DocumentsDate added
Original article:
Kapil Srivastava1,*, Anil Bidwai2, Dhiraj Srivastava3, Ramesh Thanna4
Affiliation:-
1Ex Post Graduate Student, 2Professor,3MD,Assistant Professor, 4Msc,Department of Biochemistry, Index Medical College, Indore, Madhya Pradesh, India
The name of the department(s) and institution(s) to which the work should be attributed:
Department of Biochemistry, Index Medical College, Indore, Madhya Pradesh, India
Address reprint requests to
Dr. Kapil Srivastava.
Kamaleshwar colony, Dabra, Gwalior ,Madhya Pradesh, India or at kapilgrmc@gmail.com
Article citation:
Srivastava K,Bidwai A,Shrivastava D,Thanna R. A study to assess lipid profile values in atheroscerotic patients of different age and sex groups. J Pharm Biomed Sci. 2014;04(09):A1-A7. Available at www.jpbms.info
ABSTRACT
Background: Atherosclerosis, also called hardening or blockage of the arteries, is a very common condition affecting the arteries, the thick-walled, high-pressure blood vessels that carry fresh oxygen-rich blood from the heart to the rest of the body.
Atherosclerosis occurs more frequently in men than in women. There have been studies that show the sex gap in plaque prevalence is strongly influenced by age. Objectives: Estimation of serum lipid profile in normal–male, female–healthy controls and atherosclerosis patients (male & female).
Comparison above biochemical parameters between normal male healthy control and male atherosclerosis patients (30 – 50 year & 51 – 70 year) Methodology: A Total of 53 patients full filing exclusion and inclusion criteria’s were included in the study group and 50 ages matched male and female healthy individual control groups during the period one year. Blood samples were collected from the patients and male and female healthy individual controls. This blood used for separation of serum. Serum used for estimation of lipid profile.
Results: There is significant difference in the biochemical parameters values between normal male and female healthy controls and male and female Atherosclerosis patients. There is no significant difference in the vales of serum cholesterol in both male and female atherosclerotic patients.
Conclusion: The present study hereby concludes that in comparison to normal healthy controls, atherosclerotic patients have higher serum values of TC, LDL, and TG and lower values of HDI cholesterol.
KEYWORDS: Atherosclerosis, Lipid Profile, Atherosclerotic diseases
REFERENCES
1.Sharrett AR, Patsch W, Sorlie PD. Associations of lipoprotein cholesterols, apolipoproteinsA-I and B, and triglycerides with carotid atherosclerosis and coronary heart disease: The Atherosclerosis Risk in Communities (ARIC) Study. Arterioscler Thromb 1994;14:1098-104.
2.Libermann C. Ber Deutsch Chem Gescl 1885;18:1803.
3.Tietz NW. Clinical guide to laboratory tests, 2nd ed. Saunders Co. 1991.
4.NCEP expert panel, Arch Inter Med. 1988;148:26-69.
5.Nauck M, Kramer-Guth A, Bartens W, Marz W, Wieland H, Wanner C. Is the determination of LDL cholesterol according to Friedewald accurate in CAPD and HD patients? Clin Nephrol. 1996;46:319–25.
6.Herbert K. Lipids, In clinical Chemistry: Theory, Analysis and Co – relation, Kaplan L A and Pesce A J, Eds. C. V. Mosby, Tronto. 1984. p 1182 – 1230.
7.Yazdi SAT, Rezaei A, Azari JB, Hejazi A, Shakeri MT, Shahri MK. Prevalence of Atherosclerotic Plaques in Autopsy Cases with Noncardiac Death. Iranian J Pathol 2009;4 (3):101.
8.Jablonski WK. Non-HDL Cholesterol as a Predictor of Cardiovascular Disease in Type 2 Diabetes. Diabetes Care 2003;26(1).
9.Reddy RK, Reddy S, Kumar AM. Lipid Profile levels on the second day of Acute Myocardial Infarction; is it the right time for estimation? Internet Journal of Medical Update 2012 Jan;7(1):52-5
10.Niedziela AS, Roman P. Clinical usefulness of determining C-reactive protein and fibrinogen concentrations and lipid profile in blood serum of patients undergoing surgery due to atherosclerosis. Journal of Pre-Clinical and Clinical Research.2008; 2(1):75-79.
Source of support: 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.
Research article
Priyanka Joshi1* M.Sc., Harnam Kaur2 MD, Rajesh Pandey2 MD, Jasbir Singh2 MD, Kuldip Singh Sodhi2 MD
Affiliation:-
1*MSc MLT (Intern), 2Professor, Department of Biochemistry, MMIMSR, Mullana, Ambala, Haryana., India
The name of the department(s) and institution(s) to which the work should be attributed:
Department of Biochemistry, MMIMSR, Mullana, Ambala, Haryana, India
Address reprint requests to
Priyanka Joshi
Department of Biochemistry, MMIMSR, Mullana, Ambala, Haryana, India
Criteria for inclusion in the authors'/ contributors' list: 1*Research work, data acquisition, statistical analysis, 2Concept and design, manuscript preparation and editing.
Article citation:
Joshi P, Kaur H, Pandey R, Singh J, Sodhi KS. To estimate serum vitamin C Level in non-alcoholic chronic smokers and compare it with non-smokers. J Pharm Biomed Sci. 2014;04(09):825-827. Available at www.jpbms.info
ABSTRACT
Context: Tobacco smoking is associated with deficiency of antioxidants in the body.
Aims: To estimate serum vitamin C level in non-alcoholic chronic smokers and compare it with non-smokers.
Setting and Design: Prospective cross sectional study in rural setting of Haryana.
Material and Method: The study was conducted in the Department of Biochemistry, on the staff members and students of Maharishi Markandeshwar Institute of Medical Sciences and Research, Mullana (Ambala). The study was conducted for a period of one year from March 2013 to March 2014. Total number of 60 subjects between the age of 18 to 60 years were selected and divided into two groups. Group 1: 30 subjects; healthy non-alcoholic chronic smokers and Group 2: 30 subjects, healthy non-alcoholic non-smokers. 5 ml of fasting venous blood was collected from antecubital vein under aseptic conditions from each subject into plain vials. Serum was separated and used for estimation of vitamin C by colorimetry.
Statistical analysis: By SPSS version 12 [SPSS v12 (SPSS Inc., Chicago, IL)].
Results: Serum vitamin C levels were lower in smokers (0.24 ± 0.18 mg %) as compared to non-smokers (1.38 ± 0.51 mg %) and the difference was highly significant (p = 0.000). The age, weight, height and Body Mass Index (BMI) did not affect the level of vitamin C.
Conclusion: Smokers have a significantly lower level of vitamin C as compared to non-smokers and may need supplementation.
KEYWORDS: Ascorbic acid, Vitamin C, Smokers, Reactive oxygen species, Reactive nitrogen species.
Source of support: None
REFERENCES
1.Thurnham Dl, Northrop-Clewes CA. Effects of infection on nutritional and immune status. In: Diet and human immune function, edited by: Hughes DA, Darlington LG, Bendich A. New Jersey Humana Press 2004: 35-63.
2.Church D, Pryor WA. Antioxidant. Env Health Persp. 1985, 64: 111-26.
3.Cross CE, Traber M, Eiserich J. World population prospectus. Br Med Bull 1999; 55: 691-704.
4.Pryor WA, Prier DG, Church DF. Oxidative stress. Env Health Persp. 1983; 47: 345-55.
5.Pryor WA, Stroke K. Free radicals. Atherosclerosis 1983; 168: 169-79.
6.Park EM, Park YM, Gwark YS. Immune response. Atherosclerosis 1998; 168: 169-79.
7.Pandey R, Singh M, Singhal U, Gupta KB, Aggarwal SK. Oxidative/ nitrosative stress and the pathobiology of chronic obstructive pulmonary disease. J Clin Diag Res 2013; 7(3): 580 – 8.
8.Schectman G., Kaul S., Kissebah A.H. Arterioscler Thromb Vasc Biol. 1989; 9: 345-54.
9.Halliweli B, Gutteridge JMC, Cross CE. Free radicals antioxidants and human disease: where are we now? Clin Lab Med 1992; 119: 598-620.
10.Yu BP. Cellular defenses against damage from reactive oxygen species. Physiol Rev. 1994; 74: 139-62.
11.Di Giacomo C, Acquaviva R, Lanteri R, Licat F, Licata A, Venella A. Nonproteic antioxidant status in plasma of subjects with colon cancer. Exp Biol Med. 2003; 228: 525-28.
12.Ozturk O, Gumuslu S. Change in glucose 6-phosphate dehydrogenase, copper, zinc- superoxide dismutase and Catalase activities, glutathione and its metabolizing enzymes, and lipid peroxidation in rat erythrocytes with age. Exp Geront 2004; 39: 211-16.
13.Lykkesfeldt J, Viscovich M, Poulsen HE. Ascorbic acid recycling in human erythrocytes is induced by smoking in vivo. Free Rad Biol Med. 2003; 35: 1439-47.
14.Duthic GG, Arthur JR, Beattie JA, Brown KM, Morrice PC, Robertson JD, et al. Cigarette smoking, antioxidants, lipid peroxidation, and coronary heart disease. Ann NY Acad Sci. 1993; 686: 120-9.
15.Schectman G, Byrd JC, Gruchow HW. The influence of smoking on vitamin C status in adults. Am J Public Health. 1989;79:158–62.
16.World Medical Association declaration of Helsinki. Ethical Principles for Medical Research involving Human subjects. World Medical Association available from; http://www.wma.net/e/policy/b3html. Accessed on 23/08/14.
17.Kim HA, Min HS, Ha AW, Hyun HJ, Mie H, Ro MS et al. Effects of Vitamin C and Vitamin E Supplementation on Anti-oxidative System of the Smokers and Non-smokers. J Community Nutr. 2004; 6(3): 146-54.
18.Li N, Jia X, Chen CY, Blumberg JB, Song Y, Zhang W et al. Almond consumption reduces oxidative DNA damage and lipid peroxidation in male smokers. J Nutr. 2007; 137(12): 2717–22.
19. Chow CK, Thacker RR, Changchit C, Bridges RB, Rehm SR, Humble J et al. Lower levels of vitamin C and carotenes in plasma of cigarette smokers. J Am Coll Nutr. 1986; 5(3): 305-12.
Copyright © 2014 Joshi P, Kaur H, Pandey R, Singh J, Sodhi KS. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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.
Original article
Rupal Samal 1 MD DNB(OBG), Sendhil Coumary.A2,* MD, DNB, MNAMS (OBG), Lopamudra B John3 MD, DNB (OBG), Seetesh Ghose4 MD, FICOG
Affiliation:-
1Assistant Professor,2Professor, 3Associate Professor, 4Professor and Head of Department, Department of Obstetrics and Gynaecology, Mahatma Gandhi Medical College And Research Institute, Puducherry, India
The name of the department(s) and institution(s) to which the work should be attributed:
Department of Obstetrics and Gynaecology, Mahatma Gandhi Medical College and Research Institute, Puducherry, India
Address reprint requests to
Dr. Sendhil Coumary. A,
Department of Obstetrics and Gynaecology, Mahatma Gandhi Medical College And Research Institute, Pillaiyarkuppam, Puducherry, India-607402
Article citation:
Samal R, Coumary SA, John LJ, Ghose S. Comparative study of oral, rectal misoprostol with intravenous methylergometrine in active management of third stage of labour. J Pharm Biomed Sci. 2014; 04(09):828-833. Available at www.jpbms.info
ABSTRACT
Objectives: To compare the efficacy and side effects of oral misoprostol, rectal misoprostol and intravenous methyl ergometrine in active management of third stage of labour.
Study Design: Prospective Randomised Control Study.
Study Setting: The study was conducted in Mahatma Gandhi Medical College and Research Institute, Puducherry, between November 2010 and May2012.
Method: 300 participants were randomised into three groups. Active management of third stage of labour was followed in all the participants. The uterotonic of choice divided them into groups. Group I received 0.2 mg methyl ergometrine, Group II received oral misoprostol 400 μg, and Group III received rectal misoprostol 800 μg within one minute of the delivery of the baby. Duration of third stage of labour was noted. Blood loss was measured by preweighed sponge method. Hemoglobin and hematocrit were measured 24 hours after delivery.
Outcome Measures: The parameters studied were the duration of third stage, amount of blood loss in the third stage and side effects of the drugs.
Results: The duration of third stage of labour and blood loss was significantly reduced in group III (rectal misoprostol) with p value<0.001. The difference in haemoglobin and hematocrit measured 24 hours postpartum was also significantly lesser in group III. The incidences of side effects were significantly more in group II.
Conclusion: Rectal misoprostol is an effective uterotonic and an acceptable alternative uterotonic in the Active management of the third stage of labour.
KEYWORDS: Active management of third stage labour; oral misoprostol; rectal misoprostol; methyl ergometrine; duration of third stage.
REFERENCES
1.World Health Organisation (WHO) Department of Reproductive Health and Research. Maternal mortality in 2000: Estimates developed by WHO, UNICEF,
and UNFPA.Geneva: WHO March, 2012.
2.Vora KS,Dileep VM,Ramani KV et al. Maternal Health Situation in India: A Case Study. J Health Popul Nutr. 2009 April; 27(2): 184–201.
3.Obstetrical Haemorrhage: Gray Cunningham et al. Williams Obstetrics 23rd edition. Alyssa Friedband Karen Davis editors. United State of America; Mc Graw Hill; 2010;35:759-761.
4.Placental cord drainage after vaginal delivery as part of the management of the third stage of labour (Review)Copyright © 2011: The Cochrane Collaboration. Published by John Wiley & Sons, Ltd.:2-3
5.Rogers J, Wood J, McCandlish R, Ayers S,Truesdale A, Elbourne D. Active versus expectant management of third stage of labour: the Hinchingbrooke randomised controlled trial. Lancet 1998; 351: 693–99.
6.Maughan KL, Heim SW, Galazka SS. Preventing postpartum hemorrhage: managing the third stage of labor. Am Fam Physician. 2006;73(6):1025–8.
7.Bamigboye AA, Holfmeyr GJ, Merrell Da, Mitchell Ronald. Randomised comparison of rectal misoprostol with syntometerive for mangement of third stage of labour. Acta obstet Gynecol scand 1998;77:178-181.
8.Frederic Amant, Bernard Spitz, Dirk Timmer Man, Annick Corremans, Frans Andre VA . Misoprostol compared with methyle ergometerine for the prevention of PPH a double blind randomized trial. Br J of Obstet and Gynecol .Oct 1999; 106: 1066 – 1070.
9.Parsons SM, Robert LW, Joan MG, et al. Rectal Misoprostol Versus Oxytocin in the Management of the Third Stage of Labour.J Obstet Gynaecol Can 2007; 29(9):711–718.
10.Parsons SM, Robert LW, Joan MG, et al. Oral Misoprostol versus Oxytocin in the Management of the Third Stage of Labour. J Obstet Gynaecol Can 2006; 28(1):20–26.
11.Tripti N , Balram S. 400μg oral misoprostol versus 0.2mg intravenous methyl ergometrine for the active management of third stage of labor. J Obstet Gynecol.2009; 59(3):228-234.
12.Gohil JT, Tripathi Beenu . A study to compare the efficacy of misoprostol, oxytocin, methyl ergometrine and ergometrine-oxytocin in reducing blood loss in active management of third stage of labor. J Obstet Gynecol2011; 61(4):408-412.
13.Surbek VD, Peter MF, Irene H ,Wolfgang H. Oral misoprostol in third stage of labour:A randomised placebo controlled trial. Am J Obstet Gynecol.1999;94(2):255-258.
14.Lumbiganon P, Hofmeyr GJ, Gulmezoglu AM, Pinol A, Villar J. Misoprostol dose related shivering and pyrexia in the third stage of labour. Br J Obstet Gynecol.1999;106:304-308.
15.Chan ASM, Ng PS ,Sin WK,Tang LCH, Cheung KB, Yuen PM. A multicenter randomised controlled trial of oral misoprostol and intramuscular syntometrine in the management of the third stage of labour. J Human Reprod 2001;16(1):31-35.
16.WHO Multi Center randomized trial in the management of the third stage of labour .The Lancet 2001; 358:689-95.
17.Hofmeyr JG. A randomised placebo controlled trial of oral misoprostol in the third stage of labour. Br J Obstet Gynecol 1998; 105:971-975.
18.Walley RL,Wilson JB,Crane JMG,Mathews K,Elizabeth S,Hutchens D. A double blind placebo controlled randomised trial of misoprostol and oxytocin in the management of third stage of labour. Br J Obstet Gynecol.2000;107(9):1111-1115.
Copyright © 2014 Samal R, Coumary SA, John LJ, Ghose S.This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Source of support: 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.
Original article
Samavedam Srinivasa Sarma1,Pennagaram Sarguna2,*
Affiliation:-
1Assistant Professor, 2Associate Professor, Department of Microbiology, Rangaraya Medical College, Kakinada-533005, A.P,India
The name of the department(s) and institution(s) to which the work should be attributed:
Department of Microbiology, Rangaraya Medical College, Kakinada-533005, A.P, India
Address reprint requests to
Dr.Pennagaram Sarguna,
Associate Professor, Department of microbiology, Rangaraya Medical College, Kakinada, A.P.India
Core tip: The present study was undertaken to know the microbiological profile in corneal ulcers. Majority of the infections are caused by Staphylococcus aureus. The results of antibiotic susceptibility of bacterial isolates provide information to make rationale- based decision in choosing initial treatment regimen.
Article citation:
Sarma SS, Sarguna P Microbial Keratitis - A Prospective Study. J Pharm Biomed Sci. 2014;04(09):818-824.Available at www.jpbms.info
ABSTRACT
To study the epidemiological characteristics, microbiological profile, and in vitro antibiotic susceptibility results to make rationale - based decisions in choosing initial treatment regimen of bacterial keratitis. The hospital - based prospective study of 100 consecutive patients with corneal ulcers attending the outpatient department of Government General Hospital, Kakinada, Coastal A.P. from August 2011 through June 2013 were enrolled. Standard microbiologic evaluation of corneal scraping; smear examination and culture was done to establish the etiology. Attempt was made to study the microbial profile in 30 healthy conjunctival sac. Of 100 suspected cases of microbial keratitis, 59(59%) were culture proven; pure bacterial 41(41%), pure fungal 16(16%) and mixed infection in 2(2%). Majority of the bacterial infections were caused by Staphylococcus aureus (41.86%) and Aspergillus spp. (55.54%) was the leading cause of fungal keratitis. Most of the bacterial isolates were sensitive to aminoglycosides (72.09% - 95.34%) followed by cefotaxime (69.76%). The study shows that there is a region wise variation in the predominance of corneal pathogens. Routine surveillance of microbial keratitis is necessary to know the existing & emerging pathogens. This has an important public health implication for initiation of treatment, based on formulation of antimicrobial policy and management protocol to prevent visual morbidity.
KEYWORDS: Keratitis; bacteria; fungus; anti- bacterial susceptibility.
REFERENCES
1.Bharathi MJ, Ramakrishna R, Vasu S, Meenakshi R, Palaniappan R. Aetiological, diagnosis of microbial keratitis in South India – A study of 1618 cases. Ind J Med Microbiol 2002; 20:19-24.
2.Srinivasan M, Gonzales CA, George C, Cevallos V. Epidemiology and aetiological diagnosis of corneal ulceration in Madurai, South India. Br. J. Ophthalmol 1997;81:965-71.
3.Leibowitz HM.Bacterial keratitis. In Leibowitz HM(ed): corneal disorders: clinical diagnosis and management, Philadelphia, WB saunders, 1984.p353.
4.Gopinathan U, Garg P, Fernandes M, Sharma S, AthmanathanS, Rao GN, The epidemiological features and laboratory results of fungal keratitis. A 10 year review at a referral eye care center in South India. Cornea 2002;21:555-59.
5.Bharathi MJ, Ramakrishna R, Meenakshi R, Shivakumar C, Raj DL. Analysis of risk factors predisposing to fungal, bacterial & Acanthamoeba keratitis in South India. Indian J Med Res 2009 Dec: 130(6):749-57.
6.Deshpande SD, Koppikar GV. A study of mycotic keratitis in Mumbai. Indian J Pathol microbiol 1999;42(i):81-87.
7.Ansons AM. Corneal ulceration caused by penicillin – resistant Neisseria gonorrhoeae. Arch ophthalmol 1987;105:1325.
8.Reddy M, Sharma S, Rao GN. Corneal ulcer in Dutta LC, editor. Modern Ophthalmology. 2nd ed, New Delhi, Jaypee Brothers Medical Publishers;2000 pp 200-216.
9.Jones DB, Liesegang TJ, Robinson NM, Laboratory diagnosis of ocular infections, Washington DC; Cumitech 13, American society for Microbilology:1981.
10.Sharma S, Athmanathan. Diagnostic procedures in infectious keratitis Chapter 17. In: Diagnostic procedures in Ophthalmology. eds Nema HV, Nema N, Jaypee Brothers Medical Publishers (P) Ltd., New Delhi; 2002 – PP232-253.
11.A.C.Scott. Laboratory control of antimicrobial therapy in Mackie & McCartney Practical Medical Microbiology Edited b y J.G. Collee, J.P. Duguid , A.G. Fraser, B.P. Marmion, 13th Edition, Vol.2 1989, PP161-181.
12.Asha Pichare, Neeta Patwardhan, AS Damle, AB Deshmukh. Bacteriological and mycological study of corneal ulcers in and around Aurangabad. IndianJ of pathol Microbiol 2004;47(2):284-286.
13.Basak Samar K, Basak Sukumar, Mohanta Ayan, Bhowmick Arup. Epidemiological and microbiological diagnosis of suppurative keratitis in Gangetic west Bengal, Eastern India. Indian J of Ophthalmol 2005; 53(1);17-22
14.Gulnaz Bashir, Azar shah, Manzor A Thokar, Saboa Rashid, Salman Shakeel. Bacterial and fungal profile of corneal ulcers – A Prospective Study. Indian J of Pathol Microbiol 2005; 48(2):273-277.
15.Vajpayee RB, Dada T, Saxena R, et al.Study of the first contact management profile of cases of infections keratitis: a hospital based study. Cornea 2000;19:52-6.
16.M Jayahar Bharathi, R. Ramakrishnan Samala Vasu, R Meenakshi, R Palaniappan. Epidemiological Characteristics and laboratory diagnosis of fungal keratitis. A three- year study. Indian J Ophthalmol 2003;51: 315-21.
17.Usha Gopinathan, Savitri Sharma, Prashant Garg, Gullapalli N Rao. Review of epidemiological features, microbiological diagnosis and treatment outcome of microbial keratitis: Experience of over a decade. Indian J Ophthalmol:2009;57:273-279.
18.Reema Nath, Symanta Baruah,Lahiri Saikia, Bhanu Devi, AK Borthakur, J Mahanta, Mycotic Corneal ulcers in upper Assam. India J Ophthalmol 2011;59(5):367-371.
19.A Gupta, MR Capoor,S Gupta, S Kochhar, A Tomer, V Gupta. Clinico – demographical profile of keratomycosis in Delhi, North India. Indian J. Med. Microbiol 2014; 32(3):310-314.
20.Chowdhury A, Singh K. Spectrum of fungal keratitis in North India. Cornea 2005;24:8-15.
21.Nikhil S Gokhale. Medical management approach to infectious keratitis. Indian J Ophthalmol 2008;56(3):215-220.
22.Jones DB. Decision making in the Management of microbial keratitis. Ophthalmology 1981;88:814-820.
Copyright © 2014 Srinivasa S, Sarguna P. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Source of support: 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.
Original article
Sadraddin Rasi Hashemi MD1, Hamid Noshad MD1*, Mohsen Mohammadi MD2
Affiliation:-
1Chronic Kidney disease research Center, connective tissue diseases research center, Tabriz University of Medical Sciences, Tabriz, Iran.
2Faculty of medicine, Tabriz University of Medical Sciences, Tabriz, Iran
The name of the department(s) and institution(s) to which the work should be attributed: 1.Chronic Kidney disease research Center, connective tissue diseases research center, Tabriz university of medical sciences, Tabriz, Iran
2.Faculty of medicine, Tabriz university of medical sciences, Tabriz, Iran
Address reprint requests to Dr.Hamid Noshad. Chronic kidney disease research center, Tabriz university of medical sciences, Tabriz, Iran or at Tel: 00984115415023, Mobile: 00989143115927,
Article citation:
Hashemi SR, Noshad H, Mohammadi M. The correlation of uric acid serum level and arterio-venous fistula failure in patients with ESRD. J Pharm Biomed Sci. 2014; 04(09):813-817. Available at www.jpbms.info
ABSTRACT
Introduction: In end-stage renal disease, “Uremic syndrome" leads to death unless the toxins are removed and water and electrolyte imbalances treated by renal replacement therapy (dialysis or kidney transplantation). In patients with end stage renal disease(ESRD) undergoing hemodialysis, existence of a good access line is essential. AVF is the most common accesses line and its failure may lead to life threatening events. Some risk factors are mentioned for AVF failure, one of them maybe is elevated serum uric acid level.
Methods: In this descriptive-cross sectional analysis. We studied 140 patients with ESRD, who were hemodialyzed via AVF during 3.5 years retrospectively. Their demographic characteristics, smoking, duration of HD, history of previous AVF insertion also lab data like uric acid, lipid profile, blood sugar, albumin, urea, creatinine and dialysis efficacy were recorded for further analysis.
Results: Twenty seven(27) patients had previous history of fistula failure. Mean serum uric acid level in patients with and without AVF failure was 8.05±1.78 and 6.50±1.15mg/dl respectively (P= 0.001).Cholesterol level in patients with and without AVF failure was 186.81±56.80 and 173 ±31.98 mg/ dl respectively and difference was not significant (P=0.09).
Conclusion: It seems that serum uric acid level is an important factor for AVF failures, so its control is recommended in ESRD patients. KEYWORDS: ESRD; Hemodialysis; AVF.
REFERENCES
1.Fauci AS,Braunwald E,Kasper DL,Hauser SL,Longo DL,Larry Jameson J, Loscalzo J. Harrison s principles of internal medicine,17th ed. McGraw Hill.p, New York. 2008;1761-1762,1772-1773.
2.Hehrlein C. How do AV fistulae lose function? The roles of haemodynamics, vascular remodeUing, and intimal hyperplasia. Nephrol Dial Transplant.1995; (88),1287-1290.
3.Sahasrabudhe P, Dighe T, Panse N, Patil S. Retrospective analysis of 271 arteriovenous fistulas as vascular access for hemodialysis. Indian J Nephrol. 2013; 23(3):191-5.
4.Kirkpantur A,Arici M,Altun B,Ilker Yilmaz M,Cil B,Aki T, et al. Association of Serum Lipid Profile and Arteriovenous Fistula Thrombosis in Maintenance Hemodialysis.Blood Purif, 2008; (26):322–332.
5.Feig DI,Mazzali M,Kang D-H,Nakagawa T,Price K,Kannelis J,et al. Serum Uric Acid: A Risk Factor and a Target for Treatment?. J Am Soc Nephrol.2006; (17):69-73.
6.Grossman C, Shemesh J, Koren-Morag N, Bornstein G, Ben-Zvi I, Grossman E. Serum uric acid is associated with coronary artery calcification. J Clin Hypertens (Greenwich). 2014;16(6):424-8.
7.Yong-quan W,Jue L,Yuan-xi X,Yong-liang W,Ying-yi L,Da-yi H,et al. Predictive value of serum uric acid on cardiovascular disease and all-cause mortality in urban Chinese patients. Chin Med J. 2010; 123 (11):1387-1391.
8.Puškar D, Pasini J, Saviæ I, Bedalov G, Sonicki Z. Survival of Primary Arteriovenous Fistula in 463 Patients on Chronic Hemodialysis. CMJ, 2002;3(43):306-311.
9.Malovrh M. How to increase the use of native arteriovenous fistulae for heamodialysis. Prilozi. 2011 ;32(2):53-65.
10.Ozdemir F, Akcay A, Bilgic A, Akgul A, Arat Z,Haberal M. Effects of Smoking and Blood Eosinophil Count on the Development of Arteriovenous Fistulae Thrombosis in Hemodialysis Patients. Transplantation Proceedings. 2005;(37):2918–2921. 11.Serati A,Roozbeh j,Sagheb M .Serum LDL levels are a major prognostic factor for Arteriovenous fistula thrombosis (AVFT) in hemodialysis patients.J vasc access. 2007;8(2):104-109.
12.Daniel I, Duk-Hee K, Richard J .Uric Acid and Cardiovascular Risk. N Engl J Med.2008; 17(359),1811-1821. 13.Kahn H,Medalie J,Neufeld H,Riss E,Goldbourt U. The incidence of hypertension and associated factors. Am Heart J.1972;(84):171-182. 14.Rovda I,Kazakova L,Plaksina E .Parameters of uric acid metabolism in healthy children and in patients with arterial hypertension. Pediatriia.1990;(88):19–22. 15.Feig D,Johnson R. Hyperuricemia in childhood primary hypertension.Hypertension.2003;(42):247–252.
Source of support: 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.