Levels of Selected Lipids, Apolipoproteins and Malondialdehyde In Mycobacterium Tuberculosis Infected Individuals Before, During And After Treatment
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关键词

Cardiovascular Disease
Mycobacterium tuberculosis
Lipid Profile
Free Fatty Acid
Apolipoprotein B
Apolipoprotein B 48
Apolipoprotein B 100
Malondialdehyde

摘要

Cardiovascular risk prediction is of high importance

for clinicians and patients to assess the risk of

developing cardiovascular disease (CVD), thereby

allowing for preventive interventions to be instituted

in those patients. Lipids and malondialdehyde (MDA)

status of individuals with active Mycobacterium

tuberculosis (MTB) infection were determined

before, after two, and six months’ treatment. This

prospective follow-up study recruited 159

tuberculosis (TB) treatment-naive individuals. They

were followed up on a six-month course of anti--

tuberculosis therapy (ATT).120 individuals completed

the study. Lipids and malondialdehyde were

measured before ATT, at two and six months post

treatment. MTB was detected by microscopy and

Genexpert methods. Lipids and malondialdehyde

levels were determined spectrophotometrically. The

mean levels of FFA, MDA, Apolipoprotein B, and B

48 were significantly lower in individuals with active

TB at 2 months and 6 months on ATT compared

with the baseline (p<0.05). The mean levels of

Apolipoprotein B100 were significantly higher in

individuals with active TB at 2 months and 6 months

following ATT compared with the baseline (p<0.05).

These findings showed reduced levels of MDA, Apo

B, and B 48 with increased levels of Apo B100 in

individuals with active MTB infection following

treatment. The observed significantly raised level of

Apo B100, even with treatment, indicates a higher

risk of cardiovascular disease. Lipid profile and apo

B100 levels significantly increased while

malondialdehyde, apolipoproteins B, and B 48

significantly decreased after treatment indicating a

good therapeutic response.

PDF (英语)

参考

Roth GA, Forouzanfar MH, Moran et al.

Demographic and epidemiologic drivers of global

cardiovascular mortality. N. Engl. J. Med. 2015,

, 1333–1341.

James K, Garry G. Developing a Research

Agenda for Primary Prevention of Chronic Lung

Diseases An NHLBI Perspective Am J Respir

Crit Care Med 2014, 189(7)762.

Benjamin EJ, Muntner P, Alonso et al. Heart

disease and stroke statistics—2019 update: A

report from the J. Am. Heart Assoc.Circulation

, 139, e56–e528.

Gazzola K., Reeskamp L, van den Born BJ.

Ethnicity, lipids, and cardiovascular disease. Curr.

Opin. Lipidol. 2017, 28, 225–230.

Szuszkiewicz-Garcia MM, Davidson JA.

Cardiovascular disease in diabetes mellitus, risk

factors, and medical therapy. Endocrinol. Metab.

Clin. N. Am. 2014, 43, 25–40.

Silverio A, Cavallo P, De Rosa R, Galasso G.

Big Health Data and Cardiovascular Diseases:

A Challenge for Research, an Opportunity for

Clinical Care. Front. Med. 2019, 6, 36.

Alkhalil M. Mechanistic Insights to Target

Atherosclerosis Residual Risk. Curr. Probl.

Cardiol. 2019, 46, 100432.

Arnett DK., Blumenthal RS, Albert, M.A.;

Buroker, A.B.; Goldberger, Z.D.; Hahn, E.J.;

Himmelfarb, C.D.; Khera, A.; Lloyd-Jones, D.;

McEvoy, J.W.; et al. 2019 ACC/AHA Guideline

on the Primary Prevention of Cardiovascular

Disease: A Report of the American College of

Cardiology/American Heart Association Task

Force on Clinical Practice Guidelines. J.Am. Coll.

Cardiol. 2019, 74, 1376–1414.

Hemmans MP, Ahn SA, Rousseau MF.

Atherogenic dyslipidemia [log (TG)/HDL-C] is

associated with residual vascular risk, beta–cell

function loss, and microangiopathy in type 2

diabetes females. Lipids Health Dis 2012,

(1)132.

Trompet S, Packard CJ, Jukema, JW. Plasma

apolipoprotein-B is an important risk factor for

CVD, and its assessment should be routine clinical

practice. Curr. Opin. Lipidol. 2018, 29, 51–52.

Libby P, Tabas I, Fredman, G, Fisher EA.

Inûammation and its resolution as determinants

of acute coronary syndromes. Circ. Res. 2014,

, 1867–1879.

Maguire EM, Pearce SWA, Xiao Q. Foam Cell

Formation. A New Target for Fighting

Atherosclerosis and Cardiovascular Disease.

Vascul. Pharmacol. 2019, 112, 54–71.

Constantinou C, Karavia EA, Xepapadaki et al.

Advances in high-density lipoprotein physiology:

surprises, overturns, and promises. Am J Physiol

EndocrinolMetab310: E1–E14, 2016. First

published 2015,doi:10.1152/ajpendo.00429.2015

Huaman MA, Henson D, Ticona E.Tuberculosis

and cardiovascular disease: linking the

epidemics. Tropical diseases travel medicine and

vaccines, 2015, 1(1)1. DOI 10.1186/s40794-015-

-5

Rodriguez Y, de Armas Y, Capo V, Wissmann G,

Goldani LZ, De Waard JH. Sudden death related

to tuberculous coronary arteritis. Int J Cardiol.

; 156 (2):e28–9. doi:10.1016/

j.ijcard.2011.08.002.

AC Ihim, SC Meludu, CC Onyenekwe, PO Manafa, AE Anyabolu and CN Akujobi

Nnodim, J., Anyadoh, S., Nwosu NE.(2011) The

antioxidant status and lipid peroxidation product

of newly diagnosed and six weeks follow-up

patients with pulmonary tuberculosis in Owerri,

Imo State, Nigeria. Asian Pacific Journal of

Tropical Disease, 1: 292-294.

Ihim AC, Nwosu DC, Nwanjo HU, Ozuruoke

DF, Nwobodo EI, Obi PC et al. Antioxidative

status of Nauclea latifolia leaves extract on

ciprofloxacin induced oxidative stress in rats. Int.

J. Inf. Res. Rev.2017; 04(04):33-37.

Oyedeji SO, Oguntuase N R, Esan A, Adesina

AA, Oke OT.Oxidative stress and lipid profile

status in pulmonary tuberculosis patients in South

Western Nigeria. Greener J Med Sci.2013;3 (6):

– 232.

Kapusta A, Kuczyñska B, Puppel K (2018)

Relationship between the degree of antioxidant

protection and the level of malondialdehyde in

high-performance Polish Holstein-Friesian cows

in the peak of lactation. PLoS ONE 13(3):

e 0 1 9 3 5 1 2 . h t t p s : / / d o i . o r g / 1 0 . 1 3 7 1

journal.pone.0193512 20. Chinedu IA,

Chukwuemeka MS,

Ihim AC, Meludu SC, Chinedum OC, Christian

EO. Evaluation of some antioxidants in

tuberculosis patients. Int J Health Sci Res. 2020;

(7):238246.

Liu A, Hu Y, Coates A. Sudden cardiac death

and tuberculosis - how much do we know?

Tuberculosis (Edinb). 2012; 92(4):307–13.

Doi:10.1016/ j.tube.2012.02.002.

Purnima P, Swasti J,Arvind A, Sachin M,

Devender Sc.Coronary arteritis as a cause of

sudden cardiac death in a young girl. Autops Case

Rep 2021; 11(1)67-70.

Pavic I, Radulovic P, Bujas T. Frequency of

tuberculosis at autopsies in a large hospital in

Zagreb, Croatia: a 10 year retrospective study.

Croatian Medical Journal 2012; 53(1)48-52.

Chung WS, Lin CL, Hung CT, Chu et al.

Tuberculosis increases the subsequent risk of

acute coronary syndrome: a nationwide

population-based cohort study. Int J Tuberc Lung

Dis. 2014;18(1):79–83. doi:10.5588/ijtld.13.0288.

Sheu JJ, Chiou HY, Kang JH, Chen YH, Lin HC.

Tuberculosis and the risk of ischemic stroke: a

-year follow-up study. Stroke. 2010; 41(2):244–

doi:10.1161/STROKEAHA.109.567735.

Ihim AC, Obi PC, Meludu C S, Onyenekwe CC,

Anyabolu E A, Njoku CM. Free Fatty Acid And

Lipid Profile In Active Tb, Latent Tb, Active Tb

And Hiv, Active Tb And Malaria Parasite In

Subjects In Anambra. Eur J Pharm Sci . 2018;

(11):506-511.

Ihim AC, Okeke O, Manafa PO, Ezejindu DN,

Nnodim J,Obi PC . Effect of Exposure To Soot

On Troponin I and Lipid Profile Levels. Eur J

Pharm Sci . 2016, 3(2): 05-10.

Ihim AC, Meludu SC, Onyenekwe CC, Anyabolu

AE, Akujobi CN. Serum apolipoprotein B

increased among tuberculosis patients compared

to healthy subjects. Univ Med 2021,40: 45-51.

doi: 10.18051/UnivMed.2021. v40.45-51

Curry SJ. Screening for Cardiovascular Disease

Risk With Electrocardiography US Preventive

Services Task Force Recommendation

Statement. JAMA. 2018;319(22):2308-2314.

doi:1 0 . 1 0 0 1 / ja ma . 2 0 1 8 . 6 8 4 8 :ht t p s :/ /

jamanetwork.com/ accessed on 06/28/2022

Valeska O, Soumyalekshmi N, Omar E, Claudio

A, Carlos S, Felipe A Z. Association between

insulin resistance and the development of

cardiovascular disease. Cardiovasc

Diabetol. 2018, 17: 122-127. doi: 10.1186/s12933-

-0762-4

Antonio A., Mario FM, Sandro A. Lipid

Peroxidation, Production, Metabolism, and

Signaling Mechanisms of Malondialdehyde and

-Hydroxy-2-Nonenal. Oxid Med Cell Longev

,1-31 https://doi.org/10.1155/2014/360438

Pugalendhi1V, Prema G, Panicker TMR, Paul

KM, Jagadeesan K, Tracy TAJ. Lipid

peroxidation and antioxidant status in patients of

end stage renal disease with and without

pulmonary tuberculosis. J. Int. Med. Sci. Acad.

, 25(4):225-227.

Gebremedhin G, Yemane A, Feyissa C, Atsbeha

G, Girmay M, Mistire W, Desta K. Lipid Profile

in tuberculosis Patients With and Wthout Human

Immunodeficiency Virus Infection. International

Journal of Chronic Diseases 2017, (3843291):1-

Prabakaran JJ, Biniam E, Matiwos A, Mussie

et al. Association of Dietary and Serum

Cholesterol with Active Pulmonary Tuberculosis:

A Hospital Based Study. International Journal of

Current Microbiology and Applied Sciences

,6 (12 ): 4056-4073.

Taparia P, Yadav D, Koolwal S, Mishra S. Study

of lipid profile in pulmonary tuberculosis patients

and relapse cases in relation with disease

severity.A pilot study. International Journal of

Sciences and Applied Research. 2015, 2(1): 41-

Albanna K B, Amr S, Donald W, Chantal V, Dick

M. Serum lipids as biomarkers for therapeutic

monitoring of latent tuberculosis infection. Eur.

Clin. Respir. J 2013,42: 547-550.

Lipids and Malondialdehyde in Individuals during and after Anti-Tuberculosis Therapy

Burtis AC, Ashwood ER, Bruns DE. Lipids,

Lipoproteins, Apolipoproteins and other

Cardiovascular Risk Factors in: Tietz

Fundamentals of Clinical Chemistry, 6th edition,

published by Elsevier, Sri Pratap Udyog, 274,

Capt. Gaur Marg, Sriniwaspuri, New Delhi India-

, 2008, chapter 23,pp.402-411.

Sniderman AD, Islam S, McQueen M, et al. Age

and cardiovascular risk attributable to

apolipoprotein B, low-density lipoprotein

cholesterol or non-high-density lipoprotein

cholesterol. J Am Heart Assoc 2016;5. doi.org/

1161/JAHA.116.003665