Robert H. Israel

Pulmonary toxicity induced by mitomycin C is highly responsive to glucocorticoids

The authors have studied five cases of biopsy‐proven pulmonary toxicity caused by the administration of mitomycin C (M), vincristine, and cisplatin in 64 patients with advanced non‐small cell lung cancer. The clinical triad of progressive dyspnea, rales, and pulmonary infiltrates presented in all five cases. In addition, pulmonary function tests showed hypoxemia (four/five), reduced forced vital capacity (three/four), total lung capacity (two/three), and forced expiratory volume (FEV1) (three/four) and very profound reduction in diffusion capacity (three/three). Transbronchial biopsy for tissue examination was necessary to rule out other causes. Characteristics but nonspecific pathologic changes were documented in all five cases. All the patients responded quickly and dramatically to high‐dose glucocorticoids with improvement of hypoxia, dyspnea, exercise tolerance, and sense of well being. In three patients the pulmonary infiltrates cleared. However, abrupt stopping or early withdrawal of steroid resulted in aggravation of dyspnea and pulmonary infiltrate in three cases who improved subsequently with escalation of steroid doses. The authors conclude that the treatment of choice for pulmonary toxicity induced by M or M‐containing chemotherapy regimens is a high dose of glucocorticoid and discontinuation of M at once when suspicion is raised. Cancer 57:2285–2290, 1986.

Case Report The rapid development of an aspergilloma secondary to allergic bronchopulmonary aspergillosis

Abstract A patient with allergic bronchopulmonary aspergillosis who developed a cavitary lung lesion suggestive of neoplasm is presented. At thoracotomy an aspergilloma was found. Although coexistence of these two forms of aspergillosis has been reported, the brief history of preceding asthma and the rapid developement of the aspergilloma in the absence of typical roentgenographic features are unusual. Aspergilloma should be considered when a patient with allergic bronchopulmonary aspergillosis develops a cavitary pulmonary lesion.

Tropical Pulmonary Eosinophilia Masquerading as Acute Bronchial Asthma

With the influx of immigrants from developing countries, deployment of American troops on foreign soil, and wide-ranging travel patterns of some United States citizens, one should expect an increase in the frequency of parasitic pulmonary diseases. We report a case of tropical pulmonary eosinophilia in a recent immigrant to Upstate New York from India. Tropical pulmonary eosinophilia is unfamiliar to most physicians practicing in North America, but should be included in the differential diagnosis of asthmatic bronchitis with hypereosinophilia when there is a history of recent travel to or residence in endemic areas. Furthermore, knowledge of this entity should also help in the differential diagnosis of other hypereosinophilic syndromes.

Survival of patients with pleural involvement by breast carcinoma

To determine factors which affect survival in patients with pleural involvement by breast carcinoma, we reviewed records of all patients at two community teaching hospitals presenting with malignant pleural effusion over a 6-year period. Forty-five patients had had mastectomy for breast cancer, no history of other malignancy, and cytologic confirmation of subsequent pleural metastases. All had received conventional combination systemic chemo- or hormonal therapy. Ten patients (group 1) in whom effusion was the initial and only site of recurrent disease had a median survival of 48 months. The median survival was 12 months in 35 patients (group 2) who developed effusion in association with other metastatic disease. Half of the patients in group 1 had no axillary node involvement at mastectomy. Twenty-eight patients (80%) in group 2 had had more advanced disease at initial diagnosis. This, and behavior of the effusion as regional rather than systemic disease, suggested by the high incidence of effusion on the ipsilateral side of the mastectomy, probably accounts for the better outlook in patients with effusion alone.

Recurrent Pleural and Pericardial Effusions Due to Sarcoidosis

A 54-year-old man presented with fever, shortness of breath, and left-sided pleuritic chest pain. His bilateral pleural effusions and pericardial effusion turned out to be due to sarcoidosis

Pulmonary infarction in sickle cell trait

A young black man presented with unexplained pleuritic chest pain. A hematologic evaluation revealed sickle cell trait, Chest roentgenograms, ventilation/perfusion lung scanning and a pleural-parenchymal lung biopsy documented pulmonary infarction. Sickle cell trait with resultant pulmonary infarction should be considered in black subjects with unexplained pulmonary diseases.

Bronchial Provocation Tests before and after Cessation of Smoking

We studied the effect of smoking cessation on airway reactivity. We recruited cigarette smokers who were attempting to stop smoking. Entry criteria required each subject to be smoking at least 10 cigarettes each day and report a chronic cough. Exclusion criteria included significant airflow obstruction or the presence of any medical condition contraindicating challenge testing. Carbachol challenge was performed to assess airway reactivity according to a standardized method. Baseline measurements of forced expiratory volume in 1 s (FEV1), specific airway conductance (SGaw) and the provocative dose of carbachol causing a 35% reduction in SGaw (PD35), and a 20% reduction in FEV1 (PD20) were established on entry while each subject was still smoking. Thereafter, repeat measurements were performed after 2 and 6 months of smoking cessation. Adherence to smoking cessation was checked by self-report and verified by measurement of alveolar carbon monoxide levels at each session. Of the 34 subjects who gave consent, 13 relapsed prior to the 2nd month and an additional 8 relapsed before the 6th month. Thirteen of the 34 remained abstinent throughout the 6-month study. All 13 subjects had complete resolution of their cough. The difference in reactivity on entry to that at the 2nd and 6th month was not significant. We conclude that (1) the symptom of chronic cough resolved completely after 2 months of smoking cessation, and (2) airway reactivity remained unchanged at 2 and 6 months of smoking cessation.

Adult Respiratory Distress Syndrome Associated with Acute Nitrofurantoin Toxicity

A case of adult respiratory distress syndrome associated with nitrofurantoin use is described. The patient was successfully managed with continuous positive airway pressure (CPAP) through a tightly fitting face mask; clinical deterioration followed discontinuation of the CPAP, with improvement occurring when it was restarted. Acute nitrofurantoin pleuropulmonary reactions are reviewed, and CPAP by face mask is discussed

Differentiation of tuberculous from nontuberculous cavitary lung disease.

Tuberculous and nontuberculous cavitary lung disease is often initially misdiagnosed, delaying therapy. To identify findings which might help avoid such delays, we performed a retrospective review of all patients admitted to two community hospitals over a 6-year period for infectious cavitary disease of the upper lobe or apical segment of the lower lobe. 10 patients with tuberculosis and 16 with nontuberculous infections were identified. Delays in initiating therapy were common to both. Most signs and symptoms were nonspecific. The mean duration of symptoms was greater in tuberculosis (72 days) compared to nontuberculous infections (18 days). Putrid sputum was found only in nontuberculous infections (11/16). Roentgenographic features of fibronodular infiltration and atelectasis occurred only in tuberculosis. Air fluid levels were seen only in nontuberculous disease (10/16). Leukocytosis with immature neutrophils was found only in patients with nontuberculous cavities. We conclude that the previously described clinical, laboratory, and roentgenographic features may be useful in correctly diagnosing infectious cavitary lung disease.

Insidious Onset of Acute Alveolar Hypoventilation following Intermittent Positive-Pressure Breathing (IPPB)

2 patients developing acute alveolar hypoventilation following IPPB therapy are presented. The hypoventilation occurred insidiously following therapy. It is hypothesized that respiratory center depression from excessive oxygen administration caused the hypoventilation. When the IPPB machines were driven by compressed air instead of oxygen, this complication was revealed in 1 of the patients.