Objectives: Iron deficiency (ID) and its anemia (IDA) are the most prevalent nutritional deficiency worldwide. Dysfunction of the autonomic nervous system (ANS) is a consequence of anemia regardless to its type. Many studies found ANS dysfunction in adults with ID/IDA. This study evaluated ANS function in children and adolescents with IDA as related studies are scare.Patients and Methods: This prospective study included 60 children with IDA (boys = 20; girls = 40; age: 14.50 ± 2.04 yrs.). Blood concentrations of hemoglobin, ferritin and iron were determined. ANS function testing were carried twice (at baseline and 3 months after iron therapy). They included measuring of heart rate at rest and its variation (HRV) in response to standing and breathing and blood pressure (BP) changes in response to standing, sustained handgrip and cold.Results: Manifestations of IDA included excessive fatigue, dizziness, palpitation at rest and headache. Children with IDA had significant changes in resting heart rate, blood pressure and HRV parameters compared to healthy mates indicating sympathetic hyperactivity and reduction in parasympathetic activity. Early, definite and severe ANS dysfunctions were found in 20%, 36.67% and 3.33%, respectively. For children with IDA, significant correlations were found between ferritin levels and HB and iron levels (P = 0.001), HRV to active standing, deep breathing and Valsalva maneuver (P = 0.001) and systolic and diastolic (P = 0.001) and diastolic BPs in response to sustained handgrip and cold (P = 0.001). Ferrous sulfate therapy (6 mg/kg/day) for 3 months resulted in improvement of ANS manifestations with IDA. Conclusion:ANS dysfunctions are common consequences of IDA in children and can be attributed to the increased need of tissues for oxygen, resulting in sympathetic hyperactivity. Optimal iron therapy can improve ANS consequences of IDA.

Patients with rheumatoid arthritis (RA) have a higher risk of cardiovascular disease (CVD) compared to the general population, which leads to increased morbidity and mortality. Inflammation is the key in RA and CVD. Our study aimed to refine cardiovascular (CV) risk assessment in RA patients by using carotid intima-media thickness (cIMT) as a marker of subclinical atherosclerosis. We also explored whether proinflammatory cytokines represented by tumor necrosis factor-alpha (TNF-α) and high-sensitivity cardiac troponin I (hs-cTnI), a biomarker of myocardial injury, could be correlated in RA patients. The study included 80 RA patients and 80 control subjects. TNF-α and hs-cTnI levels were measured. Subclinical atherosclerosis was evaluated by cIMT by means of carotid ultrasound. Disease activity score 28 (DAS28) was used to evaluate disease activity. hs-cTnI and TNF-α serum levels were higher in RA patients compared to controls (p=0.001). There was a significant difference in the median of cIMT between cases and controls (median (IQR) 0.9 (0.2) for cases, 0.7 (0.1) for controls, (p=0.001). A significant correlation was found between the level of TNF-α and hs-cTnI (p=0.002). Also, there was a significant correlation between the cIMT level and TNF-α and hs-cTnI (p=0.003 and p=0.002, respectively). Significant correlation was found between cIMT, TNF-α, and hs-cTnI in relation to the DAS28 score (p<0.001, p<0.001, and p=0.001, respectively). In conclusion, patients with RA are more likely to develop subclinical atherosclerosis, as reflected in increased cIMT. Higher levels of hs-cTnI in RA patients may correlate with the presence of occult cardiovascular disease. TNF-α and hs-cTnI correlations can reveal the interplay between disease activity and CVD. Thus, inflammation must be the primary target of various therapeutic approaches.

Background:Defining new predictive biomarkers in diabetic kidney disease (DKD) would provide a window of opportunity for preventive and/or therapeutic interventions to prevent or delay the onset of irreversible long-term micro and or macro vascular complications. Adiponectin (ADPN) has been variously associated with diabetic microvascular complications; however, no comprehensive clinical data exist examining the association between adipocytokines and the presence of these complications. Aim of study: we aimed to measure the plasma levels of adiponectin in patients with type 2 diabetes mellitus, to assess whether these levels vary with the different stages of DKD according to their e GFR and to evaluate its relation to their microvascular complications and glycemic control. Methods: This is a prospective observational study including 100 T2DM classified into two groups according to their albuminuria levels and estimated GFR. Participants subjected to thorough history taking and clinical examination. Serum level of ADPN was assessed in all patients. Results: Serum ADPN levels were significantly lower in T2DM patients with nephropathy (P = 0.001), while their levels were nonsignificantly higher in patients with non-proliferative retinopathy or neuropathy. Their levels were lowered with more advanced stages of DKD with nephropathy and the decrement was dependent on their severity (P<0.001). Levels of ADPN with cutoff value of < 22600 (μg/mL) had ability to diagnose microvascular complications in our diabetic patients with sensitivity (81%) and specificity (27%). Multivariate logistic regression analysis showed that the odds ratio for the presence of nephropathy in the lowest tertile of ADPN was 1.09 (95% CI; 11.45-13.08, P= 0.06), therefore, ADPN was not an independent risk factor for diabetic nephropathy. However, its higher level was independently associated with increased odds for the presence of neuropathy in particular. Conclusions: ADPN plays a role in the pathogenesis of microvasculopathy in diabetic patients and help to identify high-risk patients and modulate the therapeutic potential in the prevention of DKD.