A 37-year-old female with reported medical history of asthma was admitted with s

Question

A 37-year-old female with reported medical history of asthma was admitted with shortness of breath and thought to be due to asthma attack. She used a budesonide/formoterol inhaler daily, and short-term inhalers for exacerbations a few times per year. She had been hospitalized once prior for asthma but never intubated. The patient was in her usual state of health on the morning of admission when she boarded a flight heading from Hilo toward Togo. She was concerned about developing a blood clot on the long journey, so she took 325mg of aspirin right before take-off. Shortly thereafter, she noticed difficulty breathing, described as trouble getting air in. Symptoms persisted throughout a scheduled stopover in Los Angeles, and the patient became concerned that she would not be able to tolerate the second leg of the flight. She presented to the Emergency Department for further evaluation. She denied chest pain, palpitations, dizziness, visual change, audible wheeze, fevers, chills, sick contacts, weight gain, orthopnea, paroxysmal nocturnal dyspnea, tobacco use, or IV drug use. 3. What is causing her current symptoms? Briefly explain the mechanism that triggered the patient's asthma attack.

Explanation / Answer

Aspirin belongs to a class of medications called nonsteroidal anti-inflammatory drugs (NSAIDs). Aspirin has an important inhibitory effect on platelets in the blood. This antiplatelet effect is used to prevent blood clot that promote the clotting of blood inside arteries, particularly in individuals who have atherosclerosis (narrowing of the arteries) or are otherwise prone to develop blood clots in their arteries. People with asthma are at a higher risk for experiencing serious allergic reaction. Up to 20% of the asthmatic population is sensitive to aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) and present with a triad of rhinitis, sinusitis, and asthma when exposed to the offending drugs. This syndrome is referred to as aspirin-induced asthma (AIA). Thus, her current symptoms can be suspected for aspirin-induced asthma (AIA). An aspirin-induced asthma attack can be deadly.The attack can begin within minutes or up to two hours after taking aspirin or another NSAID. The reaction is usually dose dependent: small doses cause a mild attack and large doses cause a severe attack. Signs of an attack are runny or stuffy nose, swollen, watery or itchy eyes, redness in the face and neck, difficulty breathing, stomach pain. In very serious cases, the airways can narrow severely. The person goes into shock, becomes unconscious, or stops breathing. Asthma is an inflammatory condition of the airways characterized by the shedding of airway epithelium, sub-basement membrane fibrosis, airway smooth muscle hypertrophy, excessive secretion of mucus, and multicellular inflammation involving activated mast cells, eosinophils, neutrophils, macrophages, basophils, and lymphocytes. In this state of continuous inflammation, exposure to aspirin in a subset of asthmatic patients appears to temporarily accentuate the inflammatory process, leading to asthma exacerbations. The pathogenesis of AIA has implicated both thelipoxygenase (LO) and the cyclooxygenase (COX) pathways. By inhibiting the COX pathway, aspirin diverts arachidonic acid metabolites to the LO pathway. This also leads to a decrease in the levels of prostaglandin (PG) E2, the anti-inflammatory PG, along with an increase in the synthesis of cysteinyl leukotrienes (LTs). patients with AIA have increased activity of LTC4 synthase, the rate-limiting enzyme in the cysteinyl LT synthesis, in their bronchia, thereby tilting the balance in favor of inflammation. the hypersensitivity is mediated by a deviation of the arachidonic acid metabolic pathway toward excessive leukotriene (LT) production, which then produces all the clinical features of AIA.

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