Background
Adenoviremia adversely affects prognosis in the post-hematopoietic stem cell transplant (HSCT) setting.
Methods
We sought to determine retrospectively the cutoff load of adenovirus in the stool as a predictor of adenoviremia, in children who underwent an allogeneic HSCT. The prevalence of sapovirus, norovirus and astrovirus in the stool was also studied.
Results
The study cohort consisted of 117 patients, of which 71 (60%) had diarrhea. Adenovirus was detected in the stool in 39 out of 71 (55%) patients. Age ≤ 10 years (P = 0.05; odds ratio, 2.57; 95% confidence interval: 0.98–6.75), and male sex (P = 0.04; odds ratio 2.67; 95% confidence interval: 1.02–6.99) increased risk for detection of adenovirus in stool on univariate analysis. Co-infections with enteric pathogens were infrequent. Viral load > 106 copies / gram stool predicted adenoviremia with a sensitivity and specificity of 82%. Sapovirus, norovirus, and astrovirus were detected in 3, 4 and one patient, respectively.
Conclusions
Quantitative detection of adenovirus in stool may have implications for pre-emptive therapy. Testing for other enteric viruses may have implications for infection control.
BackgroundMethylation at C-5 (5-mdC) of CpG base pairs, the most abundant epigenetic modification of DNA, is catalyzed by 3 essential DNA methyltransferases (Dnmt1, Dnmt3a and Dnmt3b). Aberrations in DNA methylation and Dnmts are linked to different diseases including cancer. However, their role in alcoholic liver disease (ALD) has not been elucidated.Methodology/Principal FindingsDnmt1 wild type (Dnmt1
+/+) and hypomorphic (Dnmt1
N/+) male mice that express reduced level of Dnmt1 were fed Lieber-DeCarli liquid diet containing ethanol for 6 weeks. Control mice were pair-fed calorie-matched alcohol-free liquid diet, and Dnmtase activity, 5-mdC content, gene expression profile and liver histopathology were evaluated. Ethanol feeding caused pronounced decrease in hepatic Dnmtase activity in Dnmt1
+/+ mice due to decrease in Dnmt1 and Dnmt3b protein levels and upregulation of miR-148 and miR-152 that target both Dnmt1 and Dnmt3b. Microarray and qPCR analysis showed that the genes involved in lipid, xenobiotic and glutathione metabolism, mitochondrial function and cell proliferation were dysregulated in the wild type mice fed alcohol. Surprisingly, Dnmt1
N/+ mice were less susceptible to alcoholic steatosis compared to Dnmt1
+/+ mice. Expression of several key genes involved in alcohol (Aldh3b1), lipid (Ppara, Lepr, Vldlr, Agpat9) and xenobiotic (Cyp39a1) metabolism, and oxidative stress (Mt-1, Fmo3) were significantly (P<0.05) altered in Dnmt1
N/+ mice relative to the wild type mice fed alcohol diet. However, CpG islands encompassing the promoter regions of Agpat9, Lepr, Mt1 and Ppara were methylation-free in both genotypes irrespective of the diet, suggesting that promoter methylation does not regulate their expression. Similarly, 5-mdC content of the liver genome, as measured by LC-MS/MS analysis, was not affected by alcohol diet in the wild type or hypomorphic mice.Conclusions/SignificanceAlthough feeding alcohol diet reduced Dnmtase activity, the loss of one copy of Dnmt1 protected mice from alcoholic hepatosteatosis by dysregulating genes involved in lipid metabolism and oxidative stress.
A 5-year-old healthy boy had a witnessed ingestion of hematite (iron oxide rock) at school. He had self-limited gagging and blood-tinged secretions. An X-ray showed a radiopaque foreign body measuring 3.5 cm by 2.2 cm in the right upper quadrant. Due to concern for iron toxicity, (1) an iron level was obtained about 3 hours after the ingestion and was 56 mg/dL, increasing to 97 mg/dL after 3 hours. The child remained asymptomatic but because of increasing iron levels with presumed risk for toxicity, the decision was made to proceed with endoscopy for removal. It was uncertain how rapidly iron could reach toxic levels as no similar cases were found in the literature. The hematite rock was successfully removed endoscopically with a Roth Net from the gastric fundus. No injuries to the stomach or esophagus were identified. Iron poisoning is a risk after iron ingestion. (1-3) However, it is unknown how rapidly the absorption occurs when an iron-containing foreign body is retained in the gastrointestinal tract. Our case evidences a rapid increase in iron levels by 1.7-fold in 3 hours, suggesting that the potential for iron poisoning does exist with the ingestion of hematite rocks (Figs. 1 and 2).
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