Update on Diagnosis and Treatment of Mastocytosis

Brockow, Knut; Ring, Johannes

doi:10.1007/s11882-011-0199-2

Cited by 19 publications

(13 citation statements)

References 51 publications

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“…Fatal reactions may occur. This is in agreement with the observation that baseline serum tryptase levels are the best known predictor of the severity of anaphylaxis in insect sting-allergic patients (Brockow & Ring, 2011) .…”

Section: Mastocytocic and Anaphylaxissupporting

confidence: 92%

“…Factors determining the severity of reaction to hymenoptera sting include history of previous severe systemic reaction, insect type, older age, pre-existing cardiovascular and respiratory disease, and use of some medications. Mastocytosis and monoclonal mast cell activation syndrome are a risk factor for severe systemic reactions in allergic patients (Brockow & Ring, 2011).…”

Section: Venommentioning

confidence: 99%

“…As in patients without mastocytosis, the most frequently reported elicitors of anaphylaxis are insect venoms, drugs, and food. Severe and fatal reactions to hymenoptera venom have been described in patients with mastocytosis (Brockow & Ring, 2011). A variety of drugs have been reported to elicit anaphylaxis in patients with mastocytosis.…”

Section: Mastocytocic and Anaphylaxismentioning

confidence: 99%

“…Other medications leading to reactions in patients with mastocytosis are opiates (including morphine and codeine), acetylsalicylic acid, other NSAIDs, antibiotics, and radiocontrast media. In some patients with mastocytosis, anaphylaxis remains idiopathic despite an extensive search for elicitors (Brockow & Ring, 2011). The intensity of anaphylaxis in patients with mastocytosis has been described to be particularly severe.…”

Section: Mastocytocic and Anaphylaxismentioning

confidence: 99%

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Anaphylaxis: Etiology, Clinical Manifestations, Diagnosis and Management

Gelincik¹,

Büyüköztürk²

2012

Allergic Diseases - Highlights in the Clinic, Mechanisms and Treatment

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Anaphylaxis: Etiology, Clinical Manifestations, Diagnosis and Management 169 Animal modelsStudies with murine models demonstrate 2 pathways of systemic anaphylaxis: one mediated by IgE, FcεRI, mast cells, histamine, and platelet-activating factor (PAF), and the other mediated by IgG, FcγRIII, macrophages, and PAF. The former pathway requires much less antibody and antigen than the latter. As a result, IgG antibody can block IgE-mediated anaphylaxis induced by small quantities of antigen without mediating FcγRIII-dependent anaphylaxis (Finkelman et al., 2005). The IgE pathway is most likely responsible for most human anaphylaxis, which generally involves small amounts of antibody and antigen; similarities in the murine and human immune systems suggest that the IgG pathway might mediate disease in persons repeatedly exposed to large quantities of antigen. Antigen cross-linking of antigen specific IgE bound to mast cell FcεRI stimulates mast cell degranulation, with the rapid release of histamine and serotonin and the synthesis and secretion of platelet activation factor (PAF) and leukotrienes. These mediators act on target cells to increase vascular permeability which cause depletion of intravascular volume. The resulting decrease in vital organ perfusion is the primary cause of the symptoms that characterize murine anaphylaxis (Finkelman et al., 2005). The other pathway in mouse is Ig-E independent pathway. As contrary of clasical pathway, at first immunized and antigen challenged mice had anaphylaxis despite the absence of mast cells, FcεRI and IgE. This pathway is also complement independent but requires IgG antibody, macrophages, Fc RIII and PAF. Regardless which pathway takes place, mouse anaphylaxis occurs in very short time and displays similar symptoms. Potentially important differences between mouse and human anaphylaxis are proposed as follows: 1. Mouse IgG has some ability to activate mast cells, an effect that is not shared by any human IgG isotype, 2. IgE binds weakly to murine, but not human low-affinity Fc Rs, 3. Human but not mouse macrophages, Langerhans cells and dendritic cells can express FcεRI, and 4. Human platelets, B cells and natural killer cells, and neutrophils express low affinity IgG receptor (Fc RIIA, Fc RIIC, and Fc RIIIB, respectively) that are not expressed in mouse (Finkelman et al., 2005). Less antibody and antigen are required to trigger IgE dependent anaphylaxis then IgG mediated anaphylaxis. IgG and IgA blocking antibodies inhibit the ability of small quantities of antigen to induce IgE dependent anaphylaxis by neutralizing antigen before it can cross link mast cell associated IgE. IgG antibodies also inhibit IgE-dependent anaphylaxis by mediating an interaction between FcεRI and Fc RIIb on mast cells. In mice the predominant determinants that influence whether IgE dependent anaphylaxis is induced appear to be the quantity of antigen specific IgG antibody produced and the quantity of antigen used to challenge immunized mice. This suggests that IgG antibodies, in addition to me...

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Section: Mastocytocic and Anaphylaxissupporting

confidence: 92%

Section: Venommentioning

confidence: 99%

Section: Mastocytocic and Anaphylaxismentioning

confidence: 99%

Section: Mastocytocic and Anaphylaxismentioning

confidence: 99%

See 2 more Smart Citations

Anaphylaxis: Etiology, Clinical Manifestations, Diagnosis and Management

Gelincik¹,

Büyüköztürk²

2012

Allergic Diseases - Highlights in the Clinic, Mechanisms and Treatment

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“…Intermittierendes Auftreten von Juckreiz oder Flushs ist mit nicht sedierenden Antihistaminika (z. B. Loratadin, Cetirizin, Desloratadin, Levocetirizin, täglich oder bei Bedarf) meist gut beherrschbar [1,4]. Weiterhin haben sich topische Substanzen wie Polidocanol oder Cromoglycinsäure in der antipruritischen Therapie bewährt [27].…”

Section: Therapieunclassified

Mastozytosen im Kindesalter

et al. 2012

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Mastocytoses are a group of rare diseases characterized, in most cases, by a benign proliferation and accumulation of mast cells in different tissues. In children, mastocytosis affects usually exclusively the skin and differs in many aspects from adult-onset mastocytosis. Except for diffuse cutaneous mastocytosis, which is an uncommon subtype of childhood-onset mastocytosis, involvement of the bone marrow or additional extracutaneous organs is rarely seen in children. The prognosis of childhood-onset mastocytosis is usually very good. Compared to adult patients who most commonly experience chronic-stable or slowly progressive disease, mastocytosis in children is mostly transient and self-limiting. In this review, we present and discuss the subtypes of childhood-onset mastocytosis, recent advances in the understanding of their pathogenesis as well as similarities and differences between adult- and childhood-onset mastocytosis.

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