PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 9674393

Latex allergy.

E M Warshaw
View original source ↗Export metadata ↓

Abstract

UNLABELLED: Coined the next major health concern of the decade, allergy to natural rubber latex affects people routinely exposed to rubber products. Groups at highest risk include health care workers, rubber industry workers, and persons who have undergone multiple surgical procedures, especially those with spina bifida. Allergy to latex is a type I, immediate, IgE-mediated reaction, which can lead to anaphylaxis and death. Much of latex research is published in allergy journals. Dermatologists may not be aware of the prevalence, symptoms, risks, diagnosis, and treatment of latex allergy. These topics are the subject of this review. Research concerning antigenic proteins, as well as sources of latex alternatives, is also summarized. (J Am Acad Dermatol 1998;39:1-24.) LEARNING OBJECTIVE: At the completion of this learning activity, participants should have a clear understanding of the history, biology, epidemiology, mechanism, clinical characteristics, diagnostic work-up, and treatment of latex allergy. Readers should also have a greater understanding of multiple potential allergenic latex proteins and their importance in preventing future latex-sensitization.

Explore related subjects

AnaphylaxisChemical IndustryHealth PersonnelHumansHypersensitivity, ImmediateImmunoglobulin ELatexOccupational DiseasesPrevalenceRisk FactorsRubberSpinal DysraphismSurgical Procedures, OperativeJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

E M Warshaw. 1998. Latex allergy.. https://doi.org/10.1016/s0190-9622(98)70397-4

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2025

Magnesium protects against anaphylactic shock and cardiac myolysis in guinea-pigs.

The pathophysiological responses to immune stress (IS) include activation of several processes which are dependent on cytosolic Ca2+ elevation. Magnesium frequently acts as a natural Ca2+ antagonist. In this study we have observed that Mg2+ can protect guinea-pigs against IS. Antigen-sensitized guinea-pigs, which had been fed a magnesium-deficient diet, were given a single dose (15 mg) of MgCl2 intraperitoneally 1 h before antigen challenge. The development of anaphylactic shock (AS) was observed during the next 2 h, and the hearts were subsequently examined histologically for signs of cardiac myolysis (CM). Magnesium (i) reduced the incidence of CM from 40% to 10% (p < 0.05); (ii) reduced the incidence of AS from 61% to 35% (p < 0.05); (iii) attenuated the severity of the AS; and (iv) lowered mortality from 39% in the control to 19% in the Mg(2+)-treated group (p = 0.1). Serum and tissue total [Mg2+] were not affected by the administration of MgCl2. Also, the serum and heart Mg2+ levels were the same whether or not the guinea-pigs developed AS or CM. In cell culture we demonstrated that by elevating the [Mg2+] in the medium bathing sensitized rat basophilic leukemia (RBL) cells, the increase in cytosolic [Ca2+] subsequent to antigen challenge was reduced from 174 +/- 23.28% (1 mM) to 82.74 +/- 13.22% (3 mM). We conclude that a single treatment with Mg2+ can considerably diminish damage induced by immune stress, probably by its altering the Ca2+: Mg2+ ratio. Since the physiological reaction to different types of stress is similar, Mg2+ could prove beneficial in preventing stress-induced shock in general. Studies examining the mechanisms by which Mg2+ exerts its effects thus provide a scientific basis for the current clinical use of Mg2+ in acute myocardial infarction (AMI) and asthma.

Anaphylaxis↗
PubMed2007

Enhanced mast cell activation in mice deficient in the A2b adenosine receptor.

Antigen-mediated cross-linking of IgE bound to mast cells via the high affinity receptor for IgE triggers a signaling cascade that results in the release of intracellular calcium stores, followed by an influx of extracellular calcium. The collective increase in intracellular calcium is critical to the release of the granular contents of the mast cell, which include the mediators of acute anaphylaxis. We show that the sensitivity of the mast cell to antigen-mediated degranulation through this pathway can be dramatically influenced by the A2b adenosine receptor. Loss of this Gs-coupled receptor on mouse bone marrow-derived mast cells results in decreased basal levels of cyclic AMP and an excessive influx of extracellular calcium through store-operated calcium channels following antigen activation. Mice lacking the A2b receptor display increased sensitivity to IgE-mediated anaphylaxis. Collectively, these findings show that the A2b adenosine receptor functions as a critical regulator of signaling pathways within the mast cell, which act in concert to limit the magnitude of mast cell responsiveness when antigen is encountered.

Anaphylaxis↗