cardiovascular-agents and Pleural-Diseases

Drug-induced pleural disease is uncommon and less known to clinicians than drug-induced parenchymal lung disease. Pleural reactions from drugs manifest as pleural effusions, pleural thickening, or pleuritic chest pain, and may occur in the absence of parenchymal infiltrates. The clinician should be cognizant of the possibility of a drug-induced pleural reaction. A detailed drug history, temporal relationship between symptom onset and initiation of therapy, and pleural fluid eosinophilia should raise the suspicion of a drug-related process. We suspect that as new drugs are marketed in the United States, the number of drugs that result in pleuropulmonary toxicity will continue to increase. Moreover, if the cause of an exudative pleural effusion is not clinically obvious after pleural fluid analysis, drug therapy withdrawal should be a consideration if clinically appropriate before initiating an extensive diagnostic evaluation that may entail unnecessary economic burden and discomfort for the patient.

Topics: Anti-Infective Agents, Urinary; Antimetabolites, Antineoplastic; Bleomycin; Cardiovascular Agents; Clozapine; Cyclophosphamide; Eosinophilia; Humans; Immunosuppressive Agents; Interleukin-2; Methotrexate; Methysergide; Nitrofurantoin; Penicillamine; Pleural Diseases; Pleural Effusion; Serotonin Antagonists

Disorders of the heart frequently cause pulmonary dysfunction because of the close structural and functional association of the heart and lungs. The pulmonary vasculature is very commonly affected by cardiac pathology. The pulmonary vasculature is normally a low-pressure, low-resistance circuit with high compliance and tremendous vascular reserve. Although resting vascular tone is low, there are many identified mediators of pulmonary arterial tone that may help mediate pulmonary blood flow. Alveolar hypoxia is clearly a stimulus for increasing pulmonary vascular resistance although factors that mediate the response to hypoxia are not fully understood. Patients with left-to-right shunting due to congenital heart disease because of elevations in pulmonary artery flow and pressure tend to develop progressive anatomic changes in the pulmonary vasculature. This leads to an increase in pulmonary vascular resistance, irreversible pulmonary hypertension, right heart failure, reversal of shunt flow, and Eisenmenger's syndrome. The degree of anatomic vascular damage due to left-to-right shunting can be graded histologically. Lesser grades of damage are reversible with corrective surgery, whereas more severe grades show no improvement or progression with operation. Chronic left-sided congestive heart failure seen in rheumatic mitral stenosis can cause secondary changes in the pulmonary vasculature. Pulmonary hypertension and increased pulmonary vascular resistance can increase reflexly and form a "second stenosis" that further limits cardiac output. Unlike congenital heart disease, severe grades of pulmonary arterial damage are not seen in left heart failure from mitral stenosis or other causes, and consequently with surgical correction pulmonary hypertension reverses. Pulmonary function testing is adversely affected by congestive heart failure. Both restrictive (stiff lungs) and obstructive (cardiac asthma) defects are observed in congestive heart failure. DLCO is abnormally decreased. With treatment of heart failure these defects reverse. Both elevated systemic and pulmonary venous pressures affect fluid filtration in the pleural space and cause pleural fluid accumulation. The fluid is transudative with low protein, low lactate dehydrogenase, and low cell counts. Transudative effusions from heart failure resolve with treatment. With large effusions and cardiomegaly, pulmonary dysfunction results because of atelectasis from compression and space-occupying effects o

Topics: Cardiovascular Agents; Heart Defects, Congenital; Heart Diseases; Humans; Hypertension, Pulmonary; Lung Diseases; Pleural Diseases; Pulmonary Circulation; Pulmonary Embolism; Respiratory Function Tests

More than 75 drugs are known to have adverse effects on the bronchopulmonary pleural system. Many of these drug reactions are fatal unless they are recognized, administration is stopped, and other measures are instituted. No data exist on the number of adverse drug reactions on the lung, because there is no mandatory reporting system in the United States. Probably less than 5% are reported. The clinician should be aware of the drugs that can produce adverse reactions on the lungs and stop the administration as soon as possible. In this article, I have classified the drugs known to produce adverse pulmonary effects as follows: chemotherapeutic, cardiovascular, antibiotic, and anti-inflammatory agents, drugs known to induce systemic lupus erythematosus, inhalants, illicit drugs such as heroin, and miscellaneous drugs. There are no blood tests or other means of diagnosing adverse drug effects on the lung. Chest roentgenographic findings are nonspecific. Pulmonary function abnormalities generally correlate with the degree of dyspnea and chest roentgenographic changes. Therefore, the clinician trying to explain the onset of pulmonary symptoms must be aware of the drugs the patient is taking.

Topics: Animals; Anti-Bacterial Agents; Anti-Inflammatory Agents; Bronchial Diseases; Cardiovascular Agents; Drug-Related Side Effects and Adverse Reactions; Humans; Illicit Drugs; Lung Diseases; Pleural Diseases