Diabetic polyneuropathy (DPN) is a complex and multifactorial entity in which various factors besides hyperglycemia play an important role. Symptoms of DPN are sensory, motor or autonomic. Intensive research proved that oxidative stress is the common denominator for the four major destructive pathways of hyperglycemia including increased hexosamine pathway flux, activation of Protein kinase-C (PKC) pathway, increased Advanced Glycated End-products (AGEs) formation, and increased Polyol Pathway flux. National data in Egypt confirms that more than 60% of Egyptian diabetic patients suffer from neuropathy. The most common complications of DPN are Cardiac Autonomic Neuropathy (CAN), diabetic foot and ulcers, neuromuscular disability, and anxiety. In addition, DPN affects the Quality of Life (QoL). According to common clinical practice, the common diagnostic tools are bed-side diagnosis and electrophysiological tests. Early diagnosis is critical to improve the prognosis of DPN and therapeutic intervention in the early phase. In this review, we provide a clear understanding of the pathogenesis, early diagnosis and the good management of DPN. Since the pathogenesis of DPN is multifactorial, its management is based on combination therapy of symptomatic; either pharmacological or non-pharmacological treatments, and pathogenic treatment. Alpha Lipoic Acid (ALA) is a potent anti-oxidant that has several advantages as a pathogenic treatment of DPN. So, in clinical practice, ALA may be prescribed for patients with early neuropathic deficits and symptoms. Patient education has an important role in the managemement of DPN.
Background Chronic hepatitis C virus (HCV) infection affects around 170 million individuals worldwide. Egypt has one of the highest prevalence of patients with HCV worldwide. A higher prevalence of insulin resistance (IR) is found in this population. Aim The aim of this work was to study the relation between IR, metabolic syndrome (MS), and hepatitis C in nondiabetic patients and to assess their relation to the duration of HCV infection. Patients and methods This was a cross-sectional study of 50 participants matched for age (49 ± 7.6 years), sex, and BMI. These participants were divided into three groups: 20 controls, 15 patients with HCV for less than 10 years’ duration, and 15 patients with HCV for more than 10 years. We assessed patients for MS according to the AACE diagnostic criteria. Fasting and postprandial insulin levels were also assessed. IR was evaluated using the homeostasis model assessment-insulin resistance (HOMA-IR) equation. Results There was a statistically significant difference in HOMA-IR levels between controls (median 0.43 μU/ml) and those with HCV for more than 10 years (median 0.75 μU/ml; P = 0.001) as well as those with HCV for less than 10 years (median 0.89 μU/ml; P = 0.001). There was no significant difference in HOMA-IR levels between both groups of HCV (P = 0.8). The increase in the HOMA-IR test values was mainly because of increased fasting insulin levels in both groups because of the significant positive correlation between HOMA-IR and fasting insulin in patients with chronic HCV less than and those more 10 years’ duration (r = 0.902, r = 1, respectively; P = 0.001 in both groups). MS was found in four of 15 patients in each group of patients; yet, none of the controls fulfilled the diagnosis criteria. Conclusion MS and IR are significantly higher in Egyptian HCV patients when compared with normal controls irrespective of the duration of HCV.
Background Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. Diabetic nephropathy is the major microvascular complication of diabetes mellitus; one of the earliest clinical signs of diabetic nephropathy is an elevated urinary albumin excretion (UAE), referred to as microalbuminuria. Fractalkine is a large cytokine protein of 373 amino acids; it contains multiple domains. Fractalkine (CX3CL1) is a unique chemokine and the only representative of the CX3C group. It exists as a membrane-bound and soluble form. It interacts with cells expressing CX3CR1, a G-coupled protein receptor. It is also commonly known by the names fractalkine (in humans) and neurotactin (in mice). Aim Our study aimed to assess fractalkine levels in type 2 Egyptian diabetic patients with and without diabetic nephropathy and its role as a marker in the development of diabetic nephropathy. Patients and methods Our study was carried out on 75 individuals: 25 controls, 25 type 2 diabetic patients without diabetic nephropathy, and 25 type 2 diabetic patients with diabetic nephropathy. These patients were subjected to a full laboratory workup including fasting and postprandial blood glucose, glycated hemoglobin A1C, serum urea and creatinine, 24-h UAE, and fractalkine level. Results and conclusion Our study showed that the serum fractalkine concentration was significantly elevated in type 2 diabetic patients with nephropathy (1153.14±261.1) compared with type 2 diabetic patients without nephropathy (705.78±150.59) and the control group (251.5±64) (both P=0.000). There was a significant correlation between serum fractalkine level and 24-h UAE, HBA1C, and serum creatinine. Thus, this positive correlation between serum fractalkine level and UAE could be an early predictor of microvascular complications in diabetic patients. We can conclude that serum fractalkine plays a pathogenic role in the development of diabetic nephropathy.
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