Özlem Bekem

Hepatic glycogenosis: a rare cause of hepatomegaly in Type 1 diabetes mellitus

Hepatomegaly, with or without abnormal liver function tests, was a common feature of both pediatric and adult patients with diabetes mellitus. We are reporting a case of a 16-year-old diabetic boy in whom we found hepatomegaly, mildly elevated transaminases and elevated serum lipids never noticed before. Abdominal ultrasound confirmed hepatomegaly; liver biopsy pointed out a picture compatible with glycogenosis. The patients abnormal liver function tests, elevated serum lipids and hepatomegaly decreased over a period of 4 weeks with tight metabolic control. This situation was due to overinsulinization because the patient assumed an excessive quantity of food and therefore took an excessive quantity of insulin. In conclusion, hepatomegaly may be seen in diabetic patients due to hepatic glycogen accumulation as a result of excessive food and insulin consumption. In hepatic glycogenosis, the pathological findings improve in 4 weeks when good metabolic control is provided. Therefore, the other reasons must be investigated when hepatomegaly persists for a longer period.

Immunohistochemical evaluation of p53 expression and proliferative activity in children with Helicobacter pylori associated gastritis

Objectives: The aim of this study was to evaluate the significance of p53 expression and proliferative activity of glandular epithelium and intestinal metaplasia in Helicobacter pylori associated gastritis of pediatric patients. Methods: The study included endoscopic gastric biopsies of 54 children with dyspeptic complaints. Immunohistochemistry was performed for evaluation of p53 expression and Ki-67 labeling index, an indicator of proliferative activity. Grading of H. pylori density, intestinal metaplasia and inflammatory cell infiltration were performed in histologic tissue sections stained with hematoxylin-eosin, Giemsa and Alcian-blue. Results: Of 54 children, 35 (64%) were infected by H. pylori. Positive immunostaining for p53 was observed in 11 of 54 cases (20.4%). H. pylori infection was found in 10 (91%) of the p53-positive patients. There was a positive correlation between H. pylori density and Ki-67 labeling index in H. pylori infected children. H. pylori density, Ki-67 labeling index and inflammatory cell infiltration in the p53-positive group were significantly higher than in the p53-negative group. Although intestinal metaplasia was more common in H. pylori infected children (n = 11; 31.4%), there was no difference in the rate of intestinal metaplasia between the p53-positive and p53-negative groups. Conclusions: The present study shows that p53 mutations and higher proliferative activity of glandular epithelium may be related to H. pylori associated gastritis in children. Because p53 mutation does not appear to be associated with intestinal metaplasia, a precursor for gastric cancer in adults, we think that H.pylori associated p53 alterations do not initiate and promote gastric cancer that may occur in adulthood.

Resolution of Helicobacter pylori associated granulomatous gastritis in a child after eradication therapy

Granulomatous gastritis is a rare disease characterized by the presence of granulomas within the gastric mucosa or submucosa (1,2). Granulomatous gastritis is mainly found in association with Crohn disease, infections (e.g., tuberculosis, histoplasmosis, syphilis, teniasis) foreign bodies, sarcoidosis and underlying malignancy or vasculitis (1–4). Helicobacter pylori infection of the gastric mucosa is most frequently associated with chronic nonspecific gastritis in both adults and children (5,6). H. pylori infection may rarely be associated with other forms of gastritis, including the granulomatous type. This case is the first pediatric case of granulomatous gastritis that resolved completely after H. pylori eradication therapy.

Developmental Characteristics of Children Aged 1–6 Years With Food Refusal

OBJECTIVE The aim of this study was to compare the sociodemographic and developmental characteristics of children with food refusal and children with no history of feeding problems. DESIGN Cross-sectional case-control study. SAMPLE 30 children aged 1-6 years who were seen in the outpatient clinics for food refusal formed the case group, and 30 healthy children matched for age, sex, and socioeconomic status formed the control group. METHODS Anthropometric indices and early developmental characteristics of all the children in the study were evaluated and also their developmental levels were determined using the Ankara Developmental Screening Inventory. RESULTS The mean age of children with food refusal was 42.4+/-17.6 months, and the male/female ratio was 12/18. Children with food refusal had shorter mean breastfeeding durations and lower mean birth weights, body mass index, percentage height for age, and percentage weight for height values than those of the controls. There were no significant differences between the 2 groups in developmental delays. CONCLUSIONS These results suggest that food refusal may be related to lower birth weight and shorter breastfeeding duration. Further research with larger samples is needed to clarify these relationships and the effects of feeding problems on the growth and development of children.

Serum total and free carnitine levels in children with asthma

BackgroundSerum carnitine is decreased in recurrent pulmonary infections. We aimed to evaluate serum carnitine levels in asthmatic children.MethodsStudy group consisted of children with stable asthma and those with acute asthma attacks, while control group included healthy children. Attack severity was determined by the pulmonary score system. Total and free carnitine levels were studied in one blood sample from the control group and stable asthmatics and in two samples from children with acute asthma exacerbation during and after the attack.ResultsAll the 40 patients in the study group had moderate asthma including 30 with acute attack (13 mild and 17 moderate) and 10 with stable asthma. Carnitine levels were significantly lower in acute attack asthmatics than in the stable asthmatics and controls, while there was no significant difference between the latter two groups. Carnitine levels were not different between asthmatics with mild and moderate attack, and were similar during and after an acute attack.ConclusionsSerum carnitine levels decrease in children with moderate asthma during exacerbation of asthma and shortly thereafter. Further studies are needed to evaluate the effect of carnitine treatment on serum carnitine level.

Hepatoportal sclerosis in a child

Hepatoportal sclerosis (non-cirrhotic portal fibrosis) is characterised by portal hypertension, splenomegaly and variceal bleeding. It is rarely seen in childhood. We report on hepatoportal sclerosis in a patient with haematemesis as a presenting symptom. This 11-year-old male patient was admitted with upper gastrointestinal bleeding (UGB). He was observed for UGB for the first time at the age of 6 years at another hospital and was treated with sclerotherapy. Afterwards he had no bleeding from varices until admission to our hospital. At the age of 6 months, he had been admitted and treated with antibiotics and intravenous fluid because of diarrhoea. On physical examination, bodyweight and height were at the 10th–25th percentile, the spleen was enlarged (7 cm under the costal margin) but the liver was not palpable. Therewas no collateral circulation on the abdominal skin. On Doppler ultrasonography, the liver parenchyma was coarsely granular, periportal hyperechogenicity was detected, and the inferior vena cava and hepatic veins were patent.At the portal hilus, a vascular structure resembling cavernous transformation or a recanalised portal veinwas seen. The portal vein diameter was enlarged with multiple collaterals. Haemoglobin was 10.1 g/dl, leukocytes 4100/ mm, thrombocytes 145000/mm, prothrombin time 18 s (reference range 11–15 s), activated partial thromboplastin time 35 s (reference range 25–35 s), international normalised ratio (INR) 1.5, blood glucose, renal function (BUN 10 mg/dl, creatinine 0.6 mg/dl) and electrolytes