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underestimate LDL-C especially at high triglyceride levels and

low LDL-C levels. This is especially seen in patients with

diabetes due to abnormalities in lipoprotein composition and

hypertriglyceridemia. A study from our institution derived a

new formula (SMART2D formula) from a cohort of patients

with type 2 diabetes for estimation of LDL-C. The aim of this

study is to validate the use of the SMART2D formula to

estimate LDL-C in patients with and without diabetes.

Methods:

We examined 54639 lipid profiles from January 2011

to December 2014 at a Regional General Hospital. LDL-C

calculated using the Friedewald formula (F-LDL-C) and the

SMART2D formula (SMART2D-LDL-C) were compared with

direct LDL-C measurement (M-LDL-C) by an automated assay

(Roche Cobas C501). The agreement in classification into

National Cholesterol Education Program defined LDL levels

was also studied.

Results:

In patients with diabetes, the mean difference

between M-LDL-C and F-LDL-C was 0.381 ± 0.253 mmol/L and

between M-LDL-C and SMART2D-LDL-C was

0.148 ± 0.201

mmol/L. Bland Altman plots showed better agreement

between SMART2D-LDL-C and M-LDL-C (B =

0.02, p = 0.160)

than between F-LDL-C and M-LDL-C (B = 0.027, p = 0.00). By

Friedewald formula, 28.7% of patients with M-LDL-C

2.6

mmol/L were classified as F-LDL-C < 2.6 mmol/L. (Kappa:

0.389) With the SMART2D formula, 5.3% of patients with

M-LDL-C

2.6 mmol/L were classified as SMART2D-LDL-C

<2.6 mmol/L. (Kappa: 0.828) In patients with TG > 2.2 mmol/L,

45.3% were misclassified with Friedewald formula, while 8.6%

were misclassified with the SMART2D formula.

In patients without diabetes, the mean difference between

M-LDL-C and F-LDL-C was 0.361 ± 0.231 mmol/L and between

M-LDL-C and SMART2D-LDL-C was 0.001 ± 0.182 mmol/L.

Bland Altman plot showed positive bias for the SMART2D

formula (B =

0.004, p = 0.00) and negative bias for the Friede-

wald formula. (B = 0.008, p = 0.00) By Friedewald formula, 33.6%

with M-LDL-C

2.6 mmol/L were classified as F-LDL-C < 2.6

mmol/L. (Kappa: 0.451) With the SMART2D formula, 6.3% with

M-LDL-C

2.6 mmol/L were classified as LDL-C < 2.6 mmol/L.

(Kappa: 0.837) In patients with TG > 2.2 mmol/L, 54.2% were

misclassified with Friedewald formula, while 11.4% were

misclassified with the SMART2D formula.

Conclusion:

The SMART2D formula, as compared to the

Friedewald formula, provides a more accurate estimate of

LDL-C and reduces misclassification in patients with and

without diabetes.

OL07-5

Elevated hemoglobin A1c levels are associated with increased

arterial stiffness in a Taiwanese population

Chih-Jen CHANG

1

, Chung-Hao LI

2

, Yi-Ching YANG

1

,

Jin-Shang WU

1

, Chung-Hung TSAI

2

, Feng-Hwa LU

1

.

1

Department of Family Medicine, National Cheng Kung University

Hospital, Tainan,

2

Department of Family Medicine, China Medical

University-An Nan Hospital, Taiwan

Introduction:

Studies have shown that diabetes mellitus

increased brachial-ankle pulse-wave velocity (baPWV), but

the impact of two pre-diabetes conditions, impaired fasting

glucose and impaired glucose tolerance, remains controver-

sial. Recently, another surrogate for the diagnosis of diabetes

and pre-diabetes has been suggested from an oral glucose

tolerance test to hemoglobin A1c (HbA1c). The aim of this

study was to investigate the impact of different HbA1c status

on baPWV in a relatively healthy Taiwanese population.

Methods:

We enrolled 4938 apparently healthy subjects after

excluding those who were under medications for diabetes,

hypertension or hyperlipidemia; or had a history of cardio-

vascular disease; or had diagnosed anemia and peripheral

atherosclerosis with ankle brachial index (ABI) <0.95 in the

health examination center of the National Cheng Kung

University Hospital from Oct. 2006 to Aug. 2009. The baPWV

values to assess arterial stiffness were calculated as the

distance traveled by the pulse wave divided by the time

taken to travel the distance. The participants were classified

into three groups based on 2011 report by an International

Expert Committee, American Diabetes Association: normal

glucose tolerance (NGT) (HbA1C <5.7%, n = 2973), pre-diabetes

(HbA1C 5.7

6.4%, n = 1817) and newly diagnosed diabetes

(NDD) (HbA1C

6.5%, n = 148).

Results:

The mean values of baPWV were 1265.2 ± 195.0,

1386.7 ± 241.2, 1488.5 ± 278.7 cm/s in NGT, pre-diabetes and

NDD groups, respectively. Both pre-diabetes and NDD groups

had a higher baPWV value as compared with NGT group

(p < 0.001). In multiple linear regression with the reference

group of NGT, both pre-diabetes (

β

= 13.96, p = 0.002) and NDD

(

β

= 25.76, p = 0.002) groups had a significantly higher baPWV

values after adjustment for age, sex, body mass index, current

smoking, alcohol consumption, habitual exercise, systolic

blood pressure, cholesterol and high-density lipoprotein

cholesterol.

Conclusions:

Diabetic subjects with HbA1c

6.5% exhibit a

greater arterial stiffness, even in pre-diabetes with HbA1C of

5.5

6.4%.

OL07-6

Urine albumin/creatinine ratio is a significant predictor for

incident diabetic peripheral neuropathy in patients with Type

2 Diabetes: 3-year prospective study

Sharon Li Ting PEK

3

, Na LI

3

, Lee Ying YEOH

4

, Su Chi LIM

1

3

,

Chee Fang SUM

1,2

, Subramanian TAVINTHARAN

1

3

.

1

Diabetes

Centre, Khoo Teck Puat Hospital,

2

Division of Endocrinology, Khoo

Teck Puat Hospital,

3

Clinical Research Unit, Khoo Teck Puat Hospital,

4

Division of Nephrology, Khoo Teck Puat Hospital, Singapore

Introduction:

Diabetic peripheral neuropathy (DPN) is a

common complication of Type 2 Diabetes (T2D). Apart from

hyperglycemia, its pathogenesis is poorly understood. DPN

can develop despite intensive glucose control, suggesting that

other risk factors are involved in the pathophysiology of DPN.

In this study, we aim to determine baseline predictors of

incident DPN.

Methods:

We consecutively enrolled patients (n = 2058) with

T2D (21

90 years old), seen our institution

s Diabetes Centre

and a primary care polyclinic in Singapore (August 2011

March

2014). From 2014, 684 of the participants made a repeat visit

3-year from first visit. The prospective data collection is still

on-going. Anthropometric data, fasting blood, urine were

collected for biochemistry and urine albumin/creatinine

measurements (uACR). Systolic and diastolic blood pressure

(SBP and DBP) was taken fromparticipants using an automated

blood pressure monitor. Carotid-femoral Pulse wave velocity

(PWV) was determined using SphygmoCor equipment and

software. Neuropathy was considered present if an abnormal

finding in monofilament (<8 of 10 points) or neurothesiometer

testing

25 volts on at least one foot.

Results:

Baseline characteristics of 684 patients are: Age:

(57.2 ± 10.4) years, 50.1% males, ethnicity: 53.8% Chinese,

20.9% Malay, 21.5% Indian and 3.8% of others, duration of

T2D: (11.1 ± 8.6) years and HbA1c (7.71 ± 1.26) mmol/L. In these

684 patients, 599 had no DPN at baseline. On a 3-year follow-

up, 48 (8%) of them developed DPN. Patients with incident DPN

(n = 48) versus controls who did not developDPN (n = 551), were

older [(60.4 ± 8.0) vs (56.9 ± 10.6)]years (p = 0.026), had longer

duration of diabetes [(14.6 ± 10.2) vs (10.4 ± 8.2)] years (p =

0.007), increased SBP [(148.4 ± 16.5) vs (136.6 ± 17.6)] mmHg

(p < 0.0001) and DBP [(81.1 ± 9.1) vs (77.7 ± 9.4)] mmHg (p =

0.017), increased PWV [(10.8 ± 2.5) vs (9.6 ± 2.6)] m/s (p = 0.002),

lower eGFR [(75.7 ± 34.8) vs (90.5 ± 29.7)] (p = 0.001), worse uACR

[18.0(6.0

63.8) vs 51.0(20.0

334.0)] mg/g (p < 0.0001) at baseline.

There were no significant difference for patients, with incident

DPN vs those without, in their baseline HbA1c [(7.81 ± 1.35) vs

(7.65 ± 1.25)] mmol/L and fasting glucose [(7.88 ± 2.43) vs

Oral Presentations / Diabetes Research and Clinical Practice 120S1 (2016) S40

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