Using Digestive Fluid Biomarkers to Predict Acute Gastrointestinal Injury in Critically Ill Patients: A Pilot Study

2018 ◽  
Vol 27 (6) ◽  
pp. 504-507
Author(s):  
Cheng Minhua ◽  
Gao Tao ◽  
Xi Fengchan ◽  
Yu Wenkui

Background Acute gastrointestinal injury is associated with significantly increased mortality in critically ill patients. However, markers for measuring acute gastrointestinal injury are neither sensitive nor specific. Objective To determine whether enzymes in digestive fluid are predictive of the severity of acute gastrointestinal injury. Methods A prospective observational study was conducted between June 2015 and December 2015 in a surgical intensive care unit. Enrolled patients were classified by acute gastrointestinal injury grade according to the 2012 European Society of Intensive Care Medicine system. Digestive fluid was collected through nasointestinal tubes and analyzed 24 hours after the diagnosis of acute gastrointestinal injury. Intestinal markers of injury (pH, interleukin 6, interleukin 10, tumor necrosis factor α, and secretory immunoglobulin A) were measured in digestive fluid. Results Of the 76 patients included, acute gastrointestinal injury was grade I in 41, grade II in 20, grade III in 8, and grade IV in 7. Secretory immunoglobulin A was an independent predictor of grade III acute gastrointestinal injury. When data from patients with grades I and II injury and patients with grades III and IV injury were grouped together, analysis revealed that pH, interleukin 10, and secretory immunoglobulin A were independent predictors of acute gastrointestinal failure. Conclusions Secretory immunoglobulin A was predictive of grade III acute gastrointestinal injury. Digestive fluid markers of injury (pH, interleukin 10, and secretory immunoglobulin A) were predictors of acute gastrointestinal failure. Further study is required to determine if other markers are specific or sensitive for acute gastrointestinal injury.

Author(s):  
Claudia Seikrit ◽  
Oliver Pabst

AbstractAntibodies are key elements of protective immunity. In the mucosal immune system in particular, secretory immunoglobulin A (SIgA), the most abundantly produced antibody isotype, protects against infections, shields the mucosal surface from toxins and environmental factors, and regulates immune homeostasis and a peaceful coexistence with our microbiota. However, the dark side of IgA biology promotes the formation of immune complexes and provokes pathologies, e.g., IgA nephropathy (IgAN). The precise mechanisms of how IgA responses become deregulated and pathogenic in IgAN remain unresolved. Yet, as the field of microbiota research moved into the limelight, our basic understanding of IgA biology has been taking a leap forward. Here, we discuss the structure of IgA, the anatomical and cellular foundation of mucosal antibody responses, and current concepts of how we envision the interaction of SIgA and the microbiota. We center on key concepts in the field while taking account of both historic findings and exciting new observations to provide a comprehensive groundwork for the understanding of IgA biology from the perspective of a mucosal immunologist.


2000 ◽  
Vol 68 (9) ◽  
pp. 5068-5074 ◽  
Author(s):  
Sara M. Dann ◽  
Pablo C. Okhuysen ◽  
Bassam M. Salameh ◽  
Herbert L. DuPont ◽  
Cynthia L. Chappell

ABSTRACT This study examined the intestinal antibody response in 26 healthy volunteers challenged with Cryptosporidium parvum oocysts. Fecal extracts were assayed for total secretory immunoglobulin A (IgA) and C. parvum-specific IgA reactivity. Specific IgA reactivity was standardized to IgA concentration and expressed as a reactivity index (RI). Anti-C. parvum fecal IgA (fIgA) increased significantly in 17 of 26 (65.4%) following oocyst ingestion. Of those with detectable responses, 59, 76.5, and 94.1% were positive by days 7, 14, and 30, respectively. Volunteers receiving high challenge doses (>1,000 and 300 to 500 oocysts) had higher RIs (RI = 5.57 [P = 0.027] and RI = 1.68 [P = 0.039], respectively) than those ingesting low doses (30 to 100 oocysts; RI = 0.146). Subjects shedding oocysts and experiencing a diarrheal illness had the highest fIgA reactivity. When evaluated separately, oocyst excretion was associated with an increased fIgA response compared to nonshedders (RI = 1.679 versus 0.024, respectively; P = 0.003). However, in subjects experiencing diarrhea with or without oocyst shedding, a trend toward a higher RI (P = 0.065) was seen. Extracts positive for fecal IgA were further examined for IgA subclass. The majority of stools contained both IgA1 and IgA2, and the relative proportions did not change following challenge. Also, no C. parvum-specific IgM or IgG was detected in fecal extracts. Thus, fecal IgA to C. parvum antigens was highly associated with infection in subjects who had no evidence of previous exposure and may provide a useful tool in detecting recent infections.


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