The Correlation Between Uric Acid and Hba1C With NLR Values in DM Type 2 Patients
The Correlation Between Uric Acid and Hba1C With NLR Values in DM Type 2 Patients
DISCUSSION
• Uric acid levels have a average value of 6.27 mg/dL which is
interpreted as normal. The highest value of uric acid in the body has the
risk of incident diabetes risk (Male: 6-6,8 mg/dL, Female: 5-6 mg/dL)
(Shani et al, 2016)
• The Hb1Ac levels of type 2 DM patients in this study had an average of
8.76% which means that the average respondent had uncontrolled type
2 DM (>7%). Uncontrolled blood sugar levels in type 2 DM patients
are affected by carbohydrate intake that exceeds the needs. (Edgren
AR, 2004).
DISCUSSION
• NLR levels of type 2 DMP patients in this study had an average value
of 6.23% which means the NLR is above the normal or high range
(0.78-3.53%). The process of increasing neutrophil levels can mediate
insulin resistance, one of them through excessive inflammation. While
the reason for the low lymphocyte value in subjects with insulin
resistance is because the body decreases the number of CD8+
lymphocytes to suppress the body's anti-inflammatory environment
(Chernecky C & Berger JB, 2012).
DISCUSSION
• NLR is often influenced by biological conditions such as dehydration,
the severity of the metabolic syndrome, or other factors such as the
treatment and processing of blood samples. Along with an increase in
living standards, elements that cause an increase in uric acid levels also
become common. Low solubility of uric acid in the blood will result in
damage to the vascular endothelium when crystallization and settles on
the vascular wall. Increased uric acid levels also encourage lipid
oxidation and free radical formation, reduce nitric oxide production,
and damage the endothelium (Azab et al, 2012).
DISCUSSION
• HbA1c is an indicator of glucose regulation and an increase in HbA1c is
associated with an increased risk of cardiovascular complications in T2DM
patients. Leukocytes play an important role in cholesterol accumulation,
endothelial dysfunction and atherogenesis (Sefil et al, 2014).
DISCUSSION
THANK YOU