China
Africa
Explore chapters and articles related to this topic
Hypersensitivity
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
A history and physical examination will provide invaluable information in most immune disorders, and simple laboratory tests such as a full blood count, erythrocyte sedimentation rate and plasma immunoglobulin concentrations are useful.
Unusual Inherited Pulmonary Diseases Which Provide Clues to Pulmonary Physiology and Function
Published in Stephen D. Litwin, Genetic Determinants of Pulmonary Disease, 2020
Thomas Κ. C. King, Robert A. Norum
Certain findings suggest the involvement of immune, allergic, hypersensitive, or autoimmune mechanisms. A significant number of patients with idiopathic pulmonary fibrosis have elevations of the rheumatoid factor, antinuclear factor, or globulins in their blood [41,53-55,62]. In addition, some patients with pulmonary fibrosis present autoimmune features [63], while, in others, pulmonary fibrosis occurs in association with collagen vascular diseases and rheumatoid arthritis. It has been shown experimentally that the injection into the trachea of antilung serum produces histologic changes in the lung resembling those seen in idiopathic pulmonary fibrosis. It may be that the antibodies participate in the formation of immune complexes which cause lung damage. Histologically, the infiltration of lymphocytes, plasma cells, and mononuclear cells also points to an immune disorder [62]. However, attempts in identifying specific autoantibodies to lung tissue in sera of patients have been negative, nor could antigen-antibody complexes be demonstrated in lung biopsy specimens [55], The recent finding that circulating lymphocytes from patients produce lympokines on exposure to collagen may be an important clue [30]. However, the response of the lung to damage is limited and fibrosis may be a nonspecific reaction to more than one single causative factor.
Acquired Circulating Anticoagulants Other than Lupus Anticoagulants
Published in E. Nigel Harris, Thomas Exner, Graham R. V. Hughes, Ronald A. Asherson, Phospholipid-Binding Antibodies, 2020
Anticoagulants may be categorized as either specific antibodies to clotting factors or nonspecific in their function. The former class can be split into slow- or fast-acting categories. Examples of specific slow-acting anticoagulants are the classic inhibitors of factor VIII found in hemophiliacs, whereas other immunoglobulins directed against specific clotting factors are usually immediate-acting. Circulating anticoagulants or acquired inhibitors of coagulation are usually defined as “pathological substances in circulating blood that directly inhibit blood clotting factors or their interactions”.4 Characteristically their effect on clotting tests is not corrected readily by the addition of normal plasma clotting factors. The majority are immunoglobulins (although this finding is not substantiated in many studies) which may usually be subdivided further into two groups: (1) those arising in patients with an initial blood clotting factor deficiency and arising as a direct immunological response to the infusion of blood products containing a “foreign” antigen and (2) those which occur spontaneously for no apparent reason in patients with previously normal hemostatic function. It is possible that the latter patients may have, or may later develop some kind of immune disorder.
The nutritional status of relapsing-remitting multiple sclerosis (RRMS) patients compared to that of healthy people: a Turkish hospital-based study
Published in Nutritional Neuroscience, 2022
Tutku Atuk Kahraman, Müge Yılmaz, Mehmet Fatih Yetkin, Meral Mirza
Multiple sclerosis (MS) is a chronic multifactorial, inflammatory, neurodegenerative, autoimmune, demyelinating central nervous system disease, which is often seen in young adults and most often in women. Although the pathophysiology of the disease is complex and not fully understood, it is an immune disorder that occurs through the interaction of genetic and environmental factors. Environmental risk factors known to play a role in the development and progress of MS are low serum vitamin D levels, smoking, viral exposure, childhood obesity, and an unhealthy diet [1–3]. The role of diet is indicated to be a possible co-factor that affects the inflammatory process through molecular pathways and intestinal microflora [1]. Studies report that the risk of MS is high in populations having a diet rich in red meat and saturated fat from milk and dairy products, whereas it is lower in populations having a diet rich in vegetables, fish, and nuts (polyunsaturated fatty acids) [1,3].
Monitoring and safety of CAR-T therapy in clinical practice
Published in Expert Opinion on Drug Safety, 2022
José M. Serra López-Matencio, Valle Gómez Garcia de Soria, Manuel Gómez, Estefanía Alañón-Plaza, Cecilia Muñoz-Calleja, Santos Castañeda
It encompasses a group of serious immune alterations characterized by over activation of macrophages and lymphocytes, production of inflammatory cytokines and multiorgan failure. These immune disorders present the same clinical manifestations regardless of their cause. Patients who have CRS after administration of CAR-T therapy have the same clinical manifestations and laboratory tests that those with macrophage activation syndrome, including fever, multiorgan dysfunction, elevated levels of ferritin, LDH, soluble CD25, and cytokines such as IL-6 or IFN-γ or low levels of fibrinogen. Although patients with CRS often respond to supportive treatment, anti-IL-6 or steroids, MAS appears in 1% of patients, who present high mortality if the condition is not treated at the right time. It is therefore essential to establish new diagnostic criteria for MAS, in addition to the classic ones, which would allow us to distinguish the patients who will benefit from other treatments [16,19,20,37–40].
Elevated neutrophil-to-lymphocyte ratio in children and adolescents with attention-deficit/hyperactivity disorder
Published in International Journal of Psychiatry in Clinical Practice, 2021
Arif Önder, Özge Gizli Çoban, Aslı Sürer Adanır
Although this study has a fairly large sample size, it has some limitations. First, this is a cross-sectional study; therefore, a causal relationship could not be investigated. Longitudinal studies that investigate the effects of ADHD treatment on inflammation as well as NLR and PLR values may have a vast impact in this field. Second, we could not obtain the body mass indexes of the subjects, which may affect the parameters. Third, CRP levels, cytokines and subtypes of lymphocytes were not assessed, which would provide additional findings regarding inflammation. Chronic pro-inflammatory immune disorder in ADHD is likely due to a predisposing genetic background. There has been evidence from genetic studies that polymorphisms in genes related to inflammatory pathways play a role in ADHD.