ABSTRACT
OBJECTIVE: To analyze the clinical characteristics of the late-onset severe pneumonia after allogeneic hematopoietic stem cell transplantation (allo-HSCT). METHODS: A retrospective study was conducted in patients diagnosed as late-onset severe pneumonia after allo-HSCT from March, 2009 to January, 2013 in People's Hospital of Peking University. RESULTS: Of 1538 patients receiving allo-HSCT, 20 developed late-onset severe pneumonia with an incidence rate of 1.3%. Among the 20 patients, 17(85%) had human leukocyte antigen (HLA) identical donors. The other 3(15%) patients had received haplo-identical transplantation. Severe pneumonia occurred at a median time of 227(150-690) days after allo-HSCT. Blood gas tests showed that 14 patients (70%) had arterial oxygen lower than 60 mm Hg (1 mm Hg = 0.133 kPa). All patients had abnormal findings in chest X-ray or CT scan images, 18 (90%) of whom represented bilateral infiltrative lesions. None of the patients had evidence of active graft-versus-host disease before or during pneumonia. Eighteen patients did not respond to empiric antibiotics, neither did 8 patients to targeted medications who had positive pathogens by culture. Eleven patients died of respiratory failure and 9 survived. Six patients received donor lymphocyte infusion (DLI), 4 of whom obtained improvement of chest images and 3 survived till the end of follow-up. CONCLUSIONS: The late-onset severe pneumonia after allo-HSCT represents an aggressive behavior with poor prognosis. DLI might be an effective way to improve its outcome.
Subject(s)
Hematopoietic Stem Cell Transplantation/adverse effects , Pneumonia/epidemiology , Adolescent , Adult , Hematopoietic Stem Cell Transplantation/methods , Humans , Middle Aged , Retrospective Studies , Transplantation, Homologous , Young AdultABSTRACT
BACKGROUND: The protective effects of magnesium sulfate against ischemia-reperfusion injury of the small intestine in Sprague-Dawley (SD) rats have been confirmed in our previous research. However, its exact mechanism is unclear. This study was to evaluate the role of PI3K/Akt signal pathway in the protective effect of magnesium sulfate against ischemia-reperfusion injury of the small intestine in SD rats. METHODS: Rat model of intestinal ischemia-reperfusion injury was used. The SD rats were divided into four groups randomly: sham operation group, ischemia-reperfusion group, magnesium sulfate group and magnesium sulfate plus LY294002 (an inhibitor of PI3K) group. The pathological changes of intestinal mucosa were examined; the activity of diamine oxidase (DAO) in plasma, the plasma contents of malondialdehyde (MDA), and apoptosis rate of the intestinal mucosal cells were determined and compared. The expression of p-Akt was detected by Western blotting. RESULTS: There were more evident pathological changes of the intestinal mucosa (higher Chiu's score, P < 0.05), enhanced DAO activity (P < 0.05), elevated contents of MDA (P < 0.05), higher apoptosis rate (P < 0.05), and lower level of p-Akt (P < 0.05) in the ischemia-reperfusion group compared with the sham operation group. There were less evident pathological changes of the intestinal mucosa (lower Chiu's score, P < 0.05), lower DAO activity (P < 0.05), lower contents of MDA (P < 0.05), and lower apoptosis rate (P < 0.05), but higher level of p-Akt (P < 0.05) in the magnesium sulfate group compared with the ischemia-reperfusion group. There were more evident pathological changes of the intestinal mucosa (higher Chiu's score, P < 0.05), higher contents of MDA (P < 0.05), higher DAO activity (P < 0.05) and higher apoptosis rate (P < 0.05), and lower level of p-Akt (P < 0.05) in the magnesium sulfate plus LY294002 group compared with the magnesium sulfate group. CONCLUSIONS: Activation of PI3K/Akt signal pathway results in the reduction of cell apoptosis, which likely accounts for the protective effect of magnesium sulfate against intestinal ischemia-reperfusion injury.