Journal of Clinical and Diagnostic Research, ISSN - 0973 - 709X

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MBBS, MD (Pathology),
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On Aug 2018




Dr. Mamta Gupta,
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Aug 2018




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Thanking you
With sincere regards
Dr. Rajendra Kumar Ghritlaharey, M.S., M. Ch., FAIS
Associate Professor,
Department of Paediatric Surgery, Gandhi Medical College & Associated
Kamla Nehru & Hamidia Hospitals Bhopal, Madhya Pradesh 462 001 (India)
E-mail: drrajendrak1@rediffmail.com
On May 11,2011




Dr. Shankar P.R.

"On looking back through my Gmail archives after being requested by the journal to write a short editorial about my experiences of publishing with the Journal of Clinical and Diagnostic Research (JCDR), I came across an e-mail from Dr. Hemant Jain, Editor, in March 2007, which introduced the new electronic journal. The main features of the journal which were outlined in the e-mail were extensive author support, cash rewards, the peer review process, and other salient features of the journal.
Over a span of over four years, we (I and my colleagues) have published around 25 articles in the journal. In this editorial, I plan to briefly discuss my experiences of publishing with JCDR and the strengths of the journal and to finally address the areas for improvement.
My experiences of publishing with JCDR: Overall, my experiences of publishing withJCDR have been positive. The best point about the journal is that it responds to queries from the author. This may seem to be simple and not too much to ask for, but unfortunately, many journals in the subcontinent and from many developing countries do not respond or they respond with a long delay to the queries from the authors 1. The reasons could be many, including lack of optimal secretarial and other support. Another problem with many journals is the slowness of the review process. Editorial processing and peer review can take anywhere between a year to two years with some journals. Also, some journals do not keep the contributors informed about the progress of the review process. Due to the long review process, the articles can lose their relevance and topicality. A major benefit with JCDR is the timeliness and promptness of its response. In Dr Jain's e-mail which was sent to me in 2007, before the introduction of the Pre-publishing system, he had stated that he had received my submission and that he would get back to me within seven days and he did!
Most of the manuscripts are published within 3 to 4 months of their submission if they are found to be suitable after the review process. JCDR is published bimonthly and the accepted articles were usually published in the next issue. Recently, due to the increased volume of the submissions, the review process has become slower and it ?? Section can take from 4 to 6 months for the articles to be reviewed. The journal has an extensive author support system and it has recently introduced a paid expedited review process. The journal also mentions the average time for processing the manuscript under different submission systems - regular submission and expedited review.
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Overall, the publishing process with JCDR has been smooth, quick and relatively hassle free and I can recommend other authors to consider the journal as an outlet for their work."



Dr. P. Ravi Shankar
KIST Medical College, P.O. Box 14142, Kathmandu, Nepal.
E-mail: ravi.dr.shankar@gmail.com
On April 2011
Anuradha

Dear team JCDR, I would like to thank you for the very professional and polite service provided by everyone at JCDR. While i have been in the field of writing and editing for sometime, this has been my first attempt in publishing a scientific paper.Thank you for hand-holding me through the process.


Dr. Anuradha
E-mail: anuradha2nittur@gmail.com
On Jan 2020

Important Notice

Original article / research
Year : 2011 | Month : November | Volume : 5 | Issue : 6 | Page : 1237 - 1240

TNF- α is An Inflammatory Marker of Cardiovascular Risks in Non-Alcoholic Fatty Liver Disease

Khan Ruhi, Quaiser Saif, Haque S. F., Ahmad A.

Corresponding Author Senior Resident, Department of Medicine, JN Medical College, Aligarh Muslim University, Aligarh Senior Resident, Department of Medicine, JN Medical College, Aligarh Muslim University, Aligarh Assistant Professor, Department of Medicine, JN Medical College, Aligarh Muslim University, Aligarh

Correspondence Address :
S.F. Haque, MD (Med.), Ph.D. (Med.)
Associate Professor,
Department of Medicine, JN Medical College,
Aligarh Muslim University, Aligarh
Phone : 09412517518
E-mail : sfhalig@yahoo.co.in

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a common clinical condition with histological features resembling those of alcohol induced liver injury but occurs in patients who do not abuse alcohol. It is often associated with features of obesity, hypertension, dyslipidemia and type2 diabetes mellitus. NAFLD plays a central role in the pathway connecting the metabolic syndrome and cardiovascular disease.Overall, the current body of evidence strongly suggests that NAFLD is likely to be associated with increased cardiovascular disease risk, and raises the possibility that NAFLD may be not only a marker but also an early mediator of atherosclerosis.

Aims of the present study: Our study was an attempt to analyze the association between non-alcoholic fatty liver disease, and various cardiovascular risk factors & plasma biomarkers of inflammation like TNF-α in non-alcoholic subjects.

Methods: In this prospective, open label, observational study, 39 cases of non-alcoholic fatty liver diseasewere evaluated for inflammatory markers and cardiovascular risk factors. The data was analysed and the results were given in percentage in accordance with previous related studies.

Results: In patients of non-alcoholic fatty liver disease serum levels of inflammatory marker TNF-α are significantly elevated, supporting the view that inflammation plays an important role in the pathogenesis of NAFLD.

Conclusion: The study concludes that there is significant association of inflammatory markers and cardiovascular risk factors in patients of non-alcoholic fatty liver disease.

Keywords

Non-alcoholic fatty liver disease (NAFLD), Tumour necrosis factor-alpha (TNF-α).

INTRODUCTION
Non-alcoholic fatty liver disease (NAFLD) is a common clinical condition with histological features which resemble those of alcohol induced liver injury, but it occurs in patients who do not abuse alcohol. NAFLD encompasses a histological spectrum which ranges from simple steatosis to steatohepatitis, advanced fibrosis and cirrhosis. The problem of this disease is not confined to its potential to cause serious liver related morbidity and mortality, but it is often associated with the features of obesity, hypertension, dyslipidaemia and type 2 diabetes mellitus. NAFLD plays a central role in the pathway which connects the metabolic syndrome and the cardiovascular disease. The biological mechanism by which NAFLD promotes atherosclerosis is not known. The possible mechanistic pathways include increased oxidative stress, subclinical inflammation, an adipocytokine profile, endothelial dysfunction and lipid abnormalities.

Recent evidence suggests that the severity of the liver histology in the NAFLD patients is closely associated with the markers of early atherosclerosis, such as a greater carotid artery wall thickness and a lower, endothelial, flow-mediated vasodilatation, which is independent of the classical risk factors and the components of the metabolic syndrome. Overall, the current body of evidence strongly suggests that NAFLD is likely to be associated with an increased cardiovascular disease risk and that it raises the possibility that NAFLD may not only be a marker but also an early mediator of atherosclerosis(1). Patients with NAFLD appear to have an increased risk of death as compared to the general population, and it has been reported that the overall mortality among these patients was increased as compared to the general population; this was most commonly due to the cardiovascular disease and malignancy(2).

Abdominal obesity, type 2 diabetes, insulin resistance, hypertension and dyslipidaemia – the typical components of the metabolic syndrome are the co-existing pathological conditions which are frequently associated with NAFLD and their co-existence within the same individual increases the likelihood of having more advanced forms of NAFLD [3-4]. Truncal obesity is an important risk factor for NAFLD (5). Hye Soon Parka et al. (2005) (6) conducted a study on NAFLD and showed that the CRP, TNF-α and IL-6 concentrations were higher in the obese than in the non-obese individuals. Adipose tissue is an important source of cytokines, and adiposity contributes to the proinflammatory milieu (7).

Tumour necrosis factor-α (TNF-α) has been considered to be a key player in the progression from simple fatty liver to non-alcohalic steato hepatitis ( NASH). TNF-α is produced by macrophages in the adipose tissue and it is increased in obesity. Free fatty acids can induce the expression of TNF-α in hepatocytes through the activation of NF-κΒ, thereby linking the increased influx of free fatty acids which are seen in hepatic steatosis, to the progression of inflammation. In adipocytes, TNF-α down regulates the adiponectin production (8).

Our study was designed to check the association between nonalcoholic fatty liver disease, various cardiovascular risk factors and the plasma biomarkers of inflammation like TNF-α in non-alcoholic subjects (those who had less than 20 gms of alcohol per day).

Material and Methods

STUDY POPULATION
The present study was undertaken in patients who had nonalcoholic fatty liver disease which was diagnosed by ultrasound,who attended the Medicine OPD and were admitted in Medicine Indoors, at Jawaharlal Nehru Medical College, Aligarh Muslim University, Aligarh. Informed consent was obtained from all the patients at recruitment and the study was approved by the Institutional Ethics Committee.

AIMS AND OBJECTIVES:
The present study was conducted to evaluate the cardiovascular profile and the hepatic inflammatory markers like TNF-α in patients who had NAFLD and to establish the correlation, if any, between the cardiovascular risk factors and the inflammatory markers in patients with NAFLD.

INCLUSION CRITERIA:
The patients who were included in this study were those who had NAFLD, which was diagnosed by ultrasound on the basis of following criteria: Echo contrast, liver brightness, deep attenuation and vascular blurring.

EXCLUSION CRITERIA:
Patients with alcoholic hepatitis, acute or chronic viral hepatitis, cirrhotic portal hypertension, acute infection (sepsis), decompensated cardiac disease and severe renal dysfunction were excluded from the study.

STUDY DESIGN:
The sample size was 39 cases and it was a prospective, non randomised and observational study.

STATISTICAL ANALYSIS:
All the statistical data were analyzed by using the SPSS Statistical Package for Windows (Chicago Inc.) software, version 15.0. The continuous variables were expressed as mean ± standard deviation (Gaussian distribution) and the range and qualitative data was expressed as percentages. Depending on the normality distribution, the unpaired t test for independent samples was used for comparing the continuous variables between the two groups. The linear relationship between the variables was analyzed by using the Pearson’s correlation coefficient and the significance of ‘r’ was tested. All the p values were two tailed and the values of p which were <0.05 were considered to be statistically significant. All the confidence intervals were calculated at a 95% level.

Results

Age and Sex distribution:
The study group comprised of 39 patients with non-alcoholic fatty liver disease, out of which 25 were males and 14 were females. The ages of the patients in this study group ranged from 31 to 70 years (the mean age was 48.5±9.5 years). Among the males, the ages of patients ranged from 31 to 70 years (the mean age 48.1±9.5years), while among the females, the ages ranged from 31 to 60 years (the mean age 49.1±11.0 years).

TNF-α Levels:
TNF-α estimation was done by an antigen capture ELISA (Enzyme Linked Immunosorbent Assay) for its quantitative measurement in the serum.

As is evident in (Table/Fig 1), the levels of the inflammatory marker, TNF-α in patients with non alcoholic fatty liver disease were studied and any correlation with the cardiovascular risk factors wasevaluated. The mean value of TNF-α in the study group was found to be 68.9±32.9 pg/ml (Table/Fig 1).

Sex distribution: The mean value of TNF-α was 65.8±35.8 pg/ml in the female group and it was 70.7±31.8 pg/ml in the male group. No significant difference was found between the two groups.

Smoking: There were 22(56.4%) smokers and all of them were males. The mean value of TNF-α in smokers was 78.9±31.8 pg/ ml and it was 70.7±31.8 pg/ml in the non-smokers. The TNF-α levels were found to be significantly higher in the smokers, with the p-value being less than 0.05.

Hypertension: The study comprised 23 hypertensive patients. The mean value of TNF-α in the hypertensive patients was 84.1±17.8 pg/ml and it was 55.9±38.0 pg/ml in the normotensive group. In our study, the TNF-α levels were found to be significantly higher in the hypertensive group, as compared to those in normotensive group, with the p-value being less than 0.05. Thus, hypertension was found to significantly affect the levels of TNF-α.

Diabetes Mellitus: There were 27 (69.2%) diabetic patients, with a sex distribution of 17 (62.9%) males and 10 (37.1%) females. The mean value of TNF-α in the patients with diabetes mellitus was 87.6±7.4 pg/ml and it was 26.6±34.3pg/ml in the non-diabetic group. Diabetes mellitus was found to significantly affect the levels of TNF-α, with the p-value being less than 0.01.

Obesity: There were 32 (82.1%) obese patients, with a sex distribution of being 20 (62.5%) males and 12 (37.5%) females. The mean value of TNF-α in the non- obese patients was 77.5±25.9 pg/ml and it was 29.6±34.3 pg/ml in the non-obese patients. Obesity was found to significantly affect the levels of TNF-α, with the p-value being less than 0.01.

Dyslipidemia: The study comprised of 36 (92.3%) patients with dyslipidaemia, with a sex distribution being of 23 (63.9%) males and 13 (34.8%) females. The mean value of TNF-α in the patients with dyslipidaemia was 73.9±29.0pg/ml and it was 8.9±0.7 pg/ml in patients without dyslipidaemia. Dyslipidaemia was found to significantly affect the levels of TNF-α, with the p-value being less than 0.01.

Inflammatory markers in patients of metabolic syndrome and NAFLD:
In the present study, 24 patients were found to have metabolic syndrome according to the International Diabetes Foundation (IDF) criteria, out of which 8 (33.3%) were females and 16(66.7%) were males. As is evident in [Tables/Fig 2] and(Table/Fig 3), the mean values of TNF-α in patients with metabolic syndrome were 86.4±7.2 pg/ ml and 88.3±7.7 pg/ml, ie. in the females and males respectively. Thus, the TNF-α levels were found to be significantly higher in patients with metabolic syndrome (both in males and females) as compared to those in patients without metabolic syndrome.

Pearson’s Correlation of TNF-α and C-Reactive Protein with metabolic syndrome :
By using Pearson’s correlation, a significant correlation of TNF-α was found with metabolic syndrome (r=0.7), as compared to those without metabolic syndrome (Table/Fig 4).

Discussion

NAFLD is a very common disease and it occurs in persons of all ages and ethnic groups (9). Although NAFLD was originally described to be more prevalent in women, no significant difference was found in the prevalence of NAFLD among men and women in the Indian population (10). The available reports confirm that non-alcoholic steato hepatitis (NASH) is prevalent in the Indian population. Moreover, a recent, clinic-based study suggests the differences in the clinico-pathological profile of Indian patients with NAFLD (11). In India, most of the studies on the prevalence of NAFLD have been performed in highly selected clinic populations [12-13] and the generalizability of the results to the community remains uncertain. India has the largest number of people withdiabetes in the world. Moreover, Asian Indians are more prone to insulin resistance and have increased waist circumference and body fat : the Asian Indian phenotype (14).

In a majority of the cases, NAFLD has been found to be a benign condition with respect to the local liver damage; it may rarely progress to non-alcoholic steato hepatitis (NASH), cirrhosis, and hepatocellular carcinoma (15),(16). However, previous research has unravelled a number of systemic effects of NAFLD. Thus, NAFLD is associated with several atherosclerotic risk factors such as hypertension, diabetes and hypertriglyceridaemia (17).

As has been shown in a number of previous studies, Tumour Necrosis Factor-α (TNF-α) is considered to be a key player in the progression from simple fatty liver to NASH (18). Our study also showed that the serum levels of inflammatory markers like TNF-α were significantly elevated in patients with non-alcoholic fatty liver disease.

Conclusion

This study concluded that the serum levels of inflammatory markers like TNF-α were significantly elevated in patients with non-alcoholic fatty liver disease, thus supporting the view that inflammation plays an important role in the pathogenesis of NAFLD. Also, there was a significant association of the TNF-α levels with various grades of fatty liver, thus suggesting an inflammatory cytokine cascade in NAFLD.

References

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Von Eyben FE, Zeeman G. The health risk from active and passive smoking. Rev Esp Salud Publica 2003; 77: 11-36.
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Kong C, Nimmo L, Elatrozy T, Anyaoku V, Hughes C, Robinson S, et al. Smoking is associated with increased hepatic lipase activity, insulin resistance, dyslipidaemia and early atherosclerosis in type 2 diabetics. Atheroscler 2001; 156: 373-8.
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Marchesini G, Marzocchi R, Agostini F, Bugianesi E. Non-alcoholic fatty liver disease and the metabolic syndrome. Curr Opin Lipidol 2005; 16: 421–7.
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Giovanni T, Arcaro G. Non-alcoholic fatty liver disease and the increased risk of cardiovascular disease. Atheroscler 2007; 191: 235- 40.
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Park H S, Park J Y, Yu R, Relationship of obesity and visceral adiposity with the serum concentrations of CRP, TNF-alpha and IL-6 Diabetes. Res Clin Pr 2005;69: 29–35.
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Bedogn G, . Miglioli L,. Masutti F,. Tiribelli C,. Marchesini G,. Bellentani S.et al Prevalence of the risk factors for non-alcoholic fatty liver disease: the Dionysos Nutrition and Liver Study. Hepatology 2005;42: 44–52.
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Mohan V, Farooq S M, Ravikumar R, Pitchumon CS Prevalence of non-alcoholic Deepa fatty liver disease in urban south Indians with respect to the different grades of glucose intolerance and metabolic syndrome. Diabetes Res Clin Pr 2004; 84: 84-91.
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Aggarwal SR, Malhotra V, Sakhuja P, Satin SK. Clinical, biochemical and histological profiles of non-alcoholic steatohepahtis. Ind J Gastroenterol 2001; 20: 183-96.
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