Development of interstitial pneumonitis during treatment with granulocyte colony-stimulating factor

Katoh, Masako; Shikoshi, K; Takada, Masafumi; Umeda, Masanori; Tsukahara, Tetsuo; Kitagawa, Seiichi; Shirai, Toshikazu

doi:10.1007/bf01695869

Cited by 25 publications

(13 citation statements)

References 6 publications

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“…In almost all of the previously reported cases who developed pulmonary toxicity after receiving chemotherapy and G-CSF, the applied chemotherapy alone can cause pulmonary toxicity at a considerable incidence (Iki et al, 1993;Katoh et al, 1993;Matthews, 1993;Okubo et al, 1993;Dirix et al, 1994: Lei et al 1994Niitsu et al, 1995). Therefore, the contribution of G-CSF to the pulmonary toxicity in these prior cases is difficult to define clearly.…”

Section: Discussionmentioning

confidence: 99%

“…The pulmonary toxicity that develops after G-CSF-combined chemotherapy may be fatal (Iki et al, 1993;Katoh et al, 1993). Therefore, prevention, early detection and proper treatment of such cases is extremely important.…”

Section: Discussionmentioning

confidence: 99%

“…Sporadic cases have developed pulmonary toxicity after receiving chemotherapy and G-CSF (Iki et al, 1993;Katoh et al, 1993;Matthews, 1993;Dirix et al, 1994;Lei et al, 1994). The pulmonary toxicity of chemotherapeutic drugs has been attributed, at least in part, to the production of reactive oxygen species that damage the pulmonary epithelium and induce an influx of peripheral neutrophils (Kreisman et al, 1992).…”

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confidence: 99%

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Pulmonary toxicity after granulocyte colony-stimulating factor-combined chemotherapy for non-Hodgkin's lymphoma

Yokose

Ogata²,

Tamura³

et al. 1998

Br J Cancer

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Summary Sporadic cases have developed pulmonary toxicity after receiving chemotherapy and granulocyte colony-stimulating factor (G-CSF). However, because such cases received chemotherapy that alone frequently causes pulmonary toxicity, the role of G-CSF in this toxicity has been unclear. CHOP therapy (cyclophosphamide, doxorubicin, vincristine and prednisolone) only slightly induces pulmonary toxicity. However, we observed a considerable incidence of this toxicity in non-Hodgkin's lymphoma subjects receiving CHOP therapy and G-CSF (6 out of 52 subjects, 11.5%). In this cohort, among various characteristics, including the dose and interval of CHOP therapy, only the mean peak leucocyte count (MPLC) with each therapy cycle was associated with development of this toxicity (MPLC . 23.0 x 109 I-, 6 out of 29 cases; MPLC < 23.0 x 109 I-', 0 out of 23 cases; P= 0.020). These findings suggest that the effect of G-CSF is the main determinant of the pulmonary toxicity in these cases. Because the toxicity was associated with a large MPLC and did not recur in cases readministered G-CSF, an idiosyncratic reaction to G-CSF is unlikely to be the pathogenesis of this toxicity. Thus, lowering the G-CSF dose seems to be useful in the prevention of this toxicity. In all six cases, the time course of manifestation of the toxicity was the same, and early application of high-dose corticosteroid led to cure. This knowledge will be helpful in the care of similar cases.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Pulmonary toxicity after granulocyte colony-stimulating factor-combined chemotherapy for non-Hodgkin's lymphoma

Yokose

Ogata²,

Tamura³

et al. 1998

Br J Cancer

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“…Although the well-known adverse events of G-CSF are fever, bone pain and liver dysfunction, these problems are largely transient and disappear after the completion of treatment (Niitsu and Umeda, 1994). Recently, compared with many other countries, interstitial pneumonia possibly related to G-CSF administration appears to be more frequently observed in Japan (lki et al, 1993;Katoh et al, 1993;Okubo and Nakazawa 1993;Murayama et al, 1994), although the link between pneumonitis and G-CSF has not been clearly explained. GM-CSF, another haematopoietic growth factor, has been associated with adult respiratory distress syndrome (ARDS) and acute respiratory insufficiency (Wiley et al, 1993).…”

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confidence: 99%

Interstitial pneumonia in patients receiving granulocyte colony-stimulating factor during chemotherapy: survey in Japan 1991-96

Niitsu

Iki²,

Muroi³

et al. 1997

Br J Cancer

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Summary Twenty cases of interstitial pneumonia secondary to treatment with granulocyte colony-stimulating factor (G-CSF) were reviewed. Their interstitial pneumonia had the following features: (a) it occurred predominantly in patients aged 60 years or older; (b) it was prevalent among patients with haematological malignancies, particularly non-Hodgkin's lymphoma; (c) in all patients G-CSF was given after anti-cancer agents with potential to affect the lungs; (d) at the onset, many patients had symptoms such as dyspnoea and fever; and (e) the leucocyte (neutrophil) count as well as lactate dehydrogenase (LDH) and C-reactive protein (CRP) levels were usually higher than normal at the onset. These findings indicate that, when G-CSF is used in combination with pneumotoxic anti-cancer agents, respiratory function should be monitored before and during treatment. If the leucocyte (or neutrophil) count and/or LDH and CRP increase suddenly in association with dyspnoea and fever during administration of G-CSF, interstitial pneumonia should be suspected. Accordingly, a chest radiograph and pulmonary functional tests should be performed promptly. If a diagnosis of interstitial pneumonia is made, steroid pulse therapy should be commenced immediately.

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“…Drugs, such as fluoxetine [62], paclitaxel [63], ACE inhibitors [64], the cytokines interferon [65], granulocyte or granulocyte/monocyte colony-stimulating factor [66,67], have been associated with interstitial pneumonia. Penicillamine-induced bronchiolitis obliterans remained almost restricted to the patient with rheumatoid arthritis, but tiopronin [68] and gold salts [69] have been shown to induce the syndrome as well.…”

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confidence: 99%

Respiratory disease induced by drugs

Camus¹

1997

Eur Respir J

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which averages 100 clinical articles per year ( fig. 1). Collectively, of approximately 2,650 clinical articles published so far, 32% are related to chemotherapeutic agents: bleomycin (226 papers); busulphan (58); cyclophosphamide (75); methotrexate (129); and nitrosoureas (46). Adverse pulmonary effects from: amiodarone (214 articles); ergolines (54); gold salts (133); minocycline (35); nitrofurantoin (135); nonsteroidal anti-inflammatory drugs (NSAIDs) (58); and sulphasalazine (22) point to all these drugs as being common offenders of the respiratory system, in addition to angiotensin-converting enzyme (ACE) inhibitors. On this basis, a brief historical perspective on DIRD is warranted.The first notice of adverse effects of drugs on the respiratory system dates back to the years 1920-1930, when it was realized that aspirin could induce severe asthma attacks and even death [2]. In the 1940s, the then newer antibiotic drugs were associated with allergic pneumonia with or without eosinophilia or angiitis [3,4], and gold was linked to the development of interstitial lung disease [5], although most of the literature on "gold lung" was published later [6][7][8].The The 1960-1969 decade was dominated by an overwhelming number of reports on nitrofurantoin lung. In addition, a worrisome picture of medication-induced pulmonary hypertension emerged, and an epidemic of this devastating illness in young females was ascribed to the appetite-suppressant, aminorex, which was withdrawn from the market [17]. For the first time, it became clear that one drug could induce more than one pattern of respiratory reactions. In the case of nitrofurantoin, these patterns included: acute allergic pneumonia, with or without eosinophilia in the blood [18]; subacute/chronic interstitial pneumonia, with or without a desquamative or eosinophilic pattern at histology [19][20][21]

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Development of interstitial pneumonitis during treatment with granulocyte colony-stimulating factor

Cited by 25 publications

References 6 publications

Pulmonary toxicity after granulocyte colony-stimulating factor-combined chemotherapy for non-Hodgkin's lymphoma

Pulmonary toxicity after granulocyte colony-stimulating factor-combined chemotherapy for non-Hodgkin's lymphoma

Interstitial pneumonia in patients receiving granulocyte colony-stimulating factor during chemotherapy: survey in Japan 1991-96

Respiratory disease induced by drugs

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