PubMed · 15249432
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Thomas L Higgins. 2004. Timing is everything.. https://doi.org/10.1378/chest.126.1.4
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BACKGROUND: Even when treated with antiviral therapy, cytomegalovirus pneumonia (CMVp) is associated with high morbidity and mortality in immunocompromised patients. CMVp has been rarely reported in patients with lymphoma. METHODS: The authors reviewed the records of patients treated at The University of Texas M. D. Anderson Cancer Center (Houston, TX) between 1997 and 2003. Collected information included demographics, use of chemotherapy, or corticosteroids, concomitant infections, and outcome. RESULTS: Thirty-one patients with lymphoma with 36 episodes of CMVp were identified. The incidence of CMVp increased between 1997 and 2003 (0 of 1000 treated patients vs. 9 of 1000 treated patients; P = 0.07). Most episodes occurred in patients with non-Hodgkin lymphoma (89%). Most of the patients (92%) had received chemotherapy and corticosteroids (89%) before the onset of CMVp. Concomitant CMV antigenemia was detected in 11 (41%) of the 27 episodes in which testing was performed. In 19 episodes (53%), patients had coinfections within 90 days of the episode of CMVp. Coinfections were present at the onset of CMVp in 11 episodes (31%). The yield for CMV in bronchoalveolar lavage (BAL) specimens was higher with culture methods than with cytologic evaluation or immunohistochemical staining (P < 0.001). The number of CMV antigenemia tests performed increased fourfold over the study period. The CMV-attributed mortality rate was 30% (9 of 30 patients). Independent predictors of death by multivariate Cox regression analysis were high APACHE II score (> 16) at onset of CMVp (P = 0.02, hazards ratio [HR] = 15.5, 95% confidence interval [CI], 1.5-163.7), and development of toxicity to antivirals (P = 0.04, HR = 14.03, 95% CI, 1.2-169.1). CONCLUSIONS: The incidence of CMVp in patients with lymphoma is increasing. CMV detection in BAL specimens was better with culture methods than with cytologic or immunohistochemical methods. High APACHE II score and development of antiviral toxicity were associated with a fatal outcome.
OBJECTIVE: Shock induces oxidative stress by ischemia-reperfusion phenomenon. Endothelial cells are involved in the inflammatory response and oxidative stress responsible for microcirculation impairment and organ failure. We examined the potential of serum from patients to induce in vitro reactive oxygen species production by cultured human umbilical vein endothelial cells (HUVECs). PATIENTS: Three groups were compared: hemorrhagic shock trauma patients, isolated brain injured patients, and healthy volunteers. METHODS: In the hemorrhagic shock group we sought a correlation between reactive oxygen species production and severity of shock. Serum was separated and perfused in an in vitro model of perfused HUVECs. Ex vivo reactive oxygen species production was assessed by fluorescence microscopy using dichlorodihydrofluorescein, an intracellular dye oxidized by H2O2. Results are expressed in proportional change from baseline and normalized by protidemia to control for variation related to hemodilution. RESULTS: Reactive oxygen species production by endothelial cells exposed to serum from hemorrhagic shock patients (46.2+/-24.9%) was significantly greater than in those with brain injury (3.9+/-35.1%) and in healthy volunteers (-6.8+/-5.8%). In the hemorrhagic shock group dichlorodihydrofluorescein fluorescence was strongly correlated positively to Simplified Acute Physiology Score II and lactatemia and negatively to [HCO3-]. CONCLUSIONS: Serum from trauma patients with hemorrhagic shock induces reactive oxygen species formation in naive endothelial cells which is correlated to shock severity.
The innate recognition of microbial components and subsequent activation of cytokine network are important in the pathophysiology of sepsis. Recently, functional gene polymorphisms in molecules associated with these responses were demonstrated. On the other hand, it has been claimed that there are ethnic differences in genetic polymorphisms. This study investigated toll-like receptor (TLR) 4, CD14, tumor necrosis factor (TNF)-alpha and -beta, and interleukin (IL)-10 gene polymorphisms in 197 Japanese critically ill patients and 214 healthy control subjects to evaluate the influence of these polymorphisms on clinical outcome. No Japanese participant carrying TLR4Asp299Gly or Thr399Ile was detected. No association of CD14-159C/T polymorphisms with genotype frequency or sepsis mortality was observed. Frequency of TNF-alpha-308 GA genotype was significantly higher in the sepsis group than in the control group and TNF-alpha-308GA and IL-10-592CC genotypes were related to poor outcome of sepsis. Ethnic differences in genetic variations are very important issues and the frequencies in this study differ from those previously reported in Caucasians. In conclusion, this study may indicate that TNF-alpha-308G/A and IL-10-592C/A polymorphisms involved in subsequent activation of cytokine network had a larger effect on clinical outcome in patients with sepsis than TLR4Asp299Gly, Thr399Ile, and CD14-159C/T polymorphisms associated with the initial host-microbial interaction.