Aspirin-sensitive asthma and rhinitis

Where it participates (unsigned role)

1. After nasal instillation of 12 milligrams of acetylsalicylic acid, significant levels of peptide leukotrienes were detected in sensitive asthmatic patients at 60 minutes in association with a significant increase in symptoms, with no increase in either insensitive patients or healthy subjects, while inhibition of prostaglandin E2 and F2-alpha release was detected in all three groups; aspirin also inhibited prostaglandin D2 release in insensitive asthmatic patients but not in sensitive patients or healthy subjects.

   Aspirin / acetylsalicylic acid → Peptide (cysteinyl) leukotrienes source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/aspirin-research/1309968.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a81a9ed941df59e6b8aa8c7c730d9a14766e2b8bd358b712ee464ae96c67e4e2", "start_char": 0, "end_char": 1685, "text_sha256": "a81a9ed941df59e6b8aa8c7c730d9a14766e2b8bd358b712ee464ae96c67e4e2"}

   experimental_model

   Double-blind nasal lavage challenge in ten aspirin-sensitive asthmatics, ten insensitive asthmatics and seven healthy subjects

   exposure

   12 milligrams of acetylsalicylic acid instilled nasally against saline

   limitations

   Three groups including two control groups, with mediators measured directly in the target tissue. Radioimmunoassay of nasal lavage fluid, and a small number per group.

   nutrient_topic

   Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. · Aspirin / acetylsalicylic acid

   organism

   Human

   plain_language

   The drug blocks prostaglandins in everyone, but only in the sensitive patients does a flood of leukotrienes follow.

   primary_references

   [asa-p1309968] Release of peptide leukotriene into nasal secretions after local instillation of aspirin in aspirin-sensitive asthmatic patients. (1992). https://pubmed.ncbi.nlm.nih.gov/1309968/ DOI: 10.1164/ajrccm/145.1.65

   tissue_or_cell_type

   Nasal mucosa

   Aspirin: the serine it acetylates, the enzyme that acetylation creates, the dose that separates platelet from vessel wall, and the metabolite that is a different drug (2026-09-22) · lines 572–583

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind nasal lavage challenge in ten aspirin-sensitive asthmatics, ten insensitive asthmatics and seven healthy subjects · source_derived_draft · unverified_draft

   ### asa-only-sensitive-patients-release After nasal instillation of 12 milligrams of acetylsalicylic acid, significant levels of peptide leukotrienes were detected in sensitive asthmatic patients at 60 minutes in association with a significant increase in symptoms, with no increase in either insensitive patients or healthy subjects, while inhibition of prostaglandin E2 and F2-alpha release was detected in all three groups; aspirin also inhibited prostaglandin D2 release in insensitive asthmatic patients but not in sensitive patients or healthy subjects. Condition category: normal nutrient_topic: Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. plain_language: The drug blocks prostaglandins in everyone, but only in the sensitive patients does a flood of leukotrienes follow. organism: Human tissue_or_cell_type: Nasal mucosa experimental_model: Double-blind nasal lavage challenge in ten aspirin-sensitive asthmatics, ten insensitive asthmatics and seven healthy subjects limitations: Three groups including two control groups, with mediators measured directly in the target tissue. Radioimmunoassay of nasal lavage fluid, and a small number per group. exposure: 12 milligrams of acetylsalicylic acid instilled nasally against saline evidence_span: {"source_cache": "artifacts/aspirin-research/1309968.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a81a9ed941df59e6b8aa8c7c730d9a14766e2b8bd358b712ee464ae96c67e4e2", "start_char": 0, "end_char": 1685, "text_sha256": "a81a9ed941df59e6b8aa8c7c730d9a14766e2b8bd358b712ee464ae96c67e4e2"} [asa-p1309968] Release of peptide leukotriene into nasal secretions after local instillation of aspirin in aspirin-sensitive asthmatic patients. (1992). https://pubmed.ncbi.nlm.nih.gov/1309968/ DOI: 10.1164/ajrccm/145.1.65

   Complete structured claim and evidence

2. Excretion of leukotriene E4 was increased by a mean of 361% during aspirin-induced asthma episodes, but the degree of increase for individual patients did not correlate with the degree of bronchospasm or with inhibition of platelet thromboxane B2 formation, so although endogenous synthesis of potent bronchoconstrictor leukotrienes increases during aspirin-induced bronchospasm it appears unlikely that direct shunting of unmetabolised arachidonate into leukotriene synthesis represents the mechanism of aspirin-induced asthma.

   Urinary leukotriene E4 excretion → Aspirin-induced bronchospasm source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/aspirin-research/1309376.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "115a13f9e08205c2b6ea376e5a1fcb90cc6887b277041acc114908c7d85f6e05", "start_char": 0, "end_char": 1427, "text_sha256": "115a13f9e08205c2b6ea376e5a1fcb90cc6887b277041acc114908c7d85f6e05"}

   experimental_model

   Urinary leukotriene E4 measured during aspirin-induced asthma episodes across a range of provoking doses

   exposure

   Aspirin doses from 30 to 365 milligrams in individual aspirin-sensitive patients

   limitations

   Tests the shunting hypothesis by asking whether the leukotriene rise tracks the bronchospasm, which it does not. Urinary leukotriene E4 is a whole-body measure rather than an airway one.

   nutrient_topic

   Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. · Aspirin / acetylsalicylic acid

   organism

   Human

   plain_language

   The leukotrienes do rise, but how much they rise says nothing about how badly the patient wheezes.

   primary_references

   [asa-p1309376] Increased excretion of leukotriene E4 during aspirin-induced asthma. (1992). https://pubmed.ncbi.nlm.nih.gov/1309376/

   tissue_or_cell_type

   Airway and urine

   Aspirin: the serine it acetylates, the enzyme that acetylation creates, the dose that separates platelet from vessel wall, and the metabolite that is a different drug (2026-09-22) · lines 559–570

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Urinary leukotriene E4 measured during aspirin-induced asthma episodes across a range of provoking doses · source_derived_draft · unverified_draft

   ### asa-shunting-does-not-track Excretion of leukotriene E4 was increased by a mean of 361% during aspirin-induced asthma episodes, but the degree of increase for individual patients did not correlate with the degree of bronchospasm or with inhibition of platelet thromboxane B2 formation, so although endogenous synthesis of potent bronchoconstrictor leukotrienes increases during aspirin-induced bronchospasm it appears unlikely that direct shunting of unmetabolised arachidonate into leukotriene synthesis represents the mechanism of aspirin-induced asthma. Condition category: normal nutrient_topic: Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. plain_language: The leukotrienes do rise, but how much they rise says nothing about how badly the patient wheezes. organism: Human tissue_or_cell_type: Airway and urine experimental_model: Urinary leukotriene E4 measured during aspirin-induced asthma episodes across a range of provoking doses limitations: Tests the shunting hypothesis by asking whether the leukotriene rise tracks the bronchospasm, which it does not. Urinary leukotriene E4 is a whole-body measure rather than an airway one. exposure: Aspirin doses from 30 to 365 milligrams in individual aspirin-sensitive patients evidence_span: {"source_cache": "artifacts/aspirin-research/1309376.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "115a13f9e08205c2b6ea376e5a1fcb90cc6887b277041acc114908c7d85f6e05", "start_char": 0, "end_char": 1427, "text_sha256": "115a13f9e08205c2b6ea376e5a1fcb90cc6887b277041acc114908c7d85f6e05"} [asa-p1309376] Increased excretion of leukotriene E4 during aspirin-induced asthma. (1992). https://pubmed.ncbi.nlm.nih.gov/1309376/

   Complete structured claim and evidence

3. The adverse effect of aspirin in asthmatics is often attributed to inhibition of the synthesis and release of defensive modulatory endogenous prostaglandins in the lungs, removing their negative feedback on allergic mediator release, and in addition work suggests diversion of arachidonic acid metabolism via the lipoxygenase pathway after cyclooxygenase inhibition, leading to formation of hydroperoxy acids and leukotrienes whose accumulation in sensitive individuals could explain the mechanism of aspirin-induced asthma.

   Aspirin / acetylsalicylic acid → Diversion of unmetabolised arachidonate into the 5-lipoxygenase pathway source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/aspirin-research/6113615.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "184fc232146a3837f396109d951c9755155f181c524a3ffaa330645138d8a616", "start_char": 0, "end_char": 2083, "text_sha256": "184fc232146a3837f396109d951c9755155f181c524a3ffaa330645138d8a616"}

   experimental_model

   Review of arachidonate metabolism in airway hyperreactivity and aspirin-induced asthma

   exposure

   Cyclooxygenase inhibition and the proposed diversion of arachidonate into the lipoxygenase pathway

   limitations

   A review from 1981 setting out the shunting hypothesis. It is recorded as the proposal that later work tested, not as evidence that the proposal is right.

   nutrient_topic

   Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. · Aspirin / acetylsalicylic acid

   organism

   Human

   plain_language

   The standard explanation: block one pathway and the raw material spills into another that makes bronchoconstrictors.

   primary_references

   [asa-p6113615] Lipoxygenase pathway and hydroperoxy acids: possible relevance to aspirin-induced asthma and hyperirritability of airways in asthmatics. (1981). https://pubmed.ncbi.nlm.nih.gov/6113615/ DOI: 10.1016/0161-4630(81)90097-5

   tissue_or_cell_type

   Airway

   Aspirin: the serine it acetylates, the enzyme that acetylation creates, the dose that separates platelet from vessel wall, and the metabolite that is a different drug (2026-09-22) · lines 546–557

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Review of arachidonate metabolism in airway hyperreactivity and aspirin-induced asthma · source_derived_draft · unverified_draft

   ### asa-shunting-proposed The adverse effect of aspirin in asthmatics is often attributed to inhibition of the synthesis and release of defensive modulatory endogenous prostaglandins in the lungs, removing their negative feedback on allergic mediator release, and in addition work suggests diversion of arachidonic acid metabolism via the lipoxygenase pathway after cyclooxygenase inhibition, leading to formation of hydroperoxy acids and leukotrienes whose accumulation in sensitive individuals could explain the mechanism of aspirin-induced asthma. Condition category: normal nutrient_topic: Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. plain_language: The standard explanation: block one pathway and the raw material spills into another that makes bronchoconstrictors. organism: Human tissue_or_cell_type: Airway experimental_model: Review of arachidonate metabolism in airway hyperreactivity and aspirin-induced asthma limitations: A review from 1981 setting out the shunting hypothesis. It is recorded as the proposal that later work tested, not as evidence that the proposal is right. exposure: Cyclooxygenase inhibition and the proposed diversion of arachidonate into the lipoxygenase pathway evidence_span: {"source_cache": "artifacts/aspirin-research/6113615.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "184fc232146a3837f396109d951c9755155f181c524a3ffaa330645138d8a616", "start_char": 0, "end_char": 2083, "text_sha256": "184fc232146a3837f396109d951c9755155f181c524a3ffaa330645138d8a616"} [asa-p6113615] Lipoxygenase pathway and hydroperoxy acids: possible relevance to aspirin-induced asthma and hyperirritability of airways in asthmatics. (1981). https://pubmed.ncbi.nlm.nih.gov/6113615/ DOI: 10.1016/0161-4630(81)90097-5

   Complete structured claim and evidence