Granulocyte Colony-Stimulating Factor for Gastrointestinal Perforation in Patients with Leukopenia
Leukopenia in the setting of widespread infection may predispose to sepsis, which is associated with a poor prognosis. Granulocyte colony-stimulating factor (G-CSF), which restores polymorphonuclear leukocyte function and count, has been shown to have protective effects in animal models of sepsis and burns. The aim of this retrospective study was to determine whether G-CSF can reduce the morbidity and mortality of gastrointestinal perforation with leukopenia.Patients and Methods
The studied subjects were 31 patients who had reduced leukocyte and neutrophil counts before undergoing surgery for gastrointestinal perforation, including six gastroduodenal, nine small intestinal, and 16 colonic perforations, from 1986 to 1994. The patients were divided into two groups: a G-CSF(+) group (n = 8) that received G-CSF subcutaneously (150 microg/day) during the perioperative period, and a G-CSF(-) group which did not.Main Results
No significant difference was found in the pre-operative and operative factors of the two groups. The postoperative increase in the leukocyte and polymorphonuclear cell counts of the G-CSF(+) group was significantly higher than that of the G-CSF(-) group (p < 0.01). Renal, hepatic, and gastrointestinal insufficiency was significantly less common in the G-CSF(+) group than in the G-CSF(-) group. The mean number of organs that failed was reduced from 4.00 +/- 2.50 in the G-CSF(-) group to 1.88 +/- 2.03 in the G-CSF(+) group. One of the eight patients who received G-CSF died of sepsis because of panperitonitis. In contrast, in the G-CSF(-) group, 15 of 23 patients died of sepsis because of panperitonitis. The cause-specific survival rate of the G-CSF(+) group was better than that of the G-CSF(-) group (p < 0.05).Conclusion
These results suggested that G-CSF reduced the morbidity and mortality of gastrointestinal perforation in patients with leukopenia and encouraged a prospective randomized study in future.