China
Africa
Explore chapters and articles related to this topic
Anaphylaxis
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
Histamine is an important chemical mediator of allergic responses and the major clinical manifestations of anaphylaxis. Histamine is released by activated mast cells and basophils. Cutaneous histamine release causes urticaria and pruritus, while systemic release of histamine results in flushing, headache, bronchoconstriction, hypotension, tachycardia, as well as direct effects on coronary arteries and atrial and ventricular contractility (Reber et al. 2017). Histamine effects are mediated through four histamine receptors; H1, H2, H3 and H4, which are present on target cells in different organs (MacGlashan 2003). H1 and H2 receptors both mediate flushing, hypotension and headaches, whereas airway obstruction and tachycardia are primarily mediated via the H1 receptor (Kaliner et al. 1981, Vigorito et al. 1983). In animal models, H3 appears to influence cardiovascular response to norepinephrine, and H4 may be involved in chemotaxis, mast cell cytokine release and pruritus (Godot et al. 2007, Dunford et al. 2007).
Principles of Treatment for Arthropod Bites, Stings, and Other Exposure
Published in Gail Miriam Moraru, Jerome Goddard, The Goddard Guide to Arthropods of Medical Importance, Seventh Edition, 2019
Gail Miriam Moraru, Jerome Goddard
It has often been estimated that between 500 and 800 honey bee stings could cause death in humans due to the toxic effects of the venom alone. One author calculated that 1,500 honey bee stings would constitute the median lethal dose for a 75-kg person based on extrapolation from the LD50 of bee venom for mice.1 These direct toxic effects (from honey bees or other social Hymenoptera) would include release of histamine, contraction of smooth muscle, increase in capillary permeability, vasodilation with a resulting drop in blood pressure, destruction of normal tissue barriers, destruction of red blood cells, and pain. Severe cases would probably result in renal failure. Treatment strategies would include symptomatic treatment until the venom effects were diminished. As histamine is a component of bee, wasp, and hornet venoms, and as melittin (found in honey bee venom) causes histamine to be released from cells, administration of antihistamines would be indicated. In addition, therapeutic agents to counteract the ill effects of histamine release (e.g., bronchodilators) would also be helpful.
Neuromuscular care
Published in Hemanshu Prabhakar, Charu Mahajan, Indu Kapoor, Essentials of Anesthesia for Neurotrauma, 2018
Ankur Khandelwal, Hemanshu Prabhakar
Cisatracurium, the 1R cis–1′R cis isomer of atracurium, comprises approximately 15% of atracurium by weight, but more than 50% in terms of NM blocking activity. Cisatracurium 0.1 to 0.2 mg/kg produces adequate conditions for tracheal intubation within 2–3 minutes. Clinical recovery occurs in about 45 to 60 minutes. Continuous infusion dosing ranges from 1 to 3 µg/kg/min. Like atracurium, cisatracurium is metabolized by Hofmann elimination to laudanosine and a monoquaternary acrylate. In contrast, however, no ester hydrolysis of the parent molecule occurs. It is approximately four times as potent as atracurium and produces five times less laudanosine in contrast to atracurium. Moreover, it does not cause histamine release. Renal clearance is about 16% of total.
Tanshinone IIA alleviates ovalbumin-induced allergic rhinitis symptoms by inhibiting Th2 cytokine production and mast cell histamine release in mice
Published in Pharmaceutical Biology, 2022
Qing Chen, Liping Shao, Yong Li, Mian Dai, He Liu, Nan Xiang, Hui Chen
The concentration of histamine release from mast cells was determined by histamine test kit. Compound 48/80 (C48/80; C2313, Sigma-Aldrich, St. Louis, MO) can be used to facilitate histamine release (Won Jung et al. 2012). The collected human mast cell line HMC-1 in logarithmic growth phase was divided into four groups: (1) control group, (2) C48/80 group, (3) C48/80 + 5 μmol/L TIIA (TIIA-5) group and (4) C48/80 + 10 μmol/L TIIA (TIIA-10) group. Cells in each group (except for control group) were pre-treated using 0.5 μg/mL C48/80 at 37 °C for 1 h. Then, the cells in C48/80 + 5 μmol/L TIIA (TIIA-5) and C48/80 + 10 μmol/L TIIA (TIIA-10) groups, were treated with C48/80 and TIIA at different concentrations at 37 °C for 30 min, respectively. Finally, the culture supernatant was collected after centrifugation at 400×g for 5 min at 4 °C. Same as the above experimental procedures, mast cell histamine release was detected by histamine ELISA kit. The OD value of each well was measured with a microplate reader at a wavelength of 450 nm. Histamine release was calculated as the percent of total (cellular + extracellular) histamine.
Pediatric chronic spontaneous urticaria: a brief clinician’s guide
Published in Expert Review of Clinical Immunology, 2022
Martina Votto, Giovanna Achilli, Maria De Filippo, Amelia Licari, Alessia Marseglia, Alice Moiraghi, Antonio Di Sabatino, Gian Luigi Marseglia
Although the pathogenesis of CSU is not yet fully understood, it is well established that symptoms ultimately result from the activation of high-affinity IgE receptors (FcεRI) on cutaneous mast cells and basophils, leading to the release of histamine. Histamine release stimulates the sensory nerves causing itchiness and vasodilation, leading to swelling, both hallmarks of urticarial lesions. Based on recent evidence, causes of CSU include: i) type I autoimmunity (‘autoallergic mechanisms’) in which IgE-mediated hypersensitivity reactions against self-antigens promote the degranulation of basophils and mast cells; and ii) type II autoimmunity in which IgG autoantibodies against the Fc region of FcεRI receptor, or less frequently against IgE and IgE autoantigens, trigger IgE receptor activation [10,11]. The ‘autoallergic’ form of CSU is more often characterized by high C reactive protein (CRP), total serum IgE, blood eosinophils, and basophils that are reduced when the type II autoimmunity mechanisms prevail. CSU patients with type II autoimmunity are more likely to have low or very low total IgE and elevated levels of IgG anti-TPO. Thus, the high IgG anti-TPO/total IgE ratio is currently the best surrogate marker for this form of CSU [11,12]. Other underlying causes of CSU include active thyroid disease, infections, inflammatory processes, foods, and drugs, but these can be both causes and aggravating factors of the urticaria.
In vitro prediction of in vivo pseudo-allergenic response via MRGPRX2
Published in Journal of Immunotoxicology, 2021
Linu M. John, Charlotte M. Dalsgaard, Claus B. Jeppesen, Kilian W. Conde-Frieboes, Katrine Baumann, Niels P. H. Knudsen, Per S. Skov, Birgitte S. Wulff
Activation of MRGPRX2 induces mast cell degranulation and histamine release (McNeil et al. 2015; Ding et al. 2019). Histamine is one of the mediators released from mast cell granules upon activation by various toxins and is associated with symptoms of dermal edema/swelling (Garafalo and Kaplan 1981; Wei et al. 2009; Kimura et al. 2015). Histamine release has long been used as a marker of anaphylaxis or pseudo-allergenic reactions (Charitos et al. 2020). Quantitative and qualitative measurements of histamine release in the ex vivo setting have been developed to test for allergenic activity induced by a diverse array of test agents with both rodent and human ex vivo skin samples (de Antonio and Rothschild 1969; Petersen 1997, 1998; Petersen et al. 1996, 1997; Suzuki et al. 2020).