Smoking-induced Acute Eosinophilic Pneumonia Research Articles

UNILATERAL CRYSTAL METHAMPHETAMINE LUNG

TOPIC: Lung Pathology TYPE: Medical Student/Resident Case Reports INTRODUCTION: Methamphetamine is a drug manufactured from ephedrine and pseudoephedrine mixed with ingredients such as ammonia, lithium, iodine, and phosphorous but adulterants such as alcohol, acetone, and energy drinks have also been used. Smoking is the most common form of abuse with complications such as eosinophilic pneumonia, alveolar hemorrhage, acute interstitial pneumonia, and pulmonary fibrosis. We present an atypical methamphetamine-induced lung injury. CASE PRESENTATION: A 57-year-old female with a 40-pack year smoking history and polysubstance abuse presented with acute onset shortness of breath. On admission, she was hypoxic requiring 25 liters of high flow oxygen. On examination, the patient was afebrile with normal blood pressure. Chest auscultation revealed wheezing, most prominent in the left lung fields, while the rest of the systemic examination was unremarkable. Laboratories showed leukocytosis, normal liver, and renal function test. Sputum culture had no bacterial growth and Covid-19 PCR negative. Urine toxicology was positive for methamphetamine. Contrast CT chest showed diffuse interstitial thickening and ground-glass opacities throughout the right lung but normal left lung parenchyma with narrowing of the distal left mainstem bronchus by an endobronchial mass. The patient's hypoxemia improved with Methylprednisolone. Bronchoscopy showed a left mainstem lesion with near-complete obstruction of the left upper and lower lobes with biopsy revealing squamous cell carcinoma. There was normal airway mucosa on the right lung segments and scant inflammation without malignant cells on biopsy. The patient underwent successful tumor debulking with follow-up PET CT demonstrating decreased but persistence of alveolar septal thickening on the right lung with FDG positive mediastinal lymph nodes. The patient was weaned off supplemental oxygen 4 weeks later. DISCUSSION: Diagnosis of Methamphetamine-induced lung injury depends on the history of recent use, ground-glass opacities on imaging, and exclusion of other infections which was fulfilled by our patient but with the question of left lung sparing. Crystalline particles range in size from less than 250 nm-10 μm, with clusters as large as 80 μm where the obstructing mass may have prevented the flow of the drug vapor. Methamphetamine has also been postulated to release early response cytokines including TNF-alpha and IL-6 leading to recruitment of neutrophils and free radicals release causing acute lung injury. The management is mainly supportive with empiric steroids with improvement via impeding this inflammatory cascade. CONCLUSIONS: Our case demonstrates multiple learning points including particle size factor in passage through an obstructed airway, response to steroids supporting in settings of acute inflammation, and the persistence of residual lung disease on imaging in contrast to clinical improvement 4 weeks post-exposure. REFERENCE #1: Javed A, Nasrullah A, Malik K (February 08, 2021) A Rare Case of Methamphetamine-Induced Lung Injury During the Ongoing COVID-19 Pandemic. Cureus 13(2): e13215. doi:10.7759/cureus.13215 REFERENCE #2: Kinner SA, Degenhardt L. Crystal methamphetamine smoking among regular ecstasy users in Australia: increases in use and associations with harm. Drug Alcohol Rev. 2008 May;27(3):292-300. doi: 10.1080/09595230801919452. PMID: 18368611. REFERENCE #3: Lin SS, Chen YC, Chang YL, Yeh DY, Lin CC. Crystal amphetamine smoking-induced acute eosinophilic pneumonia and diffuse alveolar damage: a case report and literature review. Chin J Physiol. 2014 Oct 31;57(5):295-8. doi: 10.4077/CJP.2014.BAC201. PMID: 25241990. DISCLOSURES: No relevant relationships by Uchit Thapa, source=Web Response

Waterpipe (narghile, hookah) tobacco smoking-induced acute eosinophilic pneumonia

Acute eosinophilic pneumonia (AEP) is characterized by a febrile illness, diffuse pulmonary infiltrates, hypoxemic respiratory failure, and pulmonary eosinophilia. A temporal relationship has been described in a number of patients between the development of AEP and the recent onset of cigarette smoking. A 22-year-old male patient with no known chronic disease was admitted to the emergency service for 3 days with the complaints of cough, fever, dyspnea, and pleuritic chest pain. He was formerly a nonsmoker but was a waterpipe (narghile, hookah) tobacco smoker as a new habit once a night for the last 2 months. The erythrocyte sedimentation rate and C-reactive protein are elevated. Arterial blood gases revealed moderate hypoxemia. Computed tomography scans included bilateral, random, and patchy ground-glass opacities and also small bilateral pleural effusions. Echocardiograhic examination was normal. We had accepted the patient as an acute eosinophilic pneumonia due to rapid response to corticosteroid treatment, no microorganism in bronchoalveolar lavage (BAL) culture, and predominant eosinophilia was observed (70%–80%) in BAL.

Crystal Amphetamine Smoking-Induced Acute Eosinophilic Pneumonia and Diffuse Alveolar Damage: A Case Report and Literature Review

Eosinophilic pneumonia (EP) is a disease characterized by prominent infiltration of lung structures by eosinophils. The lung interstitium is infiltrated by eosinophils, and essentially the alveolar spaces are filled with eosinophils and a fibrinous exudate, with conservation of the global architecture of the lung. Diagnosis of EP relies on pathological demonstration of alveolar eosinophilia along with characteristic clinical manifestations of nonproductive cough, dyspnea, chest pain and/or unique imaging features. EP may be categorized according to the origin: EP of undetermined origin may overlap with well-individualized syndromes, while EP with a definite cause are mainly due to infections or drug abuse. Here, we report a case of an amphetamine abuser who developed acute EP and acute respiratory distress syndrome after amphetamine inhalation. Related studies on the pathogenesis of stimulant-related lung injury and treatment strategies are also discussed.

The relationship between the clinical course and cytokine in a patient with cigarette smoking-induced acute eosinophilic pneumonia – A case report

A 19-year-old female was admitted to our hospital because of a sudden onset fever and cough, and she was diagnosed to have acute eosinophilic pneumonia (AEP). The cause was thought to be cigarette smoking, because she had started smoking just before the development of AEP and her condition improved after cigarette smoking cessation, without corticosteroid treatment. The cytokines which are thought to be involved in eosinophilic accumulation in the lungs were analyzed using bronchoalveolar lavage fluid (BALF) and serum. Of the analyzed cytokines, only regulated on activation, normal T cell expressed and secreted (RANTES) increased in the serum after the improvement. RANTES is a unique chemokine which attracts not only eosinophils, but also T cells. Interestingly, in this case, the eosinophil count in the blood increased in parallel with the lymphocyte count after the improvement. These findings are interesting because it may help to understand the pathogenesis of AEP and the role of RANTES.

Smoking-Induced Acute Eosinophilic Pneumonia in a 15-year-old Girl: A Case Report

Acute eosinophilic pneumonia is a very rare disease that is characterized by acute febrile respiratory failure, diffuse bilateral infiltrates on chest X-ray, and eosinophilia in bronchoalveolar lavage fluid in the absence of infection. We present the case of a 15-year-old girl diagnosed with smoking-induced acute eosinophilic pneumonia. A previously healthy young girl with a 1-day history of fever presented with cough, dyspnea, and diffuse bilateral infiltrates on chest X-ray. She had started smoking only 3 weeks before presentation. She was diagnosed by bronchoalveolar lavage fluid tests and lung biopsy and dramatically improved after steroid treatment. We emphasize that acute eosinophilic pneumonia must be considered when acute pneumonia does not respond to broad-spectrum antibiotics. Effective treatment and prompt institution of therapy can obviate unnecessary morbidity and mortality.

Increased serum ADAM8 concentration in patients with drug-induced eosinophilic pneumonia-ADAM8 expression depends on a the allergen route of entry

ADAM8 (a disintegrin and a metalloprotease 8) has been linked to asthma and eosinophilic pneumonia (EP). ADAM8 cleaves a variety of substrates and is a sheddase for CD23, the low affinity IgE receptor. The concentration of soluble ADAM8 (sADAM8) is increased in bronchoalveolar lavage fluid (BALF) from patients with smoking-induced acute eosinophilic pneumonia (AEP) and chronic eosinophilic pneumonia (CEP), but not drug-induced EP (Drug-EP). In AEP, the BALF sADAM8 concentration significantly correlates with the soluble CD23 concentration (sCD23). To evaluate the involvement of ADAM8 in the pathogenesis of eosinophilic pneumonia, we measured the concentrations of sADAM8 and its substrate, soluble CD23 (sCD23), in serum from patients with AEP, CEP, and Drug-EP. We also measured the change in the sADAM8 concentration after a provocation test. In contrast to the BALF findings, serum sADAM8 concentrations were increased in Drug-EP (mean+/-SEM; 639.6+/-49.15) and serum ADAM8 levels correlated positively with the serum sCD23 levels in patients with Drug-EP (P=0.0080, R(2)=0.8465). Serum sADAM8 concentrations were also increased in AEP (409+/-76.91) and CEP (644.7+/-87.03). Serum ADAM8 concentrations were also elevated after the provocation test. Serum ADAM8 concentrations were elevated in Drug-EP, although the sADAM8 concentrations were not increased in the BALF in Drug-EP. Thus, the pathogenesis of AEP and Drug-EP may be distinct with regard to allergen exposure; AEP may be caused by the inhalation of antigens, whereas Drug-EP may be caused by bloodstream antigens. These findings indicate that ADAM8 levels reflect the route of eosinophilic inflammation in EP.

Cigarette Smoking-Induced Acute Eosinophilic Pneumonia: A Case Report Including a Provocation Test

The mechanism and cause of acute eosinophilic pneumonia are largely unknown. Many factors including the smoking of cigarettes have been suggested, but none have been proven to directly cause acute eosinophilic pneumonia. The authors report a case of acute eosinophilic pneumonia in a young Asian male who recently started smoking. The diagnosis was made based on his clinical course and results of chest radiography, lung spirometry, bronchoalveolar lavage, and transbronchial lung biopsies. After administration of methylprednisolone, his clinical course rapidly improved. A provocation test was designed to establish a connection between cigarette smoking and the development of acute eosinophilic pneumonia. After the provocation test, the patient showed identical symptoms, increase in sputum eosinophils, and worsening of pulmonary function. The results of the provocation test suggest that smoking may directly cause acute eosinophilic pneumonia, and support previous reports of cigarette smoking-induced acute eosinophilic pneumonia.

Elevated Soluble ADAM8 in Bronchoalveolar Lavage Fluid in Patients with Eosinophilic Pneumonia

Background: ADAM (a disintegrin and metalloprotease) family members, characterized by a metalloprotease and a disintegrin domain, are membrane-anchored glycoproteins involved in proteolysis and cell adhesion. ADAM8 might have an important role in allergic inflammation. It can cleave a variety of substrates and is a sheddase for VCAM-1 and CD23, the low-affinity IgE receptors. Methods: To evaluate the contribution of ADAM8 to the pathogenesis of eosinophilic pneumonia (EP), we measured the concentrations of soluble ADAM8 (sADAM8) and its substrates, soluble VCAM-1 (sVCAM-1) and soluble CD23 (sCD23), in bronchoalveolar lavage fluid from patients with smoking-induced acute eosinophilic pneumonia (AEP), chronic idiopathic eosinophilic pneumonia (CEP), and drug-induced eosinophilic pneumonia (drug-EP). Results: The sADAM8 and sVCAM-1 concentrations were increased in AEP and CEP. The sCD23 concentration was elevated in AEP. In AEP, but not CEP, the sADAM8 concentration significantly correlated with those of both sVCAM and sCD23. Conclusion: The pathogenesis of AEP, CEP, and drug-EP was distinct with regard to ADAM8. Our results are the first to associate ADAM8 with eosinophilic responses and lung inflammation in humans.

A Case of Cigarette Smoking-Induced Acute Eosinophilic Pneumonia Showing Tolerance

It has been proposed that acute eosinophilic pneumonia (AEP), which is characterized by the absence of recurrence, is associated with cigarette smoking (CS), because Japanese patients with AEP are young and have a high incidence of short-term smoking history. However, there has been no direct evidence that CS causes AEP. We hypothesized that tolerance might develop against repeated resumption of smoking cigarettes in CS-induced AEP cases. In this connection, we challenged a patient with CS-induced AEP with repeated resumption of CS, and it was demonstrated that CS induced AEP in conjunction with tolerance to repeated resumption of smoking.