Gastroparesis was the defining motility disorder that attracted me to the field of Neurogastroenterology and Motility. My career has been committed to better understanding this disease and other motility disorders in hopes that this will lead to better and more treatment options for our patients. My research and clinical work related to gastrointestinal motility disorders has led to collaborations with other specialties/conditions that affect GI motility and function such as ME/CFS, Myotonic dystrophy, Autonomic dysfunction, Migraines, Cystic fibrosis, Sjogren's disease and Scleroderma.

Clinical Focus

  • Gastroenterology
  • Gastroparesis
  • Neurogastroenterology
  • Dyspepsia
  • Esophageal Dysphagia
  • Intestinal Pseudoobstruction
  • Irritable Bowel Syndrome
  • Constipation
  • Motility
  • Small intestinal bacterial overgrowth

Academic Appointments

Administrative Appointments

  • Director, GI Motility and Neurogastroenterology, Division of Gastroenterology (2008 - Present)

Professional Education

  • Medical Education:UCLA GME Office (1999) CA
  • Residency:California Pacific Medical Center Internal Medicine Residency (2002) CA
  • Board Certification: Gastroenterology, American Board of Internal Medicine (2005)
  • Fellowship:California Pacific Medical Center (2005) CA
  • MD, UCLA School of Medicine (1999)

Research & Scholarship

Current Research and Scholarly Interests

My research interests focus on disorder of gastrointestinal motility. Specifically, those related to nausea and vomiting with or without gastroparesis, reflux and swallowing disorders, and irritable bowel syndrome. My research focuses on understanding and characterizing the abnormal motility pattern(s) that are associated with these symptoms.

Clinical Trials

  • Effect of Celiac Plexus Block on Gastric Emptying and Symptoms Caused by Gastroparesis Not Recruiting

    The investigators hypothesize that in patients with gastroparesis, gastric emptying will improve with celiac plexus block. By improving gastric emptying, symptoms related to gastroparesis including nausea, vomiting, bloating, abdominal pain, and weight loss, will also improve. In order to study this hypothesis, the investigators will enroll patients with gastroparesis who are non-responsive to the current treatments available. Patients will fill out a questionnaire to assess the severity of their symptoms then undergo Ansar testing (a non-invasive test) to measure their autonomic function respectively. Then, patients will undergo a celiac plexus block which is performed via an upper endoscopy. One week after the procedure, patients will be asked to undergo a gastric emptying study as well as repeat the Ansar testing to evaluate for any improvement in the gastric emptying and autonomic function respectively. Patient will be asked to repeat the questionnaire, one, two, three, and eight weeks after their procedure.

    Stanford is currently not accepting patients for this trial. For more information, please contact Irene Sonu, MD, 703-407-4899.

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  • Continuous Glucose Monitoring and Insulin Pump Therapy in Diabetic Gastroparesis Not Recruiting

    A pilot study to assess the safety, feasibility, and potential (uncontrolled) efficacy of continuous glucose monitoring (CGMS) in conjunction with an insulin pump to improve glycemic control for treatment of type 1 and type 2 diabetic patients with gastroparesis

    Stanford is currently not accepting patients for this trial.

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  • Impact of KUVAN® on Gastric Relaxation in Women With Diabetic Gastroparesis. Not Recruiting

    Kuvan® (sapropterin dihydrochloride) for Improving Gastric Accommodation in Women with Diabetic Gastroparesis (KIGA-DG)

    Stanford is currently not accepting patients for this trial. For more information, please contact Nighat j Ullah, 650-721-7216.

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  • Aprepitant for the Relief of Nausea in Patients With Chronic Nausea and Vomiting of Presumed Gastric Origin Trial Not Recruiting

    The principal objective of this multicenter, randomized, placebo-controlled trial is to evaluate whether 4 weeks of treatment with aprepitant will improve nausea as compared with placebo in patients with symptoms of chronic nausea and vomiting of presumed gastric origin.

    Stanford is currently not accepting patients for this trial. For more information, please contact Linda B Nguyen, MD, 650-725-3362.

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  • Vagal Nerve Stimulation for Gastroparesis Recruiting

    This study is investigating a new form of treatment for a digestive disorder called gastroparesis. Gastroparesis is thought to be caused by a mix of inflammation and neural dysfunction. The vagal nerve is a large nerve originating from the brain that regulates digestive function. Patients with gastroparesis have what is a called a low vagal tone which results in gastrointestinal motility problems and inflammation; therefore, investigators hypothesize that increasing vagal tone through a hand-held vagal nerve simulator will reduce inflammation and gastrointestinal motility problems in gastroparesis patients. Investigators will evaluate this hypothesis through the use of upper endoscopy testing, breath testing, and blood, stool, urine, heart rate variability, and saliva testing before and after 4 weeks of vagal nerve stimulation (VNS) treatment. There are 6 research visits Visit 1 and visit 2 may take up to 8 weeks (screening/baseline) Visit 3 and visit 4 will take 4 weeks (VNS treatment) visit 5 and 6 will take approximately 4 weeks (VNS followup/washout) Consequently, it is possible that if a patient were to be at the farthest ends of visit windows, they could potentially be in the study for approx 16 weeks. Visit 1 and 2 may be less than 8 weeks which would shorten the patient's overall involvement in the study. The treatment phase of the study will always be 4 weeks with an additional 4 week washout phase. Use of the VNS device takes 4 weeks. Endoscopy and blood work are taken before and after the treatment period.

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  • Study to Assess the Efficacy of VLY-686 in Relieving Symptoms of Gastroparesis Recruiting

    This is a multicenter, randomized, double-blind, placebo-controlled study to be conducted in the United States. One hundred fifty (150) subjects diagnosed with gastroparesis, who satisfy the selection criteria for the study, will be randomized to one of two treatment groups, active or placebo.

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  • Clinical Management With SPM System and Validation of the SPM 5 Hour Cutoff in Patients With Symptoms of Gastroparesis Not Recruiting

    This protocol is designed to validate use of the SPM for diagnosis of delayed gastric emptying in patients with symptoms of gastroparesis and assess impact of a SmartPill study on patient management in the gastroparetic populations. Patients with symptoms of gastroparesis will be recruited. Patients will undergo concurrent gastric scintigraphy and SPM testing to determine the presence or absence of delayed gastric emptying based on predetermined diagnostic cutoffs for each technique.

    Stanford is currently not accepting patients for this trial. For more information, please contact Emerald Poon Adler, (650) 721 - 2665.

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  • Gastroparesis Registry 2 Not Recruiting

    To expand a registry of patients for the study of the epidemiology, etiology, and degree of morbidity associated with gastroparesis.

    Stanford is currently not accepting patients for this trial. For more information, please contact Linda Nguyen, MD, 650-725-3362.

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2017-18 Courses


All Publications

  • Baseline features and differences in 48 week clinical outcomes in patients with gastroparesis and type 1 vs type 2 diabetes. Neurogastroenterology and motility Koch, K. L., Hasler, W. L., YATES, K. P., Parkman, H. P., Pasricha, P. J., Calles-Escandon, J., Snape, W. J., Abell, T. L., McCallum, R. W., Nguyen, L. A., Sarosiek, I., Farrugia, G., Tonascia, J., Lee, L., Miriel, L., HAMILTON, F. 2016; 28 (7): 1001-1015


    In studies of diabetic gastroparesis, patients with type 1 and type 2 diabetes mellitus (T1DM, T2DM) are often combined for analyses. We compared gastroparesis severity, healthcare utilization, psychological function, and quality of life in T1DM vs T2DM gastroparesis patients.Questionnaire, laboratory, and scintigraphy data from patients with gastroparesis and T1DM and T2DM from seven centers of the National Institute of Diabetes and Digestive and Kidney Diseases Gastroparesis Clinical Research Consortium Registry were compared at enrollment and after 48 weeks. Multiple regression models assessed baseline and follow-up differences between diabetes subtypes.At baseline, T1DM patients (N = 78) had slower gastric emptying, more hospitalizations, more gastric stimulator implantations, higher hemoglobin A1c (HbA1c), and more anxiety vs T2DM patients (N = 59). Independent discriminators of patients with T1DM vs T2DM included worse gastroesophageal reflux disease, less bloating, more peripheral neuropathy, and fewer comorbidities (p ? 0.05). On follow-up, gastrointestinal (GI) symptom scores decreased only in T2DM (p < 0.05), but not in T1DM patients who reported greater prokinetic, proton pump inhibitor, anxiolytic, and gastric stimulator usage over 48 weeks (p ? 0.03). Gastrointestinal symptoms at baseline and 48 weeks with both subtypes were not associated with HbA1c, peripheral neuropathy, psychological factors, or quality of life.Baseline symptoms were similar in T1DM and T2DM patients, even though T1DM patients had worse gastric emptying delays and higher HbA1c suggesting other factors mediate symptom severity. Symptom scores at 48 weeks decreased in T2DM, but not T1DM patients, despite increased medical and surgical treatment utilization by T1DM patients. Defining causes of different outcomes in diabetic gastroparesis warrants further investigation.

    View details for DOI 10.1111/nmo.12800

    View details for PubMedID 26946489

    View details for PubMedCentralID PMC5319426

  • Early Satiety and Postprandial Fullness in Gastroparesis Correlate With Gastroparesis Severity, Gastric Emptying, and Water Load Testing Digestive Disease Week (DDW) Parkman, H. P., Hallinan, E., Hasler, W. L., Farrugia, G., Pasricha, P. J., McCallum, R. W., Sarosiek, I., Koch, K. L., Snape, W. J., Abell, T. L., Nguyen, L. A., Tonascia, J., Hamilton, F. A., Clarke, J. O. W B SAUNDERS CO-ELSEVIER INC. 2016: S214?S215
  • Outcomes and Factors Associated With Reduced Symptoms in Patients With Gastroparesis GASTROENTEROLOGY Pasricha, P. J., Yates, K. P., Nguyen, L., Clarke, J., Abell, T. L., Farrugia, G., Hasler, W. L., Koch, K. L., Snape, W. J., McCallum, R. W., Sarosiek, I., Tonascia, J., Miriel, L. A., Lee, L., Hamilton, F., Parkman, H. P. 2015; 149 (7): 1762-?


    Gastroparesis is a chronic clinical syndrome characterized by delayed gastric emptying. However, little is known about patient outcomes or factors associated with reduction of symptoms.We studied adult patients with gastroparesis (of diabetic or idiopathic type) enrolled in the National Institute of Diabetes and Digestive and Kidney Diseases Gastroparesis Clinical Research Consortium Gastroparesis Registry, seen every 16 weeks and treated according to the standard of care with prescribed medications or other therapies at 7 tertiary care centers. Characteristics associated with reduced symptoms, based on a decrease of 1 or more in the gastroparesis cardinal symptom index (GCSI) score after 48 weeks of care, were determined from logistic regression models. Data were collected from patients for up to 4 years (median, 2.1 y).Of 262 patients, 28% had reductions in GCSI scores of 1 or more at 48 weeks. However, there were no significant reductions in GCSI score from weeks 48 through 192. Factors independently associated with reduced symptoms at 48 weeks included male sex, age 50 years and older, initial infectious prodrome, antidepressant use, and 4-hour gastric retention greater than 20%. Factors associated with no reduction in symptoms included overweight or obesity, a history of smoking, use of pain modulators, moderate to severe abdominal pain, a severe gastroesophageal reflex, and moderate to severe depression.Over a median follow-up period of 2.1 years, 28% of patients treated for gastroparesis at centers of expertise had reductions in GCSI scores of 1 or greater, regardless of diabetes. These findings indicate the chronic nature of gastroparesis. We identified factors associated with reduced symptoms that might be used to guide treatment. no: NCT00398801.

    View details for DOI 10.1053/j.gastro.2015.08.008

    View details for Web of Science ID 000365808100030

    View details for PubMedID 26299414

    View details for PubMedCentralID PMC4663150

  • Clinical Presentation and Pathophysiology of Gastroparesis GASTROENTEROLOGY CLINICS OF NORTH AMERICA Nguyen, L. A., Snape, W. J. 2015; 44 (1): 21-?


    Gastroparesis is a heterogeneous disorder defined by delay in gastric emptying. Symptoms of gastroparesis are nonspecific, including nausea, vomiting, early satiety, bloating, and/or abdominal pain. Normal gastric motor function and sensory function depend on a complex coordination between the enteric and central nervous system. This article discusses the pathophysiology of delayed gastric emptying and the symptoms of gastroparesis, including antropyloroduodenal dysmotility, impaired gastric accommodation, visceral hypersensitivity, and autonomic dysfunction. The underlying pathophysiology of gastroparesis is complex and multifactorial. The article discusses how a combination of these factors leads to symptoms of gastroparesis.

    View details for DOI 10.1016/j.gtc.2014.11.003

    View details for Web of Science ID 000350944600005

    View details for PubMedID 25667020

  • Association of low numbers of CD206-positive cells with loss of ICC in the gastric body of patients with diabetic gastroparesis NEUROGASTROENTEROLOGY AND MOTILITY Bernard, C. E., Gibbons, S. J., Mann, I. S., FROSCHAUER, L., Parkman, H. P., Harbison, S., Abell, T. L., Snape, W. J., Hasler, W. L., McCallum, R. W., Sarosiek, I., Nguyen, L. A., Koch, K. L., Tonascia, J., Hamilton, F. A., Kendrick, M. L., Shen, K. R., Pasricha, P. J., Farrugia, G. 2014; 26 (9): 1275-1284


    There is increasing evidence for specific cellular changes in the stomach of patients with diabetic (DG) and idiopathic (IG) gastroparesis. The most significant findings are loss of interstitial cells of Cajal (ICC), neuronal abnormalities, and an immune cellular infiltrate. Studies done in diabetic mice have shown a cytoprotective effect of CD206+ M2 macrophages. To quantify overall immune cellular infiltrate, identify macrophage populations, and quantify CD206+ and iNOS+ cells. To investigate associations between cellular phenotypes and ICC.Full thickness gastric body biopsies were obtained from non-diabetic controls (C), diabetic controls (DC), DG, and IG patients. Sections were labeled for CD45, CD206, Kit, iNOS, and putative human macrophage markers (HAM56, CD68, and EMR1). Immunoreactive cells were quantified from the circular muscle layer.Significantly fewer ICC were detected in DG and IG tissues, but there were no differences in the numbers of cells immunoreactive for other markers between patient groups. There was a significant correlation between the number of CD206+ cells and ICC in DG and DC patients, but not in C and IG and a significant correlation between iNOS+ cells and ICC in the DC group, but not the other groups. CD68 and HAM56 reliably labeled the same cell populations, but EMR1 labeled other cell types.Depletion of ICC and correlation with changes in CD206+ cell numbers in DC and DG patients suggests that in humans, like mice, CD206+ macrophages may play a cytoprotective role in diabetes. These findings may lead to novel therapeutic options, targeting alternatively activated macrophages.

    View details for DOI 10.1111/nmo.12389

    View details for Web of Science ID 000341625000007

    View details for PubMedID 25041465

    View details for PubMedCentralID PMC4149814

  • Effect of Nortriptyline on Symptoms of Idiopathic Gastroparesis The NORIG Randomized Clinical Trial JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION Parkman, H. P., Van Natta, M. L., Abell, T. L., McCallum, R. W., Sarosiek, I., Nguyen, L., Snape, W. J., Koch, K. L., Hasler, W. L., Farrugia, G., Lee, L., Unalp-Arida, A., Tonascia, J., Hamilton, F., Pasricha, P. J. 2013; 310 (24): 2640-2649


    Gastroparesis remains a challenging syndrome to manage, with few effective treatments and a lack of rigorously controlled trials. Tricyclic antidepressants are often used to treat refractory symptoms of nausea, vomiting, and abdominal pain. Evidence from well-designed studies for this use is lacking.To determine whether treatment with nortriptyline results in symptomatic improvement in patients with idiopathic gastroparesis.The NORIG (Nortriptyline for Idiopathic Gastroparesis) trial, a 15-week multicenter, parallel-group, placebo-controlled, double-masked, randomized clinical trial from the National Institute of Diabetes and Digestive and Kidney Diseases Gastroparesis Clinical Research Consortium (GpCRC), comparing nortriptyline with placebo for symptomatic relief in idiopathic gastroparesis. One hundred thirty patients with idiopathic gastroparesis were enrolled between March 2009 and June 2012 at 7 US academic medical centers. Patient follow-up was completed in October 2012. Inclusion criteria included delayed gastric emptying and moderate to severe symptom scores using the Gastroparesis Cardinal Symptom Index (GCSI). INTERVENTIONS Nortriptyline vs placebo. Study drug dose was increased at 3-week intervals (10, 25, 50, 75 mg) up to 75 mg at 12 weeks.The primary outcome measure of symptomatic improvement was a decrease from the patient's baseline GCSI score of at least 50% on 2 consecutive 3-week GCSI assessments during 15 weeks of treatment.The primary symptomatic improvement outcome did not differ between 65 patients randomized to nortriptyline vs 65 patients randomized to placebo: 15 (23% [95% CI, 14%-35%]) in the nortriptyline group vs 14 (21% [95% CI, 12%-34%]) in the placebo group (P?=?.86). Treatment was stopped more often in the nortriptyline group (19 [29% {95% CI, 19%-42%}]) than in the placebo group (6 [9%] {95% CI, 3%-19%}]) (P?=?.007), but numbers of adverse events were not different (27 [95% CI, 18-39] vs 28 [95% CI, 19-40]) (P?=?.89).Among patients with idiopathic gastroparesis, the use of nortriptyline compared with placebo for 15 weeks did not result in improvement in overall symptoms. These findings do not support the use of nortriptyline for idiopathic Identifier: NCT00765895.

    View details for DOI 10.1001/jama.2013.282833

    View details for Web of Science ID 000328818000016

    View details for PubMedID 24368464

    View details for PubMedCentralID PMC4099968

  • Massive gastrointestinal dilatation in a case of hereditary hollow visceral myopathy. Digestive and liver disease Huang, R. J., Yun, C., Nguyen, L. 2013; 45 (10): 866-?

    View details for DOI 10.1016/j.dld.2013.04.005

    View details for PubMedID 23816694

  • Factors related to abdominal pain in gastroparesis: contrast to patients with predominant nausea and vomiting. Neurogastroenterology and motility Hasler, W. L., Wilson, L. A., Parkman, H. P., Koch, K. L., Abell, T. L., Nguyen, L., Pasricha, P. J., Snape, W. J., McCallum, R. W., Sarosiek, I., Farrugia, G., Calles, J., Lee, L., Tonascia, J., Unalp-Arida, A., HAMILTON, F. 2013; 25 (5): 427-?


    Factors associated with abdominal pain in gastroparesis are incompletely evaluated and comparisons of pain vs other symptoms are limited. This study related pain to clinical factors in gastroparesis and contrasted pain/discomfort- with nausea/vomiting-predominant disease.Clinical and scintigraphy data were compared in 393 patients from seven centers of the NIDDK Gastroparesis Clinical Research Consortium with moderate-severe (Patient Assessment of Upper Gastrointestinal Disorders Symptoms [PAGI-SYM] score ? 3) vs none-mild (PAGI-SYM < 3) upper abdominal pain and predominant pain/discomfort vs nausea/vomiting.Upper abdominal pain was moderate-severe in 261 (66%). Pain/discomfort was predominant in 81 (21%); nausea/vomiting was predominant in 172 (44%). Moderate-severe pain was more prevalent with idiopathic gastroparesis and with lack of infectious prodrome (P ? 0.05) and correlated with scores for nausea/vomiting, bloating, lower abdominal pain/discomfort, bowel disturbances, and opiate and antiemetic use (P < 0.05), but not gastric emptying or diabetic neuropathy or control. Gastroparesis severity, quality of life, and depression and anxiety were worse with moderate-severe pain (P ? 0.008). Factors associated with moderate-severe pain were similar in diabetic and idiopathic gastroparesis. Compared to predominant nausea/vomiting, predominant pain/discomfort was associated with impaired quality of life, greater opiate, and less antiemetic use (P < 0.01), but similar severity and gastric retention.Moderate-severe abdominal pain is prevalent in gastroparesis, impairs quality of life, and is associated with idiopathic etiology, lack of infectious prodrome, and opiate use. Pain is predominant in one fifth of gastroparetics. Predominant pain has at least as great an impact on disease severity and quality of life as predominant nausea/vomiting.

    View details for DOI 10.1111/nmo.12091

    View details for PubMedID 23414452

    View details for PubMedCentralID PMC3907086

  • Platelet-derived growth factor receptor a (PDGFRa)-expressing "fibroblast-like cells" in diabetic and idiopathic gastroparesis of humans NEUROGASTROENTEROLOGY AND MOTILITY Grover, M., Bernard, C. E., Pasricha, P. J., Parkman, H. P., Abell, T. L., Nguyen, L. A., Snape, W., Shen, K. R., Sarr, M., Swain, J., Kendrick, M., Gibbons, S., Ordog, T., Farrugia, G. 2012; 24 (9): 844-852


    Emerging evidence suggests that "fibroblast-like cells" (FLC) may play a role in the regulation of gastrointestinal (GI) motor function. FLC are ultrastructurally distinct from other interstitial cells, including interstitial cells of Cajal (ICC), and express small-conductance Ca(2+) -activated K(+) channels (SK3). In mice, platelet-derived growth factor receptor ? (PDGFR?) antibody has also been shown to label FLC. The aims of this study were to determine the morphology and distribution of PDGFR?-immunoreactive (ir) FLC in human gastric muscle and to determine if FLC are altered in gastroparesis, where ICC are reduced.Full thickness gastric body biopsies from five healthy subjects, 10 diabetic, and 10 idiopathic gastroparesis patients were immunolabeled using SK3 and PDGFR? staining for FLC and Kit staining for ICC. Intramuscular FLC and ICC were quantified.Intramuscular PDGFR?-ir cells had slender cell bodies and long, thin processes and were more abundant in the longitudinal compared with the circular muscle. In the region of myenteric plexus, FLC had smaller, rounder cell bodies with 3-4 processes and formed networks, often around ganglia. All SK3-ir cell structures showed complete overlap with PDGFR?-ir. FLC were in close proximity to ICC, but their cell bodies did not overlap. No differences were seen in the distribution, morphology, or overall numbers of FLC in gastroparesis patients.In conclusion, PDGFR? identifies FLC in human gastric smooth muscle. FLC were not altered in distribution or overall numbers in gastroparesis. Additional studies are required to determine their role in human GI function.

    View details for DOI 10.1111/j.1365-2982.2012.01944.x

    View details for Web of Science ID 000308089000012

    View details for PubMedID 22650155

  • Clinical-histological associations in gastroparesis: results from the Gastroparesis Clinical Research Consortium NEUROGASTROENTEROLOGY AND MOTILITY Grover, M., Bernard, C. E., Pasricha, P. J., Lurken, M. S., Faussone-Pellegrini, M. S., Smyrk, T. C., Parkman, H. P., Abell, T. L., Snape, W. J., Hasler, W. L., McCallum, R. W., Nguyen, L., Koch, K. L., Calles, J., Lee, L., Tonascia, J., Uenalp-Arida, A., Hamilton, F. A., Farrugia, G. 2012; 24 (6): 531-?


    Cellular changes associated with diabetic (DG) and idiopathic gastroparesis (IG) have recently been described from patients enrolled in the Gastroparesis Clinical Research Consortium. The association of these cellular changes with gastroparesis symptoms and gastric emptying is unknown. The aim of this study was to relate cellular changes to symptoms and gastric emptying in patients with gastroparesis.Earlier, using full thickness gastric body biopsies from 20 DG, 20 IG, and 20 matched controls, we found decreased interstitial cells of Cajal (ICC) and enteric nerves and an increase in immune cells in both DG and IG. Here, demographic, symptoms [gastroparesis cardinal symptom index score (GCSI)], and gastric emptying were related to cellular alterations using Pearson's correlation coefficients.Interstitial cells of Cajal counts inversely correlated with 4 h gastric retention in DG but not in IG (r = -0.6, P = 0.008, DG, r = 0.2, P = 0.4, IG). There was also a significant correlation between loss of ICC and enteric nerves in DG but not in IG (r = 0.5, P = 0.03 for DG, r = 0.3, P = 0.16, IG). Idiopathic gastroparesis with a myenteric immune infiltrate scored higher on the average GCSI (3.6 ± 0.7 vs 2.7 ± 0.9, P = 0.05) and nausea score (3.8 ± 0.9 vs 2.6 ± 1.0, P = 0.02) as compared to those without an infiltrate.In DG, loss of ICC is associated with delayed gastric emptying. Interstitial cells of Cajal or enteric nerve loss did not correlate with symptom severity. Overall clinical severity and nausea in IG is associated with a myenteric immune infiltrate. Thus, full thickness gastric biopsies can help define specific cellular abnormalities in gastroparesis, some of which are associated with physiological and clinical characteristics of gastroparesis.

    View details for DOI 10.1111/j.1365-2982.2012.01894.x

    View details for Web of Science ID 000303995700006

    View details for PubMedID 22339929

    View details for PubMedCentralID PMC3353102

  • Gastrointestinal Dysmotility DIGESTIVE DISEASES AND SCIENCES Nimgaonkar, A., Choi, J. W., Nguyen, L., Triadafilopoulos, G. 2012; 57 (5): 1130-1133

    View details for DOI 10.1007/s10620-011-1946-x

    View details for Web of Science ID 000303385100004

    View details for PubMedID 22038542

  • Characteristics of Patients With Chronic Unexplained Nausea and Vomiting and Normal Gastric Emptying CLINICAL GASTROENTEROLOGY AND HEPATOLOGY Pasricha, P. J., Colvin, R., Yates, K., Hasler, W. L., Abell, T. L., Uenalp-Arida, A., Nguyen, L., Farrugia, G., Koch, K. L., Parkman, H. P., Snape, W. J., Lee, L., Tonascia, J., Hamilton, F. 2011; 9 (7): 567-U89


    Chronic nausea and vomiting with normal gastric emptying is a poorly understood syndrome; we analyzed its characteristics.We collected and analyzed data from 425 patients with chronic nausea and vomiting, enrolled at 6 centers by the Gastroparesis Clinical Research Consortium in the National Institute of Diabetes and Digestive and Kidney Diseases Gastroparesis Registry.Among the patients, 319 (75%) had delayed emptying, defined by the results of a standardized, low-fat meal, and 106 had normal gastric emptying. Patients with or without delayed emptying did not differ in age, sex, or race, although those with normal gastric emptying were less likely to be diabetic. Symptom severity indexes were similar between groups for nausea, retching, vomiting, stomach fullness, inability to complete a meal, feeling excessively full after meals, loss of appetite, bloating, and visibly larger stomach. There were no differences in health care utilization, quality of life indexes, depression, or trait anxiety scores. However, state anxiety scores were slightly higher among patients with delayed gastric emptying. Total gastroparesis cardinal symptom index scores were not correlated with gastric retention after 2 or 4 hours in either group. Patients with the syndrome were not adequately captured by the stand-alone criteria for the Rome III diagnoses of chronic idiopathic nausea and functional vomiting. With rare exceptions, the diagnosis remained stable after a 48-week follow-up period.Patients with nausea and vomiting with normal gastric emptying represent a significant medical problem and are, for the most part, indistinguishable from those with gastroparesis. This syndrome is not categorized in the medical literature--it might be a separate clinical entity.

    View details for DOI 10.1016/j.cgh.2011.03.003

    View details for Web of Science ID 000292467900015

    View details for PubMedID 21397732

    View details for PubMedCentralID PMC3123425

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