What Is the Connection Between Asthma and Aspirin?

Some patients develop an asthma attack within minutes to hours after taking aspirin, which is called aspirin asthma. The mechanism of aspirin asthma is that such drugs inhibit cyclooxygenase and hinder PG synthesis, but do not affect lipoxygenase, resulting in an increase in leukotrienes that cause bronchoconstriction and induce asthma.

Chinese name: Aspirin asthma
Time: Minutes after taking aspirin

Phenomenon: Presence of induced asthma
Cause: Increased leukotriene causing bronchoconstriction

Aspirin asthma I. Definition

Some patients can cause asthma attacks within a few minutes to hours after taking aspirin or other non-steroidal anti-inflammatory drugs (NSAIDS). The condition is more serious. This type of antipyretic analgesic anti-inflammatory drug Intolerance is called aspirin asthma ^[1] .

Aspirin asthma type

Aspirin asthma is generally classified into three types ^[2] :

(1) Start-up type:

No previous history of asthma. Ingestion of certain antipyretic and analgesics is the direct cause of the first asthma attack. Once asthma occurs, asthma attacks often occur without taking antipyretic and analgesics. This type is not common.

(2) Basic type of asthma:

Most patients have a history of asthma from months to years before the first antipyretic analgesic, that is to say, aspirin intolerance appears on the basis of the original asthma, and before taking aspirin (or other antipyretic analgesics) ) Will cause severe asthma attacks within a few minutes, of course, without antipyretic analgesics, other reasons can also induce asthma attacks.

(3) Basic type of rhinitis:

A few patients had no history of asthma before the asthma caused by the first antipyretic analgesic, but had a history of perennial allergic rhinitis, that is, aspirin asthma occurred on the basis of allergic rhinitis.

Aspirin asthma III. Pathogenesis

Aspirin asthma occurs at least in part because the pathway of arachidonic acid to produce prostaglandin E ₂ (PGE ₂ ) is blocked by aspirin, and the cyclooxygenase (COX) pathway is shifted to the 5-lipoxygenase (5-LO) pathway. , Cause excessive production of leukotriene, resulting in contraction of bronchial smooth muscle and stimulation of airway mucus secretion. The reduction in the production of PGE ₂ with bronchodilatory also promoted the increase in leukotriene. Leukotriene receptor antagonists and 5-LO inhibitors inhibit aspirin-induced bronchoconstriction in aspirin asthma. It also illustrates the role of leukotriene in the pathogenesis of aspirin asthma.

In non-aspirin asthma patients, NSAIDS does not cause increased leukotriene and asthma attacks. Studies have shown that the number of cells expressing leukotriene C4 (LTC4) synthetase in the bronchial biopsy tissue of aspirin asthma patients is significantly higher than that of non-aspirin asthma patients. In other words, NSAIDS can cause the same decrease in PGE ₂ synthesis in both aspirin asthma and non-aspirin asthma patients, but in aspirin asthma patients, the number of cells expressing LTC4 synthetase increases. Therefore, leukotriene synthesis increases, causing bronchoconstriction ^[3] .

Aspirin asthma IV. Clinical manifestations

1. Aspirin asthma usually occurs after taking antipyretic analgesics for 5 minutes to 2 hours or a little longer. It is often accompanied by cyanosis, conjunctival hyperemia, sweating, can't lie flat, and is restless.

2. Some patients develop nasal catarrh symptoms after taking the medicine, such as paroxysmal runny nose, itchy nose, stuffy nose, followed by asthma. Some patients may develop severe measles or angioedema at the same time as the asthma attack.

3. A few cases have symptoms of shock such as loss of consciousness and decreased blood pressure. The duration of drug action varies, ranging from 1 to 2 hours in short and 1 to 2 days in length. Correct and timely treatment can greatly reduce the duration of drug action [2].

4. Nearly 36% of the patients had nasal diseases, including chronic rhinitis, nasal polyps, paranasal sinusitis, and abnormal smell ^[3] .

Aspirin asthma V. Diagnosis

The possibility of aspirin asthma should be highly suspected when asthmatic patients:

(1) typical aspirin-induced respiratory symptoms;

(2) accompanied by chronic rhinitis;

(3) recurrent nasal polyps;

(4) Sudden asthma requiring admission to the ICU ward.

Although there is currently no gold standard for diagnosing aspirin asthma, asthma patients can be diagnosed with aspirin asthma if aspirin intolerance occurs. Aspirin intolerance can be performed by aspirin challenge test.

Here are some methods to diagnose aspirin intolerance challenge test:

1. Oral aspirin challenge test.

2. Lysine aspirin bronchial inhalation challenge test.

3. Intranasal challenge test for histamine, acetylcholine and antigen.

4. Intravenous challenge test with anti-inflammatory drugs (such as indomethacin).

Aspirin asthma

Rhinosinusography should be routinely performed on all patients with aspirin asthma. Most of the sinus cavity mucosa thickening or polyp-like hyperplasia can be seen, in severe cases see maxillary sinus effusion or total sinusitis. A sinus CT scan can more clearly show nasal polyps or sinusitis. Other special tests for allergic reactions are not specific for the diagnosis of aspirin asthma ^[3] .

Aspirin asthma VII. Treatment principles and precautions

In order to effectively prevent aspirin asthma, patients with asthma must pay attention to the following points ^[4] :

1. Asthma, especially those with nasal polyps, if fever occurs, it is advisable to first use physical methods to reduce temperature, or use Chinese medicine to reduce fever, and antipyretic and analgesics should be used with caution. Of the antipyretic and analgesics, paracetamol is the least likely to induce aspirin asthma.

2. Once aspirin asthma is diagnosed, antipyretic analgesics and non-steroidal anti-inflammatory drugs must be disabled, including aspirin, APC, phenacetin, paracetamol, aminopyrine, analgin, antipyrine, etc. Avoid the use of antiasthmatic drugs containing antipyretic and analgesic ingredients, such as compound theophylline and Yinqiao detoxification tablets. Before using a compound preparation, you must understand its pharmaceutical composition.

3. Aspirin patients with asthma are often intolerant to certain azo dyes such as lemon yellow, so foods with such dyes should be avoided, and various yellow sugar-coated tablets should be used as little as possible.

4. Aspirin with mild asthma symptoms can be taken orally or injecting aminophylline; those with severe symptoms should promptly use glucocorticoids (hormones) and anti-leukotriene drugs intravenously. If necessary, oxygen therapy should be given, and care should be taken to keep the airway open; critically ill patients should be treated with tracheal intubation and mechanical ventilation.

5. Aspirin patients with asthma are often more sensitive to hormones, so the correct and reasonable use of hormones is the key to treatment. In severe cases, methylprednisolone 40 mg can be given intravenously once every 6 hours. Critical patients can increase the dose as appropriate. Once the symptoms are relieved, they can be changed to oral hormones, and the dosage can be gradually reduced, and can be stopped for about 1 week. The long-term treatment of asthma-controlling drugs such as inhaled glucocorticoids (ICS) is very important to consolidate the efficacy and prevent future attacks. The treatment plan should follow the principles of graded treatment in the Global Asthma Prevention and Treatment Guidelines (GINA), but at least overlap with systemic hormone Use for several days.

6. If the patient has yellow sputum, fever, increased white blood cells, signs of infection, antibiotics should be added in time for treatment. In addition, adrenaline is not effective in treating aspirin asthma.