Effect of digoxin and vitamin E in preventing cardiac damage caused by doxorubicin in acute myeloid leukaemia.

Whittaker, J. A.; Al‐Ismail, Saad

doi:10.1136/bmj.288.6413.283-a

Cited by 25 publications

(14 citation statements)

References 3 publications

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“…Another study reported significantly decreased oral mucositis the vitamin E group 48. All other reports of toxicities found no significant differences in general toxicities between the 2 groups 48–51…”

Section: Resultsmentioning

confidence: 91%

“…Of note, the study of the lowest quality was the only study to not report a statistically significant decrease in toxicity. This study by Whittaker recruited 63 patients, but only 25 (7 on vitamin E) survived to be included in statistical analysis for “cardiac damage.”49 Because none of the vitamin E studies had high Jadad scores or large sample sizes, statistically significant reductions in toxicities reported by the other 4 studies cannot be generalized for clinical use. Future studies should employ larger samples and better methodology.…”

Section: Discussionmentioning

confidence: 99%

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Acute Liver Failure Is Associated With Elevated Liver Stiffness and Hepatic Stellate Cell Activation†

Dechêne¹,

Sowa²,

Gieseler³

et al. 2010

Hepatology

140

103

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Acute liver failure (ALF) is associated with massive short-term cell death, whereas chronic liver injury is accompanied by continuous cell death. Hepatic stellate cells (HSCs) contribute to tissue repair and liver fibrosis in chronic liver injury, although their role in ALF remains unexplained. Twenty-nine patients (median age 5 43 years, 17 females and 12 males) with ALF according to the Acute Liver Failure Study Group criteria were included. Upon the diagnosis of ALF and after 7 days, we determined liver stiffness (LS) with FibroScan, standard laboratory parameters, and serum levels of matrix metalloproteinase 1 (MMP-1), MMP-2, MMP-9, tissue inhibitor of metalloproteinases 1 (TIMP-1), TIMP-2, hyaluronic acid, and markers of overall cell death (M65) and apoptosis (M30). Stellate cell activation and progenitor response were analyzed immunohistochemically in biopsy samples of 12 patients with a-smooth muscle actin (a-SMA), keratin-17, and keratin-19 staining, respectively. Cell death markers (M30 level 5 2243 6 559.6 U/L, M65 level 5 3732 6 839.9 U/L) and fibrosis markers (TIMP-1 level 5 629.9 6 69.4 U/mL, MMP-2 level 5 264 6 32.5 U/mL, hyaluronic acid level 5 438.5 6 69.3 lg/mL) were significantly increased in patients versus healthy controls. This was paralleled by collagen deposition, elevated a-SMA expression, and higher LS (25.6 6 3.0 kPa). ALF was associated with ductular progenitor proliferation. Conclusion: Our results demonstrate HSC activation and a progenitor response in ALF. Positive correlations between LS, the degree of liver cell damage, and the intensity of HSC activation suggest that fibrosis is a response to ALF in an attempt to repair damaged tissue. (HEPATOLOGY 2010;52:1008-1016 A cute liver failure (ALF) is a devastating clinical syndrome associated with high mortality in the absence of immediate state-of-the-art intensive care or liver transplantation. 1 ALF can occur as a result of various etiologies (overdosing with acetaminophen or other drugs, viral hepatitis, ischemia, and other causes 1 ); in approximately 15% of adult cases and 50% of pediatric cases, the reason is unidentified. 2

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Section: Resultsmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Acute Liver Failure Is Associated With Elevated Liver Stiffness and Hepatic Stellate Cell Activation†

Dechêne¹,

Sowa²,

Gieseler³

et al. 2010

Hepatology

140

103

View full text Add to dashboard Cite

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“…Among them, 26 clinical trials used glutathione or reduced glutathione (GSH) (22–47), 11 used a type of vitamin E such as α -tocopherol or dl- α -tocopherol acetate (48–59), 5 used N -acetylcysteine (NAC; 60–64), and others ( n = 10) used vitamin C, selenium, coenzyme Q10, zinc, or a combination of antioxidants (65–74; Table 1). Since GSH, vitamin E, and NAC were studied most frequently, we further analyzed the reports that examined these antioxidant supplements.…”

Section: Resultsmentioning

confidence: 99%

Systematic Review: Generating Evidence-Based Guidelines on the Concurrent Use of Dietary Antioxidants and Chemotherapy or Radiotherapy

Nakayama¹,

Alladin

Igbokwe

et al. 2011

Cancer Investigation

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The risk–benefit ratio for concurrent use of dietary antioxidants with chemotherapy or radiation therapy is a controversial topic. In this review, the medical literature on concurrent antioxidant use with chemotherapy or radiotherapy was assessed and further steps for generating evidence-based guidelines are suggested. The clinical cancer research community should cooperate and focus new studies on the use of a specific combination of antioxidant and chemotherapy or radiotherapy, and determine optimal doses for a specific cancer setting. Mechanistic studies on the interaction between antioxidants and conventional cancer therapy could lead to novel biomarkers for assessing dose adequacy.

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“…Strophanthin, the aglycone of which is strophanthidin, prevents doxorubicininduced alterations in isolated rabbit or dog hearts (57,58), digoxin inhibits the anthracycline-induced negative inotropic effects in paced cat hearts (58), and ouabain blocks anthracycline-induced depressant activity in isolated myocytes (59). The mechanism or mechanisms by which these agents operate remain controversial (1), but in clinical studies very little protection is observed (60)(61)(62)(63).…”

Section: Ohmentioning

confidence: 99%

Amelioration of Anthracycline-Induced Cardiotoxicity by Organic Chemicals

Witiak

Herman

1994

ACS Symposium Series

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The amelioration of anthracycline-induced cardiotoxicity by numerous organic chemicals is discussed. These include ion regulators, receptor site antagonists, and inhibitors of mediator release, energy regulators, enzyme inhibitors, membrane stabilizers, anthracycline uptake inhibitors, and inactivators, antioxidants and chelating materials, and various miscellaneous substances.Of these the bis(2,6-dioxopiperazine)s remain as the potentially most useful drugs.Recently published reviews (7,2) describe the various organic chemicals that serve to ameliorate acute and chronic anthracycline-induced toxicities at the cellular, animal, and clinical levels. In this review drugs are categorized according to the rationale proposed for their protective activity. Whereas major efforts have been directed towards decreasing myocardial concentrations of anthracyclines and their metabolites and the development of less cardiotoxic anthracyclines, this summary focuses upon the concurrent administration of substances that block anthracyclineinduced toxicities.As discussed in other chapters, anthracycline antitumor activity may be attributable to multiple mechanisms (1-3) such as (a) intercalation into DNA, (b) formation of ternary complexes with DNA topoisomerase n, and (c) radical-induced DNA strand breakage. The latter may involve anthracycline semiquinone radical-induced hydroxyl radical (HO*) formation, anthracycline semiquinone radical-induced superoxide anion radical (0 2 T )generation, and/or anthracycline-ferric ion complex catalyzed Fenton reactions (J).Anthracycline-induced cardiotoxicity also is a function of multiple mechanistic possibilities (1). Acute effects such as hypotension are inhibited by antagonists of neurotransmitters (4,5). Subacute toxicity is rare, is unrelated to cumulative anthracycline dose, and manifests itself within 4 weeks as pericarditis-myocarditis with pericardial effusion and ventricular dysfunction (6). Nucleolar segregation also

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Effect of digoxin and vitamin E in preventing cardiac damage caused by doxorubicin in acute myeloid leukaemia.

Cited by 25 publications

References 3 publications

Acute Liver Failure Is Associated With Elevated Liver Stiffness and Hepatic Stellate Cell Activation†

Acute Liver Failure Is Associated With Elevated Liver Stiffness and Hepatic Stellate Cell Activation†

Systematic Review: Generating Evidence-Based Guidelines on the Concurrent Use of Dietary Antioxidants and Chemotherapy or Radiotherapy

Amelioration of Anthracycline-Induced Cardiotoxicity by Organic Chemicals

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