BackgroundType 1 diabetes mellitus (T1DM) is one of the most common chronic diseases in children that may be due to micro or macrovascular complications. Diabetic renal disease or nephropathy is a common complication of DM, clinically silent and the only detectable abnormality due to the presence of microalbuminuria.Subjects and methodsThis study was a case–control study. Participants were classified into two groups. The first group included 40 children with T1DM and the second group included 30 matched healthy controls. Serum apelin (APLN), chemerin, cholesterol, and triglycerides (TG) levels were measured for each case. Also, albumin/creatinine ratio was analyzed in random urine sample.ResultsComparison between T1DM patients and controls revealed that serum apelin, chemerin, cholesterol, TG levels, and albuminuria were significantly increased in cases compared to their controls. Significant positive correlations were found between HbA1c% and albuminuria for APLN and chemerin in the diabetic group. Whereas significant negative correlations were found between apelin and glomerular filtration rate (GFR).ConclusionIncreased levels of serum apelin and chemerin in T1DM patients may be considered as promising adipokines for the development of diabetic complication.
Background Neuropathy is one of most common complications in diabetic patients. Diagnosis of diabetic neuropathy is essential for decreasing the rate of the disability and death. Neuron-specific enolase (NSE) is released from damaged neuronal cells and enters the blood circulation through an injured blood brain barrier. Therefore, serum NSE can reflect the damage of neurons and brain tissue. Objective To evaluate peripheral polyneuropathy and cognitive function in Type 2 Diabetes Mellitus (T2DM) and correlate them with NSE level as a possible biomarker of diabetic neuropathy. Subjects and Methods Forty five T2DM patients with polyneuropathy were randomly recruited in this study compared to 45 healthy age and sex matched subjects as a control. Patients group were divided into two subgroups, 24 diabetic patients with painful peripheral neuropathy and 21 with painless peripheral neuropathy. All were subjected to clinical assessment by diabetic neuropathy symptom score, Dyck neuropathy grading, Mini-Mental State Examination (MMSE), assessment of HbA1c, NSE biomarker and neurophysiological assessment (nerve conduction study (NCS), event related potential (P300wave) and somatosensory evoked potential (SSEP) of the right median nerve). Results There were significant decrease in cognitive functions in diabetic patients compared to controls and a significant increase in NSE in diabetic patients. There were no significant difference between patients with painless and painful diabetic neuropathy as regard MMSE, HbA1c and NSE. There were significant correlation of P300 in diabetic patients with HbA1c and NSE. Conclusion Neurophysiological assessment of diabetic patients by NCS, SSEP and P300 have well evaluation of cognitive functions, painless, and painful diabetic polyneuropathy. NSE is a beneficial biomarker in diabetic patients to pick up neurological complications.
Background The link between immune system and type 2 diabetes mellitus (T2DM) pathogenesis attracted attention to demonstrate the role of immune cells and their secreted cytokines in T2DM development and its subsequent foot complications. Objective To investigate the relation between T Natural killer cell (TNK) %, Interleukin 4 (IL4) and Interferon gamma (IFN-γ) and diabetic foot infection (DFI) development in patients with diabetic foot ulcer (DFU). Patients and Methods Ninety patients with diabetes were included in this work, divided as T2DM group (n=30), DFU group (n=30), and DFI group (n=30). TNK% was detected using flow cytometry. Serum IL4 and IFN-γ were measured by ELISA. Diabetes biochemical parameters were also analyzed. Results Significant decrease was detected in TNK% and IFN-γ in DFI group compared to other 2 groups ( P <0.001). Significant decrease was detected in serum levels of IL4 in DFI group compared to T2DM group ( P =0.006). IFN-γ/IL4 was significantly decreased in DFI compared to DFU group ( P =0.020). There was a significant correlation of TNK% with both IL4 and IFN-γ (r=0.385, P <0.001; r=0.534, P <0.001, respectively). Significant negative correlation of TNK% with HbA1c and LDL was revealed (r=−0.631, P <0.001; and r=−0.261, P =0.013, respectively), while a positive correlation was seen with HDL (r=0.287, P =0.006). A significant negative correlation of IL4 with HbA1c was found (r=−0.514, P <0.001;. As for IFN-γ, a significant negative correlation with HbA1c and LDL was detected (r=−0.369, P < 0.001; r=−0.229, P =0.030). TNK % and IFN-γ level showed negative correlations with disease duration/year (r=−0.546, P < 0.001; r=−0.338, P =0.001,respectively). Conclusion Decline in TNK frequency has essential role in T2DM pathogenesis and subsequent foot complications. Downregulation of TNK% and IFN-γ level have potential roles in predicting infection of diabetic ulcer and are correlated with disease duration.
Introduction Neonatal sepsis can quickly progress to multi-organ failure with high morbidity and mortality, making early diagnosis mandatory. Although being the gold standard, the long duration of blood culture may lead to hazardous neonatal complications. Sepsis activates monocytes and changes their subset distribution with the resultant activation of lymphocytes and adaptive immune cells changing the plasma cytokines levels. Subjects and Method Percentages of monocytes subsets, pattern of monocytes surface CD86 expression and serum IL-17 compared to serum procalcitonin were measured in 30 neonates with early sepsis and compared with age and sex matched 30 apparently health neonates as a control group. Results Gestational age, neonatal weight and hemoglobin concentration were significantly low in septic neonates vs the control group. Percentages of intermediate, nonclassical and CD86 positive monocytes, the mean fluorescence intensity of CD16 on CD16 positive monocytes, and serum levels of CRP, IL-17 and procalcitonin were significantly increased in septic neonates compared with the control group. Conclusion Early neonatal sepsis was associated with increasing the percentage of CD86 positive monocytes. Serum IL-17 levels were positively correlated with increased serum procalcitonin.
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