Urinary sludge caused by ceftriaxone in a young boy

It is known that ceftriaxone administration is associated with biliary pseudolithiasis, although the development of urolithiasis has been rarely reported. We encountered a young male with bacterial meningitis complicated by urinary precipitates composed of ceftriaxone-calcium salt which is confirmed by high-performance liquid chromatography. This patient suggested that ceftriaxone significantly increased urinary excretion of calcium, which may be linked to ceftriaxone-related urolithiasis or sludge. It is therefore worthwhile to monitor the levels of urinary calcium to creatinine ratio in patients on ceftriaxone, as they may be at greater risk for developing large stones and renal damage

Oral immunotherapy combined with omalizumab for high–risk cow’s milk allergy : a randomized controlled trial

We evaluated the efficacy and safety of oral immunotherapy (OIT) combined with 24 weeks of omalizumab (OMB) at inducing desensitization in children with cow’s milk allergy (CM) compared with an untreated group. The present study was a prospective randomized controlled trial. Sixteen patients (age, 6–14 years) with high IgE levels to CM were enrolled in the present study. Patients were randomized 1:1 to receive OMB-OIT group or untreated group. The primary outcome was the induction of desensitization at 8 weeks after OMB was discontinued in OMB-OIT treated group and at 32 weeks after study entry. None of the 6 children in the untreated group developed desensitization to CM while all of the 10 children in the OIT-OMB treated group achieved desensitization (P < 0.001). A significantly decreased wheal diameter in response to a skin prick test using CM was found in the OMB-OIT treated group (P < 0.05). These data suggest that OIT combined with OMB using microwave heated CM may help to induce desensitization for children with high-risk CM allergy. This prospective randomized controlled trial was intended for 50 participants but was prematurely discontinued due to overwhelming superiority of OMB combined with microwave heated OIT over CM avoidance

A calcium-deficient diet in rat dams during gestation and nursing affects hepatic 11β-hydroxysteroid dehydrogenase-1 expression in the offspring.

BackgroundPrenatal malnutrition can affect the phenotype of offspring by changing epigenetic regulation of specific genes. Several lines of evidence demonstrate that calcium (Ca) plays an important role in the pathogenesis of insulin resistance syndrome. We hypothesized that pregnant female rats fed a Ca-deficient diet would have offspring with altered hepatic glucocorticoid-related gene expression and that lactation would modify these alterations.MethodologyWe determined the effects of Ca deficiency during pregnancy and/or lactation on hepatic 11β-hydroxysteroid dehydrogenase-1 (Hsd11b1) expression in offspring. Female Wistar rats consumed either a Ca-deficient (D: 0.008% Ca) or control (C: 0.90% Ca) diet ad libitum from 3 weeks preconception to 21 days postparturition. On postnatal day 1, pups were cross-fostered to the same or opposite dams and divided into the following four groups: CC, DD, CD, and DC (first letter: original mother's diet; second letter: nursing mother's diet). All offspring were fed a control diet beginning at weaning (day 21) and were killed on day 200 ± 7. Serum insulin and adipokines in offspring were measured using ELISA kits.Principal findingsIn males, mean levels of insulin, glucose, and Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) were higher in the DD and DC groups than in the CC group. We found no difference in HOMA-IR between the CC and CD groups in either males or females. Expression of Hsd11b1 was lower in male DD rats than in CC rats. Hsd11b1 expression in male offspring nursed by cross-fostered dams was higher than that in those nursed by dams fed the same diet; CC vs. CD and DD vs. DC. In females, Hsd11b1 expression in DC rats was higher than that in CC rats.ConclusionsThese findings indicated that maternal Ca restriction during pregnancy and/or lactation alters postnatal growth, Hsd11b1 expression, and insulin resistance in a sex-specific manner

Primer sequences used to amplify mRNA with real-time RT-PCR.

<p><i>Hsd11b1</i>, 11β-hydroxysteroid dehydrogenase 1; <i>Ppia</i>, Cyclophilin</p

A Calcium-Deficient Diet in Dams during Gestation Increases Insulin Resistance in Male Offspring

Calcium (Ca) plays an important role in the pathogenesis of insulin resistance syndrome. Osteocalcin (OC), a bone formation biomarker, acts directly on &#946;-cells and increases insulin secretion. We determined the effects of Ca deficiency during pregnancy and/or lactation on insulin resistance in offspring. Female Wistar rats consumed either a Ca-deficient or control diet ad libitum from three weeks preconception to 21 days postparturition. Pups were allowed to nurse their original mothers until weaning. The offspring were fed a control diet beginning at weaning and were killed on day 180. Serum carboxylated OC (Gla-OC) and undercarboxylated OC (Glu-OC), insulin and adipokines in offspring were measured. In males, mean levels of insulin, glucose, and HOMA-IR were higher in the Ca-deficient group than in the control group. In addition, ionized Ca (iCa) was inversely associated with serum Glu-OC and adiponectin in males. In females, mean levels of Glu-OC and Gla-OC in the Ca-deficient group were higher than in the control group. In all offspring, serum leptin levels were correlated with serum insulin levels, and inversely correlated with iCa. In conclusion, maternal Ca restriction during pregnancy and/or lactation influences postnatal offspring Ca metabolism and insulin resistance in a sex-specific manner

Hepatic mRNA expression levels of <i>Hsd11b1</i>.

<p>After delivery, foster mothers fed the same or different diets: CC, DD, CD, and DC (first letter: diet of original mother; second letter: diet of nursing mother). Data are represented as the means ± standard error. Statistically significant differences among the groups were determined with two-way analysis of variance (ANOVA), with diet and sex as the main factors. If interactions were found, the data were split and analyzed with one-way ANOVA. *P<0.05, **P<0.01.</p

Profile of male offspring on day 200.

<p>CC in which offspring of control-diet dams were nursed by control dams; DD in which offspring of Ca-deficient-diet dams were nursed by Ca-deficient-diet dams; CD in which offspring of control-diet dams were nursed by Ca-deficient-diet dams; and DC in which offspring of Ca-deficient-diet dams were nursed by control dams. No pups remained with their original birth mother; the pups in all groups came from different litters. BP: blood pressure</p><p>Statistically significant differences among the groups were determined with two-way analysis of variance (ANOVA) with diet and sex as the main factors. If interactions were found, the data were split, and a one-way ANOVA was performed. *P<0.05, **P<0.01 vs. CC.</p><p>Values are represented as means ± SE.</p

Ingredient composition of each diet fed to rats.

<p>1), 2) refer <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0084125#pone.0084125.s001" target="_blank">Table S1</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0084125#pone.0084125.s002" target="_blank">Table S2</a>.</p

Differential Diagnosis of Histiocytic Necrotizing Lymphadenitis and Malignant Lymphoma with Simple Clinical Findings

It is desirable that noninvasive differential diagnosis takes place without lymph node biopsy for histiocytic necrotizing lymphadenitis (HNL) or malignant lymphoma (ML). In this study, we propose a novel scoring model for the differential diagnosis of these diseases using clinical information and clinical findings. We retrospectively analyzed the data from 15 HNL and 13 ML pediatric patients. First, a univariate analysis identified 14 clinical factors with significant differences. Second, a subsequent analysis using receiver operating characteristic (ROC) curve analysis identified three factors among them with area under the ROC curve values of >0.95: body temperature (°C), maximum lymph node size (cm), and serum β2-microglobulin level (mg/L). Finally, the cut-off values of each of these three factors were determined and examined for the 28 cases. All 15 HNL cases were within 2–3 of the cut-off values among the three factors, no ML case was within two or more cut-off values. Thus, the diagnostic sensitivity and specificity of this novel scoring system were both 100%, indicating that clinical scoring with body temperature, maximum lymph node size, and β2-microglobulin are useful for distinguishing between HNL and ML