Different Doses Of Atorvastatin Research Articles

Different doses of atorvastatin in the treatment of patients with cardiorenal syndrome Type-2: A retrospective cohort study.

To assess the cardiorenal protective effects of different doses of atorvastatin in patients with cardiorenal syndrome (CRS) Type-2. Medical records of 113 patients with CRS Type-2, admitted to First Affiliated Hospital of Hebei North University from August 2021 to August 2022 and treated with atorvastatin, were retrospectively analyzed. Patients were retrospectively grouped based on the dosage of atorvastatin. A total of 38 patients who received 10mg/day atorvastatin were selected as a Low-dose group, 36 patients who received 20mg/day atorvastatin comprised a Medium-dose group, and 39 patients who received 40mg/day atorvastatin comprised a High-dose group. Cardiac function indicators (Left ventricular end-diastolic dimension [LVEDD], left ventricular end-stage systole diameter [LVESD], and left ventricular ejection fraction [LVEF]), renal function indicators (creatinine [SCr], serum uric acid [SUA], heme oxygenase-1 [HO-1], urinary albumin [UALB]), and inflammatory factors (Serum interleukin-6 [IL-6], hypersensitive C-reactive protein [hs-CRP], and tumor necrosis factor -α [TNF-α]) were compared between the three groups. After the treatment, levels of renal and cardiac function indicators, and inflammatory factor indicators of the three groups were significantly improved compared to the before-treatment levels. The degree of improvement in the Medium-dose and the High-dose groups was significantly higher than in the Low-dose group (p<0.05). There were no significant differences in all cardiorenal function indicators and inflammatory factors between the Medium-dose and the High-dose groups after the treatment. During the treatment process, no adverse events were reported in all three groups. In the treatment of patients with CRS Type-2, medium dose (20mg/day) atorvastatin can have the same therapeutic effect as the high dose (40mg/day) treatment. Medium dose has a good protective effect on the heart and kidneys of the patients, and helps to reduce inflammatory reactions and improve heart and kidney function.

The impact of statin use before intensive care unit admission on patients with acute kidney injury after cardiac surgery.

Background: Cardiac surgery-associated acute kidney injury (CSA-AKI) is a common and serious complication after cardiac surgery. The influence of statin use before surgery on the renal outcome of patients undergoing cardiac surgery is controversial. The purpose of this study was to evaluate the effect of statins on postoperative renal outcomes in patients undergoing cardiac surgery. Methods: We included CSA-AKI patients in the Medical Information Mart for Intensive Care (MIMIC)-IV database and were divided into statin group and non-statin group according to whether they used statins before entering intensive care units (ICU). The main outcomes were hospitalization and 30-day mortality, and the secondary outcomes were 60-day mortality and 90-day mortality. We used propensity score matching (PSM) to adjust for confounding factors. The 95% confidence interval (CI) and risk ratio (RO) were calculated by the COX proportional regression model. At the same time, stratified analysis was used to explore whether the relationship between the statins use before intensive care units and mortality was different in each subgroup and whether the relationship between different doses of Atorvastatin and mortality was different. Result: We identified 675 pre-ICU statin users and 2095 non-statin users. In the COX proportional regression model, pre-ICU statin use was associated with decreased in-hospital (HR = 0.407, 95%confidence interval 0.278-0.595, p < 0.001) and 30-day mortality (HR = 0.407, 95%CI 0.279-0.595, p < 0.001). The survival rate of patients who took statins before entering ICU was significantly higher than that of those who did not use statins at 30days, 60days and 90days. There is a significant interaction between patients with aged>65years (HR = 0.373, 95%CI 0.240-0.581, p < 0.001), Acute kidney injury grade I (HR = 0.244, 95%CI 0.118-0.428, p < 0.001), and without post-myocardial infarction syndrome (HR = 0.344, 95%CI 0.218-0.542, p < 0.001). The mortality in hospital and 60days of CSA-AKI patients treated with ≥80mg Atorvastatin before operation was significantly reduced (p < 0.05). Conclusion: The pre-ICU statin use was significantly associated with decreased risk in hospital and 30-day mortality. The preoperative use of ≥80mg Atorvastatin may improve the prognosis of CSA-AKI.

Influencing Mechanism of Large-dose of Atorvastatin in Serum Visfatin, MMP-9, and Blood Fat Levels of Patients with Acute Coronary Syndromes.

The research was conducted to analyze the clinical effects and corresponding molecular mechanisms of short-term treatment of acute coronary syndromes (ACS) by different doses of atorvastatin. In the research, a total of 90 ACS patients were included as the samples and divided into an experimental group (conventional treatment+60mg/per time/late atorvastatin), control group 1 (conventional treatment+25mg/per time/late atorvastatin), and control group 2 (25mg/per time/late atorvastatin) according to different doses of atorvastatin. After that, their blood fat and inflammatory factors before and after treatment were analyzed. Total cholesterol (TC) and high-density liptein cholesterol (HDL-C) levels of the experimental group were inferior to those of control groups 1 and 2 in the 5th and 7th days (P<0.05). After treatment, visfatin, matrix metalloproteinase-9 (MMP-9), and brain natriuretic peptide (BNP) of patients in the experimental group and control groups 1 and 2 were notably inferior to those in control groups 1 and 2 (P<0.05). Besides, interleukin-6 (IL-6) and hypersensitive C-reactive protein (hs-CRP) of patients in the experimental group and control groups 1 and 2 were inferior to those in control groups 1 and 2 after treatment (P<0.05). Based on the above results, the short-term treatment by large-dose atorvastatin could reduce blood far and inflammatory factor levels of ACS patients more effectively than by conventional dose, and further inhibit inflammatory reactions and improve patient prognosis with safety and feasibility.

Cholesterol-Related lncRNAs as Response Predictors of Atorvastatin Treatment in Chilean Hypercholesterolemic Patients: A Pilot Study

Statins are currently the treatment of choice for hypercholesterolemia. However, wide interindividual variability has been observed in the response to treatment. Recent studies have reported the role of lncRNAs in the metabolism of lipids; nevertheless, there are few studies to date that show their role in the response to treatment with statins. Thus, the aim of this study was to assess the levels of expression of three lncRNAs (RP1-13D10.2; MANTIS; lncHR1) associated with genes involved in cholesterol homeostasis in leukocyte cells of hypercholesterolemic patients after treatment with atorvastatin and compare them with levels in subjects with normal cholesterol levels. A secondary aim was to assess the levels of expression in monocytic THP-1 cells differentiated to macrophages. The study included 20 subjects with normal cholesterol (NC) levels and 20 individuals with hypercholesterolemia (HC). The HC patients were treated with atorvastatin (20 mg/day/4 weeks). THP-1 cells were differentiated to macrophages with PMA and treated with different doses of atorvastatin for 24 h. Expression of lncRNAs was determined by RT-qPCR. The lncRNAs RP1-13D10.2 (p < 0.0001), MANTIS (p = 0.0013) and lncHR1 (p < 0.0001) presented increased expression in HC subjects compared with NC subjects. Furthermore, atorvastatin had a negative regulatory effect on the expression of lncHR1 (p < 0.0001) in HC subjects after treatment. In vitro, all the lncRNAs showed significant differences in expression after atorvastatin treatment. Our findings show that the lncRNAs tested present differential expression in HC patients and play a role in the variability reported in the response to atorvastatin treatment. Further research is needed to clarify the biological impact of these lncRNAs on cholesterol homeostasis and treatment with statins.

Atorvastatin shows antitumor effect in hepatocellular carcinoma development by inhibiting angiogenesis via TGF-β1/pERK signaling pathway.

Hepatocellular carcinoma (HCC) represents 90% of liver tumors. Statins may reduce HCC incidence. Its antitumor activities may be mediated by disrupting several hepatocarcinogenic pathways. To evaluate in vivo and in vitro the antiproliferative and antiangiogenic action of atorvastatin (AT) in the development of HCC as well as its mechanisms of action.In vivo model: hexachlorobenzene (HCB) was used to promote the development of HCC in Balb/C nude mice. Number of hepatic tumor, liver cell proliferation parameters (proliferating cell nuclear antigen, PCNA), angiogenesis, and VEGF levels were analyzed. In vitro model: Hep-G2 and Ea-hy926 cells were used to evaluate the effect of different doses of AT on HCB induced cell proliferation, migration, and vasculogenesis and to analyze proliferative parameters.In vivo: AT prevented liver growth and tumor development and inhibited PCNA, TGF-β1, and pERK levels increase. AT prevented skin blood vessel formation. In vitro, AT prevented cell proliferation and migration as well as tubular formation in the endothelial cell line by inhibiting the MAPK ERK pathway. We were able to demonstrate the potential AT antiproliferative and antiangiogenic effects in an HCC model and the involvement of TGF-β1 and pERK pathways.

Effect of combination of glucocorticoid and different doses of atorvastatin on neural function, blood lipid levels and magnetic resonance imaging in patients wit h multiple sclerosis

Purpose: To determine the efficacy of the combination of glucocorticoid and different doses of atorvastatin in the treatment of patients with multiple sclerosis (MS).&#x0D; Methods: Sixty MS patients treated at Heping Hospital Affiliated to Changzhi Medical College from January 2020 to June 2021, were equally and randomly assigned to study group (OG) and control group (CG). Patients in OG were treated with glucocorticoid and atorvastatin (half in low-dose, LDG; 20 mg/day) and the other half, in high-dose atorvastatin (HDG, 40 mg/day)). Patients in CG were treated with glucocorticoid and placebo. Changes in magnetic resonance imaging (MRI), blood lipids, RhoA, and neural function were determined.&#x0D; Results: After treatment, Expanded Disability Status Scale (EDSS) score was lower in HDG than in LDG and CG (p &lt; 0.05). Total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), triglycerides (TG) and lipoprotein a (LP(a)) were significantly reduced and followed the rank order: HDG &lt; LDG &lt; CG (p &lt; 0.05). No appreciable differences occurred in HDL-C levels amongst HDG, LDG and CG (p &gt; 0.05). Furthermore, RhoA levels were lower in HDG than in LDG and CG, with lower levels in LDG than in CG (p &lt; 0.05). There were lower numbers of T2 lesions in HDG than in LDG and CG at 28 days, 3, 6 and 12 months, post-treatment (p &lt; 0.05).&#x0D; Conclusion: Glucocorticoid and high-dose atorvastatin combination is better at reducing neurological dysfunction and improving blood lipid indicators in MS patients. This finding may provide a useful guide in the determination of the optimal dose of atorvastatin.

Discussion on the Clinical Observation on Adverse Reactions of Different Doses of Atorvastatin in the Treatment of Coronary Heart Disease

Discussion on the Clinical Observation on Adverse Reactions of Different Doses of Atorvastatin in the Treatment of Coronary Heart Disease

The preventive effects of different doses of atorvastatin on contrast‐induced acute kidney injury after CT perfusion

BackgroundContrast‐induced acute kidney injury (CI‐AKI) is a severe complication among patients receiving intravascular contrast media. The purpose of this study was to investigate the preventive effects of pretreatment of atorvastatin at intensive doses on CI‐AKI after computed tomography (CT) perfusion.MethodsThe levels of serum creatinine (SCR), blood urea nitrogen (BUN), Cystatin C (CysC), estimated glomerular filtration rate (eGFR), high‐sensitivity C‐reactive protein (hs‐CRP), and interleukin‐6 (IL‐6) in patients were compared between the observation group receiving 40 mg/kg atorvastatin and the control group receiving 20 mg/kg atorvastatin before and 72 h after CT examination. In addition, the incidence of CI‐AKI was recorded.ResultsCompared with the control group, the incidence of renal injury in the observation group was significantly reduced, from 8% to 2% (χ 2 = 6.62, p = 0.010). In addition, there was no notable difference in the levels of Scr, BUN, CysC, hs‐CRP, and IL‐6 before CT examination between two groups (p > 0.05). The levels of SCR, BUN, CysC, hs‐CRP, and IL‐6 were increased, while the levels of eGFR were decreased in the control group at 72 h after CT examination (p < 0.05). At 72 h after CT enhancement, the levels of BUN, CysC, and hs‐CRP were prominently increased in the observation group (p < 0.05), while SCR, eGFR, and IL‐6 did not change (p > 0.05). Compared with the control group, the levels of SCR, BUN, CysC, eGFR, hs‐CRP, and IL‐6 in the observation group were significantly decreased at 72 h after CT examination (p < 0.05).ConclusionIntensive dose of atorvastatin pretreatment can prevent CI‐AKI undergoing CT perfusion through lowering inflammation as well as renal function indexes SCR, CysC, BUN, and eGFR.

Effect of different doses of atorvastatin on collateral formation in coronary artery disease patients with coronary atherosclerosis.

The study aimed to explore the effect of different doses of atorvastatin on collateral formation in coronary artery disease (CAD) patients with coronary atherosclerosis. The study included 218 CAD patients who received treatment between January 2017 and January 2020 at our hospital. They were assigned to the high-dose group (40 mg atorvastatin) and the low-dose group (20 mg atorvastatin) using the random table method with 109 patients per group. The blood lipid levels, TNF-α, hs-CRP, NO, and coronary atherosclerosis collateral formation before and after treatment in the two groups were compared, and favorable factors of good coronary artery collateral circulation were analyzed by multivariate logistic regression analysis. LDL-C, TG, and TC levels decreased, whereas HDL-C levels increased in the two groups after treatment. The high-dose group had lower LDL-C, TG, and TC levels but higher HDL-C levels than the low-dose group, and the difference was statistically significant ( P < 0.05). TNF-α and hs-CRP levels decreased while NO levels increased in both groups after treatment. The high-dose group had lower TNF-α and hs-CRP levels but higher NO levels than the low-dose group, and the difference was statistically significant ( P < 0.05). High-dose atorvastatin could blood lipid levels of modulate CAD patients and promote coronary atherosclerosis collateral formation. In addition, hypertension, LDL-C, HDL-C, TNF-α, hs-CRP, and NO were independent determinants of good coronary artery collateral circulation.

Preventive effects of different doses of atorvastatin on contrast-induced acute kidney injury in patients after multiple CT perfusions

The purpose of this clinical trial was to evaluate the preventive effects of different doses of atorvastatin on CI-AKI in patients after CT perfusions. 688 patients undergoing CT perfusions were administered doses of atorvastatin (20 mg/day, n = 164), atorvastatin (40 mg/day, n = 178), atorvastatin (60 mg/day, n = 176) and placebo (40 mg/day, n = 170). Several factors, urinary neutrophil gelatinase-associated lipocalin (NGAL) levels, protein kinase C (PKC), nuclear factor erythroid-2 related factor 2 (Nrf2), nicotinamide adenine dinucleotide phosphate (NADPH) responsible for contrast-induced acute kidney necrosis were recorded in this study. Postoperative administration of atorvastatin decreased the risk of CI-AKI and improved renal function. 60 mg/day of atorvastatin showed best preventive effect on CI-AKI in three groups determined by Charlson Cormobidity Index (CCI) and risk, injury, failure, loss, end-stage renal disease (RIFLE). 60 mg/day of atorvastatin significantly decreased the inflammatory cytokines interleukin (IL)-1β, transforming growth factor (TGF)-β, and tumor necrosis factor (TNF)-α compared to 20 mg/day and 40 mg/day of atorvastatin in patients after multiple CT perfusions. NADPH oxidase 4 (NOX4) and p22phox expression was reduced by atorvastatin treatment. In conclusion, these outcomes indicate that 60 mg/day of atorvastatin treatment reduces the risk of CI-AKI in patients after multiple CT perfusions.

Effects of Different Doses of Atorvastatin on Cardiovascular Complications in Patients with Type 2 Diabetes

Effects of Different Doses of Atorvastatin on Cardiovascular Complications in Patients with Type 2 Diabetes

Effects of atorvastatin doses on serum level of procalcitonin and predictors for major adverse cardiovascular events in patients with acute myocardial infarction: a pilot study and post hoc analysis.

Inflammation plays an important role in acute myocardial infarction (AMI). Procalcitonin levels rise in response to proinflammatory stimuli. This study aimed to investigate the effects of different doses of atorvastatin on the serum inflammatory profiles, especially procalcitonin and major adverse cardiovascular events (MACEs) in patients with AMI during hospitalization. The patients who were admitted to the Coronary Care Unit of The Third Medical Center of PLA General Hospital (Beijing, China) between January 2015 and December 2015 with a diagnosis of AMI were enrolled, and randomized to atorvastatin 20 mg/day postoperatively (20-mg group), 40 mg/day postoperatively (40-mg group) and 80 mg preoperatively+40 mg/day postoperatively (80/40-mg group). Serum procalcitonin and high-sensitivity C-reactive protein (hs-CRP) were evaluated before and at 1 and 3 days after percutaneous coronary intervention (PCI). A total of 112 patients with AMI (23 women and 89 men) were prospectively eligible for the study. There were no significant differences in most clinical data among the three groups. The 80/40-mg group showed significantly reduced serum procalcitonin levels at 1 and 3 days after PCI (P < 0.001) and reduced hs-CRP levels at 3 days P = 0.001) compared with 20-mg and 40-mg groups. Serum procalcitonin (OR, 4.593; 95% CI, 1.476-8.387; P = 0.005), hs-CRP (OR, 1.149; 95% CI, 1.012-1.338; P = 0.018), highly sensitive cardiac troponin T (OR, 1.255; 95% CI, 1.004-1.569, P = 0.009) and Gensini score (OR, 1.022; 95% CI, 1.045-1.062; P = 0.013) were independently associated with MACEs during hospitalization. The use of atorvastatin 80 mg before and 40 mg/day after PCI in patients with AMI can effectively reduce serum inflammatory factors. procalcitonin and hs-CRP were independently associated with in-hospital MACEs.

Atorvastatin prevents the development of diabetic neuropathic nociception by possible involvement of nitrergic system.

Diabetic neuropathy has been identified as a common complication caused by diabetes. However, its pathophysiological mechanisms are not fully understood yet. Statins, also known as HMG-CoA reductase inhibitors, alleviate the production of cholesterol. Despite this cholesterol-reducing effect of statins, several reports have demonstrated their beneficial properties in neuropathic pain. In this study, we used streptozotocin (STZ)-induced diabetic model to investigate the possible role of nitric oxide (NO) in the antineuropathic-like effect of atorvastatin. Diabetes was induced by a single injection of STZ. Male rats orally received different doses of atorvastatin for 21 days. To access the neuropathy process, the thermal threshold of rats was assessed using hot plate and tail-flick tests. Moreover, sciatic motor nerve conduction velocity (MNCV) studies were performed. To assess the role of nitric oxide, N(G)-nitro-L-arginine methyl ester (L-NAME), aminoguanidine (AG), and 7-nitroindazole (7NI) were intraperitoneally administered along with some specific doses of atorvastatin. Atorvastatin significantly reduced the hyperalgesia in diabetic rats. L-NAME pretreatment with atorvastatin showed the antihyperalgesic effect, suggesting the possible involvement of the NO pathway in atorvastatin protective action. Furthermore, co-administration of atorvastatin with AG and 7NI resulted in a significant increase in pain threshold in diabetic rats. Our results reveal that the atorvastatin protective effect on diabetic neuropathy is mediated at least in a part via the nitric oxide system.

Effects of different doses of atorvastatin, rosuvastatin, and simvastatin on elderly patients with ST-elevation acute myocardial infarction (AMI) after percutaneous coronary intervention (PCI).

To conduct a randomized double-blind prospective study to investigate effect of different doses of atorvastatin, rosuvastatin, and simvastatin on elderly patients with ST-elevation AMI after PCI. One hundred and ninety-two AMI patients over 60 years old who underwent PCI were randomly divided into six groups: the low atorvastatin group, high atorvastatin group; low rosuvastatin group; high rosuvastatin group; low simvastatin group; high simvastatin group. Demographic data and clinical information as well as coronary angiography parameters were recorded. Plasma levels of CK-MB, BNP, ALT, and TnI were measured at 12 hr, 24 hr, and 1 week after PCI. Major cardiovascular events (MACE) were recorded and analyzed using Kaplan-Meier (K-M) curve. No significant differences were observed in angiographic and procedural characteristics. In all high dose groups, all levels of CK-MB, BNP, ALT, and TnI were significantly lower. However, after 1 week of PCI, only CK-MB, BNP, and TnI showed significant difference between high and low dose groups. Patients in high dose groups had significantly lower rates for surgical or percutaneous intervention, recurrence of angina, and rehospitalization. K-M curve analysis also showed cumulative incidence freedom time of overall MACE in high dose groups was significantly longer. No significant differences were found among different drugs with the same doses. Patients with higher doses had lower level of CK-MB, BNP, ALT, and TnI and lower occurrence of MACE after PCI.

High-dose atorvastatin improves vascular endothelial function in patients with leukoaraiosis.

ObjectiveLeukoaraiosis (LA), as an age‐related white matter degeneration, is mainly caused by chronic ischemia. Our study aims to explore the efficacy of different doses of atorvastatin (ATV) in the vascular endothelial function in patients with LA.MethodsOur study enrolled 402 LA patients who were then randomly included as control or treated with ATV (10 mg), ATV (20 mg), or ATV (30 mg). The total cholesterol (TC), triglycerides (TG), high‐density lipoprotein cholesterol (HDL‐C), and low‐density lipoprotein cholesterol (LDL‐C) were detected by enzyme colorimetric assay. The high‐sensitivity C‐reactive protein (hs‐CRP) level, reactive hyperemia index (RHI), endothelin‐1 (ET‐1) content, and nitric oxide (NO) level were tested by latex agglutination test, peripheral arterial tonometry technology, radioimmunoassay, and nitrate reductase assay, respectively.ResultsAfter 8 weeks of ATV treatment, the levels of TC, LDL‐C, and HS‐CRP decreased significantly, and the trends were demonstrated in a more significant way with the increases of dose of ATV. The treatment with ATV at different doses elevated NO level and RHI and declined ET‐1 content. Gastrointestinal reaction, muscular pain, and increased aminopherase were observed after treatment with the ATV at different doses with more obvious symptoms detected accompanied by the increase of the dose. The RHI was in negative correlation with the ET‐1 and HS‐CRP while in positive correlation with NO.ConclusionOur study demonstrates that ATV can significantly improve the vascular endothelial function in LA patients with a dose‐dependent effect.

Effects of atorvastatin on serum lipids, cardiomyocyte apoptosis and related genes in rats

ObjectiveTo investigate effects of different doses of atorvastatin on serum lipids, cardiomyocyte apoptosis and related genes in rats with myocardial infarction. Methods60 SD rats were randomized into control group (n = 12) and modeling group (n = 48). The models were established by ligation of left anterior descending (LAD) in rats. 5wk later, the rates after successful modeling were divided into modeling group (n = 12) and treatment group (n = 36), and treatment group was equally divided into low dose group (20 mg/kg atorvastatin daily), medium does group (40 mg/kg atorvastatin daily) and high does group (80 mg/kg atorvastatin daily). After administration, the ratio of heart weight (HW) to body weight (BW) was calculated (HW/BW). Contents of total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDL-C) and moderate – high density lipoprotein cholesterol (HDL-C) in serum of rats were measured. Apoptosis index of rat cardiomyocytes was detected with TUNEL method. Expression levels of Caspase-3, Bax, and Bcl-2 proteins in each group were detected by Western blot. ResultsCompared with control group, heart surface of modeling group was rough, and weight of model group was significantly higher than that of control group, low, medium and high dose groups after 9 weeks of modeling (P < 0.05). TC, TG, and LDL-C in modeling group were significantly higher than those in control group (P < 0.05), HDL-C was significantly lower than those in control group (P < 0.05). Changes in blood lipid-related indicators could be improved after administration, and the higher the dose, the better the improvement effect. Apoptosis index of cardiomyocytes in modeling group, the low, medium and high dose group was significantly higher than that in control group (P < 0.05), but apoptosis of cardiomyocytes was significantly reduced in atorvastatin group at different doses. The higher the dose, the more obvious the reduction effect. The expressions of Caspase-3, Bax, and Bcl-2 proteins in modeling group, low, medium and high dose groups were significantly higher than those in control group (P < 0.05), but administration group significantly reduced apoptosis of myocardial cells, and the higher the dose, the more significant the reduction effect. ConclusionAtorvastatin can reduce TC, TG and LDL-C levels and increase HDL-C level in blood lipids, inhibit expressions of Caspase-3 and Bax and raise expression of Bcl-2 protein so as to inhibit cardiac hypertrophy, reduce cardiomyocyte apoptosis, restore myocardial function and improve myocardial infarction symptoms.

Clinical study of different doses of atorvastatin combined with febuxostat in patients with gout and carotid atherosclerosis

Objective:To evaluate the efficacy of atorvastatin combined with febuxostat in the treatment of gout patients with carotid atherosclerosis and to observe the effects on serum tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and C-reactive protein (CRP) levels, carotid plaques, and the adverse reactions.Methods:Seventy patients with gout and carotid atherosclerosis admitted to Affiliated Hospital of Hebei University from January 2014 to June 2017 were randomly divided into a treatment group and a control group. The treatment group received oral febuxostat 40 mg/day combined with atorvastatin 40 mg/day. The control group was given 40 mg/day febuxostat combined with 20 mg/day atorvastatin for 90 days. The effects of treatment on TNF-α, IL-1β, and CRP levels and carotid plaques of the patients were observed.Results:After 90 days of treatment, serum TNF-α, IL-1β, and CRP levels, as well as HUA and total cholesterol (TC), decreased in both groups after treatment. There were significant differences observed (p < 0.05). The carotid artery plaques in the two groups were significantly smaller after treatment (P<0.05). There was no significant difference in adverse reactions between the two groups (P > 0.05).Conclusion:Double doses of atorvastatin combined with febuxostat can effectively reduce uric acid to improve the inflammatory state in patients and reduce carotid plaques without increasing the incidence of adverse reactions.

Comparative studies on the effects of different doses of atorvastatin combined with aspirin on inflammatory cytokines and carotid plaques in patients with ischemic cerebrovascular disease

Objective: To make comparative studies on the effects of different doses of atorvastatin combined with aspirin on inflammatory cytokines, blood lipids, blood glucose, other biochemical indexes and carotid plaques in patients with ischemic cerebrovascular disease (ICVD) and carotid plaques.Method: One hundred and twenty patients with ICVD and carotid plaques admitted by Renmin Hospital, Hubei University of Medicine Hospital from December 2016 to December 2017 were selected and randomly divided into experimental group and control group, 60 cases in each group. Patients in the control group was asked to orally take standard dose of atorvastatin (20 mg/d) combined with aspirin enteric-coated tablets (100 mg/d). Patients in the experimental group was asked to orally take high-dose atorvastatin (40 mg/d) combined with the same amount of aspirin enteric-coated tablets. Patients in two groups were treated for 6 months averagely. The levels of inflammatory factors, changes in blood biochemical parameters and carotid plaque degrees of patients in two groups before and after treatment were inspected and compared.Results: The levels of serum high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor (TNF-a), interleukin-6 (IL-6) and homocysteine (Hcy) in patients of the experimental group after treatment were higher than those in the control group, difference with statistical significance (p < .05). The total cholesterol (TC), triglyceride (TG) and low density lipoprotein cholesterol (LDL-C) in patients of the experimental group after treatment were lower than those in the control group and before treatment. The high-density lipoprotein cholesterol (HDL-C) was higher than that of the control group and before treatment, the levels of fasting blood glucose (FBS) and glycosylated hemoglobin (HbAIc) in patients of the experimental group significantly increased compared to those before treatment, difference with statistical significance (p < .05). There was no significant change in the control group. The carotid intima-media thickness (IMT) and plaque area in patients of the experimental group were lower than those in the control group and before treatment, difference with statistical significance (p < .05).Conclusion: High-dose atorvastatin combined with aspirin for treatment of patients with ICVD can effectively reduce inflammatory inflammatory cytokine levels in serum and reduce IMT and carotid plaque area. With more obvious effect than lower dose of atorvastatin combined with aspirin, it is easy to cause blood glucose abnormality. So, it is necessary to pay attention to monitoring blood sugar during medication period.

Efficacy and adverse reaction to different doses of atorvastatin in the treatment of type II diabetes mellitus

Background: Type II diabetes mellitus (T2DM), a persistent metabolic disorder, is primarily characterized by insulin resistance, relative insulin deficiency and dyslipidemia. Here, we aimed to investigate whether different doses of atorvastatin (ATV) affect rats with T2DM. A total of 110 Sprague–Dawley rats were successfully established as T2DM models. Methods: First, the total cholesterol, triglyceride (TG), high-/low-/very-low-density lipoprotein cholesterol (HDL-c/LDL-c/VLDL-c), alanine transaminase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), creatinine (Cr), apolipoprotein Al (ApoA1) and apolipoprotein B (ApoB) levels in rat serum were analyzed. In addition, cholesteryl ester transfer protein (CETP) and retinol-binding protein 4 (RBP4) were also measured. Then, the incidence of adverse reactions was noted. Finally, the pathological study of liver and pancreatic tissues was performed. Results: Rats administered ATV at the doses of 40 and 80 mg/(kg·day) showed down-regulated TG, LDL-c, ApoB, CETP and RBP4 levels yet up-regulated HDL-c and ApoAl levels. Rats administered ATV at a dose of 80 mg/(kg·day) exhibited a higher incidence of adverse reactions and higher ALT and AST levels but lower BUN and Cr levels, which might affect liver and kidney function. Rats administered ATV at the doses of 40 and 80 mg/(kg·day) demonstrated significantly improved liver injury and pancreatic injury induced by T2DM. Conclusion: These data revealed that ATV could improve the lipid metabolism in T2DM rats and 40 mg/(kg·day) may serve as the optimal dose for the reduction of lipid levels and the incidence of adverse effects.

Effect of high dose versus low dose of atorvastatin therapy on inflammation and coagulation factors in type 2 diabetic patients; a randomized clinical trial study

Introduction: Statins are one of the most widely used therapies in different groups of patients not only because of cholesterol-lowering properties but also due to their non-lipid related mechanisms. However, the effects of atorvastatin on inflammatory and coagulation markers in type 2 diabetic patients are not well examined. Objectives: To evaluate, the effects of two different doses of atorvastatin on lipid profile, inflammatory coagulation markers, and liver enzymes in type 2 diabetic patients. Patients and Methods: In a randomized double-blinded controlled trial, 150 diabetic patients were randomly assigned to get atorvastatin 10 mg/d (n = 74) or 40 mg/d (n = 76) for 12 weeks. The concentration of biomarkers was determined both at the onset of the study as well as at the completing time of the intervention. Results: Significant differences between the mean levels of lipid profiles, fibrinogen, interleukin-1 (IL-1) and IL-6 were observed between two groups after three months treatment with atorvastatin 10 and 40 mg/d (P<0.05). Furthermore, significant improvement in all blood values after atorvastatin 40 mg/d ingestion was observed (P<0.05) except for homocysteine and creatine phosphokinase (CPK) levels (P>0.05). Conclusion: Atorvastatin therapy especially with higher dose was associated with inflammation and coagulation parameters improvement in diabetic individuals.