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

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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)
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.
Strengths of the journal: The journal has an online first facility in which the accepted manuscripts may be published on the website before being included in a regular issue of the journal. This cuts down the time between their acceptance and the publication. The journal is indexed in many databases, though not in PubMed. The editorial board should now take steps to index the journal in PubMed. The journal has a system of notifying readers through e-mail when a new issue is released. Also, the articles are available in both the HTML and the PDF formats. I especially like the new and colorful page format of the journal. Also, the access statistics of the articles are available. The prepublication and the manuscript tracking system are also helpful for the authors.
Areas for improvement: In certain cases, I felt that the peer review process of the manuscripts was not up to international standards and that it should be strengthened. Also, the number of manuscripts in an issue is high and it may be difficult for readers to go through all of them. The journal can consider tightening of the peer review process and increasing the quality standards for the acceptance of the manuscripts. I faced occasional problems with the online manuscript submission (Pre-publishing) system, which have to be addressed.
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.
On April 2011

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
On Jan 2020

Important Notice

Original article / research
Year : 2007 | Month : August | Volume : 1 | Issue : 4 | Page : 209 - 216 Full Version

Role of Atorvastatin in Anti-diabetes Management

Published: August 1, 2007 | DOI:

School of Medical Science and Technology, Indian Institute of Technology, Kharagpur, Pin code-721302, India.

Correspondence Address :
Analava Mitra, Assistant Professor, School of Medical Science and Technology, Indian Institute of Technology, Kharagpur, Pin code-721302, India. Tel.: 91-322-282656/282657(R), fax: 91-322-282631, e-mail:


The hyperinsulinaemic/insulin-resistant state is a metabolic condition linked to widespread and heterogeneous clinical syndromes like hypertension, obesity, type 2 diabetes, dyslipidaemia, atherosclerosis and coronary vascular disease. About 25% of the non-diabetic population shows abnormalities of insulin sensitivity and compensatory hyperinsulinaemia. Data from National Health and Nutrition Examination Survey (NHANES) show 50 million Americans or more had hypertension. In world scenario, it approximates 1 billion individuals and 7.1 million deaths per year. India has 4% of adult population at risk of hypertension. India is facing a diabetic explosion also. It has the world’s largest diabetic population – about 25 million, and the number is predicted to rise to 35 million by 2010 and to 57 million by 2025. The exact cause of the increase in prevalence of hyperinsulinaemic/insulin-resistant state is unknown, and both genetic and life style factors are being blamed. Beta-blockers (atenolol) and statins (atorvastatin) are widely used to combat hypertension and dyslipidaemia, particularly in obese patients who are also prone to diabetes and coronary artery disease. A 3-month study is done to compare the effects of atenolol with atenolol and atorvastatin in two groups of hypertensive volunteers. The study shows that statins improve the dyslipidaemic picture and also increases insulin sensitivity.


Beta-blockers, Diabetes, Atorvastatin

The South Asian population is known to be at risk of atherosclerosis, even though the subject does not have the clinical evidence of coronary artery disease (CAD). Atorvastatin is known for its cholesterol lowering and cardioprotective effects. In India population is vast, and there is heterogenicity of origin or race, geography and habit, socioeconomic status, dietary habits, methods of cooking and preservation, use of pesticides, etc. These factors, along with known variables like age, sex, etc., influence lipid profile of individuals. In a study with 3000 patients, CAD occurred in 50% with cholesterol level of 152 mg% and in 5% even if cholesterol level was below 140 mg%. The significant finding was elevated triglycerides (>196 mg%) and low high-density lipoprotein cholesterol (HDLC) (<39 mg%). The lipid profile in Indians may appear benign, but the high triglycerides and low HDLC levels actually increase the rate of CAD. Persons with high low-density lipoprotein (LDL), high triglyceride and low high-density lipoprotein (HDL) have a three-fold higher rate of CAD (1). Diabetes mellitus is defined as a syndrome characterised by chronic hyperglycaemia and disturbances of carbohydrate, fat and protein metabolism associated with absolute or relative deficiencies in insulin secretion and/or insulin action (2). The hyperinsulinaemic /insulin-resistant state is a metabolic condition linked to such widespread and heterogeneous clinical syndromes as hypertension, obesity, type 2 diabetes, etc. About 25% of the non-diabetic population show abnormalities of insulin sensitivity and compensatory hyperinsulinaemia. Considering the magnitude and severity of hyperinsulinaemic/insulin-resistant state, pharmaceutical measures are initiated early in an Indian and common drug to be used in hypertension and dyslipidaemia are beta-blockers and statins.

As hypertension is mainly asymptomatic, it acts as a silent killer. Even in advanced countries like U.S.A., 30% of individuals are unaware of their hypertension, other 40% do not like to be treated and 67% do not bother about the blood pressure (BP) values, which remains above 140/90 mmHg (3). About 10–15% of Indian adult receive regular antihypertensive treatment (4). Risk of hypertension, particularly systolic blood pressure (SBP), increases with advancing age, and about 50% of 60–69 years old are affected. The value becomes 75% in 70 years and above age range (3),(5). Vasan et al. (6) reported that lifetime risk of hypertension is 90% for normotensive men and women at 55 or 65 years of age and who survives up to 80–85 years. Reduction of SBP, which continues throughout life, reduces total mortality, cardiovascular mortality, stroke and heart failure events. Diastolic blood pressure (DBP) is more potent cardiovascular risk factor than SBP before 50 years of age, and afterwards SBP is more important (7). In the antihypertensive and lipid-lowering treatment to prevent heart attack trial (ALLHAT) and controlled onset verapamil investigation of cardiovascular end points (CONVINCE) trial, it is found SBP control rate is less than DBP control rate (8),(9). Physician’s ignorance may be a factor in poor control of SBP.

While body mass index in Indians was not higher, they had a significantly higher waist–hip ratio indicating that although Indians have no more general obesity than the others, they tend to put it on centrally or abdominally. They also had more hyperinsulinaemia, glucose intolerance and increased plasma activator inhibitor 1 (PAI-1). Regarding the antioxidants, Indians had a lower level of plasma vitamin C and selenium (10). These factors could be due to food habits, especially prolonged cooking at hig

Material and Methods

Selection of volunteers
Sixty-four patients are screened for the study from a random population of 90 hypertensive patients receiving atenolol as anti-hypertensive measures from BC Roy Technology Hospital of IIT, Khargpur, by a random selection process, from which 44 patents are considered based on patient compliance, intelligence to understand dietary prescriptions and directions and whether free from any other disease on initial medical testing. Naturally, the volunteers are not receiving any drugs other than mentioned and not suffered from any diseases within the study period. Written consent for the study as per protocol and institute ethical clearance is obtained. The patients are divided into two groups, of 22 patients each, by a random selection process, the experimental group receiving atenolol and atorvastatin and the control group receiving atenolol only.

Duration of study
The study duration is for 3 months.

Anthropometrical, clinical and biochemical characters of volunteers
Anthropometrical, clinical and biochemical characters of volunteers are shown in (Table/Fig 1).
Clinically, both the groups show no abnormality, other than hypertension in both groups, along with dyslipidaemia in the experimental group. Different biochemical and clinical parameters like liver function tests (LFT), total leukocyte count (TLC), differential leukocyte count (DLC), Hb, urea, creatinine, total proteins, serum electrolytes, urine tests, electro-cardiograph (ECG), X-ray of chest, etc. are almost identical and within normal range in both the groups.

Collection of blood samples
Twelve hours fasting values are taken initially and at monthly intervals for 3 months. Measurement of total cholesterol (TC), high-density lipoprotein cholesterol (HDLC), low-density lipoprotein cholesterol (LDLC), very low-density lipoprotein cholesterol (VLDLC), triglycerides (TG) and fasting blood sugar (FBS) is done by standard methods, as depicted by Boehringer Mannheim (23) and by reagents supplied to meet the standard quality at monthly intervals by an indwelling catheter placed in the anti-cubital vein. Serum insulin level is measured by radioimmunoassay by Spandan Diagnostics.

Statistical methods
For calculation of t-statistic and p-values, standard SPSS package is used. The statistical analysis is done based on paired t-test, and p-value is calculated using paired t-statistic. The normality of the parent population (from which the data have been collected) is not tested, but since the sample size is 44, which could be considered to be large, t-statistic is used, the validity of which is justified through central limit theorem.


(Table/Fig 2) shows values of blood parameters of 22 volunteers who are receiving atenolol and atorvastatin, in comparison with 22 volunteers who are receiving atenolol. It is found that in the group receiving atenolol and atorvastatin (experimental group) TC is reduced from initial values of 282 +/-18 mg/dl to 271 +/-16 mg/dl (p = 0.05). HDLC increased from 48 +/-5 mg/dl to 50 +/-7 mg/dl (p = 0.04). LDLC reduced from 195 +/-11 mg/dl to 182 +/-21 mg/dl (p = 0.05). VLDLC, TG values remain almost same, and changes are statistically insignificant. FBS values changed from initial 105 +/- 17 mg/dl to 100 +/-6 mg/dl (p = 0.04). (Table/Fig 2) also shows values of blood parameters of 22 volunteers who are receiving atenolol only (control group). It is observed that TC is from initial values of 202 +/-12 mg/dl to 200 +/-16 mg/dl. HDLC changes from 42 +/-5 mg/dl to 43 +/-7 mg/dl. LDLC changes from 139 +/-12 mg/dl to 140 +/-21 mg/dl. VLDLC, TG and FBS values remain almost same, and all the value changes are statistically insignificant. (Table/Fig 3) shows serum insulin and homeostasis model assessment of insulin resistance (HOMA 2-IR) values of different groups, in order to determine insulin sensitivity. It was observed that in the experimental group, serum insulin value initially is 32 +/-3 microU/ml and finally is 29 +/-3 microU/ml (p = 0.03), and in the control group, serum insulin value initially is 31 +/-2 microU/ml and finally is 31 +/-2 microU/ml. HOMA 2 values (insulin resistance or IR) of the two groups of patients show that in the experimental group it was 4.2 +/-0.5 initially to 3.7 +/-0.4 after 3 months, and in the control group it was 4.2 +/-0.3 initially and 4.2 +/-0.2 finally, showing increase in insulin sensitivity by atorvastatin.


The exact cause of increase in insulin sensitivity by atorvastatin is unknown. The study shows that atorvastatin increases insulin sensitivity in normal subjects. It thus corroborates the findings of Parhofer et al. (24), who found that, though uncertain, short-term statin therapy can affect insulin sensitivity in patients with insulin resistance syndrome. Compared with placebo, treatment with atorvastatin (10 mg/day) resulted in significant reductions in the HOMA index (21%), fasting C-peptides (18%) and glucose, as well as a borderline reduction of insulin. In addition, significant reductions in total and LDL cholesterol concentrations were observed in the atorvastatin group. Some subjects with a better lipid profile and more normal baseline parameters respond less. Thus, the team concludes that patients with more pronounced metabolic syndrome would benefit more than those with less pronounced changes, and the present study thus is contrary to the studies of Parhofer et al. (24). Okajima et al. (25) suggest that statins could have some impact on insulin action, and, to estimate the direct effects of statins on insulin secretion from pancreatic beta cells, MIN6 cells were treated with pravastatin, simvastatin or atorvastatin. Basal insulin secretion at low glucose concentration was unexpectedly increased at very high doses of simvastatin or atorvastatin after 24 and 48 hours of incubation, though insulin secretion at high glucose was not significantly changed, and, thus, net glucose-stimulated insulin secretion was apparently decreased by these lipophilic statins. Atorvastatin is frequently administered for the treatment of hypercholesterolemia associated with type 2 diabetes mellitus. However, a marked deterioration of glycaemic control has been reported in some patients treated with atorvastatin. Takano et al. (26) suggest a predisposition to a deterioration of glycaemic control in type 2 diabetic patients treated with atorvastatin and thus are against the evidence gained by the present study. Prasad et al. (27) hypothesised that statins influence the development of new-onset diabetes mellitus in renal transplant recipients. Yoshitomi et al. (28) assessed the relationship between IR and the changes of lipid profile in patients with hyperlipidaemia treated by atorvastatin. The IR did not affect the degree of reduction in cholesterol by atorvastatin in non-diabetic subjects. The IR may influence hypertriglyceridaemia greater than the effect of atorvastatin in non-diabetic subjects. It has been suggested that HMG Co-A reductase inhibitors (‘statins’) may reduce the risk of developing type 2 diabetes mellitus. Yee et al. (29) designed to evaluate whether use of statins would also delay progression to insulin therapy. After multivariate adjustment, however, statin use was associated with a 10-month delay before newly treated diabetic subjects needed to start insulin treatment. Whether this relationship exists for patients at high risk of developing diabetes should be examined in a randomised trial. In order to evaluate a hypothesised protective effect of the use of HMG Co-A reductase inhibitors (statins) on the development of type 2 diabetes, Jick and Bradbury (30) conducted a nested case–control study, based on data from the UK-based General Practice Research Database (GPRD). There was little evidence for a duration effect for simvastatin in these data, though there is a slight suggestion of a long-term protective effect with pravastatin. The study results are most consistent with the conclusion that there is little, if any, protective effect of statins on the development of type 2 diabetes. Ohmura et al. (31) report a patient in whom the administration of HMG CoA


Statins reduce the magnitude of hyperinsulinaemic/insulin-resistant state. Statins are believed to have an anti-infective role. The exact cause of hyperinsulinaemic/insulin-resistant state is unknown. Hyperinsulinaemic/insulin-resistant state is very common and is of explosive occurrence in India. Infective aetiology may play a role in the causation of the state, and statins reduce the infective conditions by its anti-infective role. The claim is controversial and several studies also refute the findings. Further, studies are needed in Indian context to find out a conclusive result.


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Gill G, Pickup J, Williams G. Difficult diabetes. Oxford: Blackwell Science;2001.
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Enase AE, Yusuf S, Mehta JL. Prevalence of coronary artery disease in Asian Indians. Am J Cardiol 1992;70:945–9.
Raheja BS, Talwalkar NG, Suttarwalla SK.. Ischaemic heart disease in diabetes. J Assoc Physicians India 1970 February;18(2):261–7.
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Tables and Figures
[Table / Fig - 1] [Table / Fig - 2] [Table / Fig - 3]

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