Drug-induced lung disease

2020 ◽  
pp. 4272-4281
Author(s):  
S. J. Bourke
Keyword(s):  
Lung Disease ◽  
Enzyme Inhibitors ◽  
Oral Contraceptive Pill ◽  
Drug Effects ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Vascular Involvement ◽  
Drug Induced ◽  
Converting Enzyme Inhibitors ◽  
Effect Of Treatment ◽  
Respiratory Conditions

Drug-induced lung disease is common and needs to be considered in the differential diagnosis of many respiratory conditions. The nature and timing of events often provide important clues and are sometimes sufficiently characteristic for drug-induced lung disease to be diagnosed with confidence, with resolution of symptoms on drug cessation providing further supportive evidence. Direct drug effects may arise through toxic, pharmacological, allergic, or idiosyncratic mechanisms (there may also be indirect effects). From a clinical perspective, adverse effects may be classified according to the induced disorder and the site of involvement. Asthma is the most common airway disorder to be induced or exacerbated by drugs. Cough is a well-recognized side effect of treatment with angiotensin-converting enzyme inhibitors. Pulmonary vascular involvement includes venous thromboembolism (e.g. oral contraceptive pill), and pulmonary hypertension (e.g. aminorex, now withdrawn), dasatinib, and interferons. Pleural effusions and thickening may result from drugs (e.g. dantrolene, bromocriptine, methysergide, and dasatinib).

scholarly journals Drug-Induced Cough

2020 ◽  
pp. S81-S92 ◽  
Author(s):  
J. Shim ◽  
W.-J. Song ◽  
A.H. Morice
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Chronic Cough ◽  
Side Effect ◽  
Enzyme Inhibitors ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Converting Enzyme ◽  
Drug Induced ◽  
Converting Enzyme Inhibitors ◽  
Effect Of Treatment

Since the recognition of angiotensin-converting enzyme inhibitors (ACEIs)-induced cough, drug has been considered as a potential cause of chronic cough. This review presents recent knowledge on drug-induced coughs in patients with chronic cough. The focus is placed on ACEIs, for which there are a multitude of studies documenting their associations with cough. Additional drugs are discussed for which there are reports of cough as a side effect of treatment, and the potential mechanisms of these effects are discussed.

Drug-induced lung disease

2018 ◽  
Author(s):  
Salman Siddiqui ◽  
Dhananjay Desai
Keyword(s):  
Lung Disease ◽  
Progressive Disease ◽  
Enzyme Inhibitors ◽  
Latency Period ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Symptom Development ◽  
Drug Induced ◽  
Converting Enzyme Inhibitors ◽  
Radiological Change ◽  
Radiological Changes

Pulmonary drug toxicity is being increasingly recognized as a cause of various forms of lung disease. The spectrum of disease can range from transient, minor reactions to rapidly progressive disease with fatal consequences. A large number of drugs are linked to pulmonary disease; however, causality is often difficult to establish, because the length of the latency period between exposure and the onset of disease can vary and because there can be discordance between symptom development and the appearance of radiological changes, which may not be present at all (e.g. angiotensin-converting enzyme inhibitors can cause cough-related airways disease in the absence of radiological change).

Beta-blocker/ACE inhibitor therapy differentially impacts the steady state signaling landscape of failing and non-failing hearts

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
A Sorrentino ◽  
N Bagwan ◽  
N Linscheid ◽  
P Poulsen ◽  
K Kahnert ◽  
...  
Keyword(s):  
Ace Inhibitor ◽  
Enzyme Inhibitors ◽  
Drug Effects ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Left Ventricular ◽  
Global Changes ◽  
Converting Enzyme Inhibitors ◽  
Reduced Ejection Fraction ◽  
Funding Sources ◽  
Post Surgery

Abstract Background The molecular underpinnings of heart failure with reduced ejection fraction (HFrEF) involves a complex remodeling of the contractile, metabolic and electrical functions. Current pharmacotherapy for patients presenting HFrEF includes combination of angiotensin-converting enzyme inhibitors (ACEi) and β-adrenergic receptor blockers (β-AR blockers). Yet, a knowledge gap exists regarding the molecular changes accompanying such treatment. Purpose The present study takes an omics approach to study protein and phosphorylation signaling derangement in HFrEF and to define the global changes resulting from treatment with β-AR blocker (metoprolol) and ACE inhibitor (enalapril) in control- and HFrEF hearts. Methods and results For induction of HFrEF, a tight and permanent ligature was applied to constrict the transverse aorta in male C57BL6 mice. Eight weeks post-surgery, an osmotic pump was implanted delivering either vehicle or treatment (enalapril, ACE inhibitor, and metoprolol, β-AR blocker) for a two week period. The proteome- and phosphoproteome of left ventricular tissue was resolved using high-resolution liquid chromatography-mass spectrometry. The resulting dataset covered 6,004 proteins and 14,967 phosphorylation events. HFrEF was characterized by profound downregulation of mitochondrial proteins coupled with derangement of β-adrenergic and pyruvate dehydrogenase signaling. Upon treatment, phosphorylation changes consequent to HFrEF were reversed, including a reversal of Pdhk4 activity. In controls, treatment mainly led to downregulation of canonical PKA signaling. Overall, the signaling response elicited by treatment was profoundly different for failing than for control hearts. Conclusions We used state-of-the-art proteomics and phosphoproteomics approaches to analyze changes in protein abundance and phosphorylation state of the left ventricle resulting from combination therapy with a β-AR blocker and an ACE inhibitor in failing and non-failing hearts. Our observation of divergent signaling outcomes depending on the disease state of the heart underscores the importance of evaluating drug effects within the context of the specific conditions present in the recipient heart. FUNDunding Acknowledgement Type of funding sources: Foundation. Main funding source(s): The Danish Council for independent ResearchLundbeck FoundationFondation Leducq Transatlantic Network of Excellence

Drug-induced pancreatitis: focus on drugs used to treat cardiovascular disease

2021 ◽  
pp. 37-42
Author(s):  
A. V. Filippova ◽  
O. D. Ostroumova
Keyword(s):  
Adverse Reactions ◽  
Enzyme Inhibitors ◽  
Antihypertensive Drugs ◽  
Case Series ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Angiotensin Ii Receptor ◽  
Drug Induced ◽  
Converting Enzyme Inhibitors ◽  
Treatment And Prevention ◽  
Meta Analyses

Cardiovascular diseases (CVD) are the leading cause of death worldwide and in Russia. Therefore, the question of safe and rational drug therapy is acute. But, like most drugs, drugs for the treatment of CVD have a number of adverse reactions, in particular, the development of acute pancreatitis. This adverse reactions can be both dose-dependent and depend on the duration of administration of these groups of drugs. The purpose of this review is to analyze the literature data on drugs intended for the treatment of СVD that can lead to the development of drug-induced pancreatitis (LIP), on the mechanisms of development of this pathology against the background of taking specific drugs, diagnosis, treatment and prevention. The development of LIP is associated with the use of diuretics, both loop (furosemide, etacric acid, bumetamide), and thiazide/thiazide-like (chlorothiazide, hydrochlorothiazide and chlorthalidone), antihypertensive drugs of central action (methyldopa), angiotensin converting enzyme inhibitors and angiotensin II receptor blockers, statins, antiarrhythmic drugs (amiodarone, procainamide). Literature data on the development of LIP are presented in most publications with the description of clinical case/series of cases, however, in the case of LIP associated with the use of ACEI and statins, there are also data from cohort, retrospective observational, prospective case-control, randomized controlled trials, and meta-analyses. With timely diagnosis, and the cancellation of drugs that have caused the development of OP, the symptoms of the disease regress until they completely disappear and develop serious consequences.

scholarly journals Delayed angioedema during therapy with angiotensin-converting enzyme inhibitors

2011 ◽  
Vol 68 (4) ◽  
pp. 372-376 ◽  
Author(s):  
Slobodan Jankovic ◽  
Srdjan Stefanovic
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Enzyme Inhibitors ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
First Episode ◽  
Term Therapy ◽  
Chronic Obstructive ◽  
Converting Enzyme ◽  
Drug Induced ◽  
Converting Enzyme Inhibitors ◽  
Obstructive Pulmonary Disease

Introduction. Angiotensin-converting enzyme inhibitors are leading cause of drug-induced angioedema, with incidence of 0.1 to 0.2%. The angioedema is not of immune nature; in predisposed individuals it is caused by accumulation of vasoactive mediators due to reduced activity of angiotensinconverting enzyme. Case report. We presented a 63-year old male patient suffering from hypertension and chronic obstructive pulmonary disease, who had developed two episodes of angioedema during a 5-year long therapy with enalapril. The first episode happened after three, and the second after five years of the therapy. On both occasions, the patient was admitted to the hospital and tracheotomy was avoided in the last moment. Conclusion. Long-term therapy with angiotensin-converting enzyme inhibitors could be associated with delayed angioedema, especially in patients with inflammation of airways caused by infection or chronic irritation.

scholarly journals ACE-inhibitor induced angioedema masked by nephrotic syndrome

2016 ◽  
Vol 4 (16) ◽  
pp. 67
Author(s):  
Kenneth Iwuji ◽  
Hezekiah Sobamowo ◽  
James Tarbox ◽  
Rose Egbe
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Ace Inhibitors ◽  
Ace Inhibitor ◽  
Enzyme Inhibitors ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
The United States ◽  
Converting Enzyme ◽  
Drug Induced ◽  
Converting Enzyme Inhibitors ◽  
Medical Disorders

Angiotensin-converting enzyme (ACE) inhibitors are the leading cause of drug-induced angioedema in the United States because these drugs are widely prescribed for several common medical disorders. Angiotensin-converting enzyme inhibitors cause angioedema in 0.1 to 0.7 percent of recipients. When prescribing ACE-inhibitors to patients, angioedema should always be considered as a potential adverse reaction during treatment.

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