Clinical Factors Associated With the Development of Severe Sepsis in Patients Being Treated for Acute Myeloid Leukemia (AML)
Acute leukemia is a life threatening illness that strikes people of all ages. In addition to surviving the direct effects of the disease, the treatment of leukemia generally requires chemotherapy which has its own burden. Infection is one of the most common secondary problems faced by these patients. Simple infections are common and easily treated with aggressive antibiotics. However, treated progressive infection leads to loss of vital organ function and is termed severe sepsis. Severe sepsis is associated with increased risk of death and the need for specialized care in the intensive care unit.
Besides the appropriate use of antibiotics, little is known about what clinical and patient factors are associated with the development of severe sepsis. Recent evidence has suggested that certain practices like frequent transfusion of blood products and control of glucose levels effects outcome in critically ill patients. In addition, there have been advances in our knowledge of certain genes that may predispose people to severe infections. It is possible that these factors are important in people who are not yet critically ill, but are at risk for the development of severe sepsis.
This observational study will look at genetic, clinical and therapeutic factors that are associated with the development of severe sepsis. This will help doctors understand what treatments may be helpful in preventing this serious complication.
Acute Myeloid Leukemia
|Study Design:||Observational Model: Cohort
Time Perspective: Prospective
|Official Title:||Clinical Factors Associated With the Development of Severe Sepsis in Patients Being Treated for Acute Myeloid Leukemia|
- determine the true relationship of hyperglycemia to the development of severe sepsis after chemotherapy for AML [ Time Frame: end of study ] [ Designated as safety issue: No ]
Biospecimen Retention: Samples With DNA
baseline blood sample drawn (2 tablespoons or 30 ml) at the beginning of the study. If subjects experience a fever another blood sample (10 ml up to 2 times) will be drawn at that time.
|Study Start Date:||November 2007|
|Study Completion Date:||May 2010|
|Primary Completion Date:||February 2010 (Final data collection date for primary outcome measure)|
Adult patients with AML admitted for treatment of the same
Primary hypothesis: Hyperglycemia during inpatient therapy of AML is associated with increased mortality (fewer hospital free days to Day 60, see below).
- H1a: Hyperglycemia will result in an increased risk of developing clinical signs of infection (fever).
H1b: Hyperglycemia will be associated with an increased risk of developing severe sepsis after the onset of clinical signs of infection (fever).
o H1b1: Hyperglycemia will be associated with the development of acute lung injury after the onset of signs of infection (fever).
H1c: Hyperglycemia will be associated with an increased risk of ICU admission.
o H1c1: Hyperglycemia will be associated with an increased risk of ICU admission for severe sepsis.
- H1d: Hyperglycemia will be associated with an increased risk of death in those subjects with severe sepsis (fewer hospital free days to Day 60, see below).
Secondary Aim: To investigate whether TSP-1 is important in modulating the course of sepsis-induced acute lung injury.
Secondary hypothesis: In patients with sepsis, increased levels of functional TSP-1 will be associated with a lower incidence of and a less severe course of lung injury.
- H2a: In human sepsis, increased TSP-1 levels will be associated with a lower incidence of lung-injury.
- H2b: In human sepsis, increased TSP-1 levels will be associated with a less severe course of lung-injury.
- H2c: In human sepsis, patients with the Asn682Ser polymorphism in the TSP-1 gene will be associated with a higher incidence of lung-injury.
- H2d In human sepsis, patients with the Asn682Ser polymorphism in the TSP-1 gene will be associated with a more severe course of lung-injury.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00806325
|United States, Ohio|
|The Ohio State University|
|Columbus, Ohio, United States, 43210|
|Principal Investigator:||Naeem A Ali, MD||Ohio State University|