Severe adenovirus pneumonia requiring extracorporeal membrane oxygenation support--Serotype 7 revisited.

INTRODUCTION: Adenovirus causing severe fatal pneumonia has been well described in infants, children, and patients with immunocompromised function, but reports in previously healthy adults are rare. We report 3 cases of severe adenovirus pneumonia in whom conventional mechanical ventilation failed and required extracorporeal membrane oxygenation support. METHODS: Retrospective case records review of 3 patients admitted to the medical intensive care unit, Singapore General Hospital, a tertiary care university-affiliated hospital, with severe adenovirus pneumonia requiring extracorporeal membrane oxygenation support from February to March 2013. RESULTS: All 3 patients were previously healthy immunocompetent adults from the community with negative HIV serology. Duration prior to development of respiratory failure requiring intubation and invasive mechanical ventilation was 2, 8 and 3 days. Veno-venous extracorporeal membrane oxygenation (ECMO) support as rescue ventilation was instituted in all 3 patients after 2, 16, and 5 days of conventional mechanical ventilator support. Duration on ECMO support was 16, 22, and 9 days and mechanical ventilation was 18, 62, and 19 days respectively. Length of stay in intensive care unit was 18, 68, and 21 days, and length of stay in hospital was 20, 70, and 31 days respectively. Two of the 3 patients died. CONCLUSION: The mainstay of treatment for patients with severe adenovirus pneumonia is still supportive, with the use of antivirals not apparently effective. Whilst ECMO support for rescue ventilation may be considered, the outcomes do not appear as promising as other viral pneumonias, mirroring that previously described in the paediatric population.

Comparisons of norcantharidin cytotoxic effects on oral cancer cells and normal buccal keratinocytes.

Norcantharidin (NCTD) is the demethylated analogue of cantharidin. In this study, multi-parameter assessments of morphological alterations, clonogenic efficiency, cell growth curves, DNA synthesis, and DNA strand break were employed to determine and compare the cytotoxic effects of NCTD on oral cancer KB cell line and normal buccal keratinocytes. The results showed NCTD induced significant cytotoxicity in KB cells after 24 h of exposure. Normal buccal keratinocytes were more resistant to NCTD induced cytotoxicity. The IC(50) of 24 h NCTD treatment for KB and keratinocytes were 15.06 and 216.29 microg/ml, respectively with a keratinocyte/KB selective index of 14.36. Anoikis and membrane blebbing, morphological characterization of apoptosis, were observed in about 90% of KB cells after exposure to 100 microg/ml of NCTD for 24 h compared to about 30% in keratinocytes. In addition, inhibition of colony formation was noted in KB cells even when exposed to low concentration of drug (5 microg/ml) for a short period of time (6 h). NCTD inhibited subsequent cell proliferation in KB but growth of normal keratinocytes was retarded only temporarily. NCTD inhibited DNA synthesis in both KB and normal keratinocytes. However, keratinocytes were more sensitive to DNA synthesis inhibition by low dose of NCTD. Significant DNA strand break was noted in KB cells only after cell viability was reduced to less than 60% of the control. In comparison, normal keratinocytes were resistant to NCTD induced DNA strand break. These results indicated KB cells were more sensitive to NCTD induced cytotoxicity compared to normal keratinocytes. NCTD may be of value in treating oral cancers. The underlying mechanisms of the differential actions of NCTD on these two cell types are worthy of further investigations.