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Original article
Anzar Ashraf1,Anita Chakravarti2,Priyamvada Roy2,Oves Siddiqui2,Shipra Goel2,Neeru Kapoor2,Premashish Kar3
1 Virology laboratory, Department of Microbiology, Maulana Azad Medical College, Delhi-110002, India
2 Department of Microbiology, Maulana Azad Medical College, Delhi-110002, India
3 Department of Medicine, Maulana Azad Medical College & Associated Lok Nayak Hospital, Delhi-110002, India
Address reprint requests to:
*Dr Anita Chakravarti,
Department of Microbiology, Maulana Azad Medical College, Delhi-110002, India
Article citation: Ashraf A, Chakravarti A,Roy P, Siddiqui O, Goel S, Kapoor N,Kar P. Revisiting the utility of biochemical profile in the diagnosis and management of hepatitis C virus infection: a study from India. J Pharm Biomed Sci 2016;06(09):502–507.
Abstract
Several serum analytes can be used for the management of liver diseases. The present study was carried out to assess the role of biochemical markers in the diagnosis and prognosis of HCV infection. Blood samples (5 ml) collected from 300 patients with chronic HCV infection were analyzed for the presence of HCV antibodies and HBsAg by ELISA, and the infection was reconfirmed using reverse transcription polymerase chain reaction (PCR). Genotyping was done by restriction fragment length polymorphism or direct sequencing. Quantitative detection of HCV RNA by real-time PCR and measurement of Serum Glutamic Oxaloacetic Transaminase (SGOT), Serum Glutamic Pyruvic Transaminase (SGPT), Alkaline Phosphatase
(ALP), Bilirubin, Total Protein and Albumin levels was performed before and after 6 months of therapy. Anti HCV antibodies were found in 139 samples, of which 73 were positive for HCV RNA. Genotype 3 was the commonest genotype isolated, while an initial viral load of patients was higher in genotype 1. SGPT, SGOT and bilirubin levels were significantly deranged in HCV antibody positive patients while SGPT, SGOT, albumin and ALP were markedly raised in HCV RNA positive patients. Among 139 HCV AB-positive patients, all six parameters were found to be significantly deranged in HCV RNA positive patients compared to negative patients. Pre-therapy levels of SGPT, bilirubin and ALP were significantly higher than post-therapy levels. SGOT, SGPT and bilirubin are important diagnostic markers of HCV infection, while SGPT, bilirubin and ALP are valuable indicators of response to therapy. Biochemical profile can serve as cost-effective and dependable indirect marker for HCV infection.
KEYWORDS biochemical profile, diagnosis, hepatitis C virus infection, india, prognosis
REFERENCES
1.Penin F, Dubusson J, Rey FA, Moradpour D, Pawlotsky JM.Structural biology of hepatitis C virus. Hepatology. 2004;39(1):5–19.
2.Mohd Hanafiah K, Groeger J, Flaxman AD, Wiersma ST. Global epidemiology of hepatitis C virus infection: new estimates of age-specific antibody to HCV seroprevalence. Hepatology.2013;57(4):1333–1342.
3.Goodgame B, Shaheen NJ, Galanko J, El-Serag HB. The risk of end stage liver disease and hepatocellular carcinoma among persons infected with hepatitis C virus: publication bias? Am J Gastroenterol. 2003;98(11):2535–2542.
4.Mukhopadhyaya A. Hepatitis C in India. J Biosci. 2008;33(4):465–73.
5.Chakravarti A, Verma V. Prevalence of Hepatitis C and B viral markers in patients with chronic liver disease: A study of from north India. Indian J Med Microbiol. 2005;23(4):273–274.
6.Acharya SK, Madan K, Dattagupta S, Panda SK. Viral hepatitis in India. Natl Med J India. 2006;19(4):203–217.
7.Rehan HS, Manak S, Yadav M, Chopra D, Wardhan N. Diversity of genotype and mode of spread of Hepatitis C virus in Northern India. Saudi J Gastroenterol. 2011;17(4):241–244.
8.Shiffman ML, Diago M, Tran A, Pockros P, Reindollar R, Prati D, et al. Chronic hepatitis C in patients with persistently normal alanine transaminase levels. Clin Gastroenterol Hepatol.2006;4(5):645–652.
9.Khaliq S, Latief N, Jahan S. Role of different regions of the hepatitis C virus genome in the therapeutic response to interferon- based treatment. Arch Virol. 2014;159(1):1–15.
10. Wolf PL. Biochemical diagnosis of liver disease. Indian J Clin Biochem. 1999;14(1):59–90.
11.Mellor J, Hawkins A, Simmonds P. Genotype dependence of hepatitis C virus load measurement in commercially available quantitative assays. J Clin Microbiol. 1999;37(8):2525–2532.
12.Chinchai T, Labout J, Noppornpanth S, Theamboonlers A, Haagmans BL, Osterhaus AD, et al. Comparative study of different methods to genotype hepatitis C virus type 6 variants. J Virol Methods.2003;109(2):195–201.
13.Jindal N, Jindal M, Jilani N, Kar P. Seroprevalence of hepatitis C virus (HCV) in health care workers of a tertiary care centre in New Delhi. Indian J Med Res. 2006;123(2):179–180.
14.Verma V, Chakravarti A, Kar P. Genotypic characterization of hepatitis C virus and its significance in patients with chronic liver disease from Northern India. Diagn Microbiol Infect Dis.2008;61(4):408–414.
15.Bostan N, Mahmood T. An overview about hepatitis C: a devastating virus. Crit Rev Microbiol. 2010;36(2):91–133.
16.Thomas DL. Global control of hepatitis C: where challenge meets opportunity. Nat Med. 2013;19(7):850–858.
17.Shepard CW, Finelli L, Alter MJ. Global epidemiology of hepatitis C virus infection. Lancet Infect Dis. 2005;5(9):558–567.
18.Hissar SS, Goyal A, Kumar M, Pandey C, Suneetha PV, Sood A, et al. Hepatitis C virus genotype 3 predominates in North and Central India and is associated with significant histopathologic liver disease. J Med Virol. 2006;78(4):452–458.
19.Chakravarti A, Dogra G, Verma V, Parkash AS. Distribution pattern of HCV genotypes & its association with viral load. Indian J Med Res. 2011;133(3):326–331.
20.Sarrazin C, Berg T, Lee JH, Rüster B, Kronenberger B, Roth WK, et al. Mutations in the Protein Kinase–Binding Domain of the NS5A Protein in Patients Infected with Hepatitis C Virus Type 1a are associated with treatment response. J Infect Dis. 2000;181:432–441.
21.Fried MW, Shiffman ML, Reddy KR, Smith C, Marinos G, Gonçales FL Jr, et al. Peginterferon alpha-2a plus ribavirin for chronic hepatitis C virus infection. N Engl J Med. 2002;347:975–982.
22.Sarasin-Filipowicz M. Interferon therapy of hepatitis C: molecular insights into success and failure. Swiss Med Wkly. 2010;140:3–11.
23.Shakil AO, Conry-Cantilena C, Alter HJ. Volunteer blood donors with antibody to hepatitis C Study Group. Ann Intern Med. 1995;123(5):330–337.
24.Monitoring patients who are starting hepatitis C treatment, are on treatment, or have completed therapy. American Association for the Study of Liver Diseases. 2016. http://www. hcvguidelines.org/full-report/monitoring-patients-who-arestarting-hepatitis-c-treatment- are-treatment-or-have
25.Dusheiko G, Schmilovitz-Weiss H, Brown D, McOmish F, Yap PL, Sherlock S, et al. Hepatitis C virus genotypes: an investigation of type specific differences in geographic origin and disease. Hepatology. 1994;19:13–18.
26.Idrees M, Riazuddin S. Frequency distribution of hepatitis C virus genotypes in different regions of Pakistan and their possible routes of transmission. BMC Infect Dis. 2008;8:69.
27.Interpreting HCV serology and PCR results in diagnostic HCV testing. Australasian Society for HIV Medicine. 2015.
Statement of originality of work: The manuscript has been read and approved by all the authors, the requirements for authorship have been met, and that each author believes that the manuscript represents honest and original work.
Source of funding: None.
Competing interest / Conflict of interest: The author(s) have no competing interests for financial support, publication of this research, patents and royalties through this collaborative research. All authors were equally involved in discussed research work. There is no financial conflict with the subject matter discussed in the manuscript.
Disclaimer: Any views expressed in this paper are those of the authors and do not reflect the official policy or position of the Department of Defense.
Original article
Zayneb A. Mohammed1*,Haydar F. Al-Tukmagi1,Hassan M. Abbas2
1 Clinical Pharmacy Department, College of Pharmacy, Baghdad University, Baghdad,Iraq
2 Clinical Pharmacy Department, Medical city, Baghdad, Iraq
Address reprint requests to:
*Dr. Zayneb A. Mohammed,
Clinical Pharmacy Department, College of Pharmacy,Baghdad University, Baghdad, Iraq. Tel: (+964) 7718493580
Article citation: Mohammed ZA,Al-Tukmagi HF, Abbas HM. The role of coenzyme Q10 in breast cancer.J Pharm Biomed Sci 2016;06(09):522–525.Available at www.jpbms.info
ABSTRACT
Oxidative stress plays a crucial role in pathogenesis as well as progression of all cancers including breast cancer. The aim of the present study was to explore the possible protective effects of coenzyme Q10, an antioxidant agent, on Doxorubicin induced cardiotoxicity in breast cancer patients, we also investigated the role of coenzyme Q10 on oxidative stress. Sixty-four women having histologically confirmed breast cancer participated in this study. The patients divided into two groups. Group (A) who treated with coenzyme Q10 supplement in addition to chemotherapy adriamycin plus cyclophosphamide (AC). Group (B) treated with chemotherapy only. In this study, serum coenzyme Q10, malondialdehyde (MDA), total antioxidant status (TAS), complete blood count (CBC), serum ALT, AST, creatine kinase (CK), renal functions (serum creatinine and urea), creatine phosphokinase (CPK), high sensitivity C-Reactive protein (hs-CRP) levels were determined. Ejection Fraction (EF) was determined by echocardiography for all participants at baseline as well as post treatment. Statistical analysis was performed using SPSS, version 23, USA for WINDOWS, results are defined as mean ± standard deviation SD. Serum coenzyme Q10, total antioxidant status (TAS) were low at baseline in both groups, serum malondialdehyde (MDA), high sensitivity C-reactive protein (hs-CRP) levels had decreased significantly after supplementation with coenzyme Q10. The reduction in EF was more pronounced in group B at the end of the work. The present study demonstrated that women with breast cancer have a low level of coenzyme Q10 as compared to those of healthy women. It also emphasizes the growing concern that oxidative damage may occur in those patients that exhaust the antioxidant defense of the body leading to a low levels of Coenzyme Q10 and TAS and increasing in inflammatory markers as well as oxidative stress markers which lead to cardiotoxicity. Administration of antioxidant supplements such as a coenzyme Q10 is necessary in women with breast cancer postoperative with adjuvant chemotherapy to minimizes its cardiotoxicity.
KEYWORDS breast cancer, coenzyme Q10, oxidative stress
REFERENCES
1.DeSantis C, Ma J, Bryan L, Jemal A. Breast cancer statistics, 2013. CA a Cancer J Clin. 2014;64:52–62.
2.Tao Z, Shi A, Lu C, Song T, Zhang Z, Zhao J. Breast Cancer:Epidemiology and Etiology. Cell Biochem Biophys. 2015;72:333–338.
3.Siegel RL, Miller KD, Jemal A. Cancer statistics, 2016. CA Cancer J Clin. 2016;66:7–30.
4.Malhotra GK, Zhao X, Band H, Band V. Histological, molecular and functional subtypes of breast cancers. Cancer Biol Ther.2010;10:955–960.
5.Beral V, Reeves G, Bull D, Green J. Million Women Study Collaborators. Breast cancer risk in relation to the interval between menopause and starting hormone therapy. J Natl Cancer Inst. 2011;103:296–305.
6.Thomas S. Cancer As a Metabolic Disease: On The Origin,Management, and Prevention of Cancer. John Wiley & Sons,2012.
7.Zhang S, Liu X, Bawa-Khalfe T, Lu LS, Lyu YL, Liu LF, et al. Identification of the molecular basis of doxorubicin-induced cardiotoxicity. Nat Med. 2012;18:1639–1642.
8.Takemura G, Fujiwara H. Doxorubicin-induced cardiomyopathy: from the cardiotoxic mechanisms to management. Progress in cardiovascular diseases. 2007;49(5):330–52.
9.Gönenç A, Ozkan Y, Torun M, Simşek B. Plasma malondialdehyde (MDA) levels in breast and lung cancer patients. J Clin Pharm Ther. 2001;26:141–144.
10.Czarnecka AM, Krawczyk T, Zdrożny M, Lubiński J, Arnold RS,Kukwa W, et al. Mitochondrial NADH-dehydrogenase subunit 3 (ND3) polymorphism (A10398G) and sporadic breast cancer in Poland. Breast cancer research and treatment. 2010;121(2):511–8.
11.Halliwell B. Oxidative stress and cancer: have we moved forward? Biochem J. 2007;401:1–11.
12.Valko M, Izakovic M, Mazur M, Rhodes CJ, Telser J. Role of oxygen radicals in DNA damage and cancer incidence. Mol Cell Biochem. 2004;266:37–56.
13.Maria Zowczak-Drabarczyk M, Murawa D, Kaczmarek L, Połom K, Litwiniuk M. Total antioxidant status in plasma of breast cancer patients in relation to ERβ expression. Contemp Oncol (Pozn). 2013;17:499–503.
14.Gönenç A, Erten D, Aslan S, Akinci M, Simşek B, Torun M. Lipid peroxidation and antioxidant status in blood and tissue of malignant breast tumor and benign breast disease. Cell Biol Int. 2006;30:376–380.
15.Lee BJ, Huang YC, Chen SJ, Lin PT. Effects of coenzyme Q10 supplementation on inflammatory markers (high-sensitivity C-reactive protein, interleukin-6, and homocysteine) in patients with coronary artery disease. Nutrition. 2012;28:767–772.
16.Chai W, Cooney RV, Franke AA, Shvetsov YB, Caberto CP,Wilkens LR, et al. Plasma coenzyme Q10 levels and postmenopausal breast cancer risk: the multiethnic cohort study. Cancer Epidemiology Biomarkers & Prevention. 2010;19(9):2351–6.
17.Mortensen SA, Rosenfeldt F, Kumar A, Dolliner P, Filipiak KJ,Pella D, et al. Q-SYMBIO Study Investigators. The effect of coenzyme Q10 on morbidity and mortality in chronic heart failure: results from Q-SYMBIO: a randomized double-blind trial. JACC Heart Fail. 2012:4;641–649.
18.Niklowitz P, Onur S, Fischer A, Laudes M, Palussen M, Menke F,et al. Coenzyme Q10 serum concentration and redox status in European adults: influence of age, sex, and lipoprotein concentration. J Clin Biochem Nutr. 2016;58:240–245.
19.Anna G, Toru T, Singh RB, Meester D, Wilson F, Douglas W, et al. New roles of coenzyme Q10 in cardiovascular diseases, discovered by a single group. World Heart J. 2013;5:159–171.
20.Guo YZ, Pan L, Du CJ, Ren DQ, Xie XM. Association between C-reactive protein and risk of cancer: a meta-analysis of prospective cohort studies. Asian Pac J Cancer Prev. 2013;14:243–248.
21.Portakal O, Ozkaya O, Erden Inal M, Bozan B, Koşan M, Sayek I. Coenzyme Q10 concentrations and antioxidant status in tissues of breast cancer patients. Clinical Biochem. 2000;33:279–284.
22.Kasapović J, Pejić S, Todorović A, Stojiljković V, Pajović SB. Antioxidant status and lipid peroxidation in the blood of breast cancer patients of different ages. Cell Biochem Funct. 2008;26:723–730.
23.Shilpa HD, Anita R Bijoor. Malondialdehyde as a marker of lipid peroxidation in acute myocardial infarction patients. MRIMS journal of Health Sciences. 2013;1:20–22.
24.Del Pozo-Cruz J, Rodríguez-Bies E, Navas-Enamorado I, Del Pozo-Cruz B, Navas P, López-Lluch G. Relationship between functional capacity and body mass index with plasma coenzyme Q10 and oxidative damage in community-dwelling elderly people. Exp Gerontol. 2014;52:46–54.
25.Basu S, Harris H, Larsson A, Vasson MP, Wolk A. Is there any role for serum cathepsin S and CRP levels on prognostic information in breast cancer? The Swedish mammography cohort. Antioxid Redox Signal. 2015;23:1298–302.
26.Sara JD, Zhang M, Lennon R, Herrmann J, Lerman L, Lerman A. High sensitivity C-reactive protein is an independent marker of coronary endothelial dysfunction in patients with non obstructive coronary artery disease. J Am Coll Cardiol. 2016;67:360–360
27.Tao Z, Shi A, Lu C, Song T, Zhang Z, Zhao J. Breast Cancer: epidemiology and etiology. Cell Biochem Biophys. 2015;72:333–338.
Statement of originality of work: The manuscript has been read and approved by all the authors, the requirements for authorship have been met, and that each author believes that the manuscript represents honest and original work. Source of funding: None.
Competing interest / Conflict of interest: The author(s) have no competing interests for financial support, publication of this research, patents, and royalties through this collaborative research. All authors were equally involved in discussed research work. There is no financial conflict with the subject matter discussed in the manuscript.
Disclaimer: Any views expressed in this paper are those of the authors and do not reflect the official policy or position of the Department of Defense.