Patients with gastroparesis often suffer with chronic gastrointestinal symptoms that are not adequately treated due, in part, to a lack of understanding of the underlying pathophysiology and due, in part, to a lack of effective treatments. The participation of Temple University Gastrointestinal Motility Center in the NIH/NIDDK Gastroparesis Clinical Research Consortium and the proposed studies will help achieve the broad, long term objectives of improving the diagnosis and treatment of patients with gastroparesis. Temple is exceptionally well qualified to be one of the clinical centers in this consortium. Temple has clinical expertise and an active research program in the evaluation and treatment of patients with gastroparesis. Our short-term study proposal is designed to test the hypotheses that botulinum toxin injection into the pylorus improves dyspeptic symptoms and accelerates gastric emptying in a subgroup of patients who can be identified with physiologic testing. We propose a prospective, multi-center, randomized, placebo- controlled, double blind study to assess the efficacy of botulinum toxin on symptoms and gastric emptying. We will analyze factors that may be predictive of a beneficial response including type and severity of gastroparesis, baseline pyloric pressure, gender, and specific symptom profiles. Our long-term study proposal is a longitudinal cohort study of patients with gastroparesis designed to understand the causes and improve the treatment of symptom exacerbations in patients with gastroparesis. In this study, patients'symptoms will be followed on a regular basis using an Internet-based telemedicine system. This will allow several antecedent factors to be followed that may be responsible for symptom exacerbation including glucose control, dietary intake, psychological stress, and inflammation. Additionally, the symptomatic response of patients to two agents (domperidone and desipramine) that may be effective in improving symptoms but target different pathophysiologic processes will be assessed. Domperidone is a prokinetic/antiemetic agent, whereas desipramine is a symptom modulator/antidepressant agent. The proposed protocols will help define patient populations that may respond to different types of treatments for gastroparesis. The protocols use novel diagnostic tests to better define the pathophysiology of gastroparesis. These studies will also better define the disease course of patients with gastroparesis

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Research Project--Cooperative Agreements (U01)
Project #
5U01DK073975-04
Application #
7616832
Study Section
Special Emphasis Panel (ZDK1-GRB-6 (O1))
Program Officer
Hamilton, Frank A
Project Start
2006-04-15
Project End
2011-03-31
Budget Start
2009-04-01
Budget End
2010-03-31
Support Year
4
Fiscal Year
2009
Total Cost
$349,309
Indirect Cost
Name
Temple University
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
057123192
City
Philadelphia
State
PA
Country
United States
Zip Code
19122
Parkman, H P; Hallinan, E K; Hasler, W L et al. (2017) Early satiety and postprandial fullness in gastroparesis correlate with gastroparesis severity, gastric emptying, and water load testing. Neurogastroenterol Motil 29:
Camilleri, Michael; McCallum, Richard W; Tack, Jan et al. (2017) Efficacy and Safety of Relamorelin in Diabetics With Symptoms of Gastroparesis: A Randomized, Placebo-Controlled Study. Gastroenterology 153:1240-1250.e2
Grover, M; Bernard, C E; Pasricha, P J et al. (2017) Diabetic and idiopathic gastroparesis is associated with loss of CD206-positive macrophages in the gastric antrum. Neurogastroenterol Motil 29:
Koch, K L; Hasler, W L; Yates, K P et al. (2016) Baseline features and differences in 48 week clinical outcomes in patients with gastroparesis and type 1 vs type 2 diabetes. Neurogastroenterol Motil 28:1001-15
Parkman, H P; Hallinan, E K; Hasler, W L et al. (2016) Nausea and vomiting in gastroparesis: similarities and differences in idiopathic and diabetic gastroparesis. Neurogastroenterol Motil 28:1902-1914
Parkman, Henry P (2015) Idiopathic gastroparesis. Gastroenterol Clin North Am 44:59-68
Pasricha, Pankaj J; Yates, Katherine P; Nguyen, Linda et al. (2015) Outcomes and Factors Associated With Reduced Symptoms in Patients With Gastroparesis. Gastroenterology 149:1762-1774.e4
Bernard, C E; Gibbons, S J; Mann, I S et al. (2014) Association of low numbers of CD206-positive cells with loss of ICC in the gastric body of patients with diabetic gastroparesis. Neurogastroenterol Motil 26:1275-84
Iorio, Raffaele; Lucchinetti, Claudia F; Lennon, Vanda A et al. (2013) Intractable nausea and vomiting from autoantibodies against a brain water channel. Clin Gastroenterol Hepatol 11:240-5
Camilleri, Michael; Parkman, Henry P; Shafi, Mehnaz A et al. (2013) Clinical guideline: management of gastroparesis. Am J Gastroenterol 108:18-37; quiz 38

Showing the most recent 10 out of 25 publications