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      Effect of Dexrazoxane and Amifostine on the Vertebral Bone Quality of Doxorubicin Treated Male Rats

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          Abstract

          Doxorubicin (DOX) is widely used in combination cocktails for treatment of childhood hematological cancers and solid tumors. A major factor limiting DOX usage is DOX-induced cardiotoxicity. However, it is not known whether protectants like dexrazoxane (DXR) and amifostine (AMF) can prevent DOX-mediated bone damage. The present study investigated whether administration of AMF alone or in combination with DXR would prevent any DOX-mediated bone damage. Male rat pups were treated with DOX, DXR, AMF, and their combinations. On neonate day 38, the bone mineral density (BMD), bone mineral content (BMC) and the micro-architecture of the lumbar vertebrae were analyzed. We have shown that when male rats are treated with DOX, DXR, DOX+DXR, AMF, DOX+AMF or DOX+DXR+AMF, there is a decrease in lumbar vertebral BMD (p<0.05). Furthermore, the relative bone volume (BV/TV) was decreased by DXR, DOX+DXR, and DOX+AMF treatments. Interestingly, DOX+AMF significantly increased BV/TV when compared to DXR treatment (p<0.04). The trabecular number (Tb.N) decreased with DXR and DOX+DXR and increased with DOX+AMF treatments. This information will be useful in designing better cancer combination therapies that do not lead to vertebrae deterioration.

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          Acute doxorubicin cardiotoxicity involves cardiomyocyte apoptosis.

          L-M Parvinen, L Pulkki-Råback, J Arola … (2000)
          Despite well-documented cardiotoxic effects, doxorubicin remains a major anticancer agent. To study the role of myocardial apoptosis following doxorubicin administration, male Wistar rats were exposed to 1.25, 2.5, and 5 mg/kg of i.p. doxorubicin and terminated on days 1-7 in groups of five. Doxorubicin caused a significant (P < 0.001) and dose-dependent induction of cardiomyocyte apoptosis at 24-48 h after the injection. Repeated injections of 2.5 mg/kg given every other day resulted in peaks of apoptosis at 24 h after each injection. However, no additive effect of repeated dosing was noted. In histological samples, alterations in the cytoskeletal apparatus with focal loss of contractile elements were seen after a single injection. Myocyte necrosis was absent. Thus, acute doxorubicin-induced cardiotoxicity involves cardiomyocyte apoptosis, a potentially preventable form of myocardial tissue loss.
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            Anthracycline-induced clinical heart failure in a cohort of 607 children: long-term follow-up study.

            M Offringa, P A Voûte, Janus L. Kremer … (2001)
            To determine the early and late cumulative incidence of anthracycline-induced clinical heart failure (A-CHF) after anthracycline therapy in childhood and to identify associated risk factors. The cumulative incidence of A-CHF and the risk factors of A-CHF were assessed in a cohort of 607 children who had been treated with anthracyclines between 1976 and 1996. For 96% of the cohort, we obtained the clinical status up to at least January 1997. The mean follow-up time was 6.3 years. The cumulative incidence of A-CHF was 2.8%, after a mean follow-up time of 6.3 years and a mean cumulative dose of anthracyclines of 301 mg/m(2). A cumulative dose of anthracycline higher than 300 mg/m(2) was associated with an increased risk of A-CHF (relative risk, 11.8; 95% confidence interval, 1.6 to 59.5) compared with a cumulative dose lower than 300 mg/m(2). The estimated risk of A-CHF increased with time after the start of anthracycline chemotherapy to 2% after 2 years and 5% after 15 years. Up to 5% of patients will develop A-CHF 15 years after treatment, and patients treated with a cumulative dose of anthracyclines higher than 300 mg/m(2) are at highest risk for A-CHF. This is thus a considerable and serious problem among these young patients. The findings reinforce the need for strategies for early detection of patients at risk for A-CHF and for the evaluation of other chemotherapeutic possibilities or cardioprotective agents in relation to the survival.
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              Congestive heart failure after treatment for Wilms' tumor: a report from the National Wilms' Tumor Study group.

              Maxim Y Grigoriev, B Nan, P Norkool … (2001)
              We determined the frequency of and risk factors for congestive heart failure following treatment for Wilms' tumor that included doxorubicin. Flow sheets and medical records were reviewed to identify cases of congestive heart failure in a cohort of patients treated on National Wilms' Tumor Studies (NWTS)-1, -2, -3, and -4. The frequency of congestive heart failure was estimated using the Kaplan-Meier method. A case-control study was conducted to determine the relationship among cumulative doxorubicin dose, site(s), total dose of abdominal and thoracic irradiation, sex, and the frequency of congestive heart failure. The cumulative frequency of congestive heart failure was 4.4% at 20 years after diagnosis among patients treated initially with doxorubicin and 17.4% at 20 years after diagnosis among those treated with doxorubicin for their first or subsequent relapse of Wilms' tumor. The relative risk (RR) of congestive heart failure was increased in females (RR = 4.5; P =.004) and by cumulative doxorubicin dose (RR = 3.3/100 mg/m(2); P <.001), lung irradiation (RR = 1.6/10 Gy; P =.037), and left abdominal irradiation (RR = 1.8/10 Gy; P =.013). We conclude that congestive heart failure is a risk of treatment with doxorubicin for Wilms' tumor. Additional follow-up of those children treated on NWTS-4 will be necessary to determine if the decrease in dose to 150 mg/m(2) significantly reduces this risk.
              Article 0 comments Cited 52 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Open Orthop J
                Journal ID (publisher-id): TOORTHJ
                Title: The Open Orthopaedics Journal
                Publisher: Bentham Open
                ISSN (Electronic): 1874-3250
                Publication date (Electronic): 14 July 2008
                Publication date Collection: 2008
                Volume: 2
                Pages: 115-120
                Affiliations
                [1 ]Lady Davis Institute for Medical Research, SMBD - Jewish General Hospital
                [2 ]Division of Orthopaedic Surgery, McGill University
                [3 ]McGill Spine & Scoliosis Unit, Montreal Children Hospital
                [4 ]Division of Experimental Medicine, McGill University, Lady Meredith House, Montréal, Canada
                Author notes
                [* ]Address correspondence to this author at the Division of Orthopaedic Surgery, McGill University, Lady Davis Institute for Medical Research, SMBD - Jewish General Hospital, 3755 Chemin de la Côte Ste Catherine, Montréal, QC H3T 1E2, Canada; E-mail: fmwale@ 123456ldi.jgh.mcgill.ca
                Article
                Publisher ID: TOORTHJ-2-115
                DOI: 10.2174/1874325000802010115
                PMC ID: 2687116
                PubMed ID: 19478935
                SO-VID: 1254ac2a-d694-448e-8ef3-e612d1dbc161
                Copyright © © Mwale et al.; Licensee Bentham Open.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.5/), which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 06 May 2008
                Date revision received : 02 June 2008
                Date accepted : 20 June 2008
                Categories
                Subject: Article

                ScienceOpen disciplines: Orthopedics
                Data availability:
                ScienceOpen disciplines: Orthopedics

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