Influenza-B associated rhabdomyolysis and acute renal failure.

We present a 15 year old boy who developed severe rhabdomyolysis and acute renal failure following influenza B infection. His renal function was restored after appropriate therapy for rhabdomyolysis. Although rapidly progressive pneumonia, respiratory failure, and acute respiratory distress syndrome are the most common severe complications of influenza B infection, clinicians should be aware that influenza B may be complicated with rhabdomyolysis and acute renal failure in children.

Cerebral sinovenous thrombosis associated with mastoiditis due to recurrent otitis media.

Cerebral sinovenous thrombosis (CSVT) in childhood is a rare reported. In this era of widespread antibiotic use for acute otitis media, the incidence of otogenic CSVT has markedly declined but has not been completely prevented. The current therapies for CSVT include anticoagulation, thrombolysis, hydration, surgery, and supportive care that were based on adult studies, pediatric case studies, and expert opinion. We describe the case of a 3-year-old boy who presented with manifestations of CSVT associated with mastoiditis secondary to otitis media. He completed a 3-month course of combination antibiotic and anticoagulation therapy; the CSVT was recanalized, and the mastoiditis had partially improved.

The efficacy and safety of proton pump inhibitors vs histamine-2 receptor antagonists for stress ulcer bleeding prophylaxis among critical care patients: a meta-analysis.

OBJECTIVE: To examine the efficacy and safety of proton pump inhibitors in comparison with histamine-2 receptor antagonists for stress-related upper gastrointestinal bleeding prophylaxis among critical care patients. DATA SOURCES: PubMed, EMBASE, Cochrane Library, and ClinicalTrials.gov. STUDY SELECTION: Randomized, controlled trials that directly compare proton pump inhibitors with histamine-2 receptor antagonists in prevention of stress-related upper gastrointestinal bleeding in intensive care unit patients published before May 30, 2008. DATA EXTRACTION: Two reviewers independently applied selection criteria, performed quality assessment, and extracted data. The primary outcome was the incidence of stress-related upper gastrointestinal bleeding, and the secondary outcome measures were the incidence of pneumonia and intensive care unit mortality. DATA SYNTHESIS: The random effect model was used to estimate the pooled risk difference between two treatment arms irrespective of drug, dosage, and route of administration. RESULTS: We identified seven randomized, controlled trials with a total of 936 patients for planned comparison. The overall pooled risk difference (95% confidence interval; p value; I statistics) of stress-related upper gastrointestinal bleeding comparing proton pump inhibitors vs. histamine-2 receptor antagonists was -0.04 (95% confidence interval, -0.09-0.01; p = .08; I = 66%). In the sensitivity analysis, removing the Levy study significantly reduced the heterogeneity (from I = 66% to I = 26%) and shifted the overall risk difference closer to the null (pooled risk difference, -0.02; 95% confidence interval, -0.05-0.01; p = .19). There was no difference between proton pump inhibitors and histamine-2 receptor antagonists therapy in the risk of pneumonia and intensive care unit mortality, with pooled risk differences of 0.00 (95% confidence interval, -0.04-0.05; p = .86; I = 0%) and 0.02 (95% confidence interval, -0.04-0.08; p = .50; I = 0%), respectively. CONCLUSIONS: This meta-analysis did not find strong evidence that proton pump inhibitors were different from histamine-2 receptor antagonists in terms of stress-related upper gastrointestinal bleeding prophylaxis, pneumonia, and mortality among patients admitted to intensive care units. Because of limited trial data, future well-designed and powerful randomized, clinical trials are warranted.

Econazole-evoked [Ca2+]i rise and non-Ca2+-triggered cell death in rabbit corneal epithelial cells (SIRC).

The effects of econazole, an antifungal drug applied for treatment of keratitis and mycotic corneal ulcer, on cytosolic-free Ca(2+) concentrations ([Ca(2+)](i)) and viability of corneal cells was examined by using SIRC rabbit corneal epithelial cells as model. [Ca(2+)](i) and cell viability were measured by using the fluorescent dyes fura-2 and WST-1, respectively. Econazole at concentrations > or = 1 microM increased [Ca(2+)](i) in a concentration-dependent manner. The Ca(2+) signal was reduced partly by removing extracellular Ca(2+). The econazole-induced Ca(2+) influx was insensitive to L-type Ca(2+) channel blockers and protein kinase C modulators. In Ca(2+)-free medium, after pretreatment with 20 microM econazole, [Ca(2+)](i) rises induced by 1 microM thapsigargin (an endoplasmic reticulum Ca(2+) pump inhibitor) were abolished. Conversely, thapsigargin pretreatment also abolished econazole-induced [Ca(2+)](i) rises. Inhibition of phospholipase C with 2 microM U73122 did not change econazole-induced [Ca(2+)](i) rises. At concentrations between 10 and 80 microM, econazole killed cells in a concentration-dependent manner. The cytotoxic effect of 20 microM econazole was not reversed by prechelating cytosolic Ca(2+) with BAPTA. This shows that in SIRC cells econazole induces [Ca(2+)](i) rises by causing Ca(2+) release from the endoplasmic reticulum and Ca(2+) influx from unknown pathways. Econazole-caused cytotoxicity was independent from a preceding [Ca(2+)](i) rise.

Effects of antrodia camphorata on viability, apoptosis, and [Ca2+]i in PC3 human prostate cancer cells.

Antrodia camphorata (AC) has been used as a health supplement in Asia to control different cancers; however, the cellular mechanisms of its effects are unclear. The effect of AC on cultured human prostate cancer cells (PC3) has not been explored. This study examined the effect of AC on viability, apoptosis, mitogen-activated protein kinases (MAPKs) phosphorylation and Ca2+ handling in PC3 cells. AC at concentrations of 5-50 microg/ml did not affect cell viability, but at 100-200 microg/ml decreased viability and induced apoptosis in a concentration-dependent manner. AC at concentrations of 25-200 microg/ml did not alter basal [Ca2+]i, but at a concentration of 25 microg/ml decreased the [Ca2+]i increases induced by ATP, bradykinin, histamine and thapsigargin. ATP, bradykinin and histamine increased cell viability whereas thapsigargin decreased it. AC (25 microg/ml) pretreatment inhibited ATP-, bradykinin-, and histamine-induced enhancement on viability, but reversed thapsigargin-induced cytotoxicity. Immunoblotting showed that AC (200 microg/ml) did not induce the phosphorylation of ERK, JNK, and p38 MAPKs. Collectively, in PC3 cells, AC exerted multiple effects on viability and [Ca2+]i, caused apoptosis via pathways unrelated to [Ca2+]i signal and phosphorylation of ERK, JNK and p38 MAPKs.