BackgroundElevated plasma triglycerides (TGs) are widely used as a major cardiovascular risk predictor and are thought to play an important role in the progression of coronary heart disease (CHD). It has been demonstrated that lipid lowering was associated with lower mortality in patients with CHD. The present study therefore aimed to investigate the consequences of the genetic variant c.553G > T (rs2075291) in apolipoprotein A5 gene to determination of triglycerides levels in CAD patients receiving, atorvastatin, lipid lowering drug.MethodsWe here report that a recently identified genetic variant, c.553G > T in the APOA5 gene which causes a substitution of a cysteine for a glycine residue at amino acid residue 185(G185C) is also associated with increased TG levels. To investigate theses effects, a case-control study compressing 608 subjects from the same area was performed.ResultsTG levels in T allele patients were significantly lower than the control GT allele patient (χ2 = 2.382E2a, P-value < 0.001). Overall, patients carrying T allele showed lower levels of TG than patients carrying GG allele. The homozygous patient for the T allele presented normal cholesterol levels of 134 mg/dl, and the levels in GG patients ranged from 25 to 340 mg/dl (P-value < 0.001). In summary, we demonstrated that the presence of c.553G > T variant (rs2075291); in APOA5 gene increases human plasma TG levels.ConclusionNevertheless, T allele is found to reduce TG levels in CAD patients who are on the cholesterol medication, atorvastatin. Thus, c.553G > T variant can be considered as a significant predicator of hypertriglyceridemia. In addition, it could be used as a hallmark for the diagnosis and prognosis of CAD.
Lipoprotein Lipase (LPL) is known to be a key enzyme for lipid metabolism specifically in an enzymatic glycoprotein which provide tissues without fatty-acids and eliminates triglycerides (TG) by the circulation. Mutations in LPL were proven to cause alteration in fractions within lipoprotein, causing the development of atherosclerosis which predispose to weakening coronary artery disease (CAD) and stroke. We examined the linkage between genetic variant
Hind
III in LPL on lipoprotein fractions, stroke occurrences and CAD. In this case-control study, we have recruited 315 CAD cases and 205 age-matched controls. A total of 520 genomic DNA was digested with the purified PCR products for restriction fragment length polymorphism with
Hind
III restriction enzyme. The distribution of genotypes in a decreasing order were TT, 148 (47%), GT 135 (42.9%) and GG 32 (10.2%) in CAD groups of the study while the pattern in controls were GT 91 (44.4%), TT 86 (42%) and GG 28 (13.7%). None of all the allele or genotype frequencies were found to be significant in our study (p greater than 0.05), while the biochemical levels for both TG and LDL-c were shown to be prone in CAD patients when compare with the controls. Furthermore, the occurence of strokes were more in CAD groups vs. controls: 72 (22.9%) vs. 7 (3.4%) [p 0.000]. This could indicate the influence of
Hind
III variant on plasma lipid levels, and the possibility of considering it a risk factor for atherosclerosis leading to CAD and stroke occurrence.
Attention-deficit/hyperactivity disorder (ADHD) is one of the most common neurodevelopmental disorders. Several studies have confirmed the co-existence of other neuropsychiatric disorders with ADHD. Out of 106 individuals suspected to have ADHD, eight Saudi Arabian pediatric patients were diagnosed with ADHD using a dual assessment procedure based on highly significant scores from the international criteria for diagnosis; (full form DMS) DSM-5. Then, these patients were examined for the co-existence of autism and ADHD using different international diagnostic protocols. Four patients with combined ADHD and autism and four ADHD patients without autism were examined for the presence of genetic variants. Six variants (chr1:98165091, chr6:32029183, chr6:32035603, chr6:32064098, chr8:2909992, chr16:84213434) were identified in 75% of the patients with ADHD and autism, indicating that these genes may have a possible role in causing autism. Five variants (The chr2:116525960, chr15:68624396, chr15:91452595, chr15:92647645, and chr16:82673047) may increase to the severity of ADHD. This study recommends screening these eleven variants in ADHD cases and their relevant controls to confirm the prevalence in the Saudi population. It is recommended that future studies examine the 11 variants in detail.
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