Anaphylaxis during negative penicillin skin prick testing confirmed by elevated serum tryptase

Durana, M. D. Alonso Díaz de; Fernández‐Rivas, Montserrat; Casas, María Luisa Maestro de las; Esteban, Elena; Cuevas, M.; Tejedor, M.A.

doi:10.1034/j.1398-9995.2003.00056_2.x

Cited by 18 publications

(12 citation statements)

References 8 publications

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“…(54–65). All routes of administration are potentially lethal: intra‐articular (66), intra‐uterine (67), intra‐lymphatic (64), inhalation (68, 69), rectal (70, 71), topical skin application (72–74), and even prick‐tests (75). Anaphylactoid reactions without defined immunological data have been associated with similar risk: angiotens in converting enzyme (ACE) inhibitors (76, 77), acetylcystein (78), nonhuman monoclonal antibodies (79, 80).…”

Section: Severe Drug‐induced Anaphylaxismentioning

confidence: 99%

Epidemiology of life‐threatening and lethal anaphylaxis: a review

Moneret-Vautrin

Morisset

Flabbee

et al. 2005

Allergy

342

177

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Severe anaphylaxis is a systemic reaction affecting two or more organs or systems and is due to the release of active mediators from mast cells and basophils. A four‐grade classification routinely places ‘severe’ anaphylaxis in grades 3 and 4 (death could be graded as grade 5). Studies are underway to determine the prevalence of severe and lethal anaphylaxis in different populations and the relative frequencies of food, drug, latex and Hymenoptera anaphylaxis. These studies will also analyse the risk arising from the lack of preventive measures applied in schools (personalized management protocols) and from the insufficient use of self‐injected adrenalin. Allergy‐related conditions may account for 0.2–1% of emergency consultations. Severe anaphylaxis affects 1–3 per 10 000 people, but for the United States and Australia figures are even higher. It is estimated to cause death in 0.65–2% of patients, i.e. 1–3 per million people. An increased prevalence has been revealed by monitoring hospitalized populations by reference to the international classification of disease (ICD) codes. The relative frequency of aetiological factors of allergy (food, drugs, insects and latex) varies in different studies. Food, drug and Hymenoptera allergies are potentially lethal. The risk of food‐mediated anaphylaxis can be assessed from the number of personalized management protocols in French schools: 0.065%. Another means of assessment may be the rate of adrenalin prescriptions. However, an overestimation of the anaphylaxis risk may result from this method (0.95% of Canadian children). Data from the literature leads to several possibilities. First, a definition of severe anaphylaxis should be agreed. Secondly, prospective, multicentre enquiries, using ICD codes, should be implemented. Moreover, the high number of anaphylaxis cases for which the aetiology is not identified, and the variation in aetiology in the published series, indicate that a closer cooperation between emergency specialists and allergists is essential.

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Section: Severe Drug‐induced Anaphylaxismentioning

confidence: 99%

Epidemiology of life‐threatening and lethal anaphylaxis: a review

Moneret-Vautrin

Morisset

Flabbee

et al. 2005

Allergy

342

177

View full text Add to dashboard Cite

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“…Numerous studies have shown that patients sensitive to preoperative agents [70], venom immunotherapy [71] and skin prick tests [72] exhibit very high levels of serum tryptase (hundreds of ng/ml) within an hour or less from the onset of response. Interestingly, it was indicated that elevated basal tryptase might constitute a risk factor for venom hypersensitivity, clearly a marker of clinical benefit.…”

Section: Tryptase In Anaphylaxis Sudden Infant Death Syndrome and Fatamentioning

confidence: 99%

Tryptase as an inflammatory marker in allergic disease and asthma

Bachelet¹,

Munitz²,

Levi‐Schaffer³

2005

Expert Review of Clinical Immunology

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Asthma is a chronic inflammatory disease of the airways, varying from occasional episodes of wheezing and shortness of breath, to an irreversible, life-threatening obstructive disease. While many cases are managed with relative ease, others do not respond to the traditional inhaled therapy or even to oral glucocorticosteroids. Although it cannot be cured as yet, asthma can be controlled if properly diagnosed. Usually, functional clinical parameters form the basis for estimation of the disease severity. In addition, the growing database of cytokine and mediator profiles have allowed their exploitation as molecular markers for processes underlying airway inflammation in asthma. Tryptase is a potent and versatile mediator in allergic inflammation, orchestrating both acute and chronic events by acting on a vast array of cells and tissue components. For more than a decade, tryptase has been used as a marker for allergic inflammation in asthma as well as in a variety of other airway diseases. In this review, the current advantages and disadvantages of the use of tryptase as an inflammatory marker in asthma will be discussed.

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“…Penicillin V was responsible for anaphylaxis in a case of systemic mastocytosis , and amoxicillin was identified as the cause of anaphylaxis in one patient in a German study and in a case report . Finally, a case of anaphylaxis during a penicillin skin test for suspected allergy to beta‐lactams in a woman with elevated baseline tryptase was recently described .…”

Section: Mast Cell Diseases and Use Of Antibiotics Anti‐inflammatorymentioning

confidence: 99%

Drug hypersensitivity in clonal mast cell disorders: ENDA/EAACI position paper

Bonadonna

Pagani

Aberer

et al. 2015

Allergy

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Mastocytosis is a clonal disorder characterized by the proliferation and accumulation of mast cells (MC) in different tissues, with a preferential localization in skin and bone marrow (BM). The excess of MC in mastocytosis as well as the increased releasability of MC may lead to a higher frequency and severity of immediate hypersensitivity reactions. Mastocytosis in adults is associated with a history of anaphylaxis in 22-49%. Fatal anaphylaxis has been described particularly following hymenoptera stings, but also occasionally after the intake of drugs such as nonsteroidal anti-inflammatory drugs, opioids and drugs in the perioperative setting. However, data on the frequency of drug hypersensitivity in mastocytosis and vice versa are scarce and evidence for an association appears to be limited. Nevertheless, clonal MC disorders should be ruled out in cases of severe anaphylaxis: basal serum tryptase determination, physical examination for cutaneous mastocytosis lesions, and clinical characteristics of anaphylactic reaction might be useful for differential diagnosis. In this position paper, the ENDA group performed a literature search on immediate drug hypersensitivity reactions in clonal MC disorders using MEDLINE, EMBASE, and Cochrane Library, reviewed and evaluated the literature in five languages using the GRADE system for quality of evidence and strength of recommendation.Mastocytosis is a clonal disorder characterized by the proliferation and accumulation of mast cells (MC) in different tissues, with preferential localization in skin and bone marrow (BM). The great majority of cases are associated with somatic gainof-function point mutations of KIT, a tyrosine kinase receptor (CD117). The clinical presentation of mastocytosis is heterogeneous ranging from symptoms limited to the skin (with frequent spontaneous regression in pediatric cases) to a more aggressive systemic variant (SM), typical only of adulthood. Mastocytosis patients can experience symptoms due to massive MC activation and release of mediators (e.g., generalized pruritus, urticaria/angioedema, abdominal pain, anaphylaxis), but the presence of mediator symptoms does not correlate with the allele burden of the KIT mutation (1).The current classification of mastocytosis was developed in 2000 (2) and accepted by the World Health Organization (WHO) in 2001 (3) and then updated in 2008 (4) ( Table 1). According to the WHO classification, two major categories are defined: cutaneous mastocytosis (CM), limited to the skin, and systemic mastocytosis (SM), involving extracutaneous organs, mainly BM (Table 1) (4). The diagnosis of SM requires the presence of one major criterion and one minor criterion, or alternatively three minor criteria (Table 2) Systemic variant is suspected in patients with mastocytosis in the skin (MIS) and also in patients without MIS who have systemic symptoms of MC mediator release, including anaphylaxis. Patients without MIS may be a diagnostic challenge. The European Competence Network on Mastocytosis (ECNM) recently ...

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Anaphylaxis during negative penicillin skin prick testing confirmed by elevated serum tryptase

Cited by 18 publications

References 8 publications

Epidemiology of life‐threatening and lethal anaphylaxis: a review

Epidemiology of life‐threatening and lethal anaphylaxis: a review

Tryptase as an inflammatory marker in allergic disease and asthma

Drug hypersensitivity in clonal mast cell disorders: ENDA/EAACI position paper

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