DRUG-INDUCED PLEURAL DISEASE
Section snippets
DRUG-INDUCED LUPUS PLEURITIS
Several drugs can cause a lupus erythematosis-like syndrome that is indistinguishable from patients who have native lupus.38 In fact, the administration of drugs known to cause lupus pleuritis to a patient with systemic lupus erythematosis (SLE) is contraindicated because there is a significant likelihood of aggravation of symptoms.1 The drugs that are associated with lupus pleuritis include procainamide, chlorpromazine, quinidine, isoniazid, phenytoin, and hydralazine. Antibiotic drugs such as
NITROFURANTOIN
Nitrofurantoin is an antibacterial agent that is chemically 1-5-Nitro-2-furanylmethyleneamino-2,4-imidazolidinedione.31 Nitrofurantoin is bactericidal in urine at therapeutic doses. Nitrofurantoin is reduced by bacterial flavoproteins to reactive intermediates that, in turn, inactivate or alter bacterial ribosomal proteins. It remains unclear whether that mechanism of nitrofurantoin action is involved in the acute hypersensitivity reaction that can occur in the lung parenchyma and the pleura.36
DANTROLENE
Dantrolene is a skeletal muscle relaxant that is similar to nitrofurantoin in structure. Dantrolene has been known to cause pleural effusions in patients using doses from 225 mg to 400 mg/day.60 Patients typically present with pleuritic chest pain, fever, and pleural effusions. The pleural effusion is usually unilateral, unlike nitrofurantoin-induced lung disease. It is not usually associated with pulmonary infiltrates as evaluated by routine radiograph. Pleural fluid, glucose, and amylase are
METHYSERGIDE
Methysergide maleate is a partially synthetic compound related to methylergonovine. The ergot alkaloids appear to have a common ability, both in vivo and in vitro, to block the effects of serotonin, a substance that may be involved in vascular headaches. Serotonin is a central neural humoral chemical mediator that acts directly or indirectly to lower the pain threshold. The use of methysergide for the treatment of cluster headaches or migraine has decreased somewhat but is still practiced in
BROMOCRIPTINE
Bromocriptine is an ergot derivative with potent dopamine receptor agonist activity. The active ingredient is bromocriptine mesylate. Bromocriptine activates postsynaptic dopamine receptors. The dopaminergic neurons modulate the secretion of prolactin and significantly reduce prolactin levels. The inhibition of physiologic lactation does not affect the secretion of other tropic hormones from the anterior-pituitary gland. Bromocriptine is used in patients with acromegaly, in which it lowers
PRACTOLOL
Practolol is a β-blocker not marketed in the United States that has been noted to cause sclerosis of the pleura and peritoneum. It also causes development of pleural effusion, pleuropulmonary fibrosis, peritonitis, deafness, and nephrotic syndrome.19, 25, 34 It became popular because it has several advantages over other β-blockers, including a long half-life and good volume of distribution. Long-term usage of practolol has been associated with pleuropulmonary complications, including
AMIODARONE
Amiodarone is a class III antiarrhythmic drug that blocks sodium channels at rapid pacing frequencies and exerts a noncompetitive antisympathetic action. One of its main effects is to lengthen the cardiac action potential and block cardiac potassium channels, which contribute to slowing of conduction and prolongation of refractoriness. Administration of the drug prolongs intranodal conduction and refractoriness of the atrioventricular node, but has no effect on the sinus cycle. Amiodarone is
PROCARBAZINE
Procarbazine is a hydrazine derivative and an antineoplastic agent. It is indicated in combination with other anticancer drugs for the treatment of stage III and stage IV Hodgkin's disease. It is also used as part of the MOPP (nitrogen mustard, vincristine, procarbazine, prednisone) regimen.17, 50 Procarbazine is absorbed rapidly and completely. The mechanism of action is considered to be cessation of protein synthesis associated with inhibition of DNA and RNA synthesis. In addition,
METHOTREXATE
Methotrexate is an antimetabolite used in the treatment of neoplastic diseases, psoriasis, and rheumatoid arthritis. The mechanism of action includes inhibition of dihydrofolic acid reductase. Methotrexate interferes with DNA synthesis and cellular replication. Actively proliferating tissues such as malignant cells, mucosal cells, and cells of the urinary bladder are acutely sensitive to the effects of methotrexate. When used in the treatment of rheumatoid arthritis, it is hypothesized that
BLEOMYCIN
Bleomycin is a cytotoxic glycopeptide antibiotic isolated from Streptomyces verticillus. Bleomycin is known to inhibit synthesis of DNA, RNA, and protein. Bleomycin is typically used for the treatment of squamous cell carcinoma of the head and neck, lymphomas such as Hodgkin's disease and non-Hodgkin's lymphoma, and testicular carcinoma. Interestingly, bleomycin is also used as a sclerosing agent for the treatment of recurrent pleural effusions. Adverse pleuropulmonary reactions occur in
MITOMYCIN
Mitomycin is an antibiotic agent isolated from the broth of Streptomyces caespitosus. Mitomycin inhibits synthesis of DNA and protein. It is cleared rapidly from the serum after intravenous administration and up to 10% of the drug is excreted unchanged in the urine. Mitomycin is typically used in combination chemotherapy for the treatment of disseminated adenocarcinoma of the stomach or pancreas and with appropriate surgery or radiotherapy.
Toxic effects of mitomycin include the development of
MINOXIDIL
Minoxidil is an antihypertensive agent, the side effects of which include excessive body hair growth. It acts as a peripheral vasodilator and is used to control blood pressure in severely hypertensive patients. The drug has been associated with the development of fluid in both the pericardium and the pleural space.53 The effusions, particularly in the pericardium, have been associated with tamponade. Bilateral pleural effusions have been noticed following the initiation of minoxidil therapy.
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Cited by (0)
Address reprint requests to Veena B. Antony, MD, Chief, Pulmonary and Critical Care Medicine, RL Roudebush VA Medical Center, 1481 W. 10th Street, Indianapolis, IN 46202
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Division of Pulmonary, Critical Care and Occupational Medicine, Department of Medicine, Indiana University School of Medicine; and Pulmonary and Critical Care Medicine, RL Roudebush VA Medical Center, Indianapolis, Indiana