exceeding the four years, by making a comparison with former research. We conclude that the disease fills the criteria of the phenomenon psychosomatic and that the assumption of the subjective metaphor it is held by the organism, thus confirming our hypothesis. We also arrive at conclusions which are mainly in agreement with preliminary research. Finally, we note the improvement of the health of the subjects and the stabilization or the disappearance of the repetitions during their analysis, in parallel with their medical care, which that had not been observed before, and the appropriation of the points of the pain and the suffering of their history so that it does not lead to the way of pathological pulsing’s acts and the discharge by the organism
2
Liley, Albert James. "Statistical co-analysis of high-dimensional association studies." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/270628.
Повний текст джерелаАнотація:
Modern medical practice and science involve complex phenotypic definitions. Understanding patterns of association across this range of phenotypes requires co-analysis of high-dimensional association studies in order to characterise shared and distinct elements. In this thesis I address several problems in this area, with a general linking aim of making more efficient use of available data. The main application of these methods is in the analysis of genome-wide association studies (GWAS) and similar studies. Firstly, I developed methodology for a Bayesian conditional false discovery rate (cFDR) for levering GWAS results using summary statistics from a related disease. I extended an existing method to enable a shared control design, increasing power and applicability, and developed an approximate bound on false-discovery rate (FDR) for the procedure. Using the new method I identified several new variant-disease associations. I then developed a second application of shared control design in the context of study replication, enabling improvement in power at the cost of changing the spectrum of sensitivity to systematic errors in study cohorts. This has application in studies on rare diseases or in between-case analyses. I then developed a method for partially characterising heterogeneity within a disease by modelling the bivariate distribution of case-control and within-case effect sizes. Using an adaptation of a likelihood-ratio test, this allows an assessment to be made of whether disease heterogeneity corresponds to differences in disease pathology. I applied this method to a range of simulated and real datasets, enabling insight into the cause of heterogeneity in autoantibody positivity in type 1 diabetes (T1D). Finally, I investigated the relation of subtypes of juvenile idiopathic arthritis (JIA) to adult diseases, using modified genetic risk scores and linear discriminants in a penalised regression framework. The contribution of this thesis is in a range of methodological developments in the analysis of high-dimensional association study comparison. Methods such as these will have wide application in the analysis of GWAS and similar areas, particularly in the development of stratified medicine.
3
Alves, André Oliveira. "Polimiosite - Fisiopatologia e Terapêutica." Master's thesis, 2018. http://hdl.handle.net/10316/84581.
Повний текст джерелаАнотація:
Relatório de Estágio do Mestrado Integrado em Ciências Farmacêuticas apresentado à Faculdade de Farmácia<br>A Polimiosite é uma doença que se inclui no grupo das Miopatias Inflamatórias Idiopáticase cuja etiologia continua desconhecida até ao momento. Contudo, a presença de anticorpose linfócitos T nos músculos, acompanhada por respostas positivas à terapêutica imunológica,constituem evidência de que podemos estar perante uma doença autoimune.As vias imunitárias e não imunitárias são a base do estudo da Polimiosite, sendo que aevolução destes conceitos foi crucial para uma melhor compreensão e distinção entre asdiferentes Miopatias Inflamatórias Idiopáticas.Apesar de nem sempre ser detetada morte ou degeneração celular, a nível muscular, éeste o processo que está na origem da fraqueza e diminuição do desempenho muscularcaraterísticas desta doença, sendo por isso, o primeiro alvo de estudo em caso de suspeita amesma.Ao longo dos anos foram vários os avanços ao nível do diagnóstico e terapêutica, de talforma que, ao exame físico inicial, indicativo da progressão da fraqueza muscular, foramacrescentados outros critérios de diagnóstico, tais como os níveis séricos das enzimasmusculares, características da distrofia muscular, presença de anticorpos específicos da mioseno soro e, por fim, a biópsia muscular, peça fundamental na distinção entre a Polimiosite e asrestantes Miopatias Inflamatórias Idiopáticas.A base do tratamento da Polimiosite continua a ser o reforço e eliminação da inflamaçãomuscular, em que o tratamento de primeira linha são os corticosteroides. No entanto, novasalternativas terapêuticas têm surgido, tais como a utilização de agentes imunossupressores e,mais recentemente, a bioterapia.A presente monografia consiste, assim, numa revisão da literatura sobre os estudos eavanços alcançados ao nível da fisiopatologia e terapêutica da Polimiosite, doença muito poucoconhecida atualmente.<br>Polymyositis is a disease included in the group of the Idiopathic Inflammatory Myopathiesand whose etiology remains unknown, so far. However, the presence of antibodies and Tlymphocytes in the muscles, accompanied by positive responses to the immunological therapy,evidence that this might be an autoimmune disease.The immune and non-immune pathways are the basis of the study of Polymyositis, beingthat the evolution of these concepts was crucial for a better understanding and distinctionbetween the different Idiopathic Inflammatory Myopathies.Although death or cell degeneration are not always detected at the muscular level, theyconstitute the source of weakness and decrease of muscular performance, characteristics ofthis disease, being therefore the first target of study in case of suspicion.Over the years there have been several advances in diagnosis and therapy, in such a waythat the initial physical examination, indicative of the progression of muscle weakness, is nowcomplemented by other diagnostic criteria, such as serum levels of muscle enzymes, musculardystrophy, the presence of myositis specific antibodies in the serum and, finally, muscle biopsy,a key element in the distinction between Polymyositis and the remaining IdiopathicInflammatory Myopathies.The basis for Polymyositis treatment continues to be the strengthening and eliminationof muscle inflammation, where the first treatment line are the corticosteroids. However, newtherapeutic alternatives have emerged, such as the use of immunosuppressive agents and,more recently, biotherapy.The present monography consists in a review of the literature on the studies and advancesachieved in the pathophysiology and therapeutics of Polymyositis, a disease that remains littleknown nowadays.
Книги з теми "Autoimmune and idiopathic organic disease"
1
Bending, David, Kiran Nistala, and Lucy R. Wedderburn. Pathogenesis of juvenile idiopathic arthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0060.
Повний текст джерелаАнотація:
Although the term juvenile idiopathic arthritis (JIA) encompasses a heterogeneous group of diseases, they all share a common pathological hallmark: inflammation of the synovium. Highly activated T cells, monocytes, and neutrophils are attracted to the joint and secrete mediators that not only perpetuate inflammation but also may attenuate immune regulation. In the oligoarticular and polyarticular forms of JIA, which are thought to be autoimmune conditions, dysregulated adaptive immunity is a likely factor in disease pathogenesis; the nature of the interactions between T effector (Teff) cells and T regulatory cells (Treg) is probably a key factor in controlling disease progression. Factors that affect the frequency and function of Tregs and/or the sensitivity of Teffs to mechanisms of immune suppression will therefore impact on the disease course. In the systemic form of JIA, however, dysregulation of innate immune pathways appears more central to disease pathogenesis resulting in augmented levels of interleukins IL-1β, IL-6, and IL-18. In the end, a final, common pathological pathway in JIA is the activation of monocytes and neutrophils, which are the principal mediators of joint inflammation and damage. This is supported by the fact that the therapies that have targeted innate cytokine pathways have shown greater success in the treatment of JIA.
2
Graham, Andrew. Neurological dementias. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0037.
Повний текст джерелаАнотація:
Dementia in old age is usually due to Alzheimer’s disease, cerebrovascular disease, or mixed pathology. Dementia due to other neurological disorders is uncommon, but important to recognise because management may be very different to that in primary or vascular dementia. This chapter surveys five neurological conditions that may present with dementia in later life: idiopathic normal pressure hydrocephalus (INPH); Huntington’s disease (HD); multiple sclerosis (MS); autoimmune limbic encephalitis (LE); and prion disease. For each disorder the epidemiology, clinical features, investigations & treatment are reviewed, with examples of the characteristic brain imaging changes. Accurate diagnosis of these conditions can be challenging even for physicians with a special interest in dementia, and often requires a neurological referral.
3
Parkes, Joanna E., Simon Rothwell, and Janine A. Lamb. Aetiology and pathogenesis. Edited by Hector Chinoy and Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0003.
Повний текст джерелаАнотація:
The aetiology and pathogenesis of idiopathic inflammatory myopathies (IIM) is poorly understood; IIM are thought to result from exposure to environmental factors in genetically susceptible individuals. Both innate and adaptive immune responses are involved in IIM, and there is increasing evidence that non-inflammatory mechanisms play an important role in disease pathology. Several environmental risk factors, including infectious agents, ultraviolet radiation, cigarette smoking, and exposure to statins, have been implicated. Genetic studies have identified the major histocompatibility complex as the most strongly associated region, while recent large scale genome-wide studies have implicated genes that commonly regulate the adaptive immune response, which overlap with other seropositive autoimmune diseases. Integrating data across these various fields should facilitate refined models of disease pathogenesis.
4
Steensma, David P. Benign Hematology. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0294.
Повний текст джерелаАнотація:
The major forms of benign hematologic conditions are anemia, neutropenia, transfusion reactions, Gaucher disease, and porphyria. Anemia is a sign of disease rather than a disease itself. Anemia results from 1 or more of 3 pathologic mechanisms: inadequate production of red blood cells (RBCs) by the bone marrow, blood loss, or premature destruction of RBCs. The major causes of neutropenia include hematologic neoplasm, metastatic neoplasm involving the marrow, irradiation, vitamin B12 deficiency and folate deficiency, drugs, infections, congenital or acquired primary disorders of hematopoiesis, autoimmune neutropenia, hypersplenism, hemodilution, and benign idiopathic neutropenia. The porphyrias are enzyme disorders that are autosomal dominant with low disease penetrance, except for congenital erythropoietic porphyria, which is autosomal recessive, and porphyria cutanea tarda, which may be acquired and is associated with hepatitis C and hemochromatosis.
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Forsyth, Rob, and Richard Newton. Specific conditions. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198784449.003.0004.
Повний текст джерелаАнотація:
This chapter adopts a systematic approach to common diagnoses in paediatric neurology, aetiologies, management to include investigation and treatment, and outcome. For each condition current knowledge on cause and underlying biology is summarized. A rational approach to investigation and treatment is summarized for each topic. These include: acquired brain injury; autoimmune and autoinflammatory disease of the CNS; cerebral palsy and neurodisability which covers feeding, communication, special senses, and respiratory disease; demyelinating disease; epilepsy including its impact on daily life; non-epileptic paroxysmal phenomena; functional illness, illness behaviour; headache; hydrocephalus; spina bifida and related disorders; idiopathic intracranial hypertension; infection of the CNS; congenital infection; mitochondrial disease; movement disorders; neuromuscular disease which covers neuropathy, anterior horn cell disease, and myasthenic syndromes; neurocutaneous syndromes; neurodegenerative conditions; late presentations of metabolic disease; neurotransmitter disorders; sleep disorders; stroke and intracerebral haemorrhage; tumours of the CNS; and vitamin-responsive disorders.
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Limaye, Vidya Sadanand. Overview and epidemiology. Edited by Hector Chinoy and Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0001.
Повний текст джерелаАнотація:
The term idiopathic inflammatory myopathies (IIM) encompasses a heterogeneous group of muscle-dominant systemic autoimmune syndromes, including polymyositis (PM), dermatomyositis (DM), sporadic inclusion body myositis (sIBM), and immune-mediated necrotizing myopathy (IMNM). The reported incidence of IIM ranges from 5 to 10 × 10–6. Patients with PM, DM, and IMNM characteristically present with the insidious onset of symmetric proximal weakness, while in sIBM the weakness can be asymmetric, and involve the distal upper limbs and quadriceps. Dermatomyositis may also be accompanied by a range of cutaneous manifestations. Raised serum creatine kinase levels, the presence of characteristic myositis-specific antibodies, myopathic triad on electromyography, and myoedema on muscle magnetic resonance imaging are helpful in supporting a diagnosis of IIM. Muscle biopsy is the definitive diagnostic test and serves to distinguish subsets of disease, which each have characteristic histopathological changes reflecting underlying differences in pathogenesis. Mortality remains elevated in patients with IIM, despite the advent of immunosuppressive therapies.
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Clunie, Gavin P. R., Nick Wilkinson, Elena Nikiphorou, and Deepak Jadon, eds. Oxford Handbook of Rheumatology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198728252.001.0001.
Повний текст джерелаАнотація:
The Oxford Handbook of Rheumatology, 4th edition, has been expanded and improved to incorporate paediatric and adolescent rheumatology. The format of the book is retained. The first four chapters offer a pragmatic guide to evaluating rheumatic and musculoskeletal diseases, showing how a differential diagnosis can be formed on the basis of symptoms, examination, and investigation findings, both for regional musculoskeletal and systemic generalized conditions. Part II comprises chapters on all the major rheumatic and bone diseases and autoimmune connective tissue diseases, such as rheumatoid arthritis, osteoarthritis, spondyloarthritis, systemic lupus erythematosus (lupus), crystal-induced musculoskeletal disease, juvenile idiopathic arthritis, antiphospholipid syndrome, Sjögren’s syndrome, osteoporosis, vasculitis, spinal disorders and back pain, and chronic pain syndromes, as well as new chapters on rare diseases and hereditary disorders. Part II includes chapters on drugs used in rheumatology practice, glucocorticoid injection therapy, and rheumatological emergencies. All chapters are updated to include details on paediatric and adolescent rheumatology, dealt with fairly cursorily in previous Handbook editions. Greatly expanded chapters are included on drugs used in rheumatology, pain syndromes, and the presentation of paediatric and adolescent disease.
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Chinoy, Hector, and Robert G. Cooper. Polymyositis and dermatomyositis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0124.
Повний текст джерелаАнотація:
Polymyositis (PM), dermatomyositis (DM), and inclusion body myositis (IBM) form part of the idiopathic inflammatory myopathies (IIM), a heterogeneous group of rare autoimmune diseases characterized by an acquired proximal muscle weakness, raised muscle enzymes (including creatine kinase), inflammatory cell infiltrates in muscle biopsy tissue, electrophysiological abnormalities, and presence of circulating myositis-specific/myositis-associated autoantibodies. The underlying aetiology of IIM is poorly understood, but likely involves interactions between environmental and genetic risk factors. Myositis may also manifest in association with other connective tissue disorders. The predominant clinical presentation of IIM is skeletal muscle weakness, but many extramuscular features can also occur. Access to good neuropathological support is essential in securing an accurate IIM diagnosis and excluding non-inflammatory myopathies, although IBM is often difficult to distinguish from PM. Antibody testing can help define IIM clinical subtypes, including cancer-associated myositis, predict prognosis, and help in optimizing treatment decisions. MRI can be invaluable for differentiating disease activity from damage, and detecting treatment-induced interval changes. Therapeutic effectiveness of new and existing treatments (where the evidence base remains poor) depends on making a prompt diagnosis and initiating early and appropriately aggressive treatment to prevent establishment of muscle damage. This chapter attempts to summarize the salient features of IIM and update the reader about currently used diagnostics and treatment paradigms in this rare and understudied disease.
Частини книг з теми "Autoimmune and idiopathic organic disease"
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Gartler, Stanley M., R. Scott Hansen, Vinzenz Oji, et al. "Idiopathic Autoimmune Hamolytic." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_7096.
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Froehlich, Stephan J., Carlo A. Lackerbauer, Guenter Rudolph, et al. "Neuromyotonia, Autoimmune and Idiopathic." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_1276.
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Pretis, Nicolo’ de, Yan Bi, Saurabh Mukewar, and Suresh Chari. "Steroid-Responsive Chronic Pancreatitides: Autoimmune Pancreatitis and Idiopathic Duct-Centric Chronic Pancreatitis." In Pancreas and Biliary Disease. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28089-9_5.
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Brodehl, Johannes, and P. F. Hoyer. "Ciclosporin Treatment of Idiopathic Nephrotic Syndrome in Children (Minimal Change Disease and Focal Segmental Glomerulosclerosis)." In Ciclosporin in Autoimmune Diseases. Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70607-3_64.
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Corbridge, Rogan, and Nicholas Steventon. "The inner ear." In Oxford Handbook of ENT and Head and Neck Surgery. Oxford University Press, 2009. http://dx.doi.org/10.1093/med/9780199550791.003.07.
Повний текст джерелаАнотація:
Structure and function of the inner ear 110 Hearing loss 114 Presbyacusis 116 Noise-induced hearing loss 118 Idiopathic sudden hearing loss 120 Autoimmune ear disease 122 Ototoxicity 124 Hereditary hearing loss 126 Syndromic hearing loss I 128 Syndromic hearing loss II 130 Non-organic hearing loss (NOHL) ...
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Lundberg, Ingrid E., Hector Chinoy, and Robert Cooper. "Inflammatory myopathies." In Oxford Textbook of Medicine, edited by Richard A. Watts. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0457.
Повний текст джерелаАнотація:
The idiopathic inflammatory myopathies are a heterogenous group of disorders characterized by muscle weakness, inflammation in muscle tissue, and with frequent extramuscular involvement. Autoantibodies are common, supporting the notion of these disorders being autoimmune. Typically, inflammatory cell infiltrates are found in muscle biopsies. Other organs are frequently involved such as skin, lungs, joints, gastrointestinal tract, and the heart. These heterogenous disorders can be subclassified based on clinical and histopathological features, or by autoantibody specificities. The idiopathic inflammatory myopathies have traditionally comprised polymyositis (PM), dermatomyositis (DM), juvenile DM, PM/DM overlapping with another connective tissue disease, and inclusion body myositis. More recently a subgroup with similar clinical features but with no or scarce inflammation and with pronounced muscle fibre necrosis has been identified and termed immune-mediated necrotizing myopathy.
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Gelbman, Brian, and Ronald G. Crystal. "Idiopathic and Autoimmune Interstitial Lung Disease." In The Autoimmune Diseases. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-812102-3.00067-1.
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Gelbman, Brian, and Ronald G. Crystal. "Idiopathic and Autoimmune Interstitial Lung Disease." In The Autoimmune Diseases. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-384929-8.00074-5.
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Spickett, Gavin P. "Autoimmune eye disease." In Oxford Handbook of Clinical Immunology and Allergy. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199603244.003.0011.
Повний текст джерелаАнотація:
Overview Uveitis Tubulointerstitial nephritis and uveitis (TINU) Vogt–Koyanagi–Harada disease (VKH) Cancer-associated retinopathy and uveitis Birdshot retinopathy Scleritis Ocular cicatricial pemphigoid Sympathetic ophthalmitis Idiopathic orbital inflammation (orbital pseudo-tumour) The eye has a number of interesting immunological properties which alter the propensity for immune-mediated disease, including the curious feature that antigen injected into the anterior chamber induces tolerance rather than immunity. In addition, the eye has no true lymphatics, relatively poor vascularity, and, as the retina is an extension of the CNS, there is a blood–retinal barrier which limits passage of molecules in either direction. Ocular involvement is a common feature of many connective tissue and vasculitic diseases....
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Oyama, Yu, Walter G. Barr, and Richard K. Burt. "Autologous Hematopoietic Stem Cell Transplantation for Idiopathic Inflammatory Myositis." In Stem Cell Therapy for Autoimmune Disease. CRC Press, 2019. http://dx.doi.org/10.1201/9780367813895-52.
Повний текст джерелаТези доповідей конференцій з теми "Autoimmune and idiopathic organic disease"
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Romagnoli, Micaela, Carlotta Nannini, Sara Piciucchi, et al. "Idiopathic Nonspecific Interstitial Pneumonia (NSIP): Early Lung Manifestation Of An Autoimmune Disease?" In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6002.
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Hayton, Conal, Dayle Terrington, Waqar Ahmed, et al. "Exhaled volatile organic compounds in idiopathic pulmonary fibrosis and disease progression." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.727.
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Remuzgo-Martínez, S., B. Atienza-Mateo, V. Pulito-Cueto, et al. "Endothelin-1 for the differential diagnosis between interstitial lung disease associated with autoimmune diseases and idiopathic pulmonary fibrosis." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.2310.
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Vergara, Karen, Silvana Saavedra, Felipe Reyes, Annelise Goecke, Caterina Chesta, and Sebastian Chavez. "AB1109 CHARACTERIZATION OF PATIENTS WITH INTERSTITIAL PNEUMONIA WITH AUTOIMMUNE FEATURES (IPAF) AND ITS COMPARISON WITH PATIENTS WITH SCLERODERMA-RELATED INTERSTITIAL LUNG DISEASE AND WITH IDIOPATHIC FIBROSIS." 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.7794.
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Moraes, Marianna, Fabiano Abrantes, José Luiz Pedroso, and Orlando Graziani Povoas Barsottini. "Etiological evaluation of hypertrophic pachymeningitis in a tertiary general neurology department." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.665.
Повний текст джерелаАнотація:
Introduction: Hypertrophic pachymeningitis (HP) is the thickening of the cranial or spinal dura. This process causes cranial nerve palsy, vascular events (stroke and venous thrombosis), and intracranial hypertension. The diagnosis of HP is disclosed by magnetic resonance imaging, showing dural thickening and contrast enhancement. Several etiologies are possible for HP, but infection and autoimmune diseases are the most frequent. The gold standard for diagnosis is the dural biopsy, but cerebrospinal fluid (CSF), blood and other tissues analysis are essential guides to the correct diagnosis. A quick diagnosis is crucial to early treatment and this avoid permanent deficits. However, the diagnostic approach can be a complicated process, which could delay the beginning of the treatment. Objectives: This study aims to analyze the population of patients with magnetic resonance imaging showing HP. Methods: Its epidemiological, clinical and radiological aspects was evaluated through a retrospective and descriptive study to elucidate the etiological diagnosis. Results: A total of 45 patients was included with some different etiologies: granulomatosis with polyangiitis (n = 7); idiopathic (n = 14); probable neurosarcoidosis (n = 9); seronegative rheumatoid arthritis (n = 1); neurotuberculosis (n = 1); plaque meningioma (n = 2); IgG4 related disease (n = 4); Inflammatory myofibloblastic tumor (n = 1); neurosyphilis (n = 1); diffuse B-cell lymphoma (n = 1); Erdheim-Chester disease (n = 1); iatrogenic secondary to radiotherapy (n = 1) and cryopyronopathy (n = 1). Conclusion: The diversity of etiologies found in this study demonstrates the complexity of HP and how important it is to follow a diagnostic algorithm in order to institute appropriate and early therapy for a better clinical outcome for patients.
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Santos, João Vitor Ribeiro dos, Mariana Spitz, and Ana Carolina Andorinho. "Stroke secondary to thrombotic microangiopathy." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.300.
Повний текст джерелаАнотація:
Introduction: Thrombotic thrombocytopenic purpura (TTP) is a hematological disease resulting from the ADAMTS 13 plasmatic protein deficit. It can be congenital or sporadic, and is usually autoimmune. Pathological platelet adhesion occurs, leading to microthrombi in capillary and arterial circulation, microangiopathic anemia and ischemia. The clinical picture includes thrombocytopenia, renal dysfunction, fluctuating neurological symptoms, microangiopathic hemolytic anemia, and fever. Methods: Case report of a 51-year-old male hypertensive patient, diagnosed with idiopathic thrombocytopenic purpura (ITP) 10 years ago and submitted to splenectomy 5 years ago, who developed acute cholecystitis. He underwent urgent colecistectomy, and on the fourth postoperative day presented sudden space and time disorientation, transcortical motor aphasia and right faciobrachial paresis, with ipsilateral Babinski and Hoffman signs. Results: Brain CT showed left frontoparietal hypodensity. During hospitalization, there was worsening of renal function, increased LDH, and thrombocytopenia. Hematoscopy identified signs of intravascular hemolysis (erythrocyte fragmentation, reticulocytosis, helmet erythrocytes). Direct Coombs was negative. There was no history of heparin use. TTP was diagnosed, and fresh frozen plasma and prednisone 1mg/kg were prescribed. There was resolution of thrombotic microangiopathy, with subsequent increase of platelet levels, decreased LDH and improved hematoscopy. Conclusions: This case illustrates a rare cause of stroke and an unusual association of two hematological conditions: ITP and TTP. The treatment of TTP consists of replacement of deficient ADAMTS13 protein through plasmapheresis or fresh frozen plasma. The use of immunosuppressants is also associated, initially with glucocorticoids, followed by rituximab or splenectomy in order to prevent recurrences.
Звіти організацій з теми "Autoimmune and idiopathic organic disease"
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Zhang, Yingrong, Sanchun Tan, Jieyu Wang, et al. A scoping review protocol of systematic reviews and meta-analyses to acupuncture for the treatment of peripheral facial paralysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.3.0084.
Повний текст джерелаАнотація:
Review question / Objective: To conduct a systematic comprehensive review for Acupuncture treatment of peripheral facial paralysis and to evaluate the efficacy and safety of acupuncture therapy for peripheral facial paralysis. Condition being studied: Peripheral facial paralysis, known as peripheral facial never palsy, includes Bell’s palsy and Ramsay Hunt syndrome.Any medical conditions such as infection, malignancy and autoimmune issues can result it. Idiopathic Bell's palsy is the most common disease causing peripheral facial nerve palsy, which clinical features include unilateral weakness of the facial nerve, hyperacusis, dysgeusia, dry eye or uncontrollable tears, but the etiology of it is unclear. Ramsay Hunt syndrome, less common than Bell’s palsy, is often caused by herpes zoster virus, which clinical features are unilateral weakness of face with ear herpes, tinnitus and dizziness. Facial paralysis patients with ear herpes can be diagnosed with Ramsay Hunt syndrome. Peripheral facial paralysis not only result the dyskinesia of facial muscles but also affect the quality of patient’s life.There are lot of evidence shows that Acupuncture can be used in any period and any kind of peripheral facial paralysis.However, we still lack systematic reviews to assess the efficacy and safety of acupuncture therapy. As a result, we conduct a scoping review of systematic reviews and meta-analyses to address this gap.