Significance of CD34/CD123 expression in detection of minimal residual disease in B-ACUTE lymphoblastic leukemia in children.

BACKGROUND: MRD is seen as the major cause of disease relapse. So, it gives important feedback about conventional treatment success and helps in selecting therapeutic alternatives. We aimed to compare the expression of CD34/CD123 on normal B-cell precursors in bone marrow ("hematogones") and on leukemic blasts in B-acute lymphoblastic leukemias (B-ALL) pediatric cases by flowcytometric analysis. Our study conducted on 20 children as a control and 30 B-ALL children cases at diagnosis and after 28days of induction therapy. We found that the less mature hematogones (dim CD45+) that express CD34 lack CD123 expression, whereas the more mature hematogones (moderate CD45+) lack CD34 but always express CD123. In contrast with this discordant pattern of CD34 and CD123 expression in hematogones, blasts in 24 of 30 cases (80%) of B-ALL showed concordant expression pattern of the 2 antigens: 63% (19 of 30) cases expressed both antigens, whereas 17% (5 of 30) expressed neither. Our study concluded that these distinct patterns of CD34/CD123 expression on hematogones (discordant) and B-ALL blasts (concordant) are useful in differentiating small populations of residual blasts from hematogones after induction therapy to detect MRD.

Iron deficiency anemia as a risk factor for cerebrovascular events in early childhood: a case-control study.

In recent years, iron-deficiency anemia (IDA) has been suggested to have an association with childhood-onset ischemic stroke in otherwise healthy children, but few cases have proven it thus far. In this study, we aimed to investigate whether iron-deficiency anemia is a risk factor for cerebrovascular events and childhood-onset ischemic stroke in previously healthy children. This was a case-control study that included 21 stroke cases with patients who had previously been generally healthy, and matched with age and gender of 100 healthy control subjects. Patients were included if a diagnosis of definite stroke had been made and other known etiologies of childhood onset stroke were excluded. For all subjects, iron parameters including serum iron, ferritin, transferrin, total iron binding capacity, and transferrin saturation were assessed. We screened all case patients for prothrombotic factors including level of hemoglobin S, protein C, protein S, antithrombin III, lupus anticoagulant, factor V Leiden, and prothrombin gene mutation (G20210A). Brain magnetic resonance images (MRI), magnetic resonance angiography (MRA), and magnetic resonance venography (MRV) were performed to all case patients. All case patients have normal results regarding functional, immunological, and molecular assay for prothrombotic factors screening. Our results showed that IDA was disclosed in 57.1 % of stroke cases with no identified cause, as compared to 26 % of controls. Our study suggest that previously healthy children who developed stroke are 3.8 times more likely to have IDA than healthy children, who do not develop stroke (OR, 3.8; 95 % CI:1.3-11.2 P = 0.005). In addition, there was significant interaction between IDA and thrombocytosis among studied cases (OR, 10.5; 95 % CI, 1.0-152 P = 0.02). There were nonsignificant differences between stroke patients with IDA and those with normal iron parameters regarding stroke subtype (P > 0.05). Public health messages on the importance of early detection of iron-deficiency anemia in young children, especially in our developing countries so that it can be treated before a life-threatening complication like stroke develops.

Serum hepcidin levels in Helicobacter pylori-infected children with iron-deficiency anemia: a case-control study.

Recently, hepcidin, an antimicrobial-like peptide hormone, has evolved as the master regulator of systemic iron homeostasis. Hepcidin integrates signals from diverse physiological inputs, forming a key connection between iron trafficking and response to infection. In this study, we aimed to investigate whether Helicobacter pylori infection modulates serum hepcidin level and response to oral iron therapy in children with iron-deficiency anemia. This was a case-control study including 60 children with iron-deficiency anemia (IDA; 30 H. pylori infected and 30 H. pylori noninfected) and 30 healthy children with comparable age and gender as the control group. Iron parameters including serum iron, ferritin, transferrin, total iron binding capacity, and transferrin saturation and serum hepcidin levels were assessed initially and after 3 months of oral iron therapy for IDA. Compared to the control group, serum hepcidin was significantly lower in H. pylori-noninfected children with IDA (P < 0.01) and significantly higher in H. pylori-infected children with IDA (P < 0.01). Hepcidin increased significantly in noninfected children with IDA after 3 months of oral iron therapy (P < 0.01). On the other hand, H. pylori-infected children showed nonsignificant change in hepcidin level after oral iron therapy (P > 0.05). Although hepcidin showed significant positive correlations with serum ferritin, hemoglobin (Hb), iron, and transferrin saturation in noninfected children with IDA (P < 0.01), it showed significant negative correlations with serum ferritin, Hb, iron, and transferrin saturation in H. pylori-infected children with IDA (P < 0.05). H. pylori infection upregulates serum hepcidin levels and was associated with diminished response to oral iron therapy in children with iron-deficiency anemia.

Serum trace elements in obese Egyptian children: a case-control study.

BACKGROUND: To date, only a few studies on child obesity concerned Trace Elements (TE). TE is involved in the pathogenesis of obesity and obesity related diseases. We tried to assess trace elements status [zinc (Zn), copper (Cu), selenium (Se), iron (Fe), and chromium (Cr)] in obese Egyptian children and their relationships with serum leptin and metabolic risk factors of obesity. METHODS: This was a case-control study performed with 80 obese children (BMI ≥ 95thcentile for age and gender) and 80 healthy non-obese children with comparable age and gender as the control group. For all subjects, serum Zn, Cu, Se, Fe, ferritin and Cr as well as biochemical parameters including lipid profile, serum glucose and homeostasis model assessment of insulin resistance (HOMA-IR) were assessed. Levels of serum leptin were measured by (enzyme-linked immunosorbent assay [ELISA] method), and serum insulin was measured by an electrochemiluminesce immunoassay. RESULTS: Compared to the control group, serum Zn, Se, and Fe levels were significantly lower (all P < 0.01) and serum Cu level was significantly higher (P < 0.01) in the obese children. Meanwhile, no significant differences were observed in serum ferritin or Cr levels (P > 0.05). A significant negative correlation was found between serum leptin and zinc levels in the obese children (r = -0.746; P < 0.01). Further, serum Zn showed significant negative correlations with total cholesterol TC levels (P < 0.05) and were positively correlated with high density lipoprotein- cholesterol HDL-C levels (P < 0.01) in the obese children. In addition, serum Se levels showed significant positive correlations with HOMA-IR values in the obese children (P < 0.01). CONCLUSION: The obese children may be at a greater risk of developing imbalance (mainly deficiency) of trace elements which may be playing an important role in the pathogenesis of obesity and related metabolic risk factors.

Vitamin D status in diabetic Egyptian children and adolescents: a case-control study.

BACKGROUND: Recently, studies suggesting that vitamin D deficiency correlates with the severity and frequency of Type 1 (insulin-dependent) diabetes mellitus (T1DM) and that vitamin D supplementation reduces the risk of developing T1DM have been reported. OBJECTIVE: In this study, we aimed to assess vitamin D status in Egyptian children and adolescents with T1DM. METHODS: This was a case-control study including 80 T1DM diagnosed cases aged 6 to 16 years and 40 healthy children with comparable age and gender as the control group. For all subjects, serum 25 (OH) D levels were measured by ELISA, Serum parathyroid hormone (PTH) and serum insulin were measured by an electrochemiluminesce immunoassay. Serum glucose, Glycosylated hemoglobin (HbA1c) levels and homeostasis model assessment of insulin resistance (HOMA-IR) were also assessed. RESULTS: Compared to the control group, serum vitamin D levels were not significantly lower in diabetic subjects (24.7 ± 5.6 vs 26.5 ± 4.8 ng/ml; P > 0.05). Among diabetic cases 44(55%) were vitamin D deficient; meanwhile 36(45%) cases had normal vitamin D level (P < 0.01). In addition, 26(32.5%) diabetic cases had 2ry hyperparathyroidism and 54(67.5%) cases had normal parathyroid hormone level; meanwhile, none of the control group had 2ry hyperparathyroidism (P < 0.01). Furthermore, we found a significant difference between vitamin D deficient diabetic cases and those with normal vitamin D level as regards HOMA-IR and diabetes duration (P < 0.01). CONCLUSION: Public health message on the importance of vitamin D status; especially in diabetic children and adolescents, should be disseminated to the public.