Procalcitonin is a predictor for high-grade vesicoureteral reflux in children: meta-analysis of individual patient data.

OBJECTIVE: To assess the predictive value of procalcitonin, a serum inflammatory marker, in the identification of children with first urinary tract infection (UTI) who might have high-grade (≥3) vesicoureteral reflux (VUR). STUDY DESIGN: We conducted a meta-analysis of individual data, including all series of children aged 1 month to 4 years with a first UTI, a procalcitonin (PCT) level measurement, cystograms, and an early dimercaptosuccinic acid scan. RESULTS: Of the 152 relevant identified articles, 12 studies representing 526 patients (10% with VUR ≥3) were included. PCT level was associated with VUR ≥3 as a continuous (P = .001), and as a binary variable, with a 0.5 ng/mL preferred threshold (adjusted OR, 2.5; 95% CI, 1.1 to 5.4). The sensitivity of PCT ≥0.5 ng/mL was 83% (95% CI, 71 to 91) with 43% specificity rate (95% CI, 38 to 47). In the subgroup of children with a positive results on dimercaptosuccinic acid scan, PCT ≥0.5 ng/mL was also associated with high-grade VUR (adjusted OR, 4.8; 95% CI, 1.3 to 17.6). CONCLUSIONS: We confirmed that PCT is a sensitive and validated predictor strongly associated with VUR ≥3, regardless of the presence of early renal parenchymal involvement in children with a first UTI.

Prediction of high-grade vesicoureteral reflux after pediatric urinary tract infection: external validation study of procalcitonin-based decision rule.

BACKGROUND: Predicting vesico-ureteral reflux (VUR) ≥3 at the time of the first urinary tract infection (UTI) would make it possible to restrict cystography to high-risk children. We previously derived the following clinical decision rule for that purpose: cystography should be performed in cases with ureteral dilation and a serum procalcitonin level ≥0.17 ng/mL, or without ureteral dilatation when the serum procalcitonin level ≥0.63 ng/mL. The rule yielded a 86% sensitivity with a 46% specificity. We aimed to test its reproducibility. STUDY DESIGN: A secondary analysis of prospective series of children with a first UTI. The rule was applied, and predictive ability was calculated. RESULTS: The study included 413 patients (157 boys, VUR ≥3 in 11%) from eight centers in five countries. The rule offered a 46% specificity (95% CI, 41-52), not different from the one in the derivation study. However, the sensitivity significantly decreased to 64% (95%CI, 50-76), leading to a difference of 20% (95%CI, 17-36). In all, 16 (34%) patients among the 47 with VUR ≥3 were misdiagnosed by the rule. This lack of reproducibility might result primarily from a difference between derivation and validation populations regarding inflammatory parameters (CRP, PCT); the validation set samples may have been collected earlier than for the derivation one. CONCLUSIONS: The rule built to predict VUR ≥3 had a stable specificity (ie. 46%), but a decreased sensitivity (ie. 64%) because of the time variability of PCT measurement. Some refinement may be warranted.

Plasma ghrelin levels in various stages of development of iron deficiency anemia.

OBJECTIVES: Ghrelin stimulates food intake and induces metabolic changes leading to an increase in body weight and body fat mass. Iron-deficiency anemia (IDA) is the most frequently seen cause of nutritional anemia, that is a type of starvation. There is no available study related to levels of ghrelin in IDA. The aim of this study is to show an association with ghrelin levels and iron deficiency and to demonstrate whether changes seen in iron deficiency (ID) are explained by ghrelin, as opposed to whether ghrelin levels correlate with ID. MATERIALS AND METHODS: The study group was consisted of children who were admitted in the outpatient clinic of pediatrics. Control group (C) was defined as cases with normal hemoglobin (Hb), serum iron (SI), transferrin saturation (TS), and ferritin (F) (>12 ng/mL) values; group hypoferritinemia (IDec) Hb: N, SI: N, TS: N, F<12 ng/mL; group iron deficiency (IDef), Hb: N, SI: decreased, TS

Proinflammatory cytokines and leptin are increased in serum of prepubertal obese children.

It has not yet been shown in prepubertal children how cytokines, leptin, and body mass, as well as parameters of obesity are interrelated. The aim of this study was to explore the relation between circulating levels of some cytokines with leptin and body mass index. A case control study was carried out in obese children of both sexes. An obese group was carried out with 63 school prepubertal children and a control group comprised the same number of nonobese children paired by age and by sex. Mean serum leptin concentration was significantly higher in the obese children at 19.9 +/- 7.4 ng/mL, than the control group (7.9 +/- 5.1 ng/mL). Serum IL-1beta, IL-6, and TNF-alpha levels were also significantly higher in the obese group than controls (33.0 +/- 8.9, 45.2 +/- 11.8, and 9.2 +/- 2.3 pg/mL, versus 3.6 +/- 1.0, 13.1 +/- 3.9, and 3.9 +/- 1.0 pg/mL, resp). In controversy, serum IL-2 level was diminished in the obese group as 0.4 +/- 0.1 versus 0.9 +/- 0.1 U/L. Obesity may be a low-grade systemic inflammatory disease. Obese prepubertal children have elevated serum levels of IL-1beta , IL-6, and TNF-alpha which are known as markers of inflammation.

Acute hemorrhagic leukoencephalitis manifesting as intracerebral hemorrhage associated with herpes simplex virus type I.

Acute hemorrhagic leukoencephalitis (AHL) is a rare and usually fatal disorder characterized by an acute onset of neurological abnormalities. It may occur in association with a viral illness or vaccination. Radiology and brain biopsy are essential for the diagnosis. We present a case of AHL mimicking or manifesting as intracerebral hemorrhage associated with herpes simplex virus. A 3-year-old boy was admitted to our hospital with cerebral hemorrhage. The findings of cerebrospinal fluid, MRI and electroencephalogram indicated acute hemorrhagic leukoencephalitis associated with herpes simplex virus involving the left parietal cortex (hemorrhage) and the right temporal lobe (encephalitis). The patient received intravenous dexamethasone (1.5 mg/kg/24 h divided q6 (six times a day) for 5 days, tapered slowly to discontinuation over the next 5 days) and aciclovir (15 mg/kg/every 6 h for 14 days). His clinical condition markedly improved, and after 3 weeks he was discharged from the hospital with moderate right hemiparesis. Mild hemiparesis with normal psychometric testing was determined when he was checked 6 months later. AHL remains misdiagnosed as viral encephalitis because it produces different protean clinical forms. Pediatric patients admitted with cerebral hemorrhage and infarct should be evaluated for presence of hemorrhagic encephalitis-causing agents, especially for herpes simplex. Since, as in our case, treatment with corticosteroid and acyclovir markedly improves conditions of herpes simplex-caused AHL, we suggest that early diagnosis and treatment is of importance for the prognosis.