Serum Hepcidin Levels in Childhood-Onset Ischemic Stroke: A Case-Control Study.

Recently, hepcidin, an antimicrobial-like peptide hormone, has evolved as the master regulator of iron homeostasis. Despite the growing evidence of iron imbalance in childhood-onset ischemic stroke, serum hepcidin level in those patients has not yet been researched. In this study, we aimed to estimate serum (hepcidin) level in acute ischemic stroke (AIS) patients and to investigate whether subcutaneous enoxaparin sodium, which is a low-molecular-weight heparin (LMWH) derivative, could modulate serum hepcidin level in those patients. This was a case-control study included 60 (AIS) cases, and 100 healthy children with comparable age and gender as control group. For all subjects' serum hepcidin, interleukin-6 (IL-6), and soluble transferrin receptor [sTfR]) levels were assessed by (enzyme-linked immunosorbent assay [ELISA] method). Iron parameters including (serum iron, ferritin, transferrin, and total iron binding capacity [TIBC]) were also measured. The patients were subdivided according to treatment with an LMWH derivative into 2 groups and serum hepcidin levels were assessed initially and 1 week after stroke onset for all cases. We found that AIS cases had higher serum iron, ferritin, and IL6 levels compared to the control group (all P < 0.01). Serum hepcidin was significantly higher in AIS cases (median, 36[15-73]ng/mL) compared to the control group (median, 24[10-41]ng/mL; P < 0.01). On the 1st day of AIS diagnosis, serum hepcidin levels were similar in both stroke subgroups (P > 0.05). However, on the 7th day of diagnosis serum hepcidin level decreased significantly in AIS cases treated with LMWH (group 1) (median, 36 vs 21 ng/mL; P < 0.01, respectively). Meanwhile, no significant change was observed in serum hepcidin level in AIS cases not treated with LMWH (group 2) (P > 0.05). Serum hepcidin showed significant positive correlations with serum iron, transferrin saturation, ferritin, and IL6 (r = 0.375, P < 0.05; r = 0.453, P < 0.05; r = 0.687, P < 0.01; r = 0.515, P < 0.01; respectively). Our data brought a novel observation of elevated serum hepcidin level in pediatric AIS patients and pointed out that treatment with LMWH could modulate hepcidin level in those patients.

Novel Findings in Breath-Holding Spells: A Cross-Sectional Study.

The mechanism of breath-holding spells (BHS) is not fully understood and most probably multifactorial; so, this study was designed to clarify the pathophysiology of BHS through assessing some laboratory parameters and electrocardiographic (ECG) changes which might be contributing to the occurrence of the attacks. Another aim of the study was to evaluate the differences in the pathophysiology between pallid and cyanotic types of BHS. This was a prospective study performed in Zagazig University Hospitals. Seventy-six children diagnosed with BHS were included as follows: 32 children with cyanotic BHS, 14 children with pallid BHS, and 30 healthy children as a control group. All children were subjected to the following: full history taking, clinical examination, and laboratory work up in the form of CBC, serum iron, ferritin, and zinc levels. Twenty-four hours ambulatory ECG (Holter) recording was also performed. No significant statistical difference was found between cyanotic and pallid groups regarding family history of BHS, severity, and precipitating factors of the attacks. Frequent runs of respiratory sinus arrhythmia (RSA) during 24  hours ECG were significantly higher in children with BHS; the frequency of RSA was significantly correlated with the frequency (severity) of the attacks. Low serum ferritin was significantly associated with BHS groups but not correlated with the severity of the attacks. Autonomic dysregulation evidenced by frequent RSA is considered to be an important cause of BHS in children and is correlated with the frequency of the attacks. Low serum ferritin is additional factor in the pathophysiology. Both pallid and cyanotic BHS are suggested to be types of the same disease sharing the same pathophysiology.