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Serum 25(OH) vitamin D level and its relation to diabetic peripheral neuropathy in Egyptian patients with type 2 diabetes mellitus.
Background: Some clinical studies demonstrated a significant association between vitamin D deficiency and diabetic peripheral neuropathy (DPN).
Objective: This study aims to evaluate the correlation between serum levels of 25(OH) vitamin D and DPN in Egyptian patients with type 2 diabetes mellitus (T2DM).
Patients and method: Sixty patients were known to have T2DM, which classified into the following: group I included 40 patients with DPN and group II included 20 diabetic patients, without DPN, compared with 30 apparently healthy subjects of matched age and sex as control group. Laboratory investigations including fasting and 2-h postprandial blood glucose levels, serum calcium, phosphorus, glycosylated hemoglobin (HbA1c), lipid profile, serum 25(OH) vitamin D, and nerve conduction studies were carried out for every participant to detect the existence and severity of DPN.
Results: Vitamin D deficiency was found in 73.3% of T2DM groups and in 35% of control subjects with statistical significant differences ( p < 0.005), and serum level of 25(OH) vitamin D in patients with DPN (21.09 ± 8.38) was less statistically significant than that in patients without DPN (31.12 ± 14.85) ( p = 0.001). Mean serum level of 25(OH) vitamin D in patients with painless DPN (10.047 ± 8.12) was less significant than that in patients with painful DPN (18.14 ± 3.85), ( p < 0.05). Regression analysis revealed that vitamin D deficiency is one of the independent risk factors of DPN, (OD, 0.914), ( p = 0.007).
Conclusion: Vitamin D deficiency has a significant role in the development and severity of DPN in Egyptian patients with T2DM.
Objective: This study aims to evaluate the correlation between serum levels of 25(OH) vitamin D and DPN in Egyptian patients with type 2 diabetes mellitus (T2DM).
Patients and method: Sixty patients were known to have T2DM, which classified into the following: group I included 40 patients with DPN and group II included 20 diabetic patients, without DPN, compared with 30 apparently healthy subjects of matched age and sex as control group. Laboratory investigations including fasting and 2-h postprandial blood glucose levels, serum calcium, phosphorus, glycosylated hemoglobin (HbA1c), lipid profile, serum 25(OH) vitamin D, and nerve conduction studies were carried out for every participant to detect the existence and severity of DPN.
Results: Vitamin D deficiency was found in 73.3% of T2DM groups and in 35% of control subjects with statistical significant differences ( p < 0.005), and serum level of 25(OH) vitamin D in patients with DPN (21.09 ± 8.38) was less statistically significant than that in patients without DPN (31.12 ± 14.85) ( p = 0.001). Mean serum level of 25(OH) vitamin D in patients with painless DPN (10.047 ± 8.12) was less significant than that in patients with painful DPN (18.14 ± 3.85), ( p < 0.05). Regression analysis revealed that vitamin D deficiency is one of the independent risk factors of DPN, (OD, 0.914), ( p = 0.007).
Conclusion: Vitamin D deficiency has a significant role in the development and severity of DPN in Egyptian patients with T2DM.
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