bubble_chart Overview

Aspirin intolerance triad, also known as Wielal's syndrome, is a respiratory hyperreactivity disease of unknown cause. Such patients often have nasal polyps and bronchial asthma. Nonsteroidal anti-inflammatory drugs such as aspirin and indomethacin can often induce rhinitis (sneezing, runny nose), asthma attacks, and may also be accompanied by symptoms such as urticaria and angioedema.

bubble_chart Epidemiology

Incidence This disease is more common in adults. Since patients often seek treatment from internal medicine or otolaryngology departments based on their symptoms, reported prevalence figures vary. Poole et al. (1985) provided a set of data for otolaryngology: approximately 20% of nasal polyp patients are intolerant to aspirin, 30–40% of those with nasal polyps accompanied by asthma are aspirin-intolerant, and 10% of unselected asthma patients exhibit aspirin intolerance.

bubble_chart Pathological Changes

Immunological experimental studies and clinical examinations have confirmed that this disease is not related to allergic reactions. It is now widely speculated that the shift in cell membrane arachidonic acid metabolism, leading to excessive production of leukotrienes (LTS), is the key factor in the onset of this disease. Non-steroidal anti-inflammatory drugs such as aspirin and indomethacin can cause a shift in arachidonic acid metabolism. LTS are not only potent bronchial smooth muscle constrictors but also highly bioactive inflammatory mediators, among which LT₄ exhibits strong chemotactic activity for eosinophils. In the respiratory tract, LTS can cause local mucosal edema and induce massive infiltration of eosinophils. The cytotoxic substances (primarily basic proteins) released by these cells not only injure the mucosal epithelium, increasing its sensitivity, but also damage the neural innervation of small blood vessel walls in the nasal mucosa, leading to vasodilation, increased permeability, and aggravated tissue edema, all of which contribute to polyp formation.

bubble_chart Clinical Manifestations

The disease often begins with vasomotor manifestations, with patients experiencing profuse watery nasal discharge and eosinophils in nasal secretions. Over time, hypertrophic sinusitis and nasal polyps may develop, and asthma can occur after middle age. Patients often experience induced rhinitis or asthma attacks after taking antipyretic analgesics such as aspirin. A very small number of patients may experience severe reactions, such as chest tightness, laryngeal obstruction, or even shock and death.

Based on clinical manifestations, the disease has the following characteristics: ① Recurrent sinusitis is common; ② Nasal polyps are highly prone to recurrence after surgery; ③ Asthma is often severe and typically corticosteroid-dependent; ④ Food color additives (tartrazine) and preservatives (benzyl alcohol) can also frequently trigger asthma attacks and worsen nasal polyps.

bubble_chart Diagnosis

1. All patients with nasal polyps should be asked about their history of asthma and tolerance to antipyretic analgesics.

2. Nasal examination should be considered routine for asthma patients. In asthma patients, nasal polyps can be found in 25–30% of cases (Molone, 1977). If nasal polyps are detected, this condition should be highly suspected.

3. A higher number of eosinophils are present in nasal secretions.

4. Radiographic examination reveals signs of sinusitis. Xie Yongming (1987) reported in China that 89.8% of aspirin-induced asthma patients showed sinusitis changes on X-ray plain films.

5. If asthma attacks are triggered by foods such as pastries, sausages, canned goods, or candies, further examination should be conducted.

6. **Aspirin oral provocation test**: Since this method may cause severe respiratory reactions, the following principles should be observed: ① It should be performed when the patient’s asthma is in remission. ② It should be conducted by an experienced pulmonologist under emergency-ready conditions. ③ The provocation dose starts at 3mg, increasing every 3 hours up to 650mg, administered three times daily. Lung function should be measured after each provocation. If FEV1 decreases by more than 25%, further provocation should be discontinued. ④ This test should not be performed on patients who have already provided a clear history of aspirin intolerance. {|105|}

bubble_chart Treatment Measures

1. For patients with nasal polyps and asthma attacks, avoid using antipyretic analgesics and consuming foods with color additives or preservatives.

2. For severe asthma patients, oral prednisone 30mg/d can be administered first. After asthma is controlled, switch to beclomethasone dipropionate aerosol inhalation, 3 times a day, one spray each time, with a total daily dose of 400mg.

3. For patients with larger nasal polyps, oral prednisone 30mg/d can be given first for one week. After the polyps shrink, switch to intranasal triamcinolone acetonide nasal drops or beclomethasone dipropionate aerosol for nasal inhalation.

4. For cases where large nasal polyps cause significant nasal stuffiness and show no improvement after the above treatments, surgical removal may be considered. However, systemic corticosteroids should still be used for 1–2 weeks before surgery, followed by intranasal application. Janhi-Alanko et al. (1989) reported that 59% of patients experienced improved asthma postoperatively, while 12% had worsened asthma.