RESUMO
BACKGROUND: Inflammatory processes are implicated in the etiology of cardiovascular disease (CVD). Data on the association of inflammatory markers with cardiovascular risk factors in Indian patients with CVD are limited. AIM: This study was conducted with the aim to evaluate the association of inflammatory markers with traditional and nontraditional cardiovascular risk factors in angiographically proven coronary artery disease (CAD) patients. SUBJECTS AND METHODS: We studied the association of serum highly sensitive C-reactive protein (hsCRP) (0.1-37.9 mg/l), interleukin-6 (IL-6) (2-253.2 pg/ml) and tumor necrosis factor-alpha (TNF-α) (8-525.8 pg/ml) with cardiovascular risk factors in 300 (M: 216, F: 84; mean age: 60.9 (12.4) years) CAD patients. All patients were evaluated for anthropometry and cardiovascular risk factors, and blood samples were collected for biochemical and inflammatory markers. Statistical analysis was carried out using SPSS Version 20. RESULTS: Mean hsCRP, IL-6 and TNF-α in study population were 11.7 (9.7) mg/l, 64.5 (75.2) pg/ml, and 25.3 (40.9) pg/ml respectively. A total of 73.6% (221/300) patients had hsCRP levels >3.0 mg/l. All inflammatory markers were significantly higher and showed a positive correlation with dyslipidemia, diabetes mellitus, and/or hypertension (HTN). TNF-α had a negative correlation with age and positive correlation with smoking. Only IL-6 and hsCRP had a positive correlation with insulin resistance and negative correlation with insulin secretion. Among lipid parameters, triglyceride had a positive correlation, and high density lipoprotein had a negative correlation with all inflammatory markers. There was a progressive increase in the percentage of subjects with diabetes, HTN, and dyslipidemia with increasing levels of inflammatory markers. CONCLUSIONS: Indian patients with CAD had significantly high levels of inflammatory markers, which were related to cardiovascular risk factors.
RESUMO
BACKGROUND: The relationship between bone mineral density (BMD) and type 2 diabetes mellitus (T2DM) has been controversial. Recent studies have revealed adverse impact of antidiabetic drugs on BMD in type 2 diabetic patients. However, the influence of various antihyperglycaemic agents on BMD has not been well studied. METHOD: A total of 200 patients with T2DM were screened initially for the study. Finally 67 patients (M:34, F:33) who satisfied the requirement of having been on one year of prescribed therapy were included for analysis. RESULTS: Bone mineral density was lower in diabetic patients as compared to controls (hip 0.962 ± 0.167 g/cm(2) vs 1.013 ± 0.184 g/cm(2), P = 0.05; spine 0.929 ± 0.214 g/cm(2) vs 1.113 ± 0.186 g/cm(2), P < 0.00001). In males BMD was significantly lower at spine (P < 0.00001) and in females BMD was significantly lower in both at the spine (P < 0.00001) and hip (P < 0.032). On multivariate analysis significant positive correlation was found between spine BMD and body mass index (BMI) (r = 0.372, P = 0.002), total cholesterol (r = 0.272, P = 0.026), low-density lipoprotein (r = 0.242, P = 0.047), and triglycerides (r = 0.282, P = 0.021). There was no correlation between BMD and glycosylated haemoglobin (r = 0.158, P = 0.265). A significant decrease in BMD at spine and hip was seen with the use of glitazones and metformin while increase was noted with sulphonylurea and its combination. CONCLUSION: Men and women with T2DM have lower BMD. Bone mineral density did not have correlation to glycaemic control. Glitazones, metformin, and insulin are associated with decrease in BMD at spine, and hip, while sulphonylureas are associated with increase in BMD.
RESUMO
INTRODUCTION: Growth hormone (GH) secretion and release is a complex and highly regulated process. Any alteration disturbing synthesis, secretion or biological action of GH, results into growth hormone deficiency (GHD). GHD is of two types-isolated growth hormone deficiency (IGHD) and combined pituitary hormone deficiency (CPHD), of which IGHDis more common. The genes implicated in its etiology are growth hormone 1(GH1) and receptor of growth hormone-releasing hormone (GHRHR). Mutations within the coding region and/or either entire or partial deletions of the GH1gene lead to IGHD. In addition, GH1 possesses upstream regulatory elements and a promoter with binding sites for various transcription factors, which control its expression. AIM: The study was planned with an aim to identify entire GH1 locus deletion, mutations in the GH1 coding region and sequence variations (polymorphisms) in the promoter region of the gene in patients with IGHD. MATERIALS AND METHODS: Thirty patients clinically diagnosed with IGHD and 30 healthy individuals who formed the controls were enrolled for the study. Genomic DNA was isolated from peripheral blood sample and processed for amplification of the desired regions followed by direct sequencing and/or restriction endonuclease digestion. RESULTS: Out of the 30 IGHD patients screened, 20% of the cases showed consanguinity and 16% had a positive family history. Seven percentage of the patients showed homozygous deletion of the GH1gene while rest of them had heterozygous deletion. Screening of the coding region of GH1 showed sequence variations in exon 1 in 20% of the patients whereas the promoter region showed the presence of polymorphisms-rs2005171 in 20%, rs2005172 in 15% and rs11568828 in 18% of the cases. The haplotype comprising rs2005171 and rs2005172 was observed in four patients. CONCLUSION: The present study is an attempt to characterize the GH1 locus in IGHD patients. To the best of our knowledge this is the first study of its kind where entire GH1locus, upstream regulatory elements and promoter region have been studied. Such an analysis would provide valuable information on the etiology of IGHD.
