Книги з теми "Peripheral inflammation"
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1
Schäfer, Michael, and Christoph Stein, eds. Mind over Matter - Regulation of Peripheral Inflammation by the CNS. Basel: Birkhäuser Basel, 2003. http://dx.doi.org/10.1007/978-3-0348-8039-8.
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2
De Leo, Joyce A., 1960-, Sorkin Linda S. 1953-, Watkins Linda R. 1954-, and International Association for the Study of Pain., eds. Immune and glial regulation of pain. Seattle: IASP Press, 2007.
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3
Fatima Shad, Kaneez, ed. Erythrocyte - A Peripheral Biomarker For Infection and Inflammation. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.92510.
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4
Shad, Kaneez Fatima. Erythrocyte: A Peripheral Biomarker for Infection and Inflammation. IntechOpen, 2021.
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5
Jacoby, Dr Richard, and Raquel Baldelomar. Sugar Crush: How to Reduce Inflammation, Reverse Nerve Damage, and Reclaim Good Health. Harper Wave, 2016.
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6
Baldelomar, Raquel, and Richard Jacoby. Sugar Crush: How to Reduce Inflammation, Reverse Nerve Damage, and Reclaim Good Health. HarperCollins Publishers, 2015.
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7
(Editor), Michael Schäfer, and Christoph Stein (Editor), eds. Mind over Matter - Regulation of Peripheral Inflammation by the CNS (Progress in Inflammation Research). Birkhäuser Basel, 2004.
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8
Stein, Christoph, and Michael Schäfer. Mind over Matter - Regulation of Peripheral Inflammation by the CNS. Birkhauser Verlag, 2012.
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9
Schäfer, Michael. Mind over Matter - Regulation of Peripheral Inflammation by the Cns. Springer, 2012.
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10
Siebert, Stefan, Sengupta Raj, and Alexander Tsoukas. Peripheral musculoskeletal involvement in axial spondyloarthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198755296.003.0007.
Повний текст джерелаАнотація:
In addition to the axial diseases that characterizes axial spondyloarthritis (axSpA), many patients also develop peripheral musculoskeletal involvement. This can include peripheral joint synovitis, enthesitis, and dactylitis. Peripheral musculoskeletal involvement is an important component of the disease with significant impact on function and quality of life. Many of the features may also be subtle and overlooked, unless specifically evaluated and examined. In particular, hip disease is a bad prognostic feature and, if present, may require more aggressive therapy or surgical intervention. On occasion, further imaging may be required to detect enthesitis or subtle joint inflammation in order to inform treatment decisions.
11
Fannell, Modesto. Natural Treatments for Peripheral Neuropathy : Easy Ways to Reduce Pain and Inflammation: Neuropathy in Feet and Legs Treatment. Independently Published, 2021.
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12
Leung, Doris G. Other Proven and Putative Autoimmune Disorders of the Peripheral Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0098.
Повний текст джерелаАнотація:
Myasthenia gravis is in most cases an autoimmune disorder of the neuromuscular junction in which antibodies are directed at nicotinic acetylcholine receptors or other synaptic proteins, such as the MusK protein that is involved in the formation of the formation and maturation of the motor endplate. Less commonly, myasthenia gravis can result from antibodies directed to presynaptic calcium channels as a side effect of paraneoplastic antibodies (Lambert-Eaton syndrome) or from a developmental paucity of acetylcholine receptors in the neonatal form of the disease. Treatment is usually a combination of aceetylcoholinesterase inhibitors such as pyridostigmine to prolong the life of acetylcholine released at the neuromuscular junction and/or drugs such as corticosteroids aimed at reducing inflammation.
13
Janssen, Sofie. Effects of Il-6 & Il-8 on Respiratory & Peripheral Skeletal Muscle Function: Consequences for Systemic Inflammation in Copd (Acta Biomedica Lovaniensia). Leuven Univ Pr, 2006.
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14
Price, Chane, Zahid Huq, Eellan Sivanesan, and Constantine Sarantopoulos. Pain Pathways and Pain Physiology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190457006.003.0001.
Повний текст джерелаАнотація:
Pain is a multidimensional sensory experience that is mediated by complex peripheral and central neuroanatomical pathways and mechanisms. Typically, noxious stimuli activate specific peripheral nerve terminals onto Aδ and C nerve fibers that convey pain and generate signals that are relayed and processed in the spinal cord and then conveyed via the spinothalamic tracts to the contralateral thalamus and from there to the brain. Acute pain is self-limited and resolves with the healing process, but conditions of extensive injury or inflammation sensitize the pain pathways and generate aberrant, augmented responses. Peripheral and central sensitization of neurons (as a result of spatially and temporally excessive inflammation or intense afferent signal traffic) may result in hyperexcitability and chronicity of pain, with spontaneous pain and abnormal evoked responses to stimuli (allodynia, hyperalgesia). Finally, neuropathic pain follows injury or disease to nerves as a result of hyperexcitability augmented by various sensitizing mechanisms.
15
Sommer, Claudia. Endogenous opioids mediate stress-induced analgesia. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0031.
Повний текст джерелаАнотація:
This chapter reviews the landmark paper published in 1990 by Stein et al. and entitled ‘Opioids from immunocytes interact with receptors on sensory nerves to inhibit nociception in inflammation’. Opioids, besides acting centrally as analgesics, may act peripherally upon opioid receptors located on axons and on immune cells. In the publication by Stein et al., it was shown for the first time that endogenous opioid peptides released from immune cells mediate stress-induced analgesia, potentially through opioid receptors on peripheral nerve endings. This finding has led to numerous follow-up studies on endogenous analgesia, including work showing that cannabinoid analgesia is mediated via the peripheral release of opioids, and to the concept of topical opioid analgesia, which may be a good way of using the potent analgesia that opioids can convey, without their CNS-associated side effects.
16
Parlato, Marianna, and Jean-Marc Cavaillon. Innate immunity and the inflammatory cascade. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0299.
Повний текст джерелаАнотація:
Inflammation results from a complex interaction between a large number of mediators able to induce each other and to favour the generation of other inflammatory molecules (e.g. free radicals, lipid mediators, and proteases). The perpetuation of inflammation by these cascades of mediators is favoured by their ability to induce coagulation, leukocyte recruitment, and cell and tissue alteration (apoptosis, necrosis, and barrier disruption). Other cascades of mediators occur to generate anti-inflammatory mediators favouring the healing process. A neuroendocrine loop and neuromediators from central and peripheral nervous system are also involved in the process, allowing a return to homeostasis.
17
Gardiner, Matthew D., and Neil R. Borley. Plastic and reconstructive surgery. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199204755.003.0012.
Повний текст джерелаАнотація:
This chapter begins by discussing the basic principles of acute inflammation, cutaneous wound healing, and the reconstructive ladder, before focusing on the key areas of knowledge, namely congenital conditions, emergency management of burns, emergency hand surgery, tendon injuries, peripheral nerve injuries, elective hand surgery, cutaneous malignant melanoma, non-melanoma skin cancer, and benign skin lesions. The chapter concludes with relevant case-based discussions.
18
Harrison, Mark. Wound healing. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198765875.003.0057.
Повний текст джерелаАнотація:
This chapter describes the pathology of wound healing as it applies to Emergency Medicine, and in particular the Primary FRCEM examination. The chapter outlines the key details of haemostasis, inflammation, reconstruction, epithelialization, and maturation, and the specific tissues affected, including skin, tendon, peripheral nerve, bone, myocardium, and brain. This chapter is laid out exactly following the RCEM syllabus, to allow easy reference and consolidation of learning.
19
Bunch, Chris. Lymphadenopathy. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0036.
Повний текст джерелаАнотація:
Lymph nodes are small, bean-shaped structures generally a few millimetres in size, distributed widely throughout the body and assuming a major role in the immune system. Peripheral lymph nodes are not normally palpable except in thin individuals. Enlargement of lymph nodes is called lymphadenopathy. It is important to distinguish between reactive lymphadenopathy, which is usually an appropriate response to infection or inflammation, and malignant or neoplastic lymphadenopathy.
20
Gaston, Hill. Seronegative spondyloarthropathy. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0268.
Повний текст джерелаАнотація:
Spondyloarthropathies consist of several rheumatic conditions, initially grouped together on the basis of shared clinical features, later reinforced by their strong association with HLA-B27. The distinctive features are axial involvement, including sacroiliac joints, and enthesitis—inflammation at ligament and tendon insertions—together with certain extra-articular manifestations. The presentation of a patient with combinations of inflammatory spinal pain, peripheral synovitis and/or enthesitis, and typical extra-articular manifestations, often with a family history, is characteristic.
21
Lories, Rik. Mechanisms of bone destruction and proliferation in psoriatic arthritis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0008.
Повний текст джерелаАнотація:
Psoriatic arthritis is a chronic inflammatory joint disease that can affect both the peripheral and axial skeleton. The clinical presentation of psoriatic arthritis is very heterogeneous and different subforms have been described. Structural damage to the joint is a feared complication of psoriatic arthritis. The severity of joint inflammation and subsequent damage can range from mild to extreme. Over the last decade, insights into the molecular and cellular mechanisms that underlie the skeletal changes in psoriatic arthritis have gradually increased although translational validation of concepts using patient-derived materials still lags behind. Current treatment strategies directed against key mediators of inflammation appear to have good effects on joint destruction, but their short and long-term impact on new bone formation and ankylosis is still unclear. The identification of the role that key growth factors play in the latter process identifies new opportunities for therapeutic interventions.
22
Hartigan-O’Connor, Dennis J., and Christian Brander. Immunology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0005.
Повний текст джерелаАнотація:
The key factor in HIV pathogenesis is the decline in CD4+ T cells with resultant immunodeficiency and chronic inflammation. Depletion of CD4+ T cells from the gastrointestinal mucosa followed by microbial translocation and subsequent immune activation are components of disease progression in untreated patients. Symptomatic and occult opportunistic infections including cytomegalovirus contribute to chronic inflammation in persons infected with HIV. Antiretroviral therapy (ART) results in immune reconstitution, with increases in peripheral CD4+ T cell lymphocytes in most persons infected with HIV, although immune recovery is quite variable. A subset of patients with AIDS will develop immune reconstitution inflammatory syndromes after initiation of ART. Approximately 1% of persons with HIV are able to control infection without the need for ART (“elite” controllers). A variety of immune-based therapies, including hydroxyurea, growth hormone, and statins, are being studied in clinical trials and may ultimately play a role in treating persons with HIV infection.
23
Mason, Peggy. Somatosensation. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0017.
Повний текст джерелаАнотація:
Under normal circumstances, the somatosensory system contributes more to shaping movements than to perception. Yet damage to the somatosensory system can result in spontaneous pain and other abnormal somatic perceptions. An exploration of the mechanisms and pathways involved in touch perception is slanted toward understanding the contribution of the dorsal column–medial lemniscus pathway to the generation of paresthesia and dysesthesia. Peripheral somatosensory afferents that contribute to the perception of sharp or aching pain, temperature, and itch are described. The properties of transient receptor potential (TRP) channels on nociceptors and thermoreceptors are described. Physiological and pharmacological mechanisms that lead to neurogenic inflammation are considered. How peripheral and central changes triggered by acute injury or disease can lead to long-lasting changes that support chronic pain is described. Persistent pain that occurs independently of any stimulus is termed neuropathic. Mechanisms of referred pain from deep structures including viscera are introduced.
24
Guzik, Tomasz J., and Rhian M. Touyz. Vascular pathophysiology of hypertension. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0019.
Повний текст джерелаАнотація:
Hypertension is a multifactorial disease, in which vascular dysfunction plays a prominent role. It occurs in over 30% of adults worldwide and an additional 30% are at high risk of developing the disease. Vascular pathology is both a cause of the disease and a key manifestation of hypertension-associated target-organ damage. It leads to clinical symptoms and is a key risk factor for cardiovascular disease. All layers of the vascular wall and the endothelium are involved in the pathogenesis of hypertension. Pathogenetic mechanisms, whereby vascular damage contributes to hypertension, are linked to increased peripheral vascular resistance. At the vascular level, processes leading to change sin peripheral resistance include hyper-contractility of vascular smooth muscle cells, endothelial dysfunction, and structural remodelling, due to aberrant vascular signalling, oxidative and inflammatory responses. Increased vascular stiffness due to vascular remodelling, adventitial fibrosis, and inflammation are key processes involved in sustained and established hypertension. These mechanisms are linked to vascular smooth muscle and fibroblast proliferation, migration, extracellular matrix remodelling, calcification, and inflammation. Apart from the key role in the pathogenesis of hypertension, hypertensive vasculopathy also predisposes to atherosclerosis, another risk factor for cardiovascular disease. This is linked to increased transmural pressure, blood flow, and shear stress alterations in hypertension, as well as endothelial dysfunction and vascular stiffness. Therefore, understanding the mechanisms and identifying potential novel treatments targeting hypertensive vasculopathy are of primary importance in vascular medicine.
25
Charlson, Robert W., and Matthew S. Robbins. Migraine and Other Headache Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0047.
Повний текст джерелаАнотація:
In recent years, the characterization of the neurobiology of migraine and other headache disorders has been driven by the search to better understand several key factors: genetics, the role of neuromodulators such as calcitonin gene-related peptide (CGRP), processes including central and peripheral sensitization, neurogenic inflammation, central pain networks, and areas of activation demonstrated by advancing functional neuroimaging techniques. Yet the ultimate causes of migraine remain unknown. Nonetheless, recent work has advanced our understanding of this complex disorder, and pointed toward a future where these modalities may provide an integrated understanding of its pathophysiology and provide specific treatment targets.
26
Schaible, Hans-Georg, and Rainer H. Straub. Pain neurophysiology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0059.
Повний текст джерелаАнотація:
Physiological pain is evoked by intense (noxious) stimuli acting on healthy tissue functioning as a warning signal to avoid damage of the tissue. In contrast, pathophysiological pain is present in the course of disease, and it is often elicited by low-intensity stimulation or occurs even as resting pain. Causes of pathophysiological pain are either inflammation or injury causing pathophysiological nociceptive pain or damage to nerve cells evoking neuropathic pain. The major peripheral neuronal mechanism of pathophysiological nociceptive pain is the sensitization of peripheral nociceptors for mechanical, thermal and chemical stimuli; the major peripheral mechanism of neuropathic pain is the generation of ectopic discharges in injured nerve fibres. These phenomena are created by changes of ion channels in the neurons, e.g. by the influence of inflammatory mediators or growth factors. Both peripheral sensitization and ectopic discharges can evoke the development of hyperexcitability of central nociceptive pathways, called central sensitization, which amplifies the nociceptive processing. Central sensitization is caused by changes of the synaptic processing, in which glial cell activation also plays an important role. Endogenous inhibitory neuronal systems may reduce pain but some types of pain are characterized by the loss of inhibitory neural function. In addition to their role in pain generation, nociceptive afferents and the spinal cord can further enhance the inflammatory process by the release of neuropeptides into the innervated tissue and by activation of sympathetic efferent fibres. However, in inflamed tissue the innervation is remodelled by repellent factors, in particular with a loss of sympathetic nerve fibres.
27
Hearn, Sandra. Brachial Plexitis—Parsonage-Turner Syndrome. Edited by Meghan E. Lark, Nasa Fujihara, and Kevin C. Chung. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190617127.003.0012.
Повний текст джерелаАнотація:
The chapter provides a case-based review of Parsonage-Turner syndrome. Parsonage-Turner syndrome, also known as neuralgic amyotrophy and idiopathic brachial plexitis, represents immune-mediated inflammation of neural structures within the brachial plexus and peripheral nerves of the upper limb. Classic features include sudden-onset shoulder or upper arm pain, followed by weakness in the forequarter or limb. This pattern, in addition to nonmechanical and nonradicular clinical features, should prompt consideration of Parsonage-Turner syndrome diagnosis. The diagnosis is established on clinical grounds, although electrodiagnostic data and advanced imaging can support the impression. Management is conservative. For neurosurgeons, accurate diagnosis of Parsonage-Turner syndrome can avoid unnecessary and inappropriate surgical intervention when symptoms are erroneously ascribed to another cause.
28
Khan, Muhammad Asim. Clinical features. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0011.
Повний текст джерелаАнотація:
The leading chronic progressive inflammatory disease of the sacroiliac joints and the spinal column, traditionally known as ankylosing spondylitis (AS), is a relatively common but insidious rheumatic disease that can cause progressive limitation of physical function. It is a prototype of related forms of arthritis, grouped under the term spondyloarthritis that is subdivided into predominantly axial and predominantly peripheral forms. This chapter details the clinical features of axial spondyloarthritis, a term that encompasses ankylosing spondylitis. There is a predilection for the inflammation to affect sites where the tendons and ligaments attach to the bones (entheses) and can result in gradual and progressive spinal ankylosis, with resultant physical deformity. The disease may present with a wide spectrum of clinical features, both articular and extra-articular, and can be difficult to diagnose in early stages.
29
Sieper, Joachim. Ankylosing spondylitis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0113.
Повний текст джерелаАнотація:
Ankylosing spondylitis (AS) is a chronic inflammatory disease predominantly of the sacroiliac joint (SIJ) and the spine. It starts normally in the second decade of life and has a slight male predominance. The prevalence is between 0.2 and 0.8% and is strongly dependent on the prevalence of HLA B27 in a given population. For the diagnosis of AS, the presence of radiographic sacroiliitis is mandatory. However, radiographs do not detect active inflammation but only structural bony damage. Most recently new classification criteria for axial spondyloarthritis (SpA) have been developed by the Assessement of Spondylo-Arthritis international Society (ASAS) which cover AS but also the earlier form of non-radiographic axial SpA. MRI has become an important new tool for the detection of subchondral bone marrow inflammation in SIJ and spine and has become increasingly important for an early diagnosis. HLA B27 plays a central role in the pathogenesis but its exact interaction with the immune system has not yet been clarified. Besides pain and stiffness in the axial skeleton patients suffer also from periods of peripheral arthritis, enthesitis, and uveitis. New bone formation as a reaction to inflammation and subsequent ankylosis of the spine determine long-term outcome in a subgroup of patients. Currently only non-steroidal anti-inflammatory drugs (NSAIDs) and tumour necrosis factor (TNF) blockers have been proven to be effective in the medical treatment of axial SpA, and international ASAS recommendations for the structured management of axial SpA have been published based on these two types of drugs. Conventional disease-modifying anti-rheumatic drugs (DMARDs) such as methotrexate are not effective.
30
Siebert, Stefan, Sengupta Raj, and Alexander Tsoukas. Imaging in axial spondyloarthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198755296.003.0011.
Повний текст джерелаАнотація:
Imaging has always been a key component in the diagnosis of ankylosing spondylitis as part of the modified New York criteria. With the increased availability of MRI and the development of the ASAS axial spondyloarthritis (axSpA) criteria, there has been a shift from x-ray imaging of structural damage to MRI imaging of inflammation. This information can help in both the diagnosis of axSpA and in guiding treatment decisions in patients with this diagnosis. However, imaging results must be evaluated in the context of the clinical picture and should not be acted on in isolation. Here we review the key imaging modalities used in axSpA, with the main focus on x-rays and MRI of the sacroiliac joints, spine, and peripheral structures. Advances in technology are also likely to lead to the development of even better imaging modalities for axSpA in future.
31
Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0022.
Повний текст джерелаАнотація:
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.
32
Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_002.
Повний текст джерелаАнотація:
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.
33
Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_003.
Повний текст джерелаАнотація:
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.
34
Sieper, Joachim. Axial spondyloarthropathies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0113_update_003.
Повний текст джерелаАнотація:
Axial spondyloarthritis (axSpA) is a chronic inflammatory disease predominantly of the sacroiliac joint (SIJ) and the spine. It starts normally in the second decade of life and has a slight male predominance. The prevalence is between 0.2% and 0.8% and is strongly dependent on the prevalence of HLA-B27 in a given population. AxSpA can be split in patients with radiographic axSpA (also termed ankylosing spondylitis (AS)) and in patients with non-radiographic axSpA (nr-axSpA). For the diagnosis of AS, the presence of radiographic sacroiliitis is mandatory. However, radiographs do not detect active inflammation but only structural bony damage. Most recently new classification criteria for axSpA have been developed by the Assessment of Spondylo-Arthritis International Society (ASAS) which cover AS but also the earlier form of nr-axSpA. MRI has become an important new tool for the detection of subchondral bone marrow inflammation in SIJ and spine and has become increasingly important for an early diagnosis. HLA-B27 plays a central role in the pathogenesis but its exact interaction with the immune system has not yet been clarified. Besides pain and stiffness in the axial skeleton patients suffer also from periods of peripheral arthritis, enthesitis, and uveitis. New bone formation as a reaction to inflammation and subsequent ankylosis of the spine determine long-term outcome in a subgroup of patients. Currently only non-steroidal anti-inflammatory drugs (NSAIDs) and tumour necrosis factor (TNF) blockers have been proven to be effective in the medical treatment of axial SpA, and international ASAS recommendations for the structured management of axial SpA have been published based on these two types of drugs. Conventional disease-modifying anti-rheumatic drugs (DMARDs) such as methotrexate are not effective.
35
Doré-Savard, Louis, Nicolas Beaudet, and Philippe Sarret. Mechanisms of bone cancer pain. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0037.
Повний текст джерелаАнотація:
The landmark paper discussed in this chapter focuses on pain arising from malignancy of the bone, which, whether primary or originating from a distant site, is the cause for a majority of cancer pain syndromes. Bone is an innervated organ that can relay nociceptive signals triggered by nerve damage, acidosis, inflammation, and hypoxia. The understanding of the physiopathology of skeletal pain has leaped significantly forwards over the last 15 years. The development of animal models that allowed for the visualization of bone microenvironment modifications by the tumour played an important role in recent advances. One of the most significant discoveries was the contribution of local nerve growth factor (NGF) to nerve remodelling in the bone periosteum presented by Mantyh and colleagues in 2010. NGF remains one the most promising treatment avenues for malignant bone pain, and peripheral innervation has become a therapeutic target in several skeletal pathologies.
36
van Gaalen, Floris, Désirée van der Heijde, and Maxime Dougados. Diagnosis and classification of axial spondyloarthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0003.
Повний текст джерелаАнотація:
Axial spondyloarthritis (axSpA) is a potentially disabling chronic inflammatory disease affecting the spine and sacroiliac (SI) joints. Lead symptoms are chronic back pain and stiffness. The disease is called radiographic axSpA or ankylosing spondylitis (AS) when, on plain radiographs, bone changes consistent with sacroiliitis are present. When no evidence of sacroiliitis is seen on radiographs, it is called non-radiographic axSpA. In such cases, diagnosis is made based on evidence of active inflammation of SI joints on magnetic resonance imaging (MRI) and clinical and laboratory features, or a combination of clinical and laboratory features only. Apart from affecting the spine and SI joints, axSpA may involve peripheral joints (e.g. knee, ankle) and manifest in extra-articular manifestations, for example uveitis, psoriasis, and inflammatory bowel disease. In this chapter, diagnosis and classification of axSpA is discussed, including use of MRI in detecting sacroiliitis and the difference between clinical diagnosis and disease classification.
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McGonagle, Dennis, and Iris Eshed. MRI. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0018.
Повний текст джерелаАнотація:
The features of psoriatic arthritis (PsA) are disparate—from peripheral synovitis to axial inflammation, from bone destruction to bone formation or both, and nail disease. Fat suppression magnetic resonance imaging (MRI) has had a major impact on understanding PsA. MRI suggests a unifying anatomical basis for PsA with the common denominator of disease localization to entheses and adjacent bone and other sites of high biomechanical stress. MRI has also shown that entheseal changes are not uncommon in generalized osteoarthritis and occasionally in normals, making careful clinical correlation essential for imaging interpretation. MRI is useful in predicting the course of axial spondyloarthritis but there are no specific studies in axial PsA; most data comes from ankylosing spondylitis. Additionally MRI has been used for monitoring therapeutic response in PsA where good resolution of enthesitis/osteitis has been reported. Further studies are needed to define the role of MRI in measuring biological remission of PsA.
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Vlachopoulos, Charalambos, and Nikolaos Ioakeimidis. Erectile dysfunction as a marker and predictor of cardiovascular disease. Edited by Charalambos Vlachopoulos. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0245.
Повний текст джерелаАнотація:
Erectile dysfunction (ED) is defined as the inability to obtain or maintain a penile erection to support satisfactory sexual performance. It is considered an early manifestation of generalized vascular disease and recognized as a marker of increased cardiovascular risk both acutely and chronically by predicting all-cause mortality, cardiovascular mortality, coronary events, stroke, and peripheral artery disease in men with and without known coronary artery disease. The link between ED and cardiovascular disease might reside in the interaction between androgen level, chronic inflammation, and cardiovascular risk factors that determine endothelial dysfunction and atherosclerosis both in the penile and coronary circulation. Because penile artery size is smaller compared with coronary arteries, the same degree of endothelial dysfunction and atherosclerotic burden causes a more significant reduction of blood flow in erectile tissues compared with that in coronary circulation. From a clinical standpoint, because ED may precede cardiovascular disease, it can be used as an early marker to identify men at higher risk of cardiovascular events. The average 3-year time period between the onset of ED symptoms and a cardiovascular event offers the opportunity for detailed cardiological assessment and intensive treatment of risk factors.
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McDougall, Jason J., and Joel A. Vilensky. The innervation of the joint and its role in osteoarthritis pain. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0007.
Повний текст джерелаАнотація:
Diarthrodial joints possess an extensive network of sensory and sympathetic nerve fibres whose physiological functions are varied and complex. Nerves are primarily located in the synovium but also innervate the subchondral bone, the outer third of menisci, and the superficial surface of tendons and ligaments. Large-diameter, myelinated neurons are involved in joint position sense while small-diameter neurons with thin or no myelin typically sense pain. The small-diameter nerves in conjunction with sympathetic fibres control synovial blood flow and maintain joint homeostasis. In patients with osteoarthritis (OA), the sensory nerves become sensitized and increase their firing rate in response to normal movement. This peripheral sensitization is mediated by numerous algogenic agents released into the OA knee including neuropeptides, eicosanoids, and proteinases. A portion of joint afferents fire in the absence of mechanical stimuli and encode pain at rest. Interestingly, the firing rate of joint afferents does not correlate with OA severity, indicating that pain is a poor predictor of joint pathology. Evidence is accumulating to suggest that a subpopulation of OA patients who are unresponsive to classical non-steroidal anti-inflammatory drugs may be suffering from neuropathic pain in which there is damage to the joint nerves themselves. Better understanding of the biology of joint nerves could help in the development of patient-targeted therapies to alleviate OA pain and inflammation.