Ethchlorvynol

(Chest 1992; 102:239-50) ACE = angiotension-converting enzyme; BAL = broncho-alveolar lavage; BCNU = carmustine; BOOP = bronchiolitis obliterans with organizing pneumonia; IL-2 = interleukin-2; PVOD = pulmonary veno-occlusive disease

Diagnosing drug-induced pulmonary disease remains a challenge for all pulmonologists. Keeping up with what is new in this field is also a challenge. This review is intended for the pulmonologist who has a good working knowledge of the effects of drugs on the lungs but who needs to be brought up-to-date. One of us (E. C. R.) collects monthly Med-Line searches of articles pertaining to drug-induced pulmonary disease. Interestingly, the majority of the articles referred to in this review are from journals other than the one that pulmonologists would be expected to read. There are a number of reviews of this subject for those interested in more in-depth information.[1-5] Drugs known to cause pulmonary disease are shown in Table 1. Not all the drugs known to induce pulmonary disease will be discussed in this review unless new information has become available in the past several years.

Alveolar proteinosis has been recognized in a number of patients receiving chemotherapy, primarily busulfan (Fig 4).[87-89] For the most part, these patients have chronic myelogenous leukemia. The histology of the alveolar proteinosis is identical to that seen in the spontaneous primary form, but anecdotal experience suggests that patients are less likely to respond to therapeutic lavage. Of over 200 patients with alveolar proteinosis, reviewed by Bedrossian et al,[87] nearly 15 percent had a hematologic disorder, and may were receiving chemotherapeutic agents. It has been suggested that epithelial hyperplasia caused by the drugs, particularly busulfan, is probably responsible for the induction of excessive surfactant production.

Pneumothorax has been reported following therapy with a number of chemotherapeutic agents,[90-92] but it appears that bleomycin is the one most commonly mentioned.[91-92] In one report, 30 percent of the patients receiving BCNU eventually developed pneumothorax. In one series, all four patients receiving amiodarone who developed ARDS also had pneumothoraces.[23]

Pulmonary veno-occlusive disease (PVOD) has been associated with the use of bleomycin, mitomycin-C, BCNU, etoposide, and cyclophosphamide.[93-95] There are scattered reports of this condition occurring following bone marrow transplantation. It has been noted that a high dose of methylprednisolone brought about clinical remission. The roentgenographic changes may mimic drug-induced pulmonary disease as well as many other complications. However, hemosiderinladen macrophages in BAL specimens may provide a clue to the diagnosis. In addition, the presence of Kerley B lines on the chest roentgenogram raises the suspicion of PVOD.

Classification by End-Organ Response

Bronchiolitis Obliterans with Organizing Pneumonia

Bronchiolitis obliterans with organizing pneumonia has been described as a manifestation of drug toxicity for a number of medications (Table 3).[5,48,49,67,96] Patients frequently have isolated or patchy air space opacities, which can mimic pulmonary infections or neoplasms. The morphologic changes are usually indistinguishable from those described in so-called idiopathic BOOP. Most patients recover with corticosteroid therapy.

Bronchospasm

Bronchospasm as a complication of drug-induced pulmonary disease should be considered in any asthmatic patient receiving any medication.[97,98] Table 4 lists the drugs known to cause or aggravate bronchospasm. Vinblastine is a drug that has been around for many years, but only in the last several years has it been combined with mitomycin. The two appear to act synergistically to produce bronchospasm.[59,60] A small but definite percentage of patients who have an acute nitrofurantoin reaction will have bronchospasm with or without parenchymal changes.

Acetylsalicylic acid is said to produce a worsening of bronchospasm in at least 5 percent of asthmatic patients and should always be considered a potential aggravator.[99,100] There are over 200 proprietary drugs containing acetylsalicylic acid, and patients may not mention these as drugs taken. The nonacetylated salicylates have been shown to be safe in asthmatic patients,[99] whereas nonsteroidal anti-inflammatory agents may cause bronchospasm.[101]

As noted earlier, IL-2 may aggravate bronchospasm and should be used with caution in any patient with a known history of obstructive lung disease.[54] Dipyridamole increases the concentration of adenosine, which is a bronchoconstrictive agent, and a very small percentage (less than 1 percent) of patients receiving this medication at the time of a thallium study will develop significant bronchospasm.[102] Almost all of these patients have underlying obstructive lung disease and should be protected with theophylline prior to the use of dipyridamole and certainly should be given theophylline should bronchospasm occur at the time of using this drug.

Protamine has some unusual side effects that usually occur during general anesthesia when the drug is used to reverse anticoagulant effects of coronary bypass. One of these effects is significant bronchospasm, which should be kept in mind by the anesthesiologist.[103]

Nebulizing any medication, such as pentamidine or beclomethasone, or propellant has the potential of aggravating irritable airways.[104-106] Beclomethasone is the only nebulized corticosteroid recognized to aggravate bronchospasm. There are two conflicting reports on the protective benefits of albuterol in pentamidine-induced bronchoconstriction. Quieffin et al[107] demonstrated that 34 percent of subjects had a decrease in [FEV.sub.1] of 10 percent or more, but it was effectively prevented by albuterol or ipratropium, whereas cromolyn sodium was only partially effective. They were unable to demonstrate any predictive factors. Katzman et al[108] found that 26 percent of patients developed a reduction in [FEV.sub.1] of 15 percent or more in their patients, but albuterol did not protect against this event.

Paradoxical bronchospasm in response to nebulized beta-agonists occurs rarely.[109 Intravenous hydrocortisone has been reported to cause severe asthma and is the only corticosteroid that has been recognized to do this.[98] Methotrexate has recently been implicated as a causative agent in inducing asthma.[110,111]

Cocaine has many adverse effects on the body, as well as the lung specifically, and one of them is bronchospasm.[66-69] Propafenone is a new antiarrhythmic agent with scattered reports of aggravating asthma; this should be avoided in patients at risk.[112,113]

Pleural Effusion

Table 5 lists the drugs that have been associated with pleural effusion.[114-116] The mechanism is unknown. Studies of the pleural fluid ar few and far between, such that the analysis of pleural fluid in the presence of these drugs gives little insight into the diagnostic accuracy and really serves as a source of eliminating other possible causes. A recent report of a procainamide-induced lupus pleuritis disclosed a white blood cell count of 53,200/cu mm (70 percent polymorphonuclear leukocytes), a pH of 7.195, and a lactate dehydrogenase value of 4,296 IU/L, suggesting a pleural space infection (glucose, 79 mg/dl), that cleared with discontinuation of the drug.[117]

Interestingly, with bromocriptine there is an intense lymphocytic response that is quite characteristic in this setting. Whether this is associated with other listed drugs is unknown.

Pulmonary Insufficiency

Table 6 lists the drugs associated with acute onset of pulmonary insufficiency, whether due to noncardiac pulmonary edema or an acute inflammatory reaction.[118,119] Reed and Glauser[118] reviewed the literature and summarized the drugs that are known to do this as well as suspected theories.

Table 7 lists the drugs that cause subacute respiratory insufficiency. L-Tryptophan is not discussed because it is no longer available.

Figure 5 lists known or suspected drug synergisms, most of which have been discussed already.

Table 8 outlines the results of BAL in drug-induced pulmonary disease.[120-122] Unfortunately, in most situations the results are nondiagnostic, but they are frequently useful in excluding other causes (eg, infection). [Tabular Data 8 Omitted]

References

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