Association between genetic polymorphisms and other attributing factors with lipid profiles among statin users: a cross-sectional retrospective study

Egyptian Journal of Medical Human Genetics

Table 5 Analysis of multiple independent variables and patients' probabilities of achieving the goal LDL-c level (< 2.6 mmol/L) using multivariate binary logistic regression

Dependent variable	Independent variables	P-value	OR	95% CI
Patient’s achievement of the LDL-target of 2.6 mmol/L	ABCG2 rs2231142^a	0.648	0.738	0.201–2.714
	ABCC2 rs717620^a	0.198	0.417	0.110–1.579
	APOE^a	0.955	0.977	0.428–2.229
	GATM rs9806699^a	0.778	0.863	0.308–2.415
	COQ2 rs4593075^a	0.73	1.6	0.111–23.804
	APOA5 rs662799^a	0.351	1.505	0.637–3.554
	Age	0.452	1.023	0.964–1.087
	Gender^b	0.749	0.874	0.384–1.991
	Statin types^c
	Simvastatin	0.182	–	–
	Atorvastatin	0.199	0.558	0.229–1.360
	Pravastatin	0.04	0.11	0.013–0.902
	Lovastatin	0.437	0.357	0.027–4.775
	TC^d	0.984	1.01	0.373–2.739
	HDL-c^d	0.424	0.449	0.063–3.188
	LDL-c^d	0.54	0.745	0.291–1.907
	TG^d	0.641	1.151	0.638–2.076

The P = 0.368 for Hosmer–Lemeshow test indicates that this model is fit
^aHomozygous dominant as reference category vs. Heterozygous + Homozygous recessive
^bMale as reference category
^cSimvastatin as reference category
^dBaseline lipid level at the initiation of statin treatment (baseline). P < 0.05 is considered as statistically significant (indicated by bold text)