Insights in Anaphylaxis and Clonal Mast Cell Disorders

González-de-Olano, David; Álvarez‐Twose, Iván

doi:10.3389/fimmu.2017.00792

Cited by 19 publications

(10 citation statements)

References 68 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…On the other hand, mast cells in secondary and idiopathic MCAS (increased activation) are normal, and symptoms of mast cell activation are related to other, secondary underlying conditions that activate these cells (allergies, neoplasms, inflammatory or autoimmune diseases, or unknown factors). 137 …”

Section: Patients At Riskmentioning

confidence: 99%

Anaphylaxis in the 21st century: phenotypes, endotypes, and biomarkers

Jiménez-Rodriguez

Garcia-Neuer

Alenazy

et al. 2018

JAA

109

131

View full text Add to dashboard Cite

Anaphylaxis is the most serious of all allergic reactions and can be fatal. The diagnosis is frequently delayed, and misdiagnosis often occurs with asthma or urticaria. Biomarkers such as tryptase are not routinely checked, and appropriate treatment with epinephrine is not administered in a majority of cases, increasing the risk of poor outcomes. The objective of this review is to provide a better understanding of the pathophysiology of anaphylaxis with a description of phenotypes, endotypes, and biomarkers available in both the clinical and research settings. Expanding knowledge with regard to the presentation, causes, and triggers for anaphylaxis among health care providers will improve its diagnosis and management, increase patient safety, and decrease morbidity and mortality.

show abstract

Section: Patients At Riskmentioning

confidence: 99%

Anaphylaxis in the 21st century: phenotypes, endotypes, and biomarkers

Jiménez-Rodriguez

Garcia-Neuer

Alenazy

et al. 2018

JAA

109

131

View full text Add to dashboard Cite

show abstract

“…The idiopathic group has not yet been well characterized . MCAS encompasses a wide range of systemic symptoms secondary to excessive release of MC mediators which can occasionally result in anaphylaxis . Mastocytosis is an established condition and comprises of clonal MCs in various organs and tissues (mostly the bone marrow), and can be grouped into three main categories: cutaneous mastocytosis, systemic mastocytosis (SM) and mast cell sarcoma .…”

Section: Mast Cell Disorders Misdiagnosed As Idiopathic Anaphylaxismentioning

confidence: 99%

“…Diagnosis of SM can be established if at least one major and one minor criterion are detected, or with three minor criteria . Indolent SM, especially without skin lesions, is frequently underdiagnosed, due to the “silent” nature of the condition and lack of specificity of clinical symptoms . Some patients may not meet the required criteria for SM, show no evidence of cutaneous manifestations but may have evidence for a clonal MCs on bone marrow examination .…”

Section: Mast Cell Disorders Misdiagnosed As Idiopathic Anaphylaxismentioning

confidence: 99%

“…The only available validated tool is the Spanish Network on Mastocytosis (Red Española de Mastocitosis [REMA]) scoring system . This model is based on a combined clinical (ie gender and clinical symptoms) and laboratory (baseline tryptase value with “cut‐off” of 15‐25 ng/mL) parameters, to predict underlying MC clonality in patients presenting with systemic MC activation symptoms, including anaphylaxis . Gulen et al recommended using a modified version of the REMA score with a baseline serum tryptase “cut‐off” values of 11.4‐20.0 ng/mL, instead of 15‐25 ng/mL, which resulted in a better sensitivity (93%) and specificity (94%) when retrospectively applied to their study cohort.…”

Section: Mast Cell Disorders Misdiagnosed As Idiopathic Anaphylaxismentioning

confidence: 99%

See 1 more Smart Citation

Idiopathic anaphylaxis

Bilò

Martini

Tontini

et al. 2019

Clin Experimental Allergy

View full text Add to dashboard Cite

Idiopathic anaphylaxis (IA) or spontaneous anaphylaxis is a diagnosis of exclusion when no cause can be identified. The exact incidence and prevalence of IA are not known. The clinical manifestations of IA are similar to other known causes of anaphylaxis. A typical attack is usually acute in onset and can worsen over minutes to a few hours. The pathophysiology of IA has not yet been fully elucidated, although an IgE‐mediated pathway by hitherto unidentified trigger/s might be the main underlying mechanism. Elevated concentrations of urinary histamine and its metabolite, methylimidazole acetic acid, plasma histamine and serum tryptase have been reported, consistent with mast cell activation. There is some evidence that corticosteroids reduce the frequency and severity of episodes of IA, consistent with a steroid‐responsive condition. Important differential diagnoses of IA include galactose alpha‐1,3 galactose (a carbohydrate contained in red meat) allergy, pigeon tick bite (Argax reflexus), wheat‐dependent exercise‐induced anaphylaxis, Anisakis simplex allergy and mast cell disorders. Other differential diagnoses include “allergy‐mimics” such as asthma masquerading as anaphylaxis, undifferentiated somatoform disorder, panic attacks, globus hystericus, vocal cord dysfunction, scombroid poisoning, vasoactive amine intolerance, carcinoid syndrome and phaeochromocytoma. Acute treatment of IA is the same as for other forms of anaphylaxis. Long‐term management is individualized and dictated by frequency and severity of symptoms and involves treatment with H1 and H2 receptor blockers, leukotriene receptor antagonist and consideration for prolonged reducing courses of oral corticosteroids. Patients should possess an epinephrine autoinjector with an anaphylaxis self‐management plan. There are anecdotal reports regarding the use of omalizumab. For reasons that remain unclear, the prognosis of IA is generally favourable with appropriate treatment and patient education. If remission cannot be achieved, the diagnosis should be reconsidered.

show abstract

“…Mast cells play a key role in the process of inflammation. 50 They are the major effector cells that drive allergic responses. Upon stimulation with antigens, mast cells secrete a large number of granules that contain histamine and other inflammatory mediators such as cytokines and eicosanoids.…”

Section: Tyrosine Phosphorylation Of Phb1 In Antigen-stimulated Signamentioning

confidence: 99%

Prohibitin: a potential therapeutic target in tyrosine kinase signaling

Ande

Mishra

2017

Sig Transduct Target Ther

View full text Add to dashboard Cite

Prohibitin is a pleiotropic protein that has roles in fundamental cellular processes, such as cellular proliferation and mitochondrial housekeeping, and in cell- or tissue-specific functions, such as adipogenesis and immune cell functions. The different functions of prohibitin are mediated by its cell compartment-specific attributes, which include acting as an adaptor molecule in membrane signaling, a scaffolding protein in mitochondria, and a transcriptional co-regulator in the nucleus. However, the precise relationship between its distinct cellular localization and diverse functions remain largely unknown. Accumulating evidence suggests that the phosphorylation of prohibitin plays a role in a number of cell signaling pathways and in intracellular trafficking. Herein, we discuss the known and potential importance of the site-specific phosphorylation of prohibitin in regulating these features. We will discuss this in the context of new evidence from tissue-specific transgenic mouse models of prohibitin, including a mutant prohibitin lacking a crucial tyrosine phosphorylation site. We conclude with the opinion that prohibitin can be used as a potential target for tyrosine kinase signal transduction-targeting therapy, including in insulin, growth factors, and immune signaling pathways.

show abstract

Insights in Anaphylaxis and Clonal Mast Cell Disorders

Cited by 19 publications

References 68 publications

Anaphylaxis in the 21st century: phenotypes, endotypes, and biomarkers

Anaphylaxis in the 21st century: phenotypes, endotypes, and biomarkers

Idiopathic anaphylaxis

Prohibitin: a potential therapeutic target in tyrosine kinase signaling

Contact Info

Product

Resources

About