Platelet thrombopathy in asthmatic patients with elevated immunoglobulin E

Ca, Maccia; Js, Gallagher; Ataman, G; Hi, Glueck; Sm, Brooks; Il, Bernstein

doi:10.1016/0091-6749(77)90210-x

Cited by 61 publications

(48 citation statements)

References 27 publications

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“…Depressed platelet function might be another beneficial factor. Indeed, subjects with high IgE are characterized by a prolonged bleeding time28 and impaired platelet aggregability.28 29 This mild hemostatic imbalance, similar to the one caused by aspirin ingestion, might explain28 why death from myocardial infarction in patients with atopic bronchial asthma appears to be rare. 30 31 We would like to point out, however, that in patients with acute myocardial infarction the high levels of IgE and low complication rate observed by us are only two associated events, and any causative relationship at this time is totally speculative.…”

Section: Discussionmentioning

confidence: 99%

Serum immunoglobulin E response to myocardial infarction.

Szczeklik¹,

Sładek²,

Szczerba³

et al. 1988

Circulation

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Mast cells have been implicated in the pathogenesis of coronary heart disease. They can be activated by immunoglobulin (Ig) E-mediated mechanisms to release powerful mediators affecting local blood flow. We have determined systematically serum IgE concentrations in 100 patients with acute myocardial infarction. There was a consistent pattern of change in serum IgE, characterized by a significant increase on the third and fifth day, peak values on the seventh day, and a gradual decline to initial levels by the end of the third week after infarction. The increase in serum IgE shortly after myocardial infarction was similar to the increase in blood eosinophil count, but was in contrast to serum IgG levels. After infarction, patients with high initial IgE levels (> 200 IU/ml) had a greater increase in IgE and less frequent severe complications than those whose initial IgE levels were below 200 IU/ml. In 16 subjects with acute coronary insufficiency without infarction serum IgE levels remained unchanged. It is suggested that in myocardial infarction circulating IgE sensitizes both mast cells of coronary arteries and eosinophils, invading ischemic myocardium; this facilitates release of chemical mediators. Patients with high IgE levels might be protected against complications of infarction because of a favorable ratio of locally released mediators and because of decreased platelet function. Circulation 77, No. 6, 1245No. 6, -1249No. 6, , 1988 MAST CELLS have been implicated in the pathogenesis of coronary heart disease.1 2 Their number in the adventitia of coronary arteries increases with the progression of atherosclerosis.3 Higher mast cell counts are seen in coronary arteries containing both fresh and organizing thrombi, and lower counts are observed in association with fully organized thrombi.

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Section: Discussionmentioning

confidence: 99%

Serum immunoglobulin E response to myocardial infarction.

Szczeklik¹,

Sładek²,

Szczerba³

et al. 1988

Circulation

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“…An altered functionality is manifested as heightened platelet activation in vivo, while platelets from the same allergic patients are found to be refractory to a variety of stimuli ex vivo, possibly resulting from platelet 'exhaustion', due to the inability of platelets to replenish many released mediators that require de novo synthesis because platelets lack a nucleus (Harker et al, 1980;Pareti et al, 1980). Platelet 'exhaustion' has been reported as an inability of noradrenaline and adenosine di-phosphate (ADP) to induce full aggregation of platelets, with no secondphase aggregation, an occurrence that has been correlated with increased serum immunoglobulin E (IgE) in asthmatic patients (Maccia et al, 1977;Palma-Carlos et al, 1991). However, full aggregation of platelets in vitro returns in the same patients when studies are repeated outside of the allergy (pollen) season (Maccia et al, 1977).…”

Section: Platelet Activation In Asthma and Rhinitismentioning

confidence: 99%

“…Platelet 'exhaustion' has been reported as an inability of noradrenaline and adenosine di-phosphate (ADP) to induce full aggregation of platelets, with no secondphase aggregation, an occurrence that has been correlated with increased serum immunoglobulin E (IgE) in asthmatic patients (Maccia et al, 1977;Palma-Carlos et al, 1991). However, full aggregation of platelets in vitro returns in the same patients when studies are repeated outside of the allergy (pollen) season (Maccia et al, 1977). This alteration in platelet function has been associated with bronchial hyperresponsiveness that accompanies nocturnal asthma (Gresele et al, 1993).…”

Section: Platelet Activation In Asthma and Rhinitismentioning

confidence: 99%

“…Interestingly, IgE binds to between 20 and 30% of platelets from normal individuals, this binding affinity rises up to the binding of 50% of platelets from patients with allergies (Maccia et al, 1977;Joseph et al, 1986). Platelets from atopic individuals are characterized by a much greater IgE content stored in a-granules compared to non-atopics, which correlates to serum IgE levels from atopic patients.…”

Section: Platelet Activation In Asthma and Rhinitismentioning

confidence: 99%

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Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Pitchford

2007

British J Pharmacology

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An alteration in the character and function of platelets is manifested in patients with inflammatory diseases, and these alterations have been dissociated from the well‐characterized involvement of platelets in thrombosis and haemostasis. Recent evidence reveals platelet activation is sometimes critical in the development of inflammation. The mechanisms by which platelets participate in inflammation are diverse, and offer numerous opportunities for future drug intervention. There is now acceptance that platelets act as innate inflammatory cells in immune responses, with roles as sentinel cells undergoing surveillance, responding to microbial invasion, orchestrating leukocyte recruitment, and migrating through tissue, causing damage and influencing repair processes in chronic disease. Some of these processes are targeted by drugs that are being developed to target platelet participation in atherosclerosis. The actions of platelets therefore influence the pathogenesis of diverse inflammatory diseases in various body compartments, encompassing parasitic and bacterial infection, allergic inflammation (especially asthma and rhinitis), and non‐atopic inflammatory conditions, for example, chronic obstructive pulmonary disease (COPD), rheumatoid arthritis (RA), inflammatory bowel disease (IBD) and atherosclerosis. This review will first discuss the evidence for platelet activation in these various inflammatory diseases, and secondly discuss the mechanisms by which this pathogenesis occurs and the various anti‐platelet agents which have been developed to combat platelet activation in atherosclerosis and their potential future use for the treatment of other inflammatory diseases.British Journal of Pharmacology (2007) 152, 987–1002; doi:10.1038/sj.bjp.0707364; published online 2 July 2007

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“…They have a mild hemostatic imbalance [3], resembling that produced by aspirin [4]. It is reflected by a moderately prolonged bleeding time [5], depressed platelet aggregability [5,6] and delayed generation of thrombin in clotting blood [7]. In these patients, the generation of a clot inside a critically obstructed coronary artery would be prolonged and delayed because of the late appearance of thrombin.…”

mentioning

confidence: 99%

Mast Cell, IgE and Atherothrombosis

1998

Int Arch Allergy Immunol

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Platelet thrombopathy in asthmatic patients with elevated immunoglobulin E

Cited by 61 publications

References 27 publications

Serum immunoglobulin E response to myocardial infarction.

Serum immunoglobulin E response to myocardial infarction.

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Mast Cell, IgE and Atherothrombosis

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