Component
Aspirin-induced bronchospasm
Aspirin-induced bronchospasm. Species, exposure and limitations are retained in each linked claim.
1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What acts on it
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.
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
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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.