BackgroundMalnutrition is a common cause of morbidity and mortality in children with congenital heart disease (CHD). This study aimed to identify prevalence and predictors of malnutrition in Egyptian children with symptomatic CHD.MethodsThis case–control study included 100 children with symptomatic CHD (76 acyanotic and 24 cyanotic) and 100 healthy children matched for age and sex as a control group. Clinical Evaluation and Laboratory Assessment of Nutritional Status were documented. Anthropometric measurements were recorded and Z scores for weight for age (WAZ), weight for height (WHZ), and height for age (HAZ) have been calculated. Malnutrition was defined as weight, height, and weight/height Z score ≤–2.ResultsThe overall prevalence of malnutrition was 84.0% in patients with CHD and 20% in controls. Severe malnutrition was diagnosed in 71.4% of cases. All anthropometric measurements and levels of biochemical markers of nutritional state were significantly lower in the patients group compared to controls. In patients with acyanotic CHD, stunting was proportionately higher (57.89%) than in cyanotic CHD, while wasting was predominant (45.83%) in the latter. Malnutrition correlated significantly with low hemoglobin level, low arterial oxygen saturation, heart failure, pulmonary hypertension, and poor dietary history.ConclusionMalnutrition is a very common problem in children with symptomatic CHD and predicted by the presence of low hemoglobin level, low arterial oxygen saturation, heart failure, poor dietary history, and pulmonary hypertension.

The aim of this work is to study the incidence of acute kidney injury (AKI) in neonates admitted to the neonatal intensive care unit (NICU) over a six-month period from September 2011 to March 2012. This prospective study was performed on 250 neonates admitted to the NICU at the Children's Hospital, Faculty of Medicine, Zagazig University. All neonates were subjected to detailed history taking, including pre-natal, natal and post-natal history, with stress on symptoms suggestive of AKI. All neonates were examined thoroughly and the following investigations were performed: Blood urea nitrogen (BUN), serum creatinine, sodium, potassium, calcium, complete blood count, C-reactive protein, arterial blood gases, urine sodium and urine creatinine. AKI was diagnosed in 27 cases (10.8%), including 12 females and 15 males. 40.7% of the AKI cases were born after full-term pregnancy while 59.3% were pre-term babies. 29.6% of the AKI cases had oliguria, and there was male sex predominance, with a male-female ratio of 1.3:1. The cause of AKI was pre-renal in 96.3% and intrinsic renal in 3.7% of the cases. The predisposing factors for AKI were sepsis in 63% of the cases, respiratory distress syndrome in 55.6%, mechanical ventilation in 51.9%, peri-natal asphyxia in 18.5%, dehydration in 14.8%, surgical operation in 11.1%, congenital heart disease in 7.4%, sub-galeal hematoma in 3.7%, polycythemia in 3.7% and intra-ventricular hemorrhage in 3.7% of the cases. Our data suggest that pre-renal failure was the most common form of AKI in our patients. Early recognition of risk factors such as sepsis, peri-natal asphyxia or peri-operative problems and rapid effective treatment of contributing conditions will reduce the incidence of AKI in the neonatal period.

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Iron overload causes most of the mortality and morbidity associated with thalassemia. Excess iron deposits primarily in the liver, but once a threshold level is reached, iron loading may occur in other tissues such as the heart. Magnetic resonance imaging is a well established technique to noninvasively quantify myocardial and liver iron content. More than 300 disease-causing mutations have been identified. We aimed to determine the impact of genotype on liver iron content in patients with beta thalassemia. Cross sectional study was carried on 73 patients with beta thalassemia. MRI liver and heart was performed to determine hepatic and myocardial iron overload. Genotyping was determined by DNA sequencing technique. The mean liver iron content was 17.4 mg/g dw and mean cardiac T2* was 25.5 ms in our patients. Patients with b 0 b 0 were associated with significantly higher liver and myocardial iron content compared to those with b 0 b ? and b ? b ? genotypes. There was a clear association between genotype and both hepatic and myocardial iron overload. Patients with b 0 b 0 had significantly higher liver and heart iron content compared to those with b 0 b ? and b ? b ? genotypes. Liver iron content was strongly correlated to serum ferritin levels and myocardial iron overload.

In beta thalassemia, the degree of globin chain imbalance is determined by the nature of the mutation of the β-gene. β° refers to the complete absence of production of β-globin on the affected allele. β+ refers to alleles with some residual production of β-globin. The homozygous state results in severe anemia that necessitates regular blood transfusion. On the other hand, frequent blood transfusion can lead to iron overload resulting in progressive dysfunction of the heart, Liver as well as multiple endocrinopathies. We studied the impact of genotype on the development of disease complications in patients with β thalassemia. A Cross sectional study was carried on 73 patients with beta thalassemia. Genotyping was determined by DNA sequencing technique. Routine investigations as well as MRI liver and heart were performed to assess iron overload. We found that β+β+ was the most common genotype in our patients followed by β°β° and β°β+. Mean Liver iron content (LIC) was significantly higher in β°β° compared to β°β+ and β+β+ genotypes and mean cardiac T2* was significantly lower in β°β° compared to β°β+ and β+β+ genotypes. Hepatic complications, hepatitis C, cardiac complications and some endocrinopathies were significantly higher in patients with β°β° genotype compared to other genotypes which explain the role of the underlying genetic defect in thalassemia patients in development of disease complications.