Academic literature on the topic 'Autoimmune system; Muscle'
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Journal articles on the topic "Autoimmune system; Muscle"
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Sweeney, Michael. "Autoimmune Neurologic Diseases in Children." Seminars in Neurology 38, no. 03 (June 2018): 355–70. http://dx.doi.org/10.1055/s-0038-1660520.
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AbstractAutoimmune diseases of the nervous system in children are composed of a heterogeneous group of rare disorders that can affect the central or peripheral nervous system at any level. Presentations may occur in children of any age and are typically acute or subacute in onset. Consideration of an autoimmune process as the etiology of neurologic diseases in children is important, as it may lead to early initiation of immunotherapy and an improvement in long-term neurologic outcomes. The developing nervous and immune systems in children create unique challenges in diagnosis and treatment of these rare diseases. In this review, autoimmune diseases affecting the brain, spinal cord, nerve roots, peripheral nerves, neuromuscular junction, and muscle in children are described.
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Zhang, Tan, Xin Feng, Bo Feng, Juan Dong, Karen Haas, Barbara M. Nicklas, Osvaldo Delbono, and Stephen Kritchevsky. "CARDIAC TROPONIN T MEDIATED AUTOIMMUNE RESPONSE AND ITS ROLE IN SKELETAL MUSCLE AGING." Innovation in Aging 3, Supplement_1 (November 2019): S882. http://dx.doi.org/10.1093/geroni/igz038.3231.
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Abstract Cardiac troponin T (cTnT), a key component of contractile machinery essential for muscle contraction, is also expressed in skeletal muscle under certain conditions (e.g. neuromuscular diseases and aging). We have reported that skeletal muscle cTnT regulates neuromuscular junction denervation preferentially in fast skeletal muscle of old mice. Here, we further report that cTnT is also enriched within some myofibers, and/or along microvascular walls in old mice fast skeletal muscle. Strikingly, immunoglobulin G (IgG), together with markers of complement system activation, cell death (necroptosis or apoptosis), and macrophage infiltration, were all found to be co-localized with cTnT and IgG in those areas. In addition, elevated cTnT and IgG are associated with lower dystrophin expression on muscle fiber membrane, lower muscle capillary density, and reduced muscle performance (wire hanging test). Using purified recombinant TnT proteins, we confirmed that only cTnT, but not slow or fast skeletal muscle TnT1 or TnT3, was detected by immunoblot using sera from old (but not young) mice with pre-determined elevated cTnT and IgG in their skeletal muscle, indicating the existence of anti-cTnT autoantibodies in sera (previously found in human blood) and skeletal muscle of old mice. Immunoblotting further revealed that the age related changes in skeletaI muscle cTnT and IgG are more prominent in fast skeletal muscle than in slow. Importantly, elevated cTnT and IgG were also detected in skeletal muscles from 4 older adults (65-70 yrs, IMFIT). Our finding suggests a novel autoimmune mechanism mediated by cTnT that underlies age related skeletal muscle abnormalities and dysfunction.
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Mathis, Stéphane, Laurent Magy, Philippe Corcia, Karima Ghorab, Laurence Richard, Jonathan Ciron, Mathilde Duchesne, and Jean-Michel Vallat. "Simultaneous Combined Myositis, Inflammatory Polyneuropathy, and Overlap Myasthenic Syndrome." Case Reports in Neurological Medicine 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/6108234.
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Immune-mediated neuromuscular disorders include pathologies of the peripheral nervous system, neuromuscular junction, and muscles. If overlap syndromes (or the association of almost two autoimmune disorders) are recognized, the simultaneous occurrence of several autoimmune neuromuscular disorders is rare. We describe two patients presenting the simultaneous occurrence of inflammatory neuropathy, myositis, and myasthenia gravis (with positive acetylcholine receptor antibodies). For each patient, we carried out a pathological analysis (nerve and muscle) and an electrophysiological study (and follow-up). To our knowledge, this is the first description of such a triple immune-mediated neuromuscular syndrome. We compared our observations with a few other cases of simultaneous diagnosis of two inflammatory neuromuscular disorders.
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Jacob, Saiju. "Myasthenia Gravis – A Review of Current Therapeutic Options." European Neurological Review 13, no. 2 (2018): 86. http://dx.doi.org/10.17925/enr.2018.13.2.86.
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Myasthenia gravis (MG) is an autoimmune disorder that leads to skeletal muscle weakness and fatigue. The autoimmune attack is caused by autoantibodies against the acetylcholine postsynaptic receptors at the neuromuscular junction of skeletal muscles. However, other antigenic targets that are components of the neuromuscular junction have also been implicated in the pathogenesis of MG. The current standard of care is immunosuppressive therapy; however, many existing therapeutic options have not been validated for use in MG in large randomised controlled trials. Furthermore, around 10% of patients with generalised MG are refractory to treatment. The complement system is involved in numerous inflammatory, neurodegenerative and autoimmune diseases, and is a key factor in the pathogenesis of acetylcholine receptor antibody-related MG. Targeting complement and other components involved in the underlying pathogenesis of the disease may provide useful treatment options, particularly for refractory patients.
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Amaya-Amaya, Jenny, Laura Montoya-Sánchez, and Adriana Rojas-Villarraga. "Cardiovascular Involvement in Autoimmune Diseases." BioMed Research International 2014 (2014): 1–31. http://dx.doi.org/10.1155/2014/367359.
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Autoimmune diseases (AD) represent a broad spectrum of chronic conditions that may afflict specific target organs or multiple systems with a significant burden on quality of life. These conditions have common mechanisms including genetic and epigenetics factors, gender disparity, environmental triggers, pathophysiological abnormalities, and certain subphenotypes. Atherosclerosis (AT) was once considered to be a degenerative disease that was an inevitable consequence of aging. However, research in the last three decades has shown that AT is not degenerative or inevitable. It is an autoimmune-inflammatory disease associated with infectious and inflammatory factors characterized by lipoprotein metabolism alteration that leads to immune system activation with the consequent proliferation of smooth muscle cells, narrowing arteries, and atheroma formation. Both humoral and cellular immune mechanisms have been proposed to participate in the onset and progression of AT. Several risk factors, known as classic risk factors, have been described. Interestingly, the excessive cardiovascular events observed in patients with ADs are not fully explained by these factors. Several novel risk factors contribute to the development of premature vascular damage. In this review, we discuss our current understanding of how traditional and nontraditional risk factors contribute to pathogenesis of CVD in AD.
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Troshina, Ekaterina A., Elena A. Panfilova, and Taras S. Panevin. "Autoimmune polyglandular disorders in myotonic dystrophy." Problems of Endocrinology 65, no. 3 (September 12, 2019): 155–60. http://dx.doi.org/10.14341/probl9775.
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Myotonic dystrophy (MD) is the most common muscle disorder in adults. MD is a hereditary disease with an autosomal dominant mode of inheritance, almost 100% penetrance and pronounced clinical polymorphism. The mechanism for the development of the disease is that a mutation of the DMPK (dystrophia myotonica protein kinase) gene disrupts the normal metabolism of RNA, which leads to a defect in the maturation and translation of mRNA. The disorder in the DMPK gene affects not only striated musculature, but also smooth myocytes and cardiomyocytes. The main clinical symptom that distinguishes MD from others is a spontaneous or provoked inability to relax muscles (myotonia phenomenon). Endocrine disorders arising from type 1 MD (MD1) with a higher than average frequency in the population include hypergonadotropic hypogonadism, impaired glucose tolerance with hyperinsulinism, and insulin resistance. Thyroid function may remain normal, although many cases of autoimmune thyroiditis resulting in hypothyroidism, as well as Graves’ disease, have been described. A description is given of a patient suffering from MD1 with a number of endocrine disorders, including hypergonadotropic hypogonadism, autoimmune thyroid disease, hyperinsulinism, and also impaired calcium-phosphorus metabolism. Important features are the absence of any significant complaints from the muscular system in the presence of an increase in creatine phosphokinase (CPK), which is characteristic of this disease, as well as the temporal dynamics of thyroid status and the nature of the autoimmune thyroid disease.
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Shidlovskyi, V. O., O. V. Shidlovskyi, and V. V. Kravtsiv. "The effect of autoimmune thyroiditis on the organs and systems of the body (a literature review)." INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine) 17, no. 2 (May 11, 2021): 145–54. http://dx.doi.org/10.22141/2224-0721.17.2.2021.230569.
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Background. In recent years, scientific reports on the effects of autoimmune thyroiditis on the body have been published. They concern separate organs and systems that does not allow receiving the general picture of pathological reactions of the body to autoimmune aggression. The review analyzes the literature sources about the pathological significance of autoimmune thyroiditis for the body as a whole. Sources of information. The sources of information were reports in domestic and, mainly, foreign periodicals on general medicine, pathophysiology, immunology, and endocrinology. Synthesis of evidence. The effect of autoimmune thyroiditis and hypothyroidism on the function of body systems is considered from the standpoint of the interaction of both autoimmune thyroiditis on organs and systems and body systems on the thyroid gland, in particular on the development of its autoimmune pathology. In general, autoimmune thyroiditis and its consequence — hypothyroidism affect all organs and systems of the body without exception by reducing the level of metabolic processes and the accumulation of glucosaminoglycans, mainly glucuronic acid in the tissues of the body. As a result, interstitial edema develops, mainly in muscle tissue, including the muscular layer of the hollow organs of the digestive tract. The clinical symptoms of such lesions depend on the disease severity and the depth of metabolic disorders and have significant individual differences. They concern to all the systems and organs of the body. The effects on the cardiovascular and reproductive systems, musculoskeletal system, gastrointestinal tract are the most significant for health. Conclusions. The mentioned data expand knowledge and create a holistic view of autoimmune thyroiditis not as a local autoimmune disease of the thyroid gland but as a local manifestation of general autoimmune disease of the body.
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Pejin, Radoslav, Edita Stokic, Mile Novkovic, Sofija Banic-Horvat, and Milan Cvijanovic. "Autoimmune polyglandular syndrome, type 2 associated with myasthenia gravis." Vojnosanitetski pregled 69, no. 4 (2012): 358–62. http://dx.doi.org/10.2298/vsp1204358p.
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Introduction. Autoimmune polyglandular syndrome type 2 is defined as adrenal insufficiency associated with autoimmune primary hypothyroidism and/or with autoimmune type 1 diabetes mellitus, but very rare with myasthenia gravis. Case report. We presented a case of an autoimmune polyglandular syndrome, type 2 associated with myasthenia gravis. A 49-year-old female with symptoms of muscle weakness and low serum levels of cortisol and aldosterone was already diagnosed with primary adrenal insufficiency. Primary hypothyroidism was identified with low values of free thyroxine 4 (FT4) and raised values of thyroidstumulating hormone (TSH). The immune system as a cause of hypothyroidism was confirmed by the presence of thyroid antibodies to peroxidase and TSH receptors. Myasthenia gravis was diagnosed on the basis of a typical clinical feature, positive diagnostic tests and an increased titre of antibodies against the acetylcholine receptors. It was not possible to confirm the immune nature of adrenal insufficiency by the presence of antibodies to 21- hydroxylase. The normal morphological finding of the adrenal glands was an indirect confirmation of the condition as well as the absence of other diseases that might have led to adrenal insufficiency and low levels of both serum cortisol and aldosterone. Hormone replacement therapy, anticholinergic therapy and corticosteroid therapy for myasthenia gravis improved the patient?s general state of health and muscle weakness. Conclusion. This case report indicates a need to examine each patient with an autoimmune disease carefully as this condition may be associated with another autoimmune diseases.
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Hristov, K. "OBESITY, INFLAMMATION, AND T-CELL METABOLISM." Trakia Journal of Sciences 17, no. 4 (2019): 392–98. http://dx.doi.org/10.15547/tjs.2019.04.017.
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Aim: The overview of the interdependence of the immune system and the system metabolism. Regulation of metabolism is immunomodulatory, and targeting key cellular metabolic enzymes impacts T-cell development, altering the immune functions. Background: The diet, gastrointestinal microbiota and the balanced function of liver, adipose and muscle tissues underlie the immune ecology. Chronic inflammation (macrophage, TH1, and TH17 T-cell infiltration) associates with obesity, and the development of metabolic syndrome, cardiovascular diseases, type 2 diabetes, IBD and intestinal malignancies. While naive T-cells use beta-oxidation, TCA cycle, and mitochondrial respiration to produce ATP, activated T-cells, similarly to cancer cells, employ the Warburg’s effect to power their function. The development of T-cells depends on key metabolic regulators, like mTORC1 (TH1 and TH17 T-cells) and mTORC2 (TH2 T-cells). Inhibition of HIF1-alpha (critical for TH17 T-cells) results in the development of FOXP3+ Treg T-cells, improving autoimmune disorders. Metabolic flexibility of normal cells underlines the successful treatment of neoplastic, autoimmune and hyper-sensitivity disorders. Conclusions: The immune system influences the system metabolism, and depends on the function of adipose tissue, muscles, liver, pancreas, lungs and gastro-intestinal tract. Diet and pharmacological regulation of T-cell metabolic activity influence immune function during autoimmunity, infections, and vaccinations.
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Váncsa, Andrea, and Katalin Dankó. "Újabb adatok a myositisspecifikus és -asszociált antitestekről juvenilis és felnőttkori myositisekben." Orvosi Hetilap 157, no. 30 (July 2016): 1179–84. http://dx.doi.org/10.1556/650.2016.30404.
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Myositis, which means inflammation of the muscles, is a general term used for inflammatory myopathies. Myositis is a rare idiopathic autoimmune disease. It is believed that environmental factors such as virus, bacteria, parasites, direct injuries, drugs side effect can trigger the immune system of genetically susceptible individuals to act against muscle tissues. There are several types of myositis with the same systemic symptoms such as muscle weakness, fatigue, muscle pain and inflammation. These include dermatomyositis, juvenile dermatomyositis, inclusion-body myositis, polymyositis, orbital myositis and myositis ossificans. Juvenile and adult dermatomyositis are chronic, immune-mediated inflammatory myopathies characterized by progressive proximal muscle weakness and typical skin symptoms. The aim of the authors was to compare the symptoms, laboratory and serological findings and disease course in children and adult patients with idiopathic inflammatory myopathy. Early diagnosis and aggressive immunosuppressive treatment improve the mortality of these patients. Myositis-specific autoantibodies have predictive and prognostic values regarding the associated overlap disease, response to treatment and disease course. The authors intend to lighten the clinical and pathogenetic significance of the new target autoantigens. Orv. Hetil., 2016, 157(29), 1179–1184.
Dissertations / Theses on the topic "Autoimmune system; Muscle"
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Plested, Charles Paul. "Mechanism of action of seronegative myasthenia gravis." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301392.
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Chan, Koon-ho. "Neuronal and muscle autoantibodies in paraneoplastic neurological disorders and autoimmune myasthenia gravis." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B39557091.
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Chan, Koon-ho, and 陳灌豪. "Neuronal and muscle autoantibodies in paraneoplastic neurological disorders and autoimmune myasthenia gravis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39557091.
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Hayashi, Ana Paula Tanaka. "Eficácia e segurança da suplementação de creatina em pacientes com lúpus erimatoso sistêmico de início juvenil." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5164/tde-07022014-144017/.
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Introdução: A suplementação de creatina tem surgido na literatura como uma potencial estratégia terapêutica não farmacológica em diversas condições caracterizadas por disfunções musculares e baixa massa muscular, incluindo as doenças reumatológicas pediátricas. O objetivo deste estudo foi avaliar a eficácia e a segurança da suplementação de creatina em pacientes com lúpus eritematoso sistêmico de início juvenil (LESJ). Métodos: Trata-se de um estudo duplo-cego, crossover, balanceado e controlado por placebo. Os voluntários (n = 15) foram randomizados em duas condições que receberam creatina ou dextrose por 12 semanas, interpassadas por um período de washout de 8 semanas. A função muscular foi avaliada por testes de uma repetição máxima (1 RM), Timed-Up-And-Go, Timed-Stands e de preensão manual. Ainda, foram avaliados a composição corporal, os marcadores bioquímicos do remodelamento ósseo, a aptidão aeróbia, os parâmetros de qualidade de vida e a capacidade funcional dos voluntários. As possíveis alterações no consumo alimentar foram avaliadas por três recordatórios alimentares de 24h, enquanto o conteúdo de fosforilcreatina muscular foi avaliado por meio de espectroscopia de fósforo por ressonância magnética (31P-ERM). A segurança da intervenção foi avaliada por parâmetros laboratoriais e por clearance de 51Cr-EDTA e, por fim, os eventos adversos foram registrados durante todo o estudo. Resultados: Não houve diferença significativa no conteúdo intramuscular de fosforilcreatina entre as condições, antes e após as intervenções (creatina - Pré: 20,5 ± 2,6/ Pós: 20,4 ± 4,1; placebo - Pré: 19,8 ± 2,0/ Pós: 20,2 ± 3,2 mmol/kg peso úmido; p = 0,70 para interação entre condições). Ainda, provavelmente, como consequência do conteúdo intramuscular ter se mantido inalterado, não houve diferença significativa entre as condições para todos os parâmetros analisados (p > 0,05). Além do clearance de 51Cr-EDTA não ter sido alterado com a suplementação de creatina, nenhum efeito adverso foi observado. Conclusão: O protocolo de suplementação de creatina (0,1 g/kg/d) por 12 semanas foi bem tolerado e livre de efeitos adversos. Entretanto, a suplementação de creatina não foi eficaz no aumento do conteúdo intramuscular de fosforilcreatina, na melhora da função muscular, aptidão aeróbia, composição corporal e parâmetros de qualidade de vida em pacientes com LESJIntroduction: Creatine supplementation has emerged as a promising non-pharmacological therapeutic strategy to counteract muscle dysfunction and low lean mass in a variety of conditions, including in pediatric and rheumatic diseases. The objective of this study was to examine the efficacy and safety of creatine supplementation in childhood systemic lupus erythematosus (C-SLE). Methods: C-SLE patients with mild disease activity (n=15) received placebo or creatine supplementation in a randomized fashion using a crossover, double-blind, repeated-measures design. The subjects were assessed at baseline and after 12 weeks in each arm, interspersed by a 8-week washout period. The primary outcomes was muscle function, as assessed by a battery of tests including one-maximum repetition (1-RM) tests, the Timed-Up-And-Go test, the Timed-Stands test, and the handgrip test. Secondary outcomes included body composition, biochemical markers of bone remodeling, aerobic conditioning, quality of life, and physical capacity. Possible differences in dietary intake were assessed by three 24-h dietary recalls. Muscle phosphorylcreatine content was measured through phosphorus magnetic resonance spectroscopy (31P-MRS). The safety of the intervention was assessed by laboratory parameters and kidney function was measured by the 51Cr-EDTA clearance. Additionally, self-reported adverse events were recorded throughout the trial. Results: Intramuscular phosphorylcreatine content was not significantly different between creatine and placebo before or after the intervention (creatine - Pre: 20.5 ± 2.6, Post: 20.4 ± 4.1, placebo - Pre: 19.8 ± 2.0; Post: 20.2 ± 3.2 mmol/kg wet muscle; p = 0.70 for interaction between conditions). In addition, probably as a consequence of the lack of change in intramuscular phosphorylcreatine content, there were no significant changes between placebo and creatine for any muscle function and aerobic conditioning parameters, lean mass, fat mass, bone mass, and quality of life scores (p > 0.05). The 51Cr-EDTA clearance was not altered by creatine supplementation and no side effects were noticed. Conclusion: a 12-week creatine supplementation protocol at 0.1 g/kg/d is well tolerable and free of adverse effects but did not affect intramuscular phosphorylcreatine, muscle function, free-fat mass or quality of life in C-SLE patients with mild disease activity
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Barnes, Jill Nicole. "The effects of acute muscle damage and autoimmune disease on vascular function : the potential role of inflammation." 2009. http://hdl.handle.net/2152/6529.
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Inflammation has been implicated in the development of cardiovascular disease and a
potential underlying mechanism in the pathogenesis of impaired vascular function. Two
different but complementary approaches were utilized to determine the role of
inflammation on vascular function. First, to evaluate the effect of acute inflammation, we
induced muscle damage to both small and large muscle mass and measured vascular
function every 24 hours for up to 5 days of recovery. Eccentric exercise-induced muscle
damage, in both small and large muscle mass, resulted in a transient increase in central
arterial stiffness. Next, patients with systemic lupus erythematosus (SLE) were studied
as a model of chronic inflammation. Measurements of vascular function were compared
in habitually-exercising and sedentary SLE patients, and age-matched healthy controls.
Individuals with SLE demonstrated lower vascular function than healthy controls. When SLE patients were grouped by exercise status, habitually-exercising SLE patients
exhibited similar vascular function to healthy controls, and lower overall disease activity
compared with sedentary SLE patients, supporting the beneficial effect of regular
exercise in this population. Inflammatory biomarkers were associated with measures of
macro- and microvascular function. In conclusion, acute muscle damage and chronic
disease-related inflammation have a potent effect on measures of vascular function,
suggesting that inflammation plays a role in the pathogenesis of vascular dysfunction and is an important biomarker for cardiovascular risk.text
Books on the topic "Autoimmune system; Muscle"
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Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0022.
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Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
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Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_002.
Full textAbstract:
Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
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Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_003.
Full textAbstract:
Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
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Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 68-Year-Old Female with Progressive Pain and Weakness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0027.
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Statin myopathy can occur at anytime during use. This chapter discusses an approach to diagnosis, and emphasizes management considerations, including awareness of statin metabolism by the cytochrome P-450 system. A statin must be discontinued in any patient with evidence of myopathy or myalgias. A muscle biopsy should be done in cases that do not improve clinically or by creatine kinase level. It is important to note that there are cases of apparent statin myopathy which transform into a chronic autoimmune inflammatory myopathy. Antibodies to hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase have recently been identified in the majority of patients with autoimmune statin myopathy and this test may give further weight to treat with immunotherapy.
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Mills, Gary H. Pulmonary disease and anaesthesia. Edited by Philip M. Hopkins. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0082.
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Respiratory adverse events are the commonest complications after anaesthesia and have profound implications for the recovery of the patient and their subsequent health. Outcome prediction related to respiratory disease and complications is vital when determining the risk:benefit balance of surgery and providing informed consent. Surgery produces an inflammatory response and pain, which affects the respiratory system. Anaesthesia produces atelectasis, decreases the drive to breathe, and causes muscle weakness. As the respiratory system ages, closing capacity increases and airway closure becomes an increasing issue, resulting in atelectasis. Increasing comorbidity and polypharmacy reduces the patient’s ability to eliminate drugs. The proportion of major operations on older frailer patients is rising and postoperative recovery becomes more complicated and the demand for critical care rises. At the same time, the population is becoming more obese, producing rapid decreases in end-expiratory lung volume on induction, together with a high incidence of sleep-disordered breathing. Despite this, many high-risk patients are not accurately identified preoperatively, and of those that are admitted to critical care, some are discharged and then readmitted to the intensive care unit with complications. Respiratory diseases may lead to increases in pulmonary vascular resistance and increased load on the right heart. Some lung diseases are primarily fibrotic or obstructive. Some are inflammatory, autoimmune, or vasculitic. Other diseases relate to the drive to breathe, the nerve supply to, or the respiratory muscles themselves. The range of types of respiratory disease is wide and the physiological consequences of respiratory support are complex. Research continues into the best modes of respiratory support in theatre and in the postoperative period and how best to protect the normal lung. It is therefore essential to understand the effects of surgery and anaesthesia and how this impacts existing respiratory disease, and the way this affects the balance between load on the respiratory system and its capacity to cope.
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Christadoss, Premkumar. Myasthenia Gravis: Disease Mechanism And Immunointervention. Alpha Science International, Ltd, 2000.
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Christadoss, Premkumar. Myasthenia Gravis: Disease Mechanism and Immunointervention. Springer, 2000.
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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.
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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.
Book chapters on the topic "Autoimmune system; Muscle"
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Guttmann, Oliver P., and Perry Elliott. "Specific heart muscle disorders." In Oxford Textbook of Medicine, edited by Jeremy Dwight, 3489–500. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0355.
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Systemic immune-mediated diseases are autoimmune and autoinflammatory diseases affecting at least two-organ systems. Autoinflammatory diseases are a family of conditions characterized by episodes of unprovoked inflammation in the absence of high autoantibody titres or autoreactive T lymphocytes, reflecting a primary dysfunction of the innate immune system. Autoimmune diseases are characterized by aberrant B, T, and dendritic cell responses with predominantly cell-mediated or autoantibody-mediated responses to self-antigens in genetically susceptible individuals. Cardiovascular involvement is systemic immune-mediated diseases may be occult and often goes undetected, but is associated with a poor prognosis. As any anatomical structure in the heart may be involved, patients can present with one or more features consistent with pericarditis, myocarditis, endocarditis, and vasculitis. There is often no correlation between the extent of systemic disease and cardiac involvement.
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Shibasaki, Hiroshi, Mark Hallett, Kailash P. Bhatia, Stephen G. Reich, and Bettina Balint. "Disorders of Increased Muscle Stiffness or Overactivity." In Involuntary Movements, 175–80. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190865047.003.0009.
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Increased muscle stiffness or overactivity (which differs from parkinsonian rigidity or dystonia) can be caused by a variety of disorders of central or peripheral nervous system origin and genetic, autoimmune, or infectious etiology. Increased muscle stiffness may be the cause of some joint movements, particularly when such stiffness is associated with stimulus sensitivity that causes involuntary movements. The conditions discussed in this chapter include stiff person syndrome, progressive encephalomyelitis with rigidity and myoclonus (PERM), acquired neuromyotonia (Isaacs syndrome), hereditary neuromyotonia, tetanus (which has an infectious etiology), Satoyoshi disease, neuromyotonia, and rippling muscle disease. Many of these cases are caused by decreased synaptic inhibition through an autoimmune mechanism.
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Straub, Rainer H. "Neuroendocrine system and chronic autoimmune rheumatic diseases." In Oxford Textbook of Rheumatology, 162–71. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_004.
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Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
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Miller, Aaron E., Tracy M. DeAngelis, Michelle Fabian, and Ilana Katz Sand. "Confusion, Muscle Cramps, and Weight Loss." In Neuroimmunology, 127–32. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190693190.003.0024.
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Morvan’s syndrome is a rare autoimmune antibody syndrome causing central, peripheral, and autonomic manifestations. It has been most consistently associated with Caspr2 antibodies, although LGI1 antibodies have also been found in some patients. The Caspr2 protein is located throughout the central and peripheral nervous system. This may account for the diversity of presentations that have been reported in patients with Caspr2 antibodies. The seven core symptoms of Caspr2 antibodies include cognitive dysfunction/seizures, cerebellar symptoms, peripheral nerve hyperexcitability, autonomic dysfunction, insomnia, neuropathic pain, and weight loss. Treatment of Morvan’s syndrome and other Caspr-associated antibody syndromes is largely empirical. Typically, patients are given steroids, intravenous immunoglobulin, and if necessary, other immunosuppressive agents. Prognosis for remission is very good, but relapses may occur.
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Miller, Aaron E., Tracy M. DeAngelis, Michelle Fabian, and Ilana Katz Sand. "Checks and Balances." In Neuroimmunology, 153–56. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190693190.003.0029.
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In recent years, immune checkpoint inhibitors have been shown to be effective tools in treating multiple types of cancer. In a healthy person, immune checkpoint molecules function to remove self-reactive T cells. However, cancer cells may also use these same pathways to suppress T cells. Checkpoint inhibition brings about non-specific T cell activation, which allows for a tumor-specific immune response. However, an infrequent, but potentially severe, complication of checkpoint inhibitor therapies is the formation of autoimmune conditions. Cases of new or worsened autoimmune conditions have been reported in many organ systems. In the nervous system, central and peripheral processes, as well as disorders of the neuro-muscular junction or muscle, have been identified. Treatment is targeted towards the acute episode. Chronic immunosuppression is usually not initiated because stopping the checkpoint inhibitor therapy will typically abort the autoimmune process. In the future, more of these drugs are likely to be used to treat cancer, and thus more must be known about the mechanisms that induce autoimmunity in this setting and the best strategies to treat them.
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Benarroch, Eduardo E. "Cholinergic Transmission." In Neuroscience for Clinicians, edited by Eduardo E. Benarroch, 337–51. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.003.0019.
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Acetylcholine (ACh) is a major neurotransmitter in the central and peripheral nervous systems. Cholinergic neurons in the central nervous system include the basal forebrain cholinergic group that projects to the cerebral cortex and has a major role in attention, sensory processing, and memory; the mesopontine group that projects to the thalamus, basal ganglia, and brainstem areas and is involved in arousal, reward, and control of muscle tone; and large aspiny neurons of the striatum controlling basal ganglia function. In the periphery, ACh is the neurotransmitter of motor neurons innervating skeletal muscle; preganglionic neurons innervating autonomic ganglia; and parasympathetic, enteric, and sudomotor sympathetic neurons. Acetylcholine acts via nicotinic receptors to elicit fast excitation and several subtypes of muscarinic receptors that exert a variety of modulatory actions. Given the widespread distribution and targets of ACh, cholinergic systems have a major role in a variety of neurologic disorders, including Alzheimer disease, neuromuscular transmission defects, and autonomic manifestation of autoimmune diseases, drugs, or toxins.
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M. Harvey, Evan, Murad Almasri, and Hugo R. Martinez. "Genetics of Cardiomyopathy." In Cardiomyopathy - Disease of the Heart Muscle [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97010.
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Cardiomyopathies (CMs) encompass a heterogeneous group of structural and functional (systolic and diastolic) abnormalities of the myocardium and are either confined to the cardiovascular system or are part of a systemic disorder. CMs represent a leading cause of morbidity and mortality and account for a significant percentage of death and cardiac transplantation. The 2006 American Heart Association (AHA) classification grouped CMs into primary (genetic, mixed, or acquired) or secondary (i.e., infiltrative or autoimmune). In 2008, the European Society of Cardiology classification proposed subgrouping CM into familial or genetic and nonfamilial or nongenetic forms. In 2013, the World Heart Federation recommended the MOGES nosology system, which incorporates a morpho-functional phenotype (M), organ(s) involved (O), the genetic inheritance pattern (G), an etiological annotation (E) including genetic defects or underlying disease/substrates, and the functional status (S) of a particular patient based on heart failure symptoms. Rapid advancements in the biology of cardio-genetics have revealed substantial genetic and phenotypic heterogeneity in myocardial disease. Given the variety of disciplines in the scientific and clinical fields, any desired classification may face challenges to obtaining consensus. Nonetheless, the heritable phenotype-based CM classification offers the possibility of a simple, clinically useful diagnostic scheme. In this chapter, we will describe the genetic basis of dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), arrhythmogenic cardiomyopathy (ACM), LV noncompaction cardiomyopathy (LVNC), and restrictive cardiomyopathy (RCM). Although the descriptive morphologies of these types of CM differ, an overlapping phenotype is frequently encountered within the CM types and arrhythmogenic pathology in clinical practice. CMs appear to originate secondary to disruption of “final common pathways.” These disruptions may have purely genetic causes. For example, single gene mutations result in dysfunctional protein synthesis causing downstream dysfunctional protein interactions at the level of the sarcomere and a CM phenotype. The sarcomere is a complex with multiple protein interactions, including thick myofilament proteins, thin myofilament proteins, and myosin-binding proteins. In addition, other proteins are involved in the surrounding architecture of the sarcomere such as the Z-disk and muscle LIM proteins. One or multiple genes can exhibit tissue-specific function, development, and physiologically regulated patterns of expression for each protein. Alternatively, multiple mutations in the same gene (compound heterozygosity) or in different genes (digenic heterozygosity) may lead to a phenotype that may be classic, more severe, or even overlapping with other disease forms.
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Isenberg, David A., and Ian Giles. "Introduction." In Oxford Textbook of Medicine, edited by Richard A. Watts, 4495–99. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0453.
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About 1 in 20 people develop an autoimmune disease, many of which involve the musculoskeletal system. Young women are particularly at risk, but the development at any age of symptoms such as unexplained fever, rash, polyarthritis, Raynaud’s phenomenon, or mouth ulcers should encourage serological screening for autoimmune rheumatic or vasculitic disorder. The autoimmune rheumatic diseases are a heterogeneous group of disorders characterized by clinical involvement of the joints, connective tissues, muscles, internal organs, Raynaud’s phenomenon, and cutaneous manifestations. They include a broad clinical spectrum of disease, including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), Sjögren’s syndrome, scleroderma, dermatomyositis, polymyositis, antiphospholipid syndrome (APS), and the vasculitides.
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Sultan, Shabina, and David A. Isenberg. "Inflammatory Muscle Diseases: Pathogenesis and Clinical Features." In Handbook of Systemic Autoimmune Diseases, 107–28. Elsevier, 2004. http://dx.doi.org/10.1016/s1571-5078(04)03007-7.
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Martínez-Jiménez, Santiago. "Other Autoimmune Diseases." In Chest Imaging, 361–65. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780199858064.003.0062.
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Autoimmune diseases described herein include systemic lupus erythematosus (SLE), dermatomyositis/polymyositis (DM/PM), Sjögren syndrome (SS), and mixed connective tissue disease (MCTD). SLE predominantly affects women of reproductive age. Although pleural involvement is the most common thoracic manifestation, other manifestations include pneumonia, diffuse alveolar hemorrhage and lupus pneumonitis. Interstitial lung disease in patients with SLE include non-specific interstitial pneumonia (NSIP) and usual interstitial pneumonia (UIP). DM/PM affects the skeletal muscle and may frequently result in hypoventilation and respiratory failure (respiratory muscle involvement) and aspiration (laryngeal involvement). Interstitial lung disease is also frequent, and NSIP and organizing pneumonia are the most common patterns. SS typically affects women in the 4th to 5th decades of life. Classic symptoms include xerophtalmia and xerostomia. Interstitial lung disease is among the most common thoracic manifestations; and although NSIP, UIP, organizing pneumonia and amyloidoisis can occur, lymphocytic interstitial pneumonia (LIP) is a characteristic form of interstitial lung disease in SS. MCTD combines clinical features of RS, SLE, PSS and PM/DM. Thoracic involvement typically manifests with pulmonary hypertension and interstitial lung disease (NSIP, UIP and LIP). Pulmonary hypertension can occur in any autoimmune disease and is often associated with a worse prognosis. Chest radiography and thin-section chest CT (or HRCT) are the imaging modalities of choice to detect and assess thoracic manifestations of autoimmune disease.