PNPLA 3I148M genetic variant associates with insulin resistance and baseline viral load in HCV genotype 2 but not in genotype 3 infection

Table 3 Baseline characteristics according to PNPLA3 I148M sequence variant in HCV genotype 3 patients

	II	IM	MM	P value	P value
	n = 159	n = 91	n = 6	additive	recessive
Male gender, n (%)	97 (61)	52 (57)	5 (83)	0.466	0.407
Age, years	39 (31–47)	41 (35–48)	42 (29–46)	0.128	0.653
BMI, kg/m ²	26^a (23–29)	25^a (23–28)	26 (22–28)	0.232	0.644
ALT, U/l	108 (68–175)	106^d (62–181)	69 (61–109)	0.398	0.248
Total cholesterol, mmol/L	4.0^e (3.3-4.7)	3.8^a (3.2-4.5)	3.7 (3.1-5.7)	0.909	0.452
Triglycerides, mmol/L	0.9^e (0.7-1.3)	0.9^a (0.7-1.4)	0.8 (0.6-1.1)	0.336	0.256
Glucose, mmol/L	4.9^c (4.5-5.6)	4.9^f (4.6-5.3)	4.8 (4.6-5.4)	0.147	0.882
Insulin, mIU/L	13^g (7–26)	12^h (7–25)	12 (6–39)	0.800	0.785
HOMA-IR, U	2.7ⁱ (1.5-6.1)	2.6^j (1.6-4.7)	2.5 (1.5-8.4)	0.882	0.941
Baseline HCV RNA, log ₁₀ IU/mL	6.0 (5.3-6.7)	6.2 (5.6-6.7)	6.8 (6.1-7.1)	0.030	0.100
Steatosis ¹ , n (%)	99^k (68)	68^c (82)	4^d (80)	0.068	0.989
Cirrhosis ³ , n (%)	17^k (12)	11^c (13)	1^d (20)	0.636	0.489
Diabetes mellitus, n (%)	6^c (4)	1^f (1)	0 (0)	0.520	0.996

Categorical traits, expressed as number (n) and relative proportion (%), have been compared by Fisher exact test. Continuous traits are expressed as median (interquartile range) and have been analyzed using a linear regression model. For additional information on statistical analyses, see methods.
¹Steatosis was defined as histological grade > 0. ²Cirrhosis was defined as Ishak stage 5–6.
Missing data: ^an = 4, ^bn = 18, ^cn = 8, ^dn = 1, ^en = 2, ^fn = 7, ^gn = 9, ^hn = 6, ⁱn = 16, ^jn = 11, ^kn = 14. Abbreviations: PNPLA3, patatin-like phospholipase domain-containing 3; HCV, hepatitis C virus; BMI, body mass index; ALT, alanine transferase; HOMA-IR, homeostasis model assessment for insulin resistance; II, individuals with two 148I alleles; MM, individuals with two 148 M alleles; IM, heterozygotes.

ISSN: 1471-2350