The relation between increased carotid intima-media thickness with fibrin monomers in obese children.

AIM: This study aimed to investigate the association between carotid intima-media changes that play a part in the atherosclerotic process in childhood obesity and fibrin monomers as an important indicator of fibrin plaque. METHODS: This is a cross-sectional study of obese children and non-obese healthy control subjects. Height, weight, body mass index, waist/hip ratio, systolic/diastolic blood pressures were recorded, in addition, biochemistry, haemogram, fibrin monomers and d-dimer were measured in both groups. Right and left common carotid intima-media thicknesses were measured by ultrasonography and mean carotid intima-media thickness was calculated. RESULTS: Obese children (n = 89, 46.1% girls, median age: 12.6 ± 2.3 years) and healthy control group (n = 40, 52.5% girls, median age: 13.2 ± 2.2 years) were comparable in terms of gender, age and puberty stage. Mean carotid intima-media thickness was higher in obese children than the healthy control group (P = .002). There was no difference between the two groups in terms of fibrin monomers and d-dimer levels. In obese children, there was a weak negative correlation between mean carotid intima-media thickness and fibrin monomers (P = .030, r = -0.233). CONCLUSION: In obese children, mean carotid intima-media thickness was determined higher, as an early indicator of atherosclerosis. We want to emphasise that obese children are at risk for cardiovascular disease and should be evaluated in terms of atherosclerosis. This study investigates the relation between increased carotid intima-media thickness and fibrin monomers, in children, the first time in Literature.

Characteristics of Children with Acute Carbon Monoxide Poisoning in Ankara: A Single Centre Experience.

The purpose of the study was to define characteristics of children with acute carbon monoxide poisoning. Eighty children hospitalized with acute carbon monoxide poisoning were recruited prospectively over a period of 12 months. Sociodemographic features, complaints and laboratory data were recorded. When the patient was discharged, necessary preventive measures to be taken were explained to parents. One month later, the parents were questioned during a control examination regarding the precautions that they took. The ages of the cases were between one month and 16 yr. Education levels were low in 86.2% of mothers and 52.6% of fathers. All families had low income and 48.8% did not have formal housing. The source of the acute carbon monoxide poisoning was stoves in 71.2% of cases and hot-water heaters in 28.8% of cases. Three or more people were poisoned at home in 85.1% of the cases. The most frequent symptoms of poisoning were headache and vertigo (58.8%). Median carboxyhemoglobin levels at admission to the hospital and discharge were measured as 19.5% and 1.1% (P < 0.001). When families were called for re-evaluation, it was determined that most of them had taken the necessary precautions after the poisoning incident (86.3%). This study determined that children with acute childhood carbon monoxide poisoning are usually from families with low socioeconomic and education levels. Education about prevention should be provided to all people who are at risk of carbon monoxide poisoning before a poisoning incident occurs.

Severe Clinical Course in a Patient with Congenital Amegakaryocytic Thrombocytopenia Due to a Missense Mutation of the c-MPL Gene.

Congenital amegakaryocytic thrombocytopenia (CAMT) generally begins at birth with severe thrombocytopenia and progresses to pancytopenia. It is caused by mutations in the thrombopoietin receptor gene, the myeloproliferative leukemia virus oncogene (c-MPL). The association between CAMT and c-MPL mutation type has been reported in the literature. Patients with CAMT have been categorized according to their clinical symptoms caused by different mutations. Missense mutations of c-MPL have been classified as type II and these patients have delayed onset of bone marrow failure compared to type I patients. Here we present a girl with severe clinical course of CAMT II having a missense mutation in exon 4 of the c-MPL gene who was admitted to our hospital with intracranial hemorrhage during the newborn period.