Health Professionals at Banner Good Samaritan Medical Ctr.  

March 13: Research that makes a difference (2/4)

Steve Narang  

Every day, we continue our journey to transform Banner Good Samaritan as a complex community hospital in downtown Phoenix with excellent teaching programs, to a medical center whose “why” is simple ... That we believe that our culture which values and sustains learning, scholarship and performance improvement leads directly to excellent patient care, innovation, and superior outcomes.    

Today, I’d like to share the words of our very own Dr. Steven Curry, a nationally recognized expert in toxicology, who is working with several other key leaders on an institute structure that highlights BGSMC’s expertise in critical illness and injury. This institute will tell our story around our highly differentiated programs such as trauma, critical care, toxicology and emergency medicine.

Take a few minutes and learn more about the incredible scholarship currently being created by our very own physicians here at BGSMC. It is this type of research that improves the care of our most complex patients and draws patients from all over the state and southwest to BGSMC. So many similar stories of highly differentiated care at Good Sam … so many possibilities… Thank you for your contributions.

Steve Narang, MD, is the chief executive officer at Banner Good Samaritan Medical Center.

HLH in septic patients

By Dr. Steven Curry

When confronted with an infection, it is critical that our immune systems become activated and begin producing substances, such as cytokines, that cause our body to fight off the infection by causing movement of white blood cells into areas of infection, raising body temperature, and other actions.  And it is just as important that the our bodies turns off the activated immune response once the infection is resolved.

It has long been known that some persons are born with rare genetic variations that causes their immune systems to become activated in the absence of infection, or to remain activated after an infection has resolved. The illness from which they suffer has the long name of hemophagocytic lymphohistiocytosis (HLH). There are criteria for diagnosing HLH that include specific laboratory test results and clinical findings.  Recommendations for treating some of these patients include administering corticosteroids like prednisone, and giving etoposide, a chemotherapeutic drug that is active against a type of cell involved in generating or sustaining the abnormal immune response. Still, HLH carries a high mortality.

Apart from those with congenital predisposition to HLH, some patients with serious infections appear to display signs of persistent infection (fever, low blood pressure, kidney failure, etc.), even after the infection appears to have resolved. Over the last several years, it has been recognized that these patients also display some or all of the same laboratory and pathology study results that are seen in patients with HLH.  And just as in classical HLH, these patients also experience prolonged hospitalizations and a high mortality.

There is a need to better understand how often inpatients who clinically remain ill after evidence of infection has resolved display findings similar to HLH, and whether these patients who meet criteria for HLH (whether they have HLH or a similar disease) have some predisposition to developing this disorder after infection.

In 2011, Dr. Robert Raschke and Dr. Roxanne Garcia-Orr, from BGSMC’s Department of Pulmonary and Critical Care Medicine Fellowship, published a review of HLH associated with sepsis and included descriptions of patients they cared for at BGSMC (Chest 2011;140:933-938). Now, faculty and house staff from the Pulmonary and Critical Care Medicine Fellowship, the Medical Toxicology Fellowship, and the General Surgery Residency programs at BGSMC, working together under the Institute of Critical Illness and Injury, are implementing a study in which detailed clinical data and blood samples will be obtained from patients with suspected HLH following sepsis.

Results from this study will contribute to determining how common HLH is in patients who do not rapidly improve after serious infections.  Analysis of stored blood specimens may identify markers that help explain or predict HLH in this setting.  Given the high mortality of HLH, the common finding of HLH as a sequela to serious infection may lead to trials of corticosteroids or etoposide in such patients, which might dramatically improve survival. But before such trials can be designed, essential data such as that being collected in the current study are required.


Banner Good Samaritan Medical Center
1111 E. McDowell Road
Phoenix, AZ 85006
(602) 839-2000
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