Ldl Conversion From Mmol L To Mg Dl _TOP_ Download Free
SI units Conversion Calculator. Convert Triglycerides level to mmol/L, µmol/L, mg/dL, mg/100mL, mg%, mg/L, µg/mL. Clinical laboratory units online conversion from conventional or traditional units to Si units. Table of conversion factors for Triglycerides unit conversion to mmol/L, µmol/L, mg/dL, mg/100mL, mg%, mg/L, µg/mL.
ldl conversion from mmol l to mg dl download free
SI units Conversion Calculator. Convert Uric Acid level to mmol/L, µmol/L, mg/dL, mg/100mL, mg%, mg/L, µg/mL. Clinical laboratory units online conversion from conventional or traditional units to Si units. Table of conversion factors for Uric Acid unit conversion to mmol/L, µmol/L, mg/dL, mg/100mL, mg%, mg/L, µg/mL.
The mean LDL-C concentrations were 3.9 1.09 mmol/L, 3.63 1.06 mmol/L and 3.72 1.04 mmol/L measured by a direct homogenous assay (D-LDL-C), calculated by Friedewald's formula (F-LDL-C) and calculated by Anandaraja's formula (A-LDL-C), respectively in the 1010 patients. The Student's paired t-test showed that D-LDL-C values were significantly higher than F-LDL-C and A-LDL-C values (p 0.89). Using lipoprotein values from the initial group we modified Friedewald's formula by replacing the term 2.2 with 3. The new modified formula for LDL-C estimation (S-LDL-C) showed no statistically significant difference compared to D-LDL-C. The absolute bias between these two methods was -0.06 0.37 mmol/L with a high correlation coefficient (r = 0.96).
The obtained unsatisfactory results led us to re-examine Friedewald's formula for LDL-C estimation. Following the procedure which led to Friedewald's formula derivation we re-calculated factor for VLDL-C concentration estimation. We used TC, TG, LDL-C and HDL-C concentration measurements in the initial group to calculate the VLDL-C/TG ratio for a Serbian population. We first subtracted the sum of HDL-C and LDL-C from TC for each person. This was estimation of VLDL-C concentration for each person. Thereafter, we divided the particular TG concentration with the corresponding calculated VLDL-C to determine the mean of the ratio. The TG/VLDL mean ratio was 3 compared with 2.2 according to Friedewald [8]. Therefore, the modified formula should be stated as follows: S-LDL-C (mmol/L) = TC - TG/3 - HDL-C. The percentage difference for our modified formula (%ΔS-LDL-C) was calculated in the same way as for Friedewald's and Anandaraja's formulas.
In our study we investigated if Anandaraja's formula could be applied in the Serbian population by comparing the value obtained with that of the homogenous direct method for LDL-C determination. This is the first study of its kind where the reliability and accuracy of Friedewald's formula were tested in the Serbian population. In our initial group LDL-C values from the direct measurement and from Anandaraja's formula were both higher than the values in Indian, Brazilian and Greek populations by almost 1 mmol/L [12, 24, 25]. The A-LDL-C concentration was significantly lower than the D-LDL-C concentration (Table 1). The correlation coefficient between methods was good (r = 0.89) but lower than previously published (r = 0.97) [12, 24].
In our initial population we calculated that to determine cholesterol in VLDL, TG should be divided by 3 (mmol/L) or 6.85 (mg/dL). Our modified formula was tested and its accuracy was validated in our second population. S-LDL-C showed no statistically significant difference compared to D-LDL-C in the validation group, despite the fact that there was still an underestimation. No significant difference between these two mean values was found in situations of TC 7.24 mmol/L, TG 2.26 - 2.82 mmol/L and LDL-C
According NCEP-ATP III guidelines, LDL-C concentrations 4.14 mmol/L are considered high. Medication should be administered to subjects falling into the latter group [4]. Our study demonstrated that 45%, 45% and 26% of samples from Friedewald's, Anandaraja's and our modified formula, respectively underestimated the diagnostic LDL-C level of 4.14 mmol/L and were classified one cut-off point below that indicated for therapy (data not shown).
Dyslipidemia is one of the major risk factors for cardiovascular disease in diabetes mellitus. High plasma TG, increased small dense LDL-c particles, low HDL-c are characteristic features of diabetic dyslipidemia and these lipid changes are mainly attributed to increased free fatty acid flux secondary to insulin resistance [72]. The increase in cardiovascular risk in obesity depends to a significant extent on changes in lipid profile, mainly decreased HDL-c and increased TG and insulin resistance is the central cause for these changes [73]. Prominent and known risk factors that contribute to the increased incidence of atherosclerosis in hemodialysis patients are disorders in lipoprotein metabolism and elevated plasma fibrinogen concentrations [74]. Therefore the participants we categorized as non-healthy (patients with - type 2 diabetes, End stage renal failure and on haemodialysis and obesity) are at increased risk of dyslipidemias. Zinc supplementation significantly reduces TC, LDL-c and TG and elevates HDL-c in non-healthy patients. Elevated plasma concentrations of HDL-c are associated with protection from atherosclerotic cardiovascular disease. Cardio protective effect of HDL-c is due to its role in reverse cholesterol transport in which cholesterol from peripheral tissues is returned to the liver for excretion in the bile, its protective effect on endothelial cells and its antioxidant activity [75]. All these evidence support that Zinc supplementation will effectively reduce the cardiovascular risk among non-healthy patients.
Several molecular mechanisms are believed to be involved in reduction in serum lipid levels following Zinc supplementation. In Zinc-deficient rats lowered plasma HDL-c and some apoproteins (A1, A2, C and E) but also elevated total cholesterol concentrations have been observed [76, 77]. On the other hand, Zinc supplementation has been shown to inhibit the development of atherosclerosis in rabbits fed a high cholesterol diet [78]. It is well documented that Zinc is an important mediator of insulin storage and secretion from the pancreas [78]. In addition, pancreatic beta-cells utilize a very efficient transporter (ZnT8) to accumulate Zinc inside the cells. Thus, Zinc deficiency or alterations in ZnT8 expression have a potential to depress insulin secretion [79]. Zinc enhances the phosphorylation of insulin-receptor substrates to activate a series of signal transduction, improving insulin sensitivity [80, 81]. Insulin resistance at the adipocytes results in increased release of fatty acids into the circulation and then increased free fatty acid flux to the liver stimulates the assembly and secretion of VLDL resulting in hypertriglyceridemia [82]. Zinc supplementation either improving insulin secretion or reducing insulin resistance as described above inhibits the lipolysis in adipose tissues, reduce free fatty acid release into the circulation and its availability to the liver and excessive lipoprotein synthesis. Besides Zinc contribution to insulin secretion and action, Zinc directly affects lipid metabolism. Recently it has been shown that Zinc deficiency down regulates fatty acid utilization in mitochondria and peroxisomes and up regulates lipid synthesis in the rat liver affecting the expression of genes encoding enzymes contributing to liver lipid homeostasis [83].
Although native LDL are exposed to all enzymatic and non-enzymatic oxidants, they are protected by a potent array of antioxidants in plasma. Moreover, some of these antioxidants are a part of the LDL composition. The LDL and other biomolecules are protected from free radical attack by the action of antioxidant capacity in the blood.
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For the purposes of this recommendation, dyslipidemia is defined as an LDL-C level greater than 130 mg/dL or a high-density lipoprotein cholesterol (HDL-C) level less than 40 mg/dL (to convert HDL-C values to mmol/L, multiply by 0.0259). Most participants enrolled in trials of statin use for the prevention of CVD had an LDL-C level of 130 to 190 mg/dL or a diabetes diagnosis; hypertension and smoking were also common among trial participants.6 Persons with an LDL-C level greater than 190 mg/dL were usually excluded from trial participation, as it was not considered appropriate to randomly assign them to placebo. Thus, these recommendations do not pertain to persons with very high cholesterol levels (i.e., LDL-C > 190 mg/dL) or familial hypercholesterolemia, as they were excluded from most prevention trials.
Dulaglutide is a once weekly injectable glucagon-like peptide-1 receptor agonist (GLP-1 RA). It received FDA approval for the reduction of major cardiovascular events (MACE) in adults with type 2 diabetes who have established cardiovascular disease or multiple cardiovascular risk factors3. Long-term use of dulaglutide is also associated with reduced composite renal outcomes - defined as the first occurrence of new macroalbuminuria (UACR >339 mg/mmol), a sustained decline in eGFR of 30% or more from baseline, or chronic renal replacement therapy - in people with type 2 diabetes4. Nevertheless, dulaglutide would be an unsuitable option in this scenario due to the presence of gastroparesis. GLP-1 RAs slow down gastric emptying and could therefore exacerbate gastroparesis.