[Show abstract][Hide abstract] ABSTRACT: Patent ductus arteriosus (PDA) is commonly seen in premature infants with low birth weights (LBW). It is a condition that has high mortality and morbidity rates. Early closure of the ductus arteriosus may require surgery or medical treatment. However, the decision of first medical approach for symptomatic PDA closure is still debated. In this study, we compared the surgical and medical treatments for the closure of PDA in premature LBW infants.
This study included 27 premature infants whose birth weights were lower than 1500 g, who were born in the period between 2011 and 2013 and had symptomatic PDA. Patients were separated into two groups: groups A and B. Group A included patients whose PDAs were closed with medical treatment (n = 16), and group B included patients who had undergone surgical operations for PDA closure (n = 11).
There were no statistically significant differences between groups A and B when the groups were compared in terms of birth weight, gestational age, respiratory distress syndrome (RDS), necrotizing enterocolitis (NEC), sepsis, intraventricular hemorrhage (IVH), retinopathy of prematurity (ROP), and pneumothorax. Although the mortality rate was determined to be lower in group B (2 out of 11, 18.1%) than in group A (7 out of 16, 43.7%), no statistically significant difference was found between the two groups. A statistically significant increase was determined in the incidence of kidney function loss in patient group that received Ibuprofen, a medical treatment, in comparison to the patients who had surgery.
In conclusion, surgery is a safe method to repair PDA in premature LBW infants. Although there is no remarkable difference between surgery and medical treatment, we suggest that a surgical approach may be used as a first choice to repair PDA considering the lower rate of mortality and morbidity and higher rate of closure compared to medical treatment.
Open journal of cardiovascular surgery. 01/2014; 7:1-4.
[Show abstract][Hide abstract] ABSTRACT: This study aimed to determine the frequency of Helicobacter pylori infections in children with phenylketonuria (PKU). Sixty-six children with PKU (35 boys, 31 girls; mean age, 8.2 ± 6.7 years) and 32 outpatient controls (15 boys, 17 girls; mean age, 9.6 ± 4.7 years) were studied. Socioeconomic factors did not differ between the two groups. The frequency of H. pylori infections was higher in patients with PKU (28.1%) than in healthy controls (9.4%). In particular, a higher frequency of infection was detected in patients with PKU with poor metabolic control (51.8%). The frequency of H. pylori infection in patients with PKU with good metabolic control was only 10.2%. There was no difference in the mean total WISC-R score between the poor and good metabolic control groups. A high frequency of H. pylori infection in children with PKU with poor metabolic control could be related to many factors. Advanced and standardized clinical studies on H. pylori infections in children with PKU are required.
Japanese journal of infectious diseases. 01/2013; 66(5):433-5.
[Show abstract][Hide abstract] ABSTRACT: BACKGROUND: Polymorphisms of plasminogen activator inhibitor-1 (PAI-1) and angiotensin-converting enzyme (ACE) genes have been implicated in susceptibility to asthma. In this study, we aimed to investigate whether there was any association between childhood asthma and polymorphisms of the PAI-1 and ACE genes. METHODS: Two hundred and three Turkish children aged 5-15 years, including 102 asthmatic patients and 101 healthy control subjects were included in this study. The asthma group was divided into two groups as follows: Group I: Asthmatic children with positive family history for atopy (n=53), Group II: Asthmatic children without any family history for atopy (n=49). One hundred and twenty-eight atopic family members were also included in the study. The insertion/deletion (I/D) polymorphism of the ACE and PAI-1 4G/5G gene polymorphisms was carried out by polymerase chain reaction. RESULTS: The prevalence of the PAI-1 4G allele was significantly greater in asthmatic children compared to control group (p<0.05, OR: 1.64 (1.11-2.43)) but there was no significant relation between ACE I/D genotypes and childhood asthma. No significant difference was detected between Groups I and II in terms of these ACE and PAI-1 genotypes and allele frequencies. No significant relationship was found between both gene polymorphisms and total serum IgE and skin prick test results. CONCLUSION: It has been established that PAI-1 4G allele may be a genetic risk factor for childhood asthma but ACE gene I/D polymorphisms do not play a role in the development of asthma in the sample of Turkish children.
Allergologia et Immunopathologia 02/2012; · 1.23 Impact Factor