DOCSLIB.ORG

Post-Transplant Complications Pulmonary Toxicity Syndrome Following CDEP (Cyclophosphamide, Dexamethasone, Etoposide, Cisplatin) Chemotherapy

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Post-Transplant Complications Pulmonary Toxicity Syndrome Following CDEP (Cyclophosphamide, Dexamethasone, Etoposide, Cisplatin) Chemotherapy Bone Marrow Transplantation (2001) 28, 399–403 2001 Nature Publishing Group All rights reserved 0268–3369/01 $15.00 www.nature.com/bmt Post-transplant complications Pulmonary toxicity syndrome following CDEP (cyclophosphamide, dexamethasone, etoposide, cisplatin) chemotherapy A Fassas1,3, I Gojo1, A Rapoport1, M Cottler-Fox1,3, B Meisenberg2, JC Papadimitriou2 and G Tricot1,3 1Department of Medicine, Division of Bone Marrow and Stem Cell Transplantation, Greenebaum Cancer Center; and 2Department of Pathology, University of Maryland, Baltimore, MD, USA Summary: development of this pulmonary toxicity syndrome (PTS). This is further supported by the lack of correlation between We report on three patients with multiple myeloma who severity of PTS in case of BCNU-based high-dose chemo- developed drug-induced pneumonitis 1–2. months fol- therapy with age, tobacco use or baseline pulmonary func- lowing maintenance (post autologous transplantation) tion, suggesting that other factors play a role in PTS, in chemotherapy with CDEP (cyclophosphamide, dexame- addition to chemotherapy exposure.3 thasone, etoposide, cisplatin) and 6–20 months after From this perspective, it was intriguing to observe three exposure to carmustine (BCNU) 300 mg/m2, used in patients, with a history of either proven (two) or suspected combination with melphalan 140 mg/m2, as pre-trans- (one) fungal pneumonia, who developed typical clinical, plant conditioning regimen. All patients had either a radiographic and histologic features of PTS 5–11 weeks proven (two) or suspected (one) fungal pneumonia and after treatment with CDEP (cyclophosphamide, dexame- were treated with liposomal amphotericin B. Dyspnea, thasone, etoposide, cisplatin) chemotherapy, a fairly com- fever and cough were the prominent clinical symptoms, monly used regimen which has not so far been associated while air-space disease with ground glass appearance with non-infective pulmonary toxicity. These patients had was seen radiographically. Histologic features typical a dramatic response to a brief course of corticosteroids. for drug-induced lung injury were detected. All patients There was no evidence of fungal infection at the time of had a dramatic, clinical and radiographic response to a PTS diagnosis. brief course of corticosteroids. Although CDEP-induced pneumonitis appears to be a rare complication, its early recognition and prompt treatment, as well as its possible Patients and methods association with preceding fungal infection may have important clinical implications. Bone Marrow Transplan- Between August 1997 and February 2000, 231 patients tation (2001) 28, 399–403. underwent autologous peripheral blood stem cell transplan- Keywords: non-infective pulmonary toxicity; CDEP tation (APBSCT), at our institution, for a variety of hemato- chemotherapy; fungal infection logic malignancies (multiple myeloma, 87; non-Hodgkin lymphoma, 64; Hodgkin’s disease, 11; others, 14) and solid tumors (breast carcinoma, 46; others, nine). In the vast majority (200 patients), the same conditioning regimen of Drug-induced pulmonary toxicity, not associated with BCNU at 300 mg/m2 and melphalan at 140 mg/m2 infection, is a well-described complication of different (BCNU/MEL) was applied, followed by post-transplant chemotherapeutic agents. Among them, carmustine chemotherapy starting 3 months after the APBSCT and (BCNU), cyclophosphamide, bleomycin, busulphan, mel- administered every 3 months × four courses during the year 1 phalan and total body irradiation have been implicated. following transplant (or until disease relapse). The regi- Furthermore, combinations of various agents (even the ones mens used for the post-transplant chemotherapy were rarely associated with the syndrome) may potentially lead cyclophosphamide 300 mg/m2 by continuous i.v. infusion 2 to lung injury through drug interactions. Additionally, over 24 h for 4 days, dexamethasone 40 mg p.o. daily for unrecognized host–drug interactions may contribute to the 4 days, etoposide 30 mg/m2 by continuous i.v. infusion over 24 h for 4 days and cisplatin 15 mg/m2 by continuous i.v. infusion over 24 h for 4 days (CDEP), for courses 1 and Correspondence: Dr A Fassas, Myeloma and Transplantation Center, Uni- 3, alternating with dexamethasone 40 mg p.o. daily for 4 versity of Arkansas for Medical Sciences, 4301 W Markham Street, Little days, taxol 135 mg/m2 by i.v. infusion over 6 h on day 2 Rock, AR, 72205, USA 2 3Current address: Myeloma and Transplantation Research Center, Univer- and cisplatin 75 mg/m by i.v. infusion over 24 h on day sity of Arkansas for Medical Sciences, Little Rock, AR, USA 3 of the cycle, for courses 2 and 4. The feasibility and Received 25 September 2000, accepted 15 May 2001 toxicity data on 50 patients with multiple myeloma treated Non-infectious pulmonary toxicity after CDEP chemotherapy A Fassas et al 400 with such an approach have been previously reported.4 Nystatin was discontinued in mid-November 1999, after no Eight patients (4%) developed non-infective, pulmonary further change was documented by serial computed tom- toxicity syndrome (seven lung-biopsy proven, one ography (CT) scans. Of note, the patient remained severely suspected). All had been exposed to BCNU during the pre- anemic and thrombocytopenic during the entire post-trans- transplant conditioning. While in five patients the syndrome plant period, requiring frequent red cell and platelet trans- occurred in temporal proximity to BCNU exposure (32– fusions. Despite the stormy post-transplant course and the 98 days after administration), the remaining three patients good control of his disease (with bone marrow plasma- experienced this complication 6–20 months following the cytosis р5%) maintenance chemotherapy consisting of pre-transplant conditioning and interestingly enough within CDEP was administered between 10 and 14 December 1–2. months after treatment with CDEP. The clinical 1999. Additional stem cells were infused at the completion history of these patients is presented. of this chemotherapy. Prophylaxis with itraconazole was initiated, but no prophylaxis against PCP was given. On 10 Patient 1 January 2000, the patient presented with new onset dys- pnea, malaise, non-productive cough and severe hypoxemia A 56-year-old man was diagnosed with nonsecretory mul- (PO2: 55 mmHg at room air). No blood products were tiple myeloma, stage II-A, in January 1999. He had a 20 transfused during the preceding 48 h. No fever was docu- pack-year history of smoking, but quit smoking approxi- mented. Chest CT showed a new infiltrate (Figure 1a). mately 17 years prior to diagnosis. Following two courses Bronchoscopy showed scant clear secretions in otherwise of pulse dexamethasone and mobilization chemotherapy normal airways. BAL failed to reveal any pathogens while consisting of cyclophosphamide 4500 mg/m2 and etoposide the transbronchial biopsy was consistent with chemo- 2000 mg/m2 (CTX/VP16), he received APBSCT on 27 May therapy-induced pneumonitis. Rapid and dramatic sympto- 1999, after conditioning with BCNU/MEL. Delayed matic and objective improvement (as evidenced by resol- engraftment, despite an excellent collection of stem cells, ution of dyspnea, weaning off supplemental oxygen, prompted the infusion of additional stem cells on day +19, correction of hypoxemia and resolution of the radiographic with ANC finally reaching 1500/␮l on day +31. Evaluation picture) occurred after a brief course of oral corticosteroids. for persistent neutropenic fevers revealed pulmonary nod- Due to the recent history of fungal pneumonia, a relatively ules. Bronchoalveolar lavage (BAL) was negative for low dose of methylprednisolone (total 24 mg/day) was pathogens (Pneumocystis carinii pneumonia (PCP), chosen and symptoms recurred on fast tapering. Reinsti- Legionella, acid fast bacilli, viral and fungal pathogens). tution of corticosteroids and much slower tapering led again Empiric treatment with liposomal amphotericin B was to complete resolution of the symptoms. The patient experi- initiated. A repeat bronchoscopy with BAL was performed enced no subsequent reactivation of fungal pneumonia. for evaluation of hemoptysis on 6 August 1999; silver stains of cytologic specimens were positive for fungal Patient 2 elements consistent with aspergillus. Liposomal nystatin A 53-year-old woman, without prior history of smoking, was introduced with improvement in the radiologic picture. was diagnosed with IgA ␬ multiple myeloma, stage III- Figure 1 Improvement of pulmonary infiltrates following treatment with corticosteroids. Upper panel, pre-treatment; lower panel, post-treatment. Bone Marrow Transplantation Non-infectious pulmonary toxicity after CDEP chemotherapy A Fassas et al 401 B, in March 1998. Following three courses of VAD and mobilization chemotherapy with CTX/VP16, she received APBSCT on 6 August 1998, after conditioning with BCNU/MEL. She achieved complete hematologic recovery and a partial remission of the myeloma. In November 1998, she was given CDEP chemotherapy, which was compli- cated by pneumonia with extensive bilateral infiltrates. Bronchoscopy with BAL was performed; cultures of the specimens grew Candida tropicalis only. The same patho- gen, ie Candida tropicalis, was also identified in blood cul- tures. Further maintenance chemotherapy was therefore held. Relapsing disease in September 1999, prompted the administration of a second APBSCT on 14 October 1999, after conditioning with melphalan 200 mg/m2. Prophylaxis with itraconazole was initiated prior to the transplantation
Load more

Recommended publications
  • Pulmonary Toxicity Following Carmustine-Based Preparative Regimens and Autologous Peripheral Blood Progenitor Cell Transplantation in Hematological Malignancies
    Bone Marrow Transplantation (2000) 25, 309–313 2000 Macmillan Publishers Ltd All rights reserved 0268–3369/00 $15.00 www.nature.com/bmt Pulmonary toxicity following carmustine-based preparative regimens and autologous peripheral blood progenitor cell transplantation in hematological malignancies EP Alessandrino1, P Bernasconi1, A Colombo1, D Caldera1, G Martinelli1, P Vitulo2, L Malcovati1, C Nascimbene2, M Varettoni1, E Volpini2, C Klersy3 and C Bernasconi1 1Centro Trapianti di Midollo Osseo, Istituto di Ematologia, 2Divisione di Pneumologia, 3Biometry-Scientific Direction IRCCS, Policlinico S Matteo, Pavia, Italy Summary: the use of BCNU is suspected to be caused by damage to the glutathione system.2 BCNU has been included in high- Sixty-five patients with hematological malignancies (25 dose conditioning regimens for gliomas, breast cancer, multiple myeloma, 18 Hodgkin’s disease, 22 non-Hodg- Hodgkin’s disease, non-Hodgkin’s lymphomas, multiple kin’s lymphomas) who received a carmustine-based myeloma. Toxic pulmonary reactions have been recognized regimen followed by autologous PBPC transplantation, in as many as 16–64% of patients;3–13 onset generally were studied retrospectively to evaluate the incidence of occurs within 1 year of starting BCNU. Events occurring post-transplant non-infective pulmonary complications up to 17 years later have been reported.14 The drug seems (NIPCs), risk factors predictive of NIPCs, and response to cause pulmonary damage in a dose-related manner:5,10,11 to steroids. Carmustine (BCNU) given i.v. at a dose of Phillips et al6 reported a 9.5% incidence of fatal pulmonary 600 mg/m2 was combined with etoposide and cyclophos- toxicity in patients receiving BCNU doses as high as 1.200 phamide in 40 patients (BCV regimen) and with etopo- mg/m2 as a single agent; another report suggests no pul- side and melphalan in 25 patients (BEM regimen).
    [Show full text]
  • Adcetris, INN-Brentuximab Vedotin
    ANNEX I SUMMARY OF PRODUCT CHARACTERISTICS 1 This medicinal product is subject to additional monitoring. This will allow quick identification of new safety information. Healthcare professionals are asked to report any suspected adverse reactions. See section 4.8 for how to report adverse reactions. 1. NAME OF THE MEDICINAL PRODUCT ADCETRIS 50 mg powder for concentrate for solution for infusion. 2. QUALITATIVE AND QUANTITATIVE COMPOSITION Each vial contains 50 mg of brentuximab vedotin. After reconstitution (see section 6.6), each mL contains 5 mg of brentuximab vedotin. ADCETRIS is an antibody-drug conjugate composed of a CD30-directed monoclonal antibody (recombinant chimeric immunoglobulin G1 [IgG1], produced by recombinant DNA technology in Chinese Hamster ovary cells) that is covalently linked to the antimicrotubule agent monomethyl auristatin E (MMAE). Excipient with known effect Each vial contains approximately 13.2 mg of sodium. For the full list of excipients, see section 6.1. 3. PHARMACEUTICAL FORM Powder for concentrate for solution for infusion. White to off-white cake or powder. 4. CLINICAL PARTICULARS 4.1 Therapeutic indications Hodgkin lymphoma ADCETRIS is indicated for adult patients with previously untreated CD30+ Stage IV Hodgkin lymphoma (HL) in combination with doxorubicin, vinblastine and dacarbazine (AVD) (see sections 4.2 and 5.1). ADCETRIS is indicated for the treatment of adult patients with CD30+ HL at increased risk of relapse or progression following autologous stem cell transplant (ASCT) (see section 5.1). ADCETRIS is indicated for the treatment of adult patients with relapsed or refractory CD30+ Hodgkin lymphoma (HL): 1. following ASCT, or 2. following at least two prior therapies when ASCT or multi-agent chemotherapy is not a treatment option.
    [Show full text]
  • Immunotherapy Associated Pulmonary Toxicity: Biology Behind Clinical and Radiological Features
    cancers Review Immunotherapy Associated Pulmonary Toxicity: Biology Behind Clinical and Radiological Features Michele Porcu 1 , Pushpamali De Silva 2,3 , Cinzia Solinas 2,4,*, Angelo Battaglia 4, Marina Schena 4, Mario Scartozzi 5, Dominique Bron 3, Jasjit S. Suri 6,7, Karen Willard-Gallo 2, Dario Sangiolo 8,9 and Luca Saba 1 1 Department of Radiology, University Hospital of Cagliari, 09042 Monserrato (Cagliari), Italy; [email protected] (M.P.); [email protected] (L.S.) 2 Molecular Immunology Unit, Institut Jules Bordet, Universitè Libre de Bruxelles (ULB), 1000 Brussels, Belgium; [email protected] (P.D.S.); [email protected] (K.W.-G.) 3 Clinical and Experimental Hematology, Institute Jules Bordet, Universitè Libre de Bruxelles (ULB), 1000 Brussels, Belgium; [email protected] 4 Department of Medical Oncology and Hematology, Regional Hospital of Aosta, 11100 Aosta, Italy; [email protected] (A.B.); [email protected] (M.S.) 5 Department of Medical Oncology, University Hospital of Cagliari, 09042 Monserrato (Cagliari), Italy; [email protected] 6 Lung Diagnostic Division, Global Biomedical Technologies, Inc., Roseville, CA 95661, USA; [email protected] 7 AtheroPoint™ LLC, Roseville, CA 95661, USA 8 Department of Oncology, University of Torino, 10043 Orbassano (Torino), Italy; [email protected] 9 Division of Medical Oncology, Experimental Cell Therapy, Candiolo Cancer Institute FPO-IRCCS, 10060 Candiolo (Torino), Italy * Correspondence: [email protected] Received: 16 January 2019; Accepted: 26 February 2019; Published: 5 March 2019 Abstract: The broader use of immune checkpoint blockade in clinical routine challenges clinicians in the diagnosis and management of side effects which are caused by inflammation generated by the activation of the immune response.
    [Show full text]
  • Methotrexate-Induced Pulmonary Toxicity
    CLINICO-PATHOLOGIC CONFERENCES Methotrexate-induced pulmonary toxicity Baruch D Jakubovic BA1, Andrea Donovan MD FRCPC2, Peter M Webster MD FRCPC3, Neil H Shear MD FRCPC4 BD Jakubovic, A Donovan, PM Webster, NH Shear. Methotrexate- Une toxicité pulmonaire induite par le induced pulmonary toxicity. Can Respir J 2013;20(3):153-155. méthotrexate Methotrexate is a widely used medication with an array of recognized side Le méthotrexate est un médicament largement utilisé qui s’associe à une effects. The present report describes a case of methotrexate-induced pneu- foule d’effets secondaires reconnus. Le présent rapport décrit un cas de monitis in a patient with psoriasis, and demonstrates the hallmark clinical pneumonite induite par le méthotrexate chez un patient ayant un psoriasis and investigational findings that support this infrequently encountered et présente les observations cliniques et les résultats d’examens caractéris- diagnosis. The ensuing discussion reviews the pathogenesis, management tiques en appui à ce diagnostic peu courant. L’exposé qui s’ensuit aborde la and prevention of this adverse drug reaction. pathogenèse, la prise en charge et la prévention de cet effet indésirable du médicament. Key Words: Methotrexate; Pneumonitis; Pulmonary toxicity Learning objectives ● To recognize that methotrexate (MTX) causes pneumonitis that is associated with a constellation of nonspecific findings. CanMEDS Competency: Medical expert ● To gain familiarity with the management and prevention of MTX-induced pneumonitis. CanMEDS Competency: Medical expert & communicator Pretest ● What are the major clinical features supporting a diagnosis of MTX-induced pneumonitis? ● How can MTX-induced pneumonitis be managed and prevented? CASE PRESENTATION A 62-year-old Scottish-born woman presented to hospital experien- cing progressive, nonproductive exertional cough accompanied by chest pain and dyspnea for the past four months.
    [Show full text]
  • MYLERAN® (Busulfan) 2-Mg Scored Tablets
    PRESCRIBING INFORMATION MYLERAN® (busulfan) 2-mg Scored Tablets WARNING MYLERAN is a potent drug. It should not be used unless a diagnosis of chronic myelogenous leukemia has been adequately established and the responsible physician is knowledgeable in assessing response to chemotherapy. MYLERAN can induce severe bone marrow hypoplasia. Reduce or discontinue the dosage immediately at the first sign of any unusual depression of bone marrow function as reflected by an abnormal decrease in any of the formed elements of the blood. A bone marrow examination should be performed if the bone marrow status is uncertain. SEE WARNINGS FOR INFORMATION REGARDING BUSULFAN-INDUCED LEUKEMOGENESIS IN HUMANS. DESCRIPTION MYLERAN (busulfan) is a bifunctional alkylating agent. Busulfan is known chemically as 1,4-butanediol dimethanesulfonate and has the following structural formula: CH3SO2O(CH2)4OSO2CH3 Busulfan is not a structural analog of the nitrogen mustards. MYLERAN is available in tablet form for oral administration. Each scored tablet contains 2 mg busulfan and the inactive ingredients magnesium stearate and sodium chloride. The activity of busulfan in chronic myelogenous leukemia was first reported by D.A.G. Galton in 1953. CLINICAL PHARMACOLOGY Studies with 35S-busulfan: Following the intravenous administration of a single therapeutic dose of 35S-busulfan, there was rapid disappearance of radioactivity from the blood; 90% to 95% of the 35S-label disappeared within 3 to 5 minutes after injection. Thereafter, a constant, low level of radioactivity (1% to 3% of the injected dose) was maintained during the subsequent 48-hour period of observation. Following the oral administration of 35S-busulfan, there was a lag period of ½ to 2 hours prior to the detection of radioactivity in the blood.
    [Show full text]
  • Pulmonary Toxicity of High-Dose Chemotherapy for Breast Cancer: a Non-Invasive Approach to Diagnosis and Treatment
    Bone Marrow Transplantation, (1997) 20, 1063–1067 1997 Stockton Press All rights reserved 0268–3369/97 $12.00 Pulmonary toxicity of high-dose chemotherapy for breast cancer: a non-invasive approach to diagnosis and treatment L Chap1, R Shpiner2, M Levine2, L Norton1, M Lill1 and J Glaspy1 Divisions of 1Hematology/Oncology, and 2Pulmonary and Critical Care Medicine, UCLA Medical Center, Los Angeles, CA, USA Summary: ive dyspnea on exertion (DOE), a nonproductive cough ± fever, restrictive changes in pulmonary function and Drug-induced pulmonary toxicity is one of the most fre- occasional radiographic infiltrates.2 The optimal approach quent non-hematologic toxicities in breast cancer to diagnosis and treatment, however, has not been eluci- patients receiving high-dose chemotherapy with cyclo- dated. phosphamide, cisplatin and BCNU (CY/CDDP/BCNU). Studies of new approaches for the prevention and early A non-invasive clinical scoring system was utilized in an diagnosis of pulmonary toxicity will depend upon the attempt to diagnose and treat early lung toxicity in 64 development of valid, reproducible and objective diagnostic consecutive breast cancer patients undergoing criteria. This study was intended to develop a noninvasive CY/CDDP/BCNU supported by peripheral blood pro- model to aid in the diagnosis and treatment of chemo- genitor cells. Following hospital discharge, patients who therapy-associated pulmonary toxicity by which points developed symptoms suggestive of lung toxicity were were assigned for abnormal results of pulmonary function evaluated with physical examination, DLCO, 2-min tests and physical examination. walking oximetry and a chest radiograph. Clinically weighted scores were assigned as follows: crackles on lung exam, 2; decrease in corrected DLCO by .10% Patients and methods from baseline, 3; decrease in O2 saturation by >4% with a 2-min walk, 3; and interstitial infiltrates on chest Patients radiograph, 3.
    [Show full text]
  • Rare Diseases C 8 Organising Pneumonia
    318 Thorax 2000;55:318–328 Rare diseases c 8 Thorax: first published as 10.1136/thorax.55.4.318 on 1 April 2000. Downloaded from Series editors: A E Tattersfield, R M du Bois Organising pneumonia Jean-François Cordier Organising pneumonia is defined pathologi- infectious pneumonia, lung abscess, empyema, cally by the presence in the distal air spaces of lung cancer, bronchiectasis, broncholithiasis, buds of granulation tissue progressing from chronic pulmonary fibrosis, aspiration pneu- fibrin exudates to loose collagen containing monia (giant cells and foreign bodies usually fibroblasts (fig 1).12 The lesions occur pre- are present), adult respiratory distress syn- dominantly within the alveolar spaces but are drome, pulmonary infarction, and middle lobe often associated with buds of granulation tissue syndrome.34 occupying the bronchiolar lumen (bronchioli- Organising pneumonia may be classified into tis obliterans). This pathological pattern is not three categories according to its cause: organis- specific for any disorder or cause, but reflects ing pneumonia of determined cause; organis- one type of inflammatory process resulting ing pneumonia of undetermined cause but from lung injury. It may also be a feature of the occurring in a specific and relevant context; organising stage of adult respiratory distress and cryptogenic (idiopathic) organising pneu- syndrome and may be an accessory finding in monia. Several possible causes and/or associ- other inflammatory disorders such as vasculi- ated disorders may coexist in the same patient. tis. However, organising pneumonia is the par- There are no clear distinguishing clinical and ticular pathological hallmark of a characteristic radiological features between cryptogenic and clinicoradiological entity called cryptogenic secondary organising pneumonia.5 organising pneumonia.
    [Show full text]
  • A Rare Complication After Intravesical Mitomycin-C Treatment for Bladder Tumor
    Yeni Üroloji Dergisi - The New Journal of Urology 2017; 12 (1): 44-47 Olgu / Case Interstitial pneumonia: A rare complication after intravesical Mitomycin-C treatment for bladder tumor İnterstisyel pnömoni: Mesane tümörü için uygulanan mesane içi Mitomycin-C tedavisinden sonra gelişen nadir bir komplikasyon Adem Emrah Coguplugil1, Alper Gundogan2, Nesrin Ocal2, Ibrahim Yildirim1, Seyfettin Gumus2, Turgay Ebiloglu1, Zafer Demirer1, Engin Kaya1, Giray Ergin1 1 Department of Urology, Gulhane Military Medical Academy, Ankara, Turkey 2 Department of Respiratory Medicine, Gulhane Military Medical Academy, Ankara, Turkey Özet Abstract Transüretral mesane tümörü rezeksiyo- Sixty six years-old male patient, who un- nu sonrası mesane içi Mitomycin-C instilas- derwent transurethral resection of bladder yonu başlanan 66 yaşında bir erkek hastada tumor and consequent intravesical Mitomy- interstisyel pnömoni gelişti. Hastaya haftalık cin-C chemotherapy, developed interstitial 40 mg mesane içi Mitomycin-C uygulanmıştı pneumonia. Forty mg intravesical Mitomy- ve üçüncü uygulamadan 4 gün sonra hasta cin-C was instillated weekly. Four days after acil servise ilerleyici dispne şikayeti ile baş- the third instillation, the patient presented vurdu. Çekilen yüksek çözünürlüklü toraks to emergency service with the complaint of tomografisinde akciğerin sağ üst ve her iki progressive dyspnea. High resolution tho- alt loblarında buzlu cam görüntüsü, iki taraflı rax tomography demonstrated ground glass plevral efüzyon ve interlobuler septal kalın- opacity in the right upper and bilateral lower laşma görüntülendi. Akciğer infeksiyonu lobes, bilateral pleural effusion and interlob- Geliş tarihi (Submitted): 18.03.2016 ve kollajen vasküler hastalıklar dışlandı. İn- ular septal thickening. Infection and collagen Kabul tarihi (Accepted): 01.05.2016 terstisyel pnömoni öntanısıyla Mitomycin-C vascular disease were excluded.
    [Show full text]
  • Pulmonary Toxicity After Intraperitoneal Mitomycin C: a Case Report of a Rare Complication of HIPEC Melissa L
    Abel et al. World Journal of Surgical Oncology (2017) 15:49 DOI 10.1186/s12957-016-1047-6 CASEREPORT Open Access Pulmonary toxicity after intraperitoneal mitomycin C: a case report of a rare complication of HIPEC Melissa L. Abel1, George Kokosis2 and Dan G. Blazer2* Abstract Background: Cytoreductive surgery combined with hyperthermic intraperitoneal chemotherapy (CRS/HIPEC) has become a common treatment approach for disseminated appendiceal neoplasms. Systemic absorption of intraperitoneal chemotherapeutics may lead to drug-induced toxicity, most commonly neutropenia. Mitomycin C has been the most commonly used chemotherapeutic in HIPEC for the past several decades. Case presentation: Here, we describe a rare pulmonary complication secondary to intraperitoneal administration of mitomycin C. Conclusions: While rare, intraperitoneal mitomycin C has the potential to cause serious pulmonary toxicity that should be considered with administration. To our knowledge, this report represents only the second case described in the literature. Keywords: Appendiceal cancer, Intraperitoneal chemotherapy, Mitomycin C, Pulmonary toxicity, ARDS Background cause dose-dependent interstitial lung disease, but re- Aggressive surgical approaches to patients with periton- ports of pulmonary toxicity secondary to intraperitoneal eal carcinomatosis from nongynecologic malignancies administration are rare [11–13]. Here, we present a case have become increasingly common, abrogating some of of acute respiratory distress syndrome (ARDS) secondary the historic nihilism
    [Show full text]
  • Amiodarone-Induced Pulmonary Toxicity
    arm Ph ac f ov l o i a g n il r a n u c o e J Vasic et al., J Pharmacovigilance 2014, 2:4 Journal of Pharmacovigilance DOI: 10.4172/2329-6887.1000137 ISSN: 2329-6887 CaseResearch Report Article OpenOpen Access Access Amiodarone-Induced Pulmonary Toxicity Mimicking Metastatic Lung Disease: Case Report Nada Vasic1 Branislava Milenkovic1,2 Ruza Stevic2,3 Dragana Jovanovic1,2 Verica Djukanovic1 1Clinic for lPulmonary Diseases, Clinical Centre of Serbia, Serbia 2Faculty of Medicine, University of Belgrade, Serbia 3Center for Radiology and MRI, Clinical Centre of Serbia, Serbia Abstract Amiodarone is an antiarrhythmic drug that is commonly used for the treatment of ventricular and supraventricular arrhythmias. It is an iodine-containing compound, and has a tendency to accumulate in certain organs, including in the lungs. We describe a case of amiodarone induced pulmonary toxicity with concurrent lung cancer which demonstrated good treatment response. A sixty nine-year old male smoker presented to our emergency department with a four-month history of progressive dyspnea, cough and 5 kilogram weight loss. Chest x-ray at admission showed enlarged heart shadow and prominent hilum bilaterally; CT revealed ground glass opacities in right lung and enlarged mediastinal lymph nodes. His past medical history was significant for dilated myocardiopathy and atrial fibrillation (for which he had been taking amiodarone for 5 years). Radiological findings, decrease in total lung capacity (TLC=84%), decrease in lung diffusing capacity (DLCOc=73%), and corneal epithelial opacities suggested amiodarone-induced pulmonary toxicity (APT) and/or advanced malignant disease. Amiodarone was eliminated from his medication profile due to suspicion of drug toxicity.
    [Show full text]
  • Association of High-Dose Cyclophosphamide, Cisplatin, And
    698 Vol. 8, 698–705, March 2002 Clinical Cancer Research Association of High-dose Cyclophosphamide, Cisplatin, and Carmustine Pharmacokinetics with Survival, Toxicity, and Dosing Weight in Patients with Primary Breast Cancer1 William P. Petros,2,3 Gloria Broadwater, sition was not found to be different in those developing -Kaplan-Meier anal .(0.96 ؍ P ;25 ؍ Donald Berry,4 Roy B. Jones,5 pulmonary toxicity (n James J. Vredenburgh, Colleen J. Gilbert, ysis (median follow-up of 5.9 years) demonstrated that pa- tients with lower cyclophosphamide AUC (faster parent John P. Gibbs, O. Michael Colvin, and drug clearance to potentially cytotoxic compounds) survived 6 .(0.031 ؍ William P. Peters longer (P Bone Marrow Transplant Program, Duke University Medical Center, Inter-individual differences in the pharmacokinetic dis- Durham, North Carolina 27710 position of high-dose chemotherapy may explain variability in both response and toxicity. Prospective strategies, which attempt to individualize AUC, should be evaluated in this ABSTRACT setting. This report investigates relationships between the phar- macokinetics and pharmacodynamics of high-dose alkyla- tors used for the treatment of primary breast cancer. INTRODUCTION Eighty-five women with primary breast cancer involv- Utilization of high-dose chemotherapy with hematopoietic ing >10 lymph nodes received four cycles of standard-dose stem cell support has resulted in improvement in the treatment chemotherapy followed by a high-dose regimen consisting of malignancies such as some lymphomas and leukemias (1–3). -of: cyclophosphamide (1875 mg/m2 once daily ؋ 3), cisplatin However, inter-patient variability in the pharmacokinetic dispo (165 mg/m2 given over 72 h), carmustine (600 mg/m2), and sition of the agents used in the high-dose regimens may result in stem cell transplantation.
    [Show full text]
  • Chest CT for Suspected Pulmonary Complications of Oncologic Therapies: How I Review and Report Stefan Diederich
    Diederich Cancer Imaging (2016) 16:7 DOI 10.1186/s40644-016-0066-4 REVIEW Open Access Chest CT for suspected pulmonary complications of oncologic therapies: how I review and report Stefan Diederich Abstract In cancer patient during or following oncologic therapies with respiratory symptoms and pulmonary pathology at chest CT the differential diagnosis includes infection, therapy-induced disease and tumour progression. Although CT morphology may be typical or even pathognomonic in some conditions the diagnosis is usually made by a synopsis of imaging, clinical and laboratory features. Close communication with referring colleagues and a good knowledge of potential side effects of therapeutic concepts, their time course and CT morphology is crucial in the differential diagnosis. This review describes a personal approach to the radiological diagnosis of therapy-induced pulmonary abnormalities in cancer patients. Keywords: Lung, Radiation pneumonitis, Drug toxicity, Infection, Cryptogenic organizing pneumonia, Oedema, Computed tomography, Image interpretation, Image display Background infectious complications but its toxicity particularly Why imaging for pulmonary complications of oncologic of antifungal therapy may be detrimental in cases of therapy? non-infectious disease. Unnecessary discontinuation In patients during or following therapy for cancer pul- of an effective drug will obviously result in a nega- monary symptoms are common. These may, obviously, tive effect for the patient. be due to a variety of causes such as progression of ma- Furthermore, in cancer patients pulmonary disease lignancy involving the chest as well as infectious or non- may have a more aggressive and potentially lethal course infectious complications of surgery, radiation or medical than in otherwise healthy patients. therapy.
    [Show full text]