Maximizing Quality of Life for New Colostomy (AKA, Ostomy/Stoma) Patients and Their Partners

Co-Principal Investigators: Vitaliy Y. Poylin, MD, MBA, Associate Professor of Surgery (Gastrointestinal Surgery), Northwestern Medicine, Northwestern Feinberg School of Medicine Rachel Hendee, PA-C, Certified Physician Assistant, Department of Surgery (Gastrointestinal Surgery), Northwestern Medicine, Northwestern Feinberg School of Medicine Stephanie Brenner, LCSW Every year, some 100,000 Americans must undergo life-saving ostomy surgery to create an opening (stoma) in the abdominal wall to allow waste (fecal and urine) to leave the body and be collected in an attached or internal ostomy pouch. A variety of urinary or digestive system problems may require the rerouting of bodily waste to avoid life threatening infection and sepsis. Whether temporary or permanent, a new stoma can have a physical and psychosocial impact on patients and their interpersonal relationships that can significantly affect their quality of life. Patients who have built resilience through pre- and post-op in-hospital training often experience less depression and are better prepared to cope with their new stoma. Current guidelines recommend pre-surgical education for patients, with partners often welcomed, but not required to participate. Helping patients best prepare and adapt to their new stomas with the strong support of their partners has not been well documented. The Northwestern researchers believe that standardizing education and intensifying resiliency training for both patients and their partners can improve patient and partner quality of life, and may in turn reduce rates of hospital readmission, emergency room and clinic visits, and complications. Awarded this year’s DHF grant, the researchers plan to evaluate the impact of enhanced training for patients and their partners at Northwestern Medicine in hopes of reducing the need for urgent interventions, as well as...

Innovating an Endoscopy Approach for Staging Unique Liver Disease

Principal Investigator: Dempsey L. Hughes, MD, Assistant Professor of Medicine (Gastroenterology and Hepatology), Northwestern Medicine, Northwestern Feinberg School of Medicine A new and aggressive form of chronic liver disease has developed in young adult survivors born with congenital, single ventricle heart disease. Until the 1970s, most babies born with essentially half a heart died in infancy until the introduction of a life-saving surgical technique called the Fontan procedure. While highly successful in correcting this cardiac defect early in life, the Fontan procedure has led to unanticipated, unfortunate outcomes – Fontan-associated Liver Disease (FALD) caused by abnormal blood flow in and out of the liver due to the heart disorder. FALD can progress from cirrhosis (irreversible liver scarring) to liver cancer, with the only cure being a massively risky heart transplant or combined heart-liver transplant. Accurate assessments of liver function could better guide treatment to improve the quality of life and survival of those developing FALD. Unfortunately, traditional liver MR imaging cannot be used in the presence of cardiac devices such as pacemakers, which many of these patients rely on. Thus, the best way of evaluating and tracking liver function in this at-risk population of Fontan patients is tragically unavailable due to their implanted medical devices that are saving their life. This year, a DHF award is supporting Dr. Hughes’ team in conducting a first-of-its-kind pilot on the use of endohepatology, a common upper endoscopy procedure, for liver disease staging in the FALD patient population. The researchers hope this novel use of endohepatology will greatly advance the clinical understanding of FALD by offering a vital alternative to MR imaging to...

Understanding a Protective Protein’s Role in Stopping Primary Sclerosing Cholangitis (PSC)

Co-Principal Investigators: Xiaoying Liu, PhD, Research Assistant Professor of Medicine (Gastroenterology and Hepatology), Northwestern Medicine, Northwestern Feinberg School of Medicine Richard M. Green, MD, Professor of Medicine (Gastroenterology and Hepatology), Northwestern Medicine, Northwestern Feinberg School of Medicine A chronic disease of the liver that currently doesn’t have any treatment, primary sclerosing cholangitis (PSC) causes destructive scarring of the ducts that carry bile to the small intestine to help digest fats. Affecting some 50,000 Americans, PSC can occur alone, but is associated with ulcerative colitis or Crohn’s disease in 80% of PSC cases (Only about 6% of IBD patients have PSC). While the exact reason for this overlap still eludes scientists, thankfully, the inevitable progression of PSC toward cirrhosis is not worsened by IBD or treatment for IBD. Limited understanding of PSC has meant that, currently, there aren’t any effective medical therapies to stop dangerous disease progression. Ultimately, PSC patients develop liver cirrhosis, need a liver transplant, or die from their disease. X-box binding protein 1 (XBP1) is a protein that protects cells from injury. In previous studies, the Liu/Green team found in an animal model that when mice lacked XBP1 in their liver, they were more prone to develop liver damage. Granted the DHF award this year, the investigators plan to explore their hypothesis that progressive PSC results when the XBP1 signaling pathway fails to adequately activate to protect the liver. toThis study will be the first of its kind to use liver biopsies from patients with PSC to measure the XBP1 pathway in several different liver cell types injured by the disease. By identifying the role of XBP1...

Advancing the Diagnosis of EoE Using Artificial Intelligence

Principal Investigators: Sourav Halder, PhD, Postdoctoral Scholar, Northwestern Medicine, Division of Gastroenterology and Hepatology, Northwestern Feinberg School of Medicine Wenjun Kou, PhD, Research Assistant Professor of Medicine (Gastroenterology and Hepatology) Every year, diagnoses are growing of eosinophilic esophagitis (EoE), a chronic, destructive allergic condition with many sub-types, that causes white blood cells (eosinophils) normally found elsewhere in the body to accumulate in the esophagus. Their presence causes inflammation, scarring, and stiffening of the esophagus. This damage impairs the ability of the esophagus to move foods and liquids from the throat to the stomach via esophageal muscle contractions—a process called peristalsis. Problems swallowing is the hallmark of EoE, which contributes to thousands of food impactions requiring urgent endoscopies each year. An innovative diagnostic tool recently developed by Northwestern gastroenterology investigators called FLIP Panometry has provided a novel method for diagnosing EoE through contraction patterns. This year’s DHF grant will support Dr. Halder’s team in their efforts to better define and classify the many different forms of the disease EoE. By harnessing the power of artificial intelligence to analyze FLIP data, the researchers hope to improve the current one-size-fits-all diagnostic approach by personalizing treatments to specific types of EoE and offering patients their best quality of...

Decoding the Genetics of Difficult-to-Treat Eosinophilic Esophagitis (EoE)

Principal Investigator: Marie-Pier Tetreault, PhD, Assistant Professor of Medicine (Gastroenterology and Hepatology), Northwestern Medicine, Northwestern Feinberg School of Medicine A dangerous immune system condition that affects children and adults, eosinophilic esophagitis (EoE) occurs when allergic reactions inflame and scar the esophagus. The normally flexible esophagus, that connects the opening of the mouth down to the entry of the stomach, becomes stiff and unable to pass food and liquids down to the stomach. This leads to problems swallowing, heartburn, vomiting, pain, and malnutrition. Despite gains in treating EoE, many patients still have difficulties swallowing or they no longer respond to available therapies. A type of cell overgrowth called basal cell hyperplasia (BCH) has been blamed for progressive esophageal stiffening. While BCH is strongly linked to disease severity,little is known about the molecular and cellular changes that drive BCH. Uncovering the molecular underpinnings of EoE to develop more effective therapies, Dr. Marie-Pier Tetreault’s team recently published a study that points the finger at two genes: SOX2 and KLF5. The researchers hypothesize that the elevation of SOX2 and KLF5 expression correlates with disease outcomes after treatment. With funding from this year’s DHF award, the investigators intend to analyze already biobanked (from the DHF BioRepository) esophageal tissue samples from patients undergoing diverse therapies. The team will look to connect the dots between changes in biomarker expression, treatment responses, and clinical outcomes. Using cutting-edge imaging techniques and clinical assessments, the group hopes to better understand EoE to pave the way toward more personalized and targeted therapies for current and future patients. Better, more effective treatment can preserve remaining esophageal function and prevent further esophageal...