DeCure for Asthma, nasal polyps, and aspirin intolerance
DeCure's autonomous Respiratory AI scientist is researching a drug-repurposing hypothesis for asthma, nasal polyps, and aspirin intolerance — screening already-approved drugs against its 1-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleAsthma, nasal polyps, and aspirin intolerance maps to a 1-gene Open Targets module — the target space DeCure's AI scientist screens approved drugs against.
DeCure.ai methodSignature reversal (LINCS) plus network proximity (STRING) rank already-approved drugs likely to perturb this module — the same engine that produces DeCure.ai's repurposing hypotheses.
Repurposing thesisScreening approved medicines against this disease module, then publishing the evidence for the strongest candidate. Known pharmacology and human exposure data make the first question sharper — they do not establish safety or efficacy in a new indication.
Research record
01
ResearchComing soon
Candidate research + dossier — target rationale, drug-repurposing thesis and evidence pack.proof: Published dossier + on-chain hash
02
ValidationComing soon
In-vitro biological validation at a contract research org (CRO).proof: CRO contract + in-vitro report
03
Peer review & paperComing soon
Peer-reviewed paper published open-access (preprint + journal).proof: DOI + open-access link + on-chain hash
Current lead
No approved-drug candidate for asthma, nasal polyps, and aspirin intolerance is corroborated in the literature DeepSearch retrieved. Some conditions are managed with non-pharmacological care — a device, surgery or physical therapy — rather than a medicine; that may be the case here, or the literature we found may simply be too sparse yet to support a drug-repurposing angle.
What the evidence adds up to
In a retrospective study of 445 patients with nasal polyps, 21 per cent had asthma. Two per cent of all patients had nasal polyps, asthma and hypersensitivity to aspirin (the ASA triad). Ten per cent of those with polyps and asthma were hypersensitive to aspirin. Asthma developed more commonly before polypectomy than after in a ratio of 2.5:1. Around 1 per cent of first polypectomies were followed by the development of asthma within a few months. The average age of onset of polyps was 39 years and of asthma was 38 years. A 1986 review notes that asthma and aspirin intolerance usually occur at the same time in life, followed by nasal polyps about ten years later, and describes the condition as a non-allergic, steroid-dependent asthma.
An open study of thirteen patients with aspirin-intolerant asthma and resistant nasal polyps, all but one of whom had undergone numerous polypectomies and were uncontrolled on standard therapy, examined the effect of intranasal lysine-aspirin administration. After three months, nasal inspiratory peak flow rate improved from 103.3 to 140.0 l/min (p = 0.014), while peak expiratory flow rate did not change significantly (438.7 vs 440.0 l/min, p = 0.700). Nasal nitric oxide levels rose significantly (p = 0.028), and nasal polyp scores on nasendoscopic examination were significantly reduced (right side p = 0.027, left side p = 0.018). Compared with the preceding three months, adding intranasal lysine-aspirin decreased nasal polyp volume (right side p = 0.031, left side p = 0.016). Nasal blockage symptoms tended to decrease, but other nasal symptoms were unchanged. A 2014 non-systematic review notes that oral and topical steroids form the mainstay of medical therapy for nasal polyps, that recurrences are common in aspirin-sensitive patients, and that topical nasal lysine-aspirin is an area under debate for use in both aspirin-sensitive and aspirin-tolerant patients.
A 1986 review states that desensitisation to aspirin is possible but does not improve asthma, and that polypectomy does not aggravate or cause asthma. A case report from 1987 describes a 44-year-old woman with aspirin-induced asthma whose polyp showed remarkable oedema and eosinophilic infiltration compared with nasal polyps in five patients without asthma.
What is still missing is a placebo-controlled, double-blind trial of intranasal lysine-aspirin, which the 2007 open study itself calls for. The 2014 review notes that diagnosis of aspirin sensitivity is rarely undertaken in routine practice, and that any adjunctive therapy to prevent or prolong recurrence would be welcome. No trial has yet stratified patients by aspirin sensitivity status in a controlled design, and no funding for such a trial is reported in these abstracts.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
The Journal of Laryngology & Otology · 1977 · 84 citations
Nasal polyps, nasal polypectomy, asthma, and aspirin sensitivity
AbstractIn a retrospective study of 445 patients with nasal polyps, 95 (21 per cent) had asthma. Forty-two (44 per cent) of the patients with asthma had been skin tested and 27 (60 per cent) had positive reactions. Nasal polyps were twice as common in men as women, though a woman with nasal polyps was twice as likely to have asthma as a man. The average age of onset of polyps was 39 years and of asthma was 38 years. No significant difference was found in the age of onset of polyps or asthma in various groups of patients. Two per cent of all the patients in the series had nasal polyps, asthma and hypersensitivity to aspirin (the ASA triad). Ten per cent of those with polyps and asthma were hypersensitive to aspirin and thus had the full triad. Overall, 6 per cent of all the patients in the series were recorded as being allergic to aspirin. Asthma developed more commonly before polypectomy than after in the ratio of 2.5:1. Around 1 per cent of first polypectomies and 0.5 per cent of all polypectomies were followed by the development of asthma within a few months. The onset of asthma was found to occur most frequently just before or just after the first polypectomy. Those who developed asthma after polypectomy had significantly more polypectomies than both non-asthmatics and those whose asthma preceded their polyps. Though it is possible polypectomy may on rare occasions precipitate asthma, it is felt that it does not cause it.
The Journal of Laryngology & Otology · 2007 · 49 citations · open access
Intranasal lysine-aspirin administration decreases polyp volume in patients with aspirin-intolerant asthma
AbstractINTRODUCTION: Nasal polyposis associated with aspirin-intolerant asthma tends to be difficult to control, with frequent recurrences. We examined the effect of intranasal lysine-aspirin administration on resistant nasal polyps of asthmatic, aspirin-intolerant patients, when used in addition to routine therapy. PATIENTS AND METHODS: Thirteen patients with asthma and intolerance to aspirin were recruited. All but one had undergone numerous polypectomies and were uncontrolled on standard therapy with intranasal corticosteroids, leukotriene receptor antagonists and nasal douching. Aspirin treatment involved one drop (100 microl) of 30 mg/ml lysine-aspirin solution to each nostril, initially daily, increased every two or three days up to a maximal of 18 drops (54 mg lysine-aspirin) a day. Nasal symptoms, nitric oxide level, nasal inspiratory peak flow rate, peak expiratory flow rate and nasendoscopic grading were assessed prior to therapy and three months later. We also compared the change in endoscopic polyp scores during three months of lysine-aspirin administration with the changes which had occurred during the three months prior to administration (during which time other therapies had been identical). RESULTS: Nasal blockage symptoms tended to decrease; other nasal symptoms were unchanged. Significant changes were seen in nasal inspiratory peak flow rate (103.3 +/- 18.9 and 140.0 +/- 16.7 l/min before and after aspirin, respectively; p = 0.014), but not in peak expiratory flow rate (438.7 +/- 33.4 and 440.0 +/- 28.4 l/min before and after aspirin, respectively; p = 0.700). Nasal nitric oxide levels rose significantly (in both sides, p = 0.028). Expired chest nitric oxide levels did not change. Nasal polyp scores on nasendoscopic examination were significantly reduced (right side, p = 0.027; left side, p = 0.018). Compared with the preceding three months, adding intranasal lysine-aspirin application had the effect on decreasing nasal polyp volume (right side, p = 0.031; left side, p = 0.016). CONCLUSION: This open study suggests that intranasal lysine-aspirin administration reduces nasal polyp volume in aspirin-intolerant patients, without any adverse affect on concomitant asthma. This was a preliminary study and should be followed by a placebo-controlled, double-blind trial.
Rhinology Journal · 2011 · 31 citations · open access
Aspirin desensitization for ASA triad patients--prospective study of the rhinologist's perspective
AbstractUNLABELLED: OBJECTIVES/PROBLEM: To determine the sinonasal effect of aspirin salicylic acid (ASA) desensitization in patients with nasal polyps, asthma and aspirin intolerance (ASA triad). METHODS OF STUDY: Patients with ASA triad were recruited from the outpatient otolaryngology clinic. They underwent a program of ASA desensitization (2005 - 2008) with prospective assessment of subjective and objective responses. Incremental doses of aspirin were given to reach a target of 625 mg twice daily during a period of 3 - 5 days. A maintenance dose was then given for the study period. The patients also received inhaled and topical nasal steroids, antihistamines and beta agonists for asthma control, but no systemic steroid treatment. MAIN RESULTS: Of the original 27 enrolled subjects, 10 elected to discontinue treatment and five dropped out because of treatment complications. The objective evaluation of the polypoid sinonasal disease in the remaining 12 patients (4 males, 8 females, age range 22 - 63 years) revealed only mild improvement. In contrast, the patients` subjective feeling of nasal congestion, nasal discharge and overall discomfort improved significantly. CONCLUSIONS: Aspirin desensitization has a favorable subjective effect on certain nasal symptoms among ASA triad patients, but the objective effect on polypoid mass is not significant.
Allergy and Asthma Proceedings · 1986 · 21 citations
Asthma, Aspirin Intolerance and Nasal Polyps
AbstractAsthma associated with aspirin intolerance (bronchospastic type) and nasal polyps is a special type of asthma with well established characteristics. Asthma and aspirin intolerance in these patients usually occurs at the same time in life followed by nasal polyps about 10 years later. Classically, it is a non allergic steroid-dependent asthma. Desensitization to aspirin is possible but does not improve asthma. Polypectomy does not aggravate or cause asthma. The pathogenic mechanism may involve arachidonic acid metabolism.
Expert Review of Clinical Immunology · 2014 · 16 citations
Topical nasal lysine aspirin in aspirin-sensitive and aspirin-tolerant chronic rhinosinusitis with nasal polyposis
AbstractChronic rhinosinusitis patients with nasal polyps can be aspirin sensitive or aspirin tolerant. The majority belong to the latter group. They tolerate intake of aspirin or other non-steroidal anti-inflammatory drugs, whereas aspirin-sensitive patients have an adverse reaction (asthma, rhinitis and/or urticaria). Diagnosis of aspirin sensitivity is important for the patient, but is rarely undertaken in routine ENT or respiratory medicine practice. Treatment of nasal polyps is by a combination of medical therapy and surgery. Oral and topical steroids form the mainstay of medical therapy, which is aimed at reducing inflammation and symptom improvement. Surgery helps with polyps causing severe nasal obstruction. Despite these therapies, recurrences are common in aspirin sensitive patients. Any adjunctive therapy to prevent or prolong recurrence would be welcome. One such possibility is topical nasal lysine-aspirin. This is an area under current debate and this non-systematic review aims to provide evidence of its use, to date, in aspirin sensitive and aspirin tolerant nasal polyp patients.
Efficacy of Aspirin Therapy After Desensitization on Chronic Rhinosinusitis With Nasal Polyps Patients With Asthma and Non‐steroidal Anti‐inflammatory Drug Exacerbated Respiratory Disease —A Randomized Clinical Trial
AbstractNon-steroidal anti-inflammatory drug (NSAID) exacerbated respiratory disease (N-ERD) is a chronic inflammatory condition typically involving hypersensitivity to NSAIDs, asthma, and/or chronic rhinosinusitis (CRS) with nasal polyps (CRSwNP). N-ERD increases the risk for severe hypersensitivity reactions, recurring sinonasal surgeries, or the need for systemic corticosteroid treatment. Aspirin (ASA) treatment after desensitization (ATAD) is a treatment option for N-ERD. Desensitization to ASA is reached with increasing ASA doses over a few days, followed by a long-term treatment. This study evaluated the efficacy of ATAD with an ASA dose of 250 mg in adult CRSwNP patients with asthma and N-ERD. Forty-one CRSwNP patients with comorbid asthma and N-ERD were recruited for this randomized double-blind clinical trial. Twenty-six patients had successful ASA desensitization, were randomized into placebo and ASA arms, and continued to 11 months of daily ASA, with a target dose of 250 mg. The outcome measures, including Sino-Nasal Outcome Test 22 (SNOT-22), nasal polyp score (NPS), Asthma Control Test (ACT), and EPOS 2012 CRS clinical control assessment, were evaluated at control visits at 1, 5, 11, and 12 months after the start of the treatment. In the linear mixed effects model, p-values for the combined effect of group and time showed no difference between placebo and ATAD for SNOT-22, ACT, and NPS, with p-values 0.17, 0.45, and 0.18, respectively. Neither group showed significant improvement in the EPOS 2012 CRS control assessment. In conclusion, no significant clinical difference was observed between ATAD and placebo in the treatment of CRSwNP patients with asthma and N-ERD.
AbstractWe treated a case of aspirin-induced asthma in a 44-year-old woman who complained of nasal obstruction. Her nasal disturbance first occurred in 1978, and she developed bronchial asthma in 1982. In 1985, she was diagnosed as having aspirininduced asthma. Both nasal polypectomy and ethmoid sinus operation were performed in June,1986. In this patient, a polyp showed remarkable edema and eosinophilic infiltration compared with nasal polyps in five patients without asthma.
Disease module: DeepOracle (Open Targets). Structures: RDKit from PubChem SMILES. Literature: retrieved by DeepSearch across 234,678,978 indexed works (targeted per-candidate search), resolved on OpenAlex.
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