Study Results
Results pending
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Basic Information
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Recruitment Status
COMPLETED
Clinical Phase
NA
Total Enrollment
14 participants
Study Classification
INTERVENTIONAL
Study Start Date
2017-11-08
Study Completion Date
2020-12-31
Brief Summary
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Non-alcoholic fatty liver disease (NAFLD) is a frequent disease affecting up to 25% of the USA population, 2-44% in Europe and up to 42,6-69,5% in patients with type 2 diabetes. It is a disease that could progress from simple steatosis to non-alcoholic steatohepatitis (NASH), hepatic cirrhosis and hepatocarcinoma. NASH is part of continuum of metabolic syndrome and constitutes a serious public health concern manifesting by premature cardiovascular disease, end stage diabetes complication and will likely become the first cause of end stage liver disease. Insuline resistance is the hallmark of NASH. Some recent studies both in animals and humans have demonstrated abnormal hypertrophy of the duodenal mucosa, changes in enteroendocrine cell density and number, endocrine hyperplasia, and alterations in gut hormone signaling highlighting the role of the upper intestine gut in glucose homeostasis and thus insulin sensitizing. Given these physiological and pathophysiological features, abrasion of duodenal mucosa was assessed both in animals and humans. The investigators reported an improvement in both glucose homeostasis and transaminases levels suggesting possibly an improvement of NASH. Until now, lifestyle medication is the only recognized efficient treatment for fatty liver disease. Unfortunately, only a minority of patients achieve a significant weight loss and lifestyle modifications. The investigators aim to study the duodenal mucosal resurfacing procedure in patients with NASH biopsy proven in a proof of concept study allowing to assess this technique as a potential treatment to NASH.
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Detailed Description
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Introduction
Non-alcoholic fatty liver disease (NAFLD) is a frequent disease affecting up to 25% of the USA population, 2-44% in Europe and up to 42,6-69,5% in patients with type 2 diabetes. It is a disease that could progress from simple steatosis to non-alcoholic steatohepatitis (NASH), hepatic cirrhosis and hepatocarcinoma. NASH is part of continuum of a metabolic syndrome and constitutes a serious public health concern, manifesting by premature cardiovascular disease, end stage diabetes complication and will likely become the first cause of end stage liver disease.
Insulin resistance is the hallmark of NASH. Some recent studies both in animals and humans have demonstrated abnormal hypertrophy of the duodenal mucosa, changes in enteroendocrine cell density and number, endocrine hyperplasia, and alterations in gut hormone signaling highlighting the role of the upper intestine gut in glucose homeostasis and thus insulin sensitizing.
Given these physiological and pathophysiological features, abrasion of duodenal mucosa was assessed both in animals and humans. The investigators reported an improvement in both glucose homeostasis and transaminases levels suggesting possibly an improvement of NASH.
Until now, lifestyle medication is the only recognized efficient treatment for fatty liver disease. Unfortunately, only a minority of patients achieve a significant weight loss and lifestyle modifications.
The investigators aim to study the duodenal mucosal resurfacing procedure in patients with NASH biopsy proven in a proof of concept study allowing to assess this technique as a potential treatment to NASH.
Design of study The study is designed as a single arm, proof of concept, non-randomized, open label trial to be conducted at one investigational site. All patients with biopsy proven NASH will undergo an upper endoscopy to perform a duodenal mucosal resurfacing procedure. Evolution of liver steatosis (assessed by MRI), insulin resistance (assessed by oral glucose tolerance test), liver damage (evaluated by blood tests), liver elastography (assessed by fibroscan, fibrotest), biometric parameters will be performed pre- and post-procedure.
Primary outcome :
\- Feasability and safety of duodenal mucosal resurfacing, using Revita ™ duodenal mucosal resurfacing after submucosal injection, in patients with NASH.
Secondary outcomes:
* Evolution of steatosis assessed by MRI 6 months after the procedure.
* Evolution of liver fibrosis (assessed by Fibroscan, Fibrotest, Fibrosis four score (FIB-4) and NAFLD fibrosis score) at 6 and 12 months after the procedure.
* Evolution of liver tests at 6 and 12 months after the procedure.
* Evolution of insulin resistance at 1,3,6 and 12 months after the procedure.
Non-alcoholic fatty liver disease (NAFLD) is a frequent disease affecting up to 25% of the USA population, 2-44% in Europe and up to 42,6-69,5% in patients with type 2 diabetes. It is a disease that could progress from simple steatosis to non-alcoholic steatohepatitis (NASH), hepatic cirrhosis and hepatocarcinoma. NASH is part of continuum of a metabolic syndrome and constitutes a serious public health concern, manifesting by premature cardiovascular disease, end stage diabetes complication and will likely become the first cause of end stage liver disease.
Insulin resistance is the hallmark of NASH. Some recent studies both in animals and humans have demonstrated abnormal hypertrophy of the duodenal mucosa, changes in enteroendocrine cell density and number, endocrine hyperplasia, and alterations in gut hormone signaling highlighting the role of the upper intestine gut in glucose homeostasis and thus insulin sensitizing.
Given these physiological and pathophysiological features, abrasion of duodenal mucosa was assessed both in animals and humans. The investigators reported an improvement in both glucose homeostasis and transaminases levels suggesting possibly an improvement of NASH.
Until now, lifestyle medication is the only recognized efficient treatment for fatty liver disease. Unfortunately, only a minority of patients achieve a significant weight loss and lifestyle modifications.
The investigators aim to study the duodenal mucosal resurfacing procedure in patients with NASH biopsy proven in a proof of concept study allowing to assess this technique as a potential treatment to NASH.
Design of study The study is designed as a single arm, proof of concept, non-randomized, open label trial to be conducted at one investigational site. All patients with biopsy proven NASH will undergo an upper endoscopy to perform a duodenal mucosal resurfacing procedure. Evolution of liver steatosis (assessed by MRI), insulin resistance (assessed by oral glucose tolerance test), liver damage (evaluated by blood tests), liver elastography (assessed by fibroscan, fibrotest), biometric parameters will be performed pre- and post-procedure.
Primary outcome :
\- Feasability and safety of duodenal mucosal resurfacing, using Revita ™ duodenal mucosal resurfacing after submucosal injection, in patients with NASH.
Secondary outcomes:
* Evolution of steatosis assessed by MRI 6 months after the procedure.
* Evolution of liver fibrosis (assessed by Fibroscan, Fibrotest, Fibrosis four score (FIB-4) and NAFLD fibrosis score) at 6 and 12 months after the procedure.
* Evolution of liver tests at 6 and 12 months after the procedure.
* Evolution of insulin resistance at 1,3,6 and 12 months after the procedure.
Conditions
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NASH - Nonalcoholic Steatohepatitis
Study Design
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Allocation Method
NA
Intervention Model
SINGLE_GROUP
Primary Study Purpose
TREATMENT
Blinding Strategy
NONE
Study Groups
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DMR procedure
Group Type
EXPERIMENTAL
DMR
Intervention Type
DEVICE
Procedure: DMR Procedure The Fractyl DMR procedure using the Revita System utilizes an over the wire endoscopic approach to ablate the duodenum. The procedure may be completed in an endoscopic suite or in an operating room depending on the facilities and support at each investigative site. All subjects are monitored and anesthetized by conscious sedation per each facility's standard protocol. A full DMR procedure is defined as 5 complete ablations or 9 axial centimeters of circumferentially ablated tissue in the duodenum. Subjects who do not receive any ablations during the DMR procedure will be followed for safety through the 4 week visit and then discontinued from the study.
Other Names:
DMR Revita
Interventions
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DMR
Procedure: DMR Procedure The Fractyl DMR procedure using the Revita System utilizes an over the wire endoscopic approach to ablate the duodenum. The procedure may be completed in an endoscopic suite or in an operating room depending on the facilities and support at each investigative site. All subjects are monitored and anesthetized by conscious sedation per each facility's standard protocol. A full DMR procedure is defined as 5 complete ablations or 9 axial centimeters of circumferentially ablated tissue in the duodenum. Subjects who do not receive any ablations during the DMR procedure will be followed for safety through the 4 week visit and then discontinued from the study.
Other Names:
DMR Revita
Intervention Type
DEVICE
Other Intervention Names
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Revita
Eligibility Criteria
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Inclusion Criteria
1. Adult subjects (male and female), age 28 to 75 years.
2. NASH histological diagnosis according to the currently accepted definition of both EASL and AASLD, requiring the combined presence of steatosis (any degree\> 5%) + lobular inflammation of any degree + liver cell ballooning of any amount, on a liver biopsy performed ≤ 6 months before screening in the study and confirmed by central reading during the periode and (apendix 1)
1. SAF (steatosis, activity, fibrosis) activity score of 3 or 4 (\>2)
2. SAF steatosis score ≥ 1
3. SAF fibrosis score \< 4
3. No other causes of chronic liver disease and compensated liver disease.
4. If applicable, have a type 2 diabetes with HbA1c \<10.0 %
5. BMI (body mass index) ≥ 24 and ≤ 40 kg/m2.
6. Willing to sign an informed consent form.
7. Willing to comply with study requirements
2. NASH histological diagnosis according to the currently accepted definition of both EASL and AASLD, requiring the combined presence of steatosis (any degree\> 5%) + lobular inflammation of any degree + liver cell ballooning of any amount, on a liver biopsy performed ≤ 6 months before screening in the study and confirmed by central reading during the periode and (apendix 1)
1. SAF (steatosis, activity, fibrosis) activity score of 3 or 4 (\>2)
2. SAF steatosis score ≥ 1
3. SAF fibrosis score \< 4
3. No other causes of chronic liver disease and compensated liver disease.
4. If applicable, have a type 2 diabetes with HbA1c \<10.0 %
5. BMI (body mass index) ≥ 24 and ≤ 40 kg/m2.
6. Willing to sign an informed consent form.
7. Willing to comply with study requirements
Exclusion Criteria
1. Evidence of another cause of liver disease.
2. History of sustained alcohol ingestion defined as: daily alcohol consumption \> 30 g/day for males and \> 20 g/day for females.
3. Previous gastrointestinal surgery such as subjects who have had Billroth 2, Roux-en-Y gastric bypass, or other similar procedures or conditions.
4. Known autoimmune disease, including celiac disease, or symptoms of systemic lupus eythematosus, sleroderma or other auto-immune connective tissue disorder.
5. For type 2 diabetes subjects, no current use of insulin or GLP-1 analogues.
6. Type 1 diabetes.
7. Probable insulin production failure defined as fasting C peptide serum \< 1 ng/ml.
8. History of acute or chronic pancreatitis.
9. Active malignancy.
10. Persistent anemia defined as Hb \< 10 g/dl.
11. Use of anticoagulation therapy which cannot be discontinued for 7 days before and 14 days after the procedure.
12. Use of P2Y12 inhibitors (clopidrogel, prasugrel, ticagrelor) which cannot be discontinued for 14 days before and14 days after the procedure.
13. History of coagulopathy or upper gastro-intestinal bleeding conditions likely to bleed.
14. Taking corticosteroids or drugs which possibly affect gastrointestinal motility or liver.
15. Unable to discontinue NSAIDs (non-steroidal anti- inflammatory drugs) during the treatment up to 4 weeks after procedure.
16. Use of weight loss medications.
17. Presence of liver cirrhosis (defined by histology)
18. Platelet count \< 120 x 109/L.
19. Clinical evidence of hepatic decompensation or severe liver impairment as defined by the presence of any of the following abnormalities:
20. Serum albumin \< 32 g/L.
21. INR\> 1.3.
22. Direct bilirubin\> 1.3 mg/L.
23. ALT or AST \> 5x ULN.
24. Alkaline Phosphatase \> 3x ULN.
25. History of esophageal varices, ascites or hepatic encephalopathy.
26. Splenomegaly.
27. Human immunodeficiency virus.
28. Contraindications to MRI as defined below.
2. History of sustained alcohol ingestion defined as: daily alcohol consumption \> 30 g/day for males and \> 20 g/day for females.
3. Previous gastrointestinal surgery such as subjects who have had Billroth 2, Roux-en-Y gastric bypass, or other similar procedures or conditions.
4. Known autoimmune disease, including celiac disease, or symptoms of systemic lupus eythematosus, sleroderma or other auto-immune connective tissue disorder.
5. For type 2 diabetes subjects, no current use of insulin or GLP-1 analogues.
6. Type 1 diabetes.
7. Probable insulin production failure defined as fasting C peptide serum \< 1 ng/ml.
8. History of acute or chronic pancreatitis.
9. Active malignancy.
10. Persistent anemia defined as Hb \< 10 g/dl.
11. Use of anticoagulation therapy which cannot be discontinued for 7 days before and 14 days after the procedure.
12. Use of P2Y12 inhibitors (clopidrogel, prasugrel, ticagrelor) which cannot be discontinued for 14 days before and14 days after the procedure.
13. History of coagulopathy or upper gastro-intestinal bleeding conditions likely to bleed.
14. Taking corticosteroids or drugs which possibly affect gastrointestinal motility or liver.
15. Unable to discontinue NSAIDs (non-steroidal anti- inflammatory drugs) during the treatment up to 4 weeks after procedure.
16. Use of weight loss medications.
17. Presence of liver cirrhosis (defined by histology)
18. Platelet count \< 120 x 109/L.
19. Clinical evidence of hepatic decompensation or severe liver impairment as defined by the presence of any of the following abnormalities:
20. Serum albumin \< 32 g/L.
21. INR\> 1.3.
22. Direct bilirubin\> 1.3 mg/L.
23. ALT or AST \> 5x ULN.
24. Alkaline Phosphatase \> 3x ULN.
25. History of esophageal varices, ascites or hepatic encephalopathy.
26. Splenomegaly.
27. Human immunodeficiency virus.
28. Contraindications to MRI as defined below.
Minimum Eligible Age
28 Years
Maximum Eligible Age
75 Years
Eligible Sex
ALL
Accepts Healthy Volunteers
No
Sponsors
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Fractyl Health Inc.
INDUSTRY
Sponsor Role
collaborator
Erasme University Hospital
OTHER
Sponsor Role
lead
Responsible Party
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Responsibility Role
SPONSOR
Principal Investigators
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Jacques Deviere, PhD, MD
Role: PRINCIPAL_INVESTIGATOR
Erasme hospital
Locations
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Erasme Hospital
Brussels, , Belgium
Site Status
Countries
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Belgium
References
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Li Y, Jadhav K, Zhang Y. Bile acid receptors in non-alcoholic fatty liver disease. Biochem Pharmacol. 2013 Dec 1;86(11):1517-24. doi: 10.1016/j.bcp.2013.08.015. Epub 2013 Aug 26.
Reference Type
BACKGROUND
Blachier M, Leleu H, Peck-Radosavljevic M, Valla DC, Roudot-Thoraval F. The burden of liver disease in Europe: a review of available epidemiological data. J Hepatol. 2013 Mar;58(3):593-608. doi: 10.1016/j.jhep.2012.12.005.
Reference Type
BACKGROUND
Tilg H, Moschen AR. Evolution of inflammation in nonalcoholic fatty liver disease: the multiple parallel hits hypothesis. Hepatology. 2010 Nov;52(5):1836-46. doi: 10.1002/hep.24001.
Reference Type
BACKGROUND
Chalasani N, Younossi Z, Lavine JE, Diehl AM, Brunt EM, Cusi K, Charlton M, Sanyal AJ; American Gastroenterological Association; American Association for the Study of Liver Diseases; American College of Gastroenterologyh. The diagnosis and management of non-alcoholic fatty liver disease: practice guideline by the American Gastroenterological Association, American Association for the Study of Liver Diseases, and American College of Gastroenterology. Gastroenterology. 2012 Jun;142(7):1592-609. doi: 10.1053/j.gastro.2012.04.001. Epub 2012 May 15. No abstract available.
Reference Type
BACKGROUND
Vernon G, Baranova A, Younossi ZM. Systematic review: the epidemiology and natural history of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis in adults. Aliment Pharmacol Ther. 2011 Aug;34(3):274-85. doi: 10.1111/j.1365-2036.2011.04724.x. Epub 2011 May 30.
Reference Type
BACKGROUND
Boza C, Riquelme A, Ibanez L, Duarte I, Norero E, Viviani P, Soza A, Fernandez JI, Raddatz A, Guzman S, Arrese M. Predictors of nonalcoholic steatohepatitis (NASH) in obese patients undergoing gastric bypass. Obes Surg. 2005 Sep;15(8):1148-53. doi: 10.1381/0960892055002347.
Reference Type
BACKGROUND
Higuera-de la Tijera F, Servin-Caamano AI. Pathophysiological mechanisms involved in non-alcoholic steatohepatitis and novel potential therapeutic targets. World J Hepatol. 2015 Jun 8;7(10):1297-301. doi: 10.4254/wjh.v7.i10.1297.
Reference Type
BACKGROUND
Schneck AS, Anty R, Patouraux S, Bonnafous S, Rousseau D, Lebeaupin C, Bailly-Maitre B, Sans A, Tran A, Gugenheim J, Iannelli A, Gual P. Roux-En Y Gastric Bypass Results in Long-Term Remission of Hepatocyte Apoptosis and Hepatic Histological Features of Non-alcoholic Steatohepatitis. Front Physiol. 2016 Aug 19;7:344. doi: 10.3389/fphys.2016.00344. eCollection 2016.
Reference Type
BACKGROUND
Hannah WN Jr, Harrison SA. Effect of Weight Loss, Diet, Exercise, and Bariatric Surgery on Nonalcoholic Fatty Liver Disease. Clin Liver Dis. 2016 May;20(2):339-50. doi: 10.1016/j.cld.2015.10.008. Epub 2016 Feb 17.
Reference Type
BACKGROUND
Klebanoff MJ, Corey KE, Chhatwal J, Kaplan LM, Chung RT, Hur C. Bariatric surgery for nonalcoholic steatohepatitis: A clinical and cost-effectiveness analysis. Hepatology. 2017 Apr;65(4):1156-1164. doi: 10.1002/hep.28958. Epub 2017 Feb 21.
Reference Type
BACKGROUND
Lassailly G, Caiazzo R, Buob D, Pigeyre M, Verkindt H, Labreuche J, Raverdy V, Leteurtre E, Dharancy S, Louvet A, Romon M, Duhamel A, Pattou F, Mathurin P. Bariatric Surgery Reduces Features of Nonalcoholic Steatohepatitis in Morbidly Obese Patients. Gastroenterology. 2015 Aug;149(2):379-88; quiz e15-6. doi: 10.1053/j.gastro.2015.04.014. Epub 2015 Apr 25.
Reference Type
BACKGROUND
Ferrannini E, Mingrone G. Impact of different bariatric surgical procedures on insulin action and beta-cell function in type 2 diabetes. Diabetes Care. 2009 Mar;32(3):514-20. doi: 10.2337/dc08-1762. No abstract available.
Reference Type
BACKGROUND
Klein S, Fabbrini E, Patterson BW, Polonsky KS, Schiavon CA, Correa JL, Salles JE, Wajchenberg BL, Cohen R. Moderate effect of duodenal-jejunal bypass surgery on glucose homeostasis in patients with type 2 diabetes. Obesity (Silver Spring). 2012 Jun;20(6):1266-72. doi: 10.1038/oby.2011.377. Epub 2012 Jan 19.
Reference Type
BACKGROUND
Rubino F, Marescaux J. Effect of duodenal-jejunal exclusion in a non-obese animal model of type 2 diabetes: a new perspective for an old disease. Ann Surg. 2004 Jan;239(1):1-11. doi: 10.1097/01.sla.0000102989.54824.fc.
Reference Type
BACKGROUND
Rubino F, Forgione A, Cummings DE, Vix M, Gnuli D, Mingrone G, Castagneto M, Marescaux J. The mechanism of diabetes control after gastrointestinal bypass surgery reveals a role of the proximal small intestine in the pathophysiology of type 2 diabetes. Ann Surg. 2006 Nov;244(5):741-9. doi: 10.1097/01.sla.0000224726.61448.1b.
Reference Type
BACKGROUND
Verdam FJ, Greve JW, Roosta S, van Eijk H, Bouvy N, Buurman WA, Rensen SS. Small intestinal alterations in severely obese hyperglycemic subjects. J Clin Endocrinol Metab. 2011 Feb;96(2):E379-83. doi: 10.1210/jc.2010-1333. Epub 2010 Nov 17.
Reference Type
BACKGROUND
Gniuli D, Calcagno A, Dalla Libera L, Calvani R, Leccesi L, Caristo ME, Vettor R, Castagneto M, Ghirlanda G, Mingrone G. High-fat feeding stimulates endocrine, glucose-dependent insulinotropic polypeptide (GIP)-expressing cell hyperplasia in the duodenum of Wistar rats. Diabetologia. 2010 Oct;53(10):2233-40. doi: 10.1007/s00125-010-1830-9. Epub 2010 Jun 30.
Reference Type
BACKGROUND
Rajagopalan H, Cherrington AD, Thompson CC, Kaplan LM, Rubino F, Mingrone G, Becerra P, Rodriguez P, Vignolo P, Caplan J, Rodriguez L, Galvao Neto MP. Endoscopic Duodenal Mucosal Resurfacing for the Treatment of Type 2 Diabetes: 6-Month Interim Analysis From the First-in-Human Proof-of-Concept Study. Diabetes Care. 2016 Dec;39(12):2254-2261. doi: 10.2337/dc16-0383. Epub 2016 Aug 12.
Reference Type
BACKGROUND
Gollisch KS, Lindhorst A, Raddatz D. EndoBarrier Gastrointestinal Liner in Type 2 Diabetic Patients Improves Liver Fibrosis as Assessed by Liver Elastography. Exp Clin Endocrinol Diabetes. 2017 Feb;125(2):116-121. doi: 10.1055/s-0042-118961. Epub 2016 Dec 22.
Reference Type
BACKGROUND
Other Identifiers
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P2017/302
Identifier Type: -
Identifier Source: org_study_id
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