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Camilleri M, Zheng T, Vosoughi K, Lupianez-Merly C, Eckert D, Busciglio I, Burton D, Dilmaghani S. Optimal measurement of gastric emptying of solids in gastroparesis or functional dyspepsia: evidence to establish standard test. Gut 2023; 72:2241-2249. [PMID: 37726164 PMCID: PMC10872889 DOI: 10.1136/gutjnl-2023-330733] [Citation(s) in RCA: 9] [Impact Index Per Article: 4.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/20/2023] [Accepted: 08/31/2023] [Indexed: 09/21/2023]
Abstract
OBJECTIVE Symptoms in gastroparesis (Gp) and functional dyspepsia (FD) overlap; using egg protein substitute to measure gastric emptying of solids (GES), ~40% of patients are reclassified from Gp to FD, and vice versa. Our aim was to assess inter-individual and intra-individual coefficients of variation (COV) in GES in symptomatic patients with Gp or FD with documented slow or normal GES, respectively. DESIGN Scintigraphic GES (T1/2 and GE% at 2 and 4 hours) using a 320 kcal real egg meal (30% fat) was tested in the following: single measurements in 20 patients with diabetes mellitus (10 each type 1 and type 2); repeat GES to estimate COVintra measured: 3 days apart in 9 Gp, 4 weeks apart in 21 Gp and 18 with FD with normal GE assigned to placebo and in 70 patients at 94.3 weeks (median) apart. RESULTS COVinter for GE% at 4 hours and GE T1/2 were respectively 14.2% and 23.5% in FD and 27.5% and 33% in Gp; COVintra for GE% at 4 hours and GE T1/2 up to 4 weeks apart were 23.4% and 37.9% in FD and 20.1% and 33% in Gp. GE% at 2 hours showed less consistent results. However, >85% retained original diagnosis as normal or delayed. From clinical GES to baseline research for Gp group, repeat GES (after treatment) showed the COVintra for GE% at 4 hours was 37.3% at median 94.3 weeks, with 26/70 changed diagnoses. CONCLUSION The 320 kcal (30% fat) GES scintigraphic test provides consistent diagnosis in >85% and should be the standard test for suspected gastric emptying disorders.
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Affiliation(s)
| | - Ting Zheng
- Gastroenterology, Mayo Clinic, Rochester, Minnesota, USA
| | - Kia Vosoughi
- Gastroenterology, Mayo Clinic, Rochester, Minnesota, USA
| | | | - Deborah Eckert
- Gastroenterology, Mayo Clinic, Rochester, Minnesota, USA
| | | | - Duane Burton
- Gastroenterology, Mayo Clinic, Rochester, Minnesota, USA
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2
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Yan C, Dai C, Liu N, Qian W, Yang P, Hou X. Effects of Simo decoction on gastric motility of diabetic rats. Neurogastroenterol Motil 2022; 34:e14450. [PMID: 36111645 DOI: 10.1111/nmo.14450] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/11/2022] [Revised: 06/27/2022] [Accepted: 07/27/2022] [Indexed: 02/08/2023]
Abstract
BACKGROUND To investigate the effects of simo decoction (SMD) on the gastric motility of diabetic rats. METHODS Diabetic rats were gavaged with various doses of SMD (0.15, 1.5, and 3.0 ml/kg/d) or saline, and their blood glucose levels and body weight were monitored. Gastric emptying and antral motility were assessed by phenol red retention and contractions of antral strips, respectively. The levels of substance P (SP), vasoactive intestinal peptide (VIP), and neurogenic nitric oxide synthase (nNOS) in the gastric antrum were determined by real-time polymerase chain reaction and Western blot. RESULTS Gastric emptying was delayed in diabetic rats (p < 0.01 vs. non-diabetic controls) but accelerated after SMD administration (p < 0.01). The contractions of antral strips were reduced in diabetic rats (p < 0.01 vs. non-diabetic controls) but improved after SMD intervention (p < 0.05). The mRNA expressions of SP, VIP, and nNOS in diabetic rats were downregulated compared with non-diabetic controls (all p < 0.01). Simo decoction treatment did not affect the expression of these factors in diabetic rats. The protein levels of SP, VIP, and nNOS in diabetic rats were decreased (p < 0.01), increased (p < 0.01), and comparable (p > 0.05), respectively, in comparison with non-diabetic controls. Simo decoction administration increased SP protein expression (p < 0.01) and decreased the levels of VIP (p < 0.01) and nNOS (p < 0.01) in diabetic rats. CONCLUSIONS Simo decoction improved gastric dysmotility of diabetic rats possibly by upregulating SP and downregulating VIP and nNOS.
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Affiliation(s)
- Caihua Yan
- Department of Gastroenterology, Renhe Hospital Affiliated to China Three Gorges University, Yichang, China
| | - Chibing Dai
- Department of Gastroenterology, Renhe Hospital Affiliated to China Three Gorges University, Yichang, China
| | - Na Liu
- Department of Gastroenterology, Union Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Wei Qian
- Department of Gastroenterology, Union Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Pengchun Yang
- Department of Gastroenterology, Renhe Hospital Affiliated to China Three Gorges University, Yichang, China
| | - Xiaohua Hou
- Department of Gastroenterology, Union Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
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3
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Meling S, Bertoli D, Sangnes DA, Brock C, Drewes A, Ejskjaer N, Dimcevski G, Søfteland E. Diabetic Gastroenteropathy: Soothe the Symptoms or Unravel a Cure? Curr Diabetes Rev 2022; 18:e220321192412. [PMID: 34225633 DOI: 10.2174/1573399817666210322154618] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/16/2020] [Revised: 01/19/2021] [Accepted: 02/13/2021] [Indexed: 11/22/2022]
Abstract
Autonomic neuropathy in patients with diabetes mellitus, and especially complications related to gastrointestinal neuropathy, are often overlooked in the clinic. Diabetic gastroenteropathy affects every segment of the gastrointestinal tract and generates symptoms that may include nausea, early satiety, vomiting, abdominal pain, constipation, and diarrhea. Severe cases can be complicated by weight loss, dehydration, and electrolyte disturbances. The pathophysiology is complex, the diagnostics and treatment options are multidisciplinary, and there is generally a lack of evidence for the treatment options. The aims for this review are first to summarize the pathophysiology and describe possible and expected symptoms and complications.Further, we will try to supply the clinician with a straightforward tool for diagnostics, and then, we shall summarize established treatment options, including diet recommendations, pharmacological and non-pharmacological options. Finally, we will explore the multiple possibilities of novel treatment, looking at medications related to the pathophysiology of neuropathy, other manifestations of autonomic neuropathies, and symptomatic treatment for other gastrointestinal disorders, also including new knowledge of endosurgical and neuromodulatory treatment. The overall goal is to increase awareness and knowledge on this frequent diabetic complication and to provide better tools for diagnosis and treatment. Ultimately, we hope to encourage further research in this field, as there are clear shortcomings in terms of biomarkers, pathophysiology, as well as treatment possibilities. In conclusion, diagnosis and management of diabetic gastroenteropathy are challenging and often require multidisciplinary teams and multimodal therapies. Treatment options are sparse, but new pharmacological, endoscopic, and neuromodulatory techniques have shown promising results in initial studies.
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Affiliation(s)
- Sondre Meling
- Department of Medicine, Stavanger University Hospital, Stavanger, Norway
- Department of Clinical Medicine, University of Bergen, Bergen, Norway
| | - Davide Bertoli
- Department of Gastroenterology and Hepatology, Aalborg University Hospital, Aalborg, Denmark
| | - Dag A Sangnes
- Department of Clinical Medicine, University of Bergen, Bergen, Norway
- Department of Medicine, Haukeland University Hospital, Bergen, Norway
| | - Christina Brock
- Department of Gastroenterology and Hepatology, Aalborg University Hospital, Aalborg, Denmark
- Steno Diabetes Center North Jutland, Aalborg, Denmark
| | - Asbjørn Drewes
- Department of Gastroenterology and Hepatology, Aalborg University Hospital, Aalborg, Denmark
- Steno Diabetes Center North Jutland, Aalborg, Denmark
| | - Niels Ejskjaer
- Steno Diabetes Center North Jutland, Aalborg, Denmark
- Department of Clinical Medicine and Endocrinology, Aalborg University Hospital, Aalborg, Denmark
| | - Georg Dimcevski
- Department of Clinical Medicine, University of Bergen, Bergen, Norway
| | - Eirik Søfteland
- Department of Clinical Medicine, University of Bergen, Bergen, Norway
- Department of Medicine, Haukeland University Hospital, Bergen, Norway
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A Meta-Analysis of the Efficacy of Prokinetic Agents against Glycemic Control. Gastroenterol Res Pract 2019; 2019:3014973. [PMID: 31582970 PMCID: PMC6754912 DOI: 10.1155/2019/3014973] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/15/2019] [Revised: 07/02/2019] [Accepted: 08/19/2019] [Indexed: 02/07/2023] Open
Abstract
Background Prokinetic agents are used in diabetic gastroparesis patients to improve gastric emptying and upper gastrointestinal (GI) symptoms. However, the efficacy of prokinetic agents against glycemic control is questionable. Therefore, we conducted a systemic review and meta-analysis to determine the efficacy of prokinetic agents against glycemic control. Methods Randomized controlled trials (RCTs) evaluating the effect of prokinetics were identified by searching PubMed, Embase, and the Cochrane Library databases until April 2018. The primary outcome was changes in the mean value of glycosylated hemoglobin (HbA1c), fasting blood sugar (FBS), and fasting serum insulin (FINS). The pooled standardized mean differences (SMD) with 95% confidence intervals (CIs) were calculated by evaluating the strength of the association. We used the random effect models to analyze these markers. The effects of each component of the prokinetic agents on glycemic control were separately analyzed. Results Five RCTs with 190 patients met the criteria and were included in the meta-analysis. There were statistically significant SMD between prokinetics and placebo-controlled groups with respect to the reduction of HbA1c (-1.141, 95% CI -1.843, -0.438; P < 0.01). No statistically significant differences were noted between the two groups for FBS (-1.270, 95% CI -2.613, -0.074; P = 0.06) and FINS (0.359, 95% CI -1.205~1.923; P = 0.65). Conclusions Prokinetics have a positive effect on glycemic control. Further large-scale prospective studies are needed.
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Abstract
PURPOSE OF REVIEW The goal of this review is to review the current status of prokinetics and to place it in historical context. Impaired motility and thus propulsion have long been thought to play important roles in the pathogenesis of a number of gastrointestinal disorders including gastroesophageal reflux disease (GERD), gastroparesis, chronic idiopathic pseudo-obstruction, and constipation. Historically, disordered motility was also thought to contribute to a number of functional gastrointestinal disorders such as functional dyspepsia (FD) and irritable bowel syndrome (IBS). RECENT FINDINGS As we learn more of the pathophysiology of FD, IBS, GERD, constipation, and gastroparesis, the limitations of a therapeutic strategy based on the stimulation of motility (i.e., the use of a prokinetic) have become apparent and the disappointments of the past explained. The development of prokinetic drugs has also been hampered by the non-selective nature of many of the agents studied to date which resulted in some unexpected side effects. There is still an unmet need for an effective and safe prokinetic, but drug development in this area must be mindful of the challenges of the area and the need for selectivity for a given target receptor.
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Affiliation(s)
- Eamonn M M Quigley
- Lynda K and David M Underwood Center for Digestive Disorders, Houston, TX, USA.
- Division of Gastroenterology and Hepatology, The Methodist Hospital, 6550 Fannin St, SM 1201, Houston, TX, 77030, USA.
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Parthasarathy G, Kudva YC, Low PA, Camilleri M, Basu A, Bharucha AE. Relationship Between Gastric Emptying and Diurnal Glycemic Control in Type 1 Diabetes Mellitus: A Randomized Trial. J Clin Endocrinol Metab 2017; 102:398-406. [PMID: 27880079 PMCID: PMC5413165 DOI: 10.1210/jc.2016-2809] [Citation(s) in RCA: 24] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/26/2016] [Accepted: 11/22/2016] [Indexed: 12/13/2022]
Abstract
CONTEXT In type 1 diabetes (T1D), delayed gastric emptying (GE) may predispose to a mismatch between insulin delivery and glucose absorption. Previous studies evaluated, only partly, the relationship between delayed GE and postprandial, but not diurnal, glycemia. OBJECTIVE To assess the relationship between GE disturbances and glycemic control in T1D and the effects of accelerating GE on glycemic control. DESIGN, SETTING, AND PARTICIPANTS This was a randomized placebo-controlled trial in 30 patients with T1D on an insulin pump at an academic medical center. INTERVENTION(S) GE was evaluated with a [13C]-Spirulina breath test at baseline (GEbaseline), during intravenous saline or erythromycin (2 or 3 mg/kg; GEiv), and after 7 days of oral erythromycin or placebo (GEoral). Weighed meals were provided throughout the study. MAIN OUTCOME MEASURE(S) These were GE and continuous glucose monitoring (CGM). RESULTS The baseline glycosylated hemoglobin was 7.6% ± 0.8% (60 ± 8.7 mmol/mol); 12 patients (40%) had delayed GE; faster GE was associated with a greater postprandial CGM-based glucose, but slower GE was not associated with postprandial hypoglycemia (<70 mg/dL). Intravenous (3 mg/kg) but not oral erythromycin accelerated GE. The relationship between GE and glycemia differed between the postprandial periods and the entire day. After adjusting for carbohydrate intake and insulin consumption, faster GE was associated with more hyperglycemia during the postprandial period but lower glucose values across the entire study. CONCLUSIONS In T1D, pharmacologically mediated acceleration of GE increases postprandial CGM-based glucose. In contrast, delayed GE is associated with greater CGM-based glucose values over the entire day.
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Affiliation(s)
| | - Yogish C. Kudva
- Division of Endocrinology, Department of Internal Medicine, and
| | - Phillip A. Low
- Department of Neurology, Mayo Clinic, Rochester, Minnesota 55905
| | | | - Ananda Basu
- Division of Endocrinology, Department of Internal Medicine, and
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Quigley EMM. Prokinetics in the Management of Functional Gastrointestinal Disorders. J Neurogastroenterol Motil 2015; 21:330-6. [PMID: 26130629 PMCID: PMC4496896 DOI: 10.5056/jnm15094] [Citation(s) in RCA: 31] [Impact Index Per Article: 3.1] [Reference Citation Analysis] [Abstract] [Key Words] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/01/2015] [Accepted: 06/23/2015] [Indexed: 12/12/2022] Open
Abstract
A variety of common and some not common gastrointestinal syndromes are thought to be based on impaired gut motility. For some, the role of motility is well defined, for others and the functional gastrointestinal disorders, in particular, the role of hypo- or dysmotility remains unclear. Over the years pharmacological and physiological laboratories have developed drugs which stimulate gut motility; many have been evaluated in motility and functional disorders with what can best be described as mixed results. Lack of receptor specificity and resultant expected and unexpected adverse events have led to the demise of some of these agents. Newer, more selective agents offer promise but the heterogeneity of the clinical disorders they target continues to pose a formidable challenge to drug development in this area.
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Affiliation(s)
- Eamonn M M Quigley
- Division of Gastroenterology and Hepatology, Department of Medicine, Houston Methodist Hospital, Houston, Texas, USA
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8
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Plummer MP, Jones KL, Cousins CE, Trahair LG, Meier JJ, Chapman MJ, Horowitz M, Deane AM. Hyperglycemia potentiates the slowing of gastric emptying induced by exogenous GLP-1. Diabetes Care 2015; 38:1123-1129. [PMID: 25784665 DOI: 10.2337/dc14-3091] [Citation(s) in RCA: 24] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/30/2014] [Accepted: 02/23/2015] [Indexed: 02/05/2023]
Abstract
OBJECTIVE Acute hyperglycemia markedly slows gastric emptying. Exogenous GLP-1 also slows gastric emptying, leading to diminished glycemic excursions. The primary objective was to determine whether hyperglycemia potentiates the slowing of gastric emptying induced by GLP-1 administration. RESEARCH DESIGN AND METHODS Ten healthy participants were studied on 4 separate days. Blood glucose was clamped at hyperglycemia using an intravenous infusion of 25% dextrose (∼12 mmol/L; hyper) on 2 days, or maintained at euglycemia (∼6 mmol/L; eu) on 2 days, between t = -15 and 240 min. During hyperglycemic and euglycemic days, participants received intravenous GLP-1 (1.2 pmol/kg/min) and placebo in a randomized double-blind fashion. At t = 0 min, subjects ingested 100 g beef mince labeled with 20 MBq technetium-99m-sulfur colloid and 3 g 3-O-methyl-glucose (3-OMG), a marker of glucose absorption. Gastric emptying was measured scintigraphically from t = 0 to 240 min and serum 3-OMG taken at regular intervals from t = 15 to 240 min. The areas under the curve for gastric emptying and 3-OMG were analyzed using one-way repeated-measures ANOVA with Bonferroni-Holm adjusted post hoc tests. RESULTS Hyperglycemia slowed gastric emptying (eu/placebo vs. hyper/placebo; P < 0.001) as did GLP-1 (eu/placebo vs. eu/GLP-1; P < 0.001). There was an additive effect of GLP-1 and hyperglycemia, such that gastric emptying was markedly slower compared with GLP-1 administration during euglycemia (eu/GLP-1 vs. hyper/GLP-1; P < 0.01). CONCLUSIONS Acute administration of exogenous GLP-1 profoundly slows gastric emptying during hyperglycemia in excess of the slowing induced by GLP-1 during euglycemia. Studies are required to determine the effects of hyperglycemia on gastric emptying with the subcutaneously administered commercially available GLP-1 agonists in patients with type 2 diabetes.
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Affiliation(s)
- Mark P Plummer
- Discipline of Acute Care Medicine, University of Adelaide, Adelaide, Australia Department of Critical Care Services, Royal Adelaide Hospital, Adelaide, Australia
| | - Karen L Jones
- Discipline of Medicine, University of Adelaide, Adelaide, Australia
| | - Caroline E Cousins
- Department of Critical Care Services, Royal Adelaide Hospital, Adelaide, Australia
| | | | - Juris J Meier
- Diabetes Division, St. Josef-Hospital, Ruhr-University Bochum, Bochum, Germany
| | - Marianne J Chapman
- Discipline of Acute Care Medicine, University of Adelaide, Adelaide, Australia Department of Critical Care Services, Royal Adelaide Hospital, Adelaide, Australia
| | - Michael Horowitz
- Discipline of Medicine, University of Adelaide, Adelaide, Australia
| | - Adam M Deane
- Discipline of Acute Care Medicine, University of Adelaide, Adelaide, Australia Department of Critical Care Services, Royal Adelaide Hospital, Adelaide, Australia
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Abstract
OPINION STATEMENT Gastroparesis is defined as the presence of delayed gastric emptying in the absence of mechanical obstruction, with a variety of upper gastrointestinal symptoms. Although measurement of gastric emptying is necessary for the diagnostic labeling, this finding has little impact in terms of explaining the symptom pattern and determining the prognosis and therapeutic approach. Clinical management is based on ruling out of mechanical causes and serum electrolyte imbalances, followed by initial medical treatment with a gastroprokinetic agent in most cases. However, the evidence that these drugs provide substantial symptomatic benefit is weak. Recent attempts to establish efficacy with newer prokinetics, including serotonin-4, motilin, and ghrelin receptor agonists, have seen few successes, but a new group of agents is under evaluation. More recently, also, no benefit was found with treatment with a tricyclic antidepressant in idiopathic gastroparesis. In refractory cases, especially when there is weight loss, invasive therapeutics such as insertion of feeding tubes, intrapyloric injection of botulinum toxin, implantable gastric electrical stimulation, or surgical (partial) gastrectomy are occasionally considered, but there is little evidence of efficacy, and these are not devoid of potentially major complications. Gastroparesis is likely to remain a challenging condition in the clinic in the foreseeable future.
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Abstract
BACKGROUND Gastroparesis (GP) is characterized by delayed gastric emptying in the absence of mechanical outlet obstruction. Symptoms may include nausea, vomiting, bloating, early satiety, abdominal pain, and weight loss. Delayed gastric emptying of a solid-phase meal assessed by radionuclear scintigraphy is the criterion standard for diagnosis. The prevalence of GP is difficult to estimate due to the lack of a validated, widely available diagnostic test that can be applied in primary care. The extent of this problem in children is unknown. METHODS We studied a cohort of children with GP diagnosed by radionuclear scintigraphy to identify demographics, symptoms, comorbidities, treatment, and outcomes. A retrospective analysis of 239 patients between ages 0 and 21 years was performed. RESULTS The mean age of presentation was 7.9 years, and boys and girls were almost equally affected, that is, 48.5% and 51.5%, respectively. Vomiting was the most frequent presenting symptom (68%), followed by abdominal pain (51%), nausea (28%), weight loss (27%), early satiety (25%), and bloating (7%). Almost 75% of patients responded to intravenous erythromycin administered provocatively during gastric scintigraphy. In a majority of the patients, no cause was identified, that is, idiopathic GP (70%), followed by drugs (18%) and postsurgical (12.5%) causes. Only 4% patients had diabetic GP, and our population was essentially narcotic naïve (2%). After an average of 24 months' follow-up, the most common complication was esophageal reflux (67%). Despite different therapeutic modalities, by the end of the follow-up period, a significant improvement in symptoms was reported by an average of 60%, regardless of sex, age, or degree of emptying delay. CONCLUSIONS GP has a good prognosis in childhood despite different etiologies, symptom presentation, and therapy.
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Ducrotté P, Gourcerol G. [Gastroparesis: pathophysiology and management]. Presse Med 2011; 41:721-9. [PMID: 22154929 DOI: 10.1016/j.lpm.2011.09.028] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/29/2011] [Accepted: 09/05/2011] [Indexed: 01/17/2023] Open
Abstract
The prevalence of gastroparesis is increasing. Diabetes mellitus and sequelae of œsogastric surgery are the two main causes of gastroparesis. In some patients, gastroparesis seems a postinfectious disease after its sudden onset after a viral infection. In about one third of the patients, gastroparesis is considered as idiopathic. In diabetic patients, gastroparesis impairs glycaemic control. Due to the low positive predictive value of symptoms, a gastric emptying study is often necessary to confirm a suspected diagnosis of gastroparesis. The symptomatic efficacy of erythromycin is higher than that of other prokinetics. This efficacy is higher when erythromycin is given intravenously. Hyperglycaemia impairs this symptomatic effect. Due to a tachyphylaxis phenomenon, the clinical effect of erythromycin decreases with the duration of treatment. In refractory gastroperis, either duodenal or jejunal enteral feeding, or high-frequency gastric electrical stimulation are possible therapeutic options while endoscopic alternatives (intrapyloric botulinum injection or pyloric balloon dilation) give unsatisfactory results.
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Affiliation(s)
- Philippe Ducrotté
- Faculté de médecine et de pharmacie, ADEN EA 4311 hôpital Charles-Nicolle, département d'hépatogastroentérologie et de nutrition, Rouen cedex, France.
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12
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Keld R, Kinsey L, Athwal V, Lal S. Pathogenesis, investigation and dietary and medical management of gastroparesis. J Hum Nutr Diet 2011; 24:421-30. [DOI: 10.1111/j.1365-277x.2011.01190.x] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/24/2022]
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Dive AM. Prokinétiques chez le patient de réanimation : quand et lesquels ? MEDECINE INTENSIVE REANIMATION 2011. [DOI: 10.1007/s13546-011-0281-8] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/18/2022]
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Gao XK, Yu Y, Yang Y, Chen J, Wang QM. High concentration of glucose enhances the expression of P2X 7 purine receptor in interstitial cells of Cajal in vitro. Shijie Huaren Xiaohua Zazhi 2010; 18:1211-1216. [DOI: 10.11569/wcjd.v18.i12.1211] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
AIM: To investigate the effects of high concentration of glucose on the expression of P2X7 purine receptor in the interstitial cells of Cajal (ICC) in vitro and to explore the mechanisms underlying gastrointestinal dysmotility in diabetic mellitus.
METHODS: ICC were isolated from the intestine of newborn mice by enzymatic dissociation and centrifugation and cultured in an incubator containing 50 mL/L CO2. Cultured ICC were identified by immunofluorescence staining using antibodies directed against c-Kit receptor and P2X7 receptor. ICC were then divided into two groups: control group and experimental group, which were treated with normal and high concentrations of glucose, respectively. After treatment, cell morphology was observed under an inverted light microscope. The expression of P2X7 receptor and c-Kit receptor mRNAs in ICC was detected by reverse transcription-polymerase chain reaction (RT-PCR).
RESULTS: Immunofluorescence staining demonstrated that both P2X7 receptor and c-Kit receptor were positive on ICC cells. After treatment with high concentration of glucose, ICC became bigger, and cell processes became shorter. RT-PCR analysis proved the expression of P2X7 receptor in ICC. The expression level of c-Kit receptor mRNA was weaker and that of P2X7 receptor mRNA was stronger in the experimental group than in the control group.
CONCLUSION: P2X7 receptor is expressed in ICC. Hyperglycemia may alter cell morphology, decrease the expression of c-Kit receptor, enhance the expression of P2X7 receptor in ICC, and thereby play a role in the pathogenesis of gastrointestinal dysmotility in diabetic mellitus.
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15
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Abstract
Delayed gastric emptying in the absence of mechanical obstruction is referred to as gastroparesis. Symptoms that are often attributed to gastroparesis include postprandial fullness, nausea, and vomiting. Although tests of gastric motor function may aid diagnostic labeling, their contribution to determining the treatment approach is often limited. Although clinical suspicion of gastroparesis warrants the exclusion of mechanical causes and serum electrolyte imbalances, followed by empirical treatment with a gastroprokinetic such as domperidone or metoclopramide, evidence that these drugs are effective for patients with gastroparesis is far from overwhelming. In refractory cases with severe weight loss, invasive therapeutics such as inserting a feeding jejunostomy tube, intrapyloric injection of botulinum toxin, surgical (partial) gastrectomy, and implantable gastric electrical stimulation are occasionally considered.
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Affiliation(s)
- Tatsuhiro Masaoka
- Center for Gastroenterological Research, University of Leuven, Leuven, Belgium
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Chapman MJ, Fraser RJL, Matthews G, Russo A, Bellon M, Besanko LK, Jones KL, Butler R, Chatterton B, Horowitz M. Glucose absorption and gastric emptying in critical illness. Crit Care 2009; 13:R140. [PMID: 19712450 PMCID: PMC2750198 DOI: 10.1186/cc8021] [Citation(s) in RCA: 58] [Impact Index Per Article: 3.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/30/2009] [Revised: 08/17/2009] [Accepted: 08/27/2009] [Indexed: 02/07/2023] Open
Abstract
INTRODUCTION Delayed gastric emptying occurs frequently in critically ill patients and has the potential to adversely affect both the rate, and extent, of nutrient absorption. However, there is limited information about nutrient absorption in the critically ill, and the relationship between gastric emptying (GE) and absorption has hitherto not been evaluated. The aim of this study was to quantify glucose absorption and the relationships between GE, glucose absorption and glycaemia in critically ill patients. METHODS Studies were performed in nineteen mechanically-ventilated critically ill patients and compared to nineteen healthy subjects. Following 4 hours fasting, 100 ml of Ensure, 2 g 3-O-methyl glucose (3-OMG) and 99mTc sulphur colloid were infused into the stomach over 5 minutes. Glucose absorption (plasma 3-OMG), blood glucose levels and GE (scintigraphy) were measured over four hours. Data are mean +/- SEM. A P-value < 0.05 was considered significant. RESULTS Absorption of 3-OMG was markedly reduced in patients (AUC240: 26.2 +/- 18.4 vs. 66.6 +/- 16.8; P < 0.001; peak: 0.17 +/- 0.12 vs. 0.37 +/- 0.098 mMol/l; P < 0.001; time to peak; 151 +/- 84 vs. 89 +/- 33 minutes; P = 0.007); and both the baseline (8.0 +/- 2.1 vs. 5.6 +/- 0.23 mMol/l; P < 0.001) and peak (10.0 +/- 2.2 vs. 7.7 +/- 0.2 mMol/l; P < 0.001) blood glucose levels were higher in patients; compared to healthy subjects. In patients; 3-OMG absorption was directly related to GE (AUC240; r = -0.77 to -0.87; P < 0.001; peak concentrations; r = -0.75 to -0.81; P = 0.001; time to peak; r = 0.89-0.94; P < 0.001); but when GE was normal (percent retention240 < 10%; n = 9) absorption was still impaired. GE was inversely related to baseline blood glucose, such that elevated levels were associated with slower GE (ret 60, 180 and 240 minutes: r > 0.51; P < 0.05). CONCLUSIONS In critically ill patients; (i) the rate and extent of glucose absorption are markedly reduced; (ii) GE is a major determinant of the rate of absorption, but does not fully account for the extent of impaired absorption; (iii) blood glucose concentration could be one of a number of factors affecting GE.
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Affiliation(s)
- Marianne J Chapman
- Department of Anaesthesia and Intensive Care, Royal Adelaide Hospital, North Terrace, Adelaide, SA 5000, Australia
- School of Medicine, University of Adelaide, Adelaide, SA 5000, Australia
| | - Robert JL Fraser
- School of Medicine, University of Adelaide, Adelaide, SA 5000, Australia
- Investigation & Procedures Unit, Repatriation General Hospital, Daws Road, Daw Park, SA 5041, Australia
| | - Geoffrey Matthews
- Centre for Paediatric and Adolescent Gastroenterology, Women's and Children's Hospital; 72 King William Road, Adelaide, SA 5006, Australia
| | - Antonietta Russo
- School of Medicine, University of Adelaide, Adelaide, SA 5000, Australia
| | - Max Bellon
- Department of Nuclear Medicine, Royal Adelaide Hospital, North Terrace, Adelaide, SA 5000, Australia
| | - Laura K Besanko
- Investigation & Procedures Unit, Repatriation General Hospital, Daws Road, Daw Park, SA 5041, Australia
| | - Karen L Jones
- School of Medicine, University of Adelaide, Adelaide, SA 5000, Australia
| | - Ross Butler
- Centre for Paediatric and Adolescent Gastroenterology, Women's and Children's Hospital; 72 King William Road, Adelaide, SA 5006, Australia
| | - Barry Chatterton
- Department of Nuclear Medicine, Royal Adelaide Hospital, North Terrace, Adelaide, SA 5000, Australia
| | - Michael Horowitz
- School of Medicine, University of Adelaide, Adelaide, SA 5000, Australia
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17
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Abstract
Gastric emptying is frequently abnormal in patients with long-standing type 1 and type 2 diabetes mellitus. Symptoms commonly associated with disordered gastric emptying include nausea, vomiting, bloating and epigastric pain, while patients are also at risk of malnutrition, weight loss, impaired drug absorption, disordered glycaemic control and poor quality of life. Although often attributed to the presence of irreversible autonomic neuropathy, acute hyperglycaemia represents a potentially reversible cause of gastric dysfunction in diabetes. Scintigraphy represents the gold standard for measuring gastric emptying. The management of diabetic gastroparesis is less than optimal, partly because the pathogenesis has not been clearly defined. Treatment approaches include dietary modification and optimization of glycaemia, and the use of prokinetic drugs, while novel therapies such as gastric electrical stimulation are the subject of ongoing investigation.
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Affiliation(s)
- Jing Ma
- University of Adelaide Discipline of Medicine, Royal Adelaide Hospital, Adelaide, South Australia, Australia
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18
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Abstract
Gastroparesis is a relatively common and often disabling condition that is characterized by a broad range of clinical presentation ranging from dyspeptic symptoms to nausea, vomiting, abdominal pain, malnutrition, frequent hospitalizations and incapacitation. The treatment of gastroparetic symptoms can be challenging to the gastroenterologist and the intensity of therapy varies with the physician's knowledge. Hence the determination that a patient is refractory to 'standard medical therapy' is an assessment that is subspeciality-based and could differ around the world depending on medications available. In this article, we review the use of available prokinetics, antiemetic agents, the approach for analgesia in the context of gastroparesis, and also discuss potential and evolving pharmacotherapies. The progress has been relatively limited as far as availability of new medications for gastroparesis is concerned; however, active research in developing newer prokinetics holds great promise for the future of management of this challenging entity.
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Affiliation(s)
- Savio C Reddymasu
- University of Kansas Medical Center, Division of Gastrointestinal Motility, Department of Medicine, Kansas City, 3901 Rainbow Boulevard, KS-66160-7350, USA
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19
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Waseem S, Moshiree B, Draganov PV. Gastroparesis: Current diagnostic challenges and management considerations. World J Gastroenterol 2009; 15:25-37. [PMID: 19115465 PMCID: PMC2653292 DOI: 10.3748/wjg.15.25] [Citation(s) in RCA: 104] [Impact Index Per Article: 6.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
Gastroparesis refers to abnormal gastric motility characterized by delayed gastric emptying in the absence of mechanical obstruction. The most common etiologies include diabetes, post-surgical and idiopathic. The most common symptoms are nausea, vomiting and epigastric pain. Gastroparesis is estimated to affect 4% of the population and symptomatology may range from little effect on daily activity to severe disability and frequent hospitalizations. The gold standard of diagnosis is solid meal gastric scintigraphy. Treatment is multimodal and includes dietary modification, prokinetic and anti-emetic medications, and surgical interventions. New advances in drug therapy, and gastric electrical stimulation techniques have been introduced and might provide new hope to patients with refractory gastroparesis. In this comprehensive review, we discuss gastroparesis with emphasis on the latest developments; from the perspective of the practicing clinician.
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20
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Stevens JE, Russo A, Maddox AF, Rayner CK, Phillips L, Talley NJ, Giguère M, Horowitz M, Jones KL. Effect of itopride on gastric emptying in longstanding diabetes mellitus. Neurogastroenterol Motil 2008; 20:456-463. [PMID: 18179609 DOI: 10.1111/j.1365-2982.2007.01058.x] [Citation(s) in RCA: 26] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
Delayed gastric emptying (GE) occurs in 30-50% of patients with longstanding type 1 or 2 diabetes, and represents a major cause of morbidity. Current therapeutic options are limited. We aimed at evaluating the effects of itopride on GE in patients with longstanding diabetes. Twenty-five patients (20 type 1, 5 type 2; 10 males, 15 females; mean age 45.2 +/- 2.7 years; body mass index 27.5 +/- 0.9 kg m(-2); duration of diabetes 20.2 +/- 2.4 years) were enrolled in a double-blind, placebo-controlled, randomized, crossover trial. Subjects received both itopride (200 mg) and placebo t.i.d. for 7 days, with a washout of 7-14 days. GE (scintigraphy), blood glucose (glucometer) and upper gastrointestinal (GI) symptoms (questionnaire) were measured following each treatment period. The test meal comprised 100 g ground beef (99mTc-sulphur colloid) and 150 mL of 10% dextrose [67Ga-ethylenediaminetetraacetic acid (EDTA)]. There was a slight trend for itopride to accelerate both solid (P = 0.09) and liquid (P = 0.09) GE. With itopride treatment, the emptying of both solids and liquids tended to be more accelerated, as the emptying with placebo was slower (solids: r = 0.39, P = 0.057; liquids: r = 0.44, P < 0.03). Twelve (48%) patients had delayed solid and/or liquid GE on placebo and in this group, itopride modestly accelerated liquid (P < 0.05), but not solid (P = 0.39), emptying. Itopride had no effect on mean blood glucose during the GE measurement (placebo: 9.8 +/- 0.6 mmol L(-1) vs itopride: 9.6 +/-0.6 mmol L(-1)), or GI symptoms (placebo: 1.4 +/- 0.4 vs itopride: 1.8 +/- 0.5). Itopride, in a dose of 200 mg t.i.d. for 7 days, tends to accelerate GE of liquids and solids in longstanding diabetes. The magnitude of this effect appears to be modest and possibly dependent on the rate of GE without itopride.
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Affiliation(s)
- J E Stevens
- Discipline of Medicine, University of Adelaide, Royal Adelaide Hospital, Adelaide, Australia
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21
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Abstract
BACKGROUND Gastroparesis is a chronic disorder caused by stomach pump failure and characterized by profound nausea, vomiting and epigastric pain. Most often, the cause is unapparent and of the known associations, diabetes is the most common. Diagnosis is usually made using an isotope-labelled test meal. Treatment is incremental and includes education, dietary support, prokinetic and antiemetic agents. There are novel approaches including gastric neurostimulation. AIM To review current concepts of gastric motor function, aetiology, investigation and treatment of gastroparesis. METHODS A systematic web-based review of the literature was undertaken using a lexicon of terms associated with gastroparesis. RESULTS There are few controlled studies of this condition. Little is known about causation or underlying nerve, muscle or pacemaker pathology. Idiopathic gastroparesis occurs most commonly in women and gastric emptying is often abnormal in diabetes. Isotopic gastric scintigraphy remains the gold standard investigation, but alternative tests are being developed. Treatment is multimodal and includes education, and nutritional support. There are no adequately powered controlled trials to support a particular drug regimen. In intractable gastroparesis, gastric neurostimulation appears to offer benefit. CONCLUSION Despite a significant progress in the past decade, further controlled trials are required into the therapeutic options available for treating this intriguing condition.
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Affiliation(s)
- A Patrick
- Centre for Gastroenterology, Royal Free Hampstead NHS Trust, London, UK
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22
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Sellin JH, Chang EB. Therapy Insight: gastrointestinal complications of diabetes--pathophysiology and management. ACTA ACUST UNITED AC 2008; 5:162-71. [PMID: 18268523 DOI: 10.1038/ncpgasthep1054] [Citation(s) in RCA: 33] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/06/2007] [Accepted: 12/10/2007] [Indexed: 12/26/2022]
Abstract
Patients with diabetes often have gastrointestinal symptoms, but the extent and severity of this problem and the specificity of the symptoms are not nearly as well defined as frequently assumed. Any part of the gastrointestinal tract can be affected, and the presenting symptoms depend on the composite of dysfunctional elements. Gastroesophageal reflux, Candida esophagitis, gastroparesis, diarrhea and constipation are among the many common gastrointestinal complications of diabetes. No specific risk factor for the development of these complications has been identified and their etiology is most likely to be multifactorial, involving both reversible and irreversible processes. Treatment should be directed at tighter glycemic and symptom control, which can bring about clinical improvement for many patients. For other patients, however, effective clinical management is problematic because no therapies are available to prevent or correct the underlying disease mechanisms. Studies now suggest that reduced levels of key trophic factors cause transdifferentiation of pacemaker interstitial cells of Cajal into a smooth-muscle-like phenotype. If this really is the case, therapies directed at restoring the normal milieu of trophic signals could correct the dysfunction of the interstitial cells of Cajal and resolve many gastrointestinal complications. Advances in stem cell technology also hold promise to provide a cure for diabetes and to correct abnormalities in gastrointestinal pathology.
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Affiliation(s)
- Joseph H Sellin
- Inflammatory Bowel Disease Center at the University of Texas Medical Branch, Galveston, TX, USA
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23
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Intagliata N, Koch KL. Gastroparesis in type 2 diabetes mellitus: prevalence, etiology, diagnosis, and treatment. Curr Gastroenterol Rep 2007; 9:270-9. [PMID: 17883973 DOI: 10.1007/s11894-007-0030-3] [Citation(s) in RCA: 30] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/20/2022]
Abstract
The worldwide epidemic of type 2 diabetes mellitus (T2DM) is a substantial economic and social burden. Although gastroparesis associated with type 1 diabetes mellitus (T1DM) has been recognized for years, only recently have studies shown that patients with T2DM also have high rates of gastroparesis. Individuals with T2DM constitute 90% to 95% of the diabetic population. Unique characteristics that distinguish this population are obesity, insulin resistance, and associated comorbidities. These features highlight the importance of investigating gastric emptying in individuals with T2DM and upper gastrointestinal symptoms. The purpose of this review is to examine the literature pertaining to diabetes and the effect of diabetes on gastric neuromuscular function, with a focus on T2DM. An understanding of gastric motility in T2DM is important to diagnose gastroparesis, to treat upper gastrointestinal symptoms, and to restore normal gastric motility, which may lead, in turn, to improved glucose control.
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Affiliation(s)
- Nicolas Intagliata
- Section on Gastroenterology, Wake Forest University Medical Center, Nutrition Building, E-115, Medical Center Boulevard, Winston-Salem, NC 27157, USA
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24
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Bradshaw LA, Sims JA, Richards WO. Noninvasive assessment of the effects of glucagon on the gastric slow wave. Am J Physiol Gastrointest Liver Physiol 2007; 293:G1029-38. [PMID: 17884978 PMCID: PMC2726773 DOI: 10.1152/ajpgi.00054.2007] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/31/2023]
Abstract
Hyperglycemic effects on the gastric slow wave are not well understood, and no studies have examined the effects that hyperglycemia has on gastric slow wave magnetic fields. We recorded multichannel magnetogastrograms (MGGs) before and after intravenous administration of glucagon and subsequent modest hyperglycemia in 20 normal volunteers. Normal slow waves were evident in baseline MGG recordings from all 20 subjects, but within 15 min after glucagon had been given, we noted significant effects on MGG signals. In addition to an overall decrease in the slow wave frequency from 2.9 +/- 0.5 cycles per min (cpm) to 2.2 +/- 0.1 cpm (P < 0.05), we observed significant changes in the number and range of spectral peaks recorded. Furthermore, the propagation velocity determined from surface current density maps computed from the multichannel MGG decreased significantly (7.1 +/- 0.8 mm/s to 5.0 +/- 0.3 mm/s, P < 0.05). This is the first study of biomagnetic effects of hyperglycemia in normal subjects. Our results suggest that the analysis of the MGG provides parameter quantification for gastric electrical activity specific to and characteristic of slow wave abnormalities associated with increased serum glucose by injection of glucagon.
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Affiliation(s)
- L Alan Bradshaw
- Department of Surgery, Vanderbilt University, Nashville, TN, USA.
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25
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Abstract
Dopamine antagonists, such as metoclopramide and domperidone, and the motilin receptor agonist erythromycin have been the cornerstones in drug treatment of severe gastroparesis for more than a decade. No new drugs have been approved for treatment of this disorder in this period. Instead, the 5-HT4 agonist cisapride has been withdrawn due to side-effects. The effectiveness of intrapyloric botulinum toxin for gastroparesis remains to be shown. In the last decade, gastric electrical stimulation (GES) with a fully implantable device has evolved as a promising treatment, with significant effects on nausea and vomiting in most patients with severe, drug-refractory diabetic gastroparesis and postsurgical gastroparesis. A proportion of patients with severe idiopathic gastroparesis and patients with idiopathic nausea and vomiting also respond. More research is needed to achieve precise selection of responders/non-responders to GES, and to study the potential benefit of GES in other patient groups suffering from severe nausea or vomiting.
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Affiliation(s)
- Hasse Abrahamsson
- Department of Internal Medicine, Sahlgrenska University Hospital, S-413 45 Göteborg, Sweden.
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26
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Maia Bosca M, Martí L, Mínguez M. [Diagnostic and therapeutic approach to patients with gastroparesis]. GASTROENTEROLOGIA Y HEPATOLOGIA 2007; 30:351-9. [PMID: 17662220 DOI: 10.1157/13107570] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 05/16/2023]
Abstract
Gastroparesis is a chronic alteration of gastric motility characterized by symptoms suggestive of mechanical obstruction and delayed gastric emptying in the absence of obstruction. Gastroparesis can be idiopathic or attributable to neuropathy or myopathy as in diabetes mellitus and scleroderma or can occur after vagotomy. Diagnosis is based on symptoms (nausea, vomiting, abdominal distension and early satiety), physical examination (capotement) and on complementary investigations, the procedure of choice being isotope gastric emptying tests. Treatment depends on the clinical repercussions. In most patients, gastroparesis can be controlled by prokinetic drugs, dietary measures, exclusion of drugs that alter gastric emptying, and exhaustive control of blood glucose levels. In patients with severe gastroparesis, hospital nutritional measures (intravenous and/or enteral), gastric decompression and intravenous antiemetic and prokinetic agents are required. Aggressive nutritional therapies (parenteral or enteral nasojejunal nutrition), intrapyloric injection of botulinum toxin, implantation of a gastric stimulation device, or gastrectomy should only be used in patients unresponsive to conservative treatment or if there is selective alteration of gastric motility.
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Affiliation(s)
- Marta Maia Bosca
- Servicio de Gastroenterología, Hospital Clínico Universitario de Valencia, Valencia, España.
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27
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Abstract
Gastroparesis is often difficult to manage. First of all, exact criteria for making a diagnosis of gastroparesis have not been established, and merely finding delayed gastric emptying does not justify the label. Furthermore, the relationship between symptoms and gastric emptying rate is poor, and the number of therapies with proven efficacy is extremely limited. A number of technical investigations are helpful to establish the anatomy and motor function of the upper gastrointestinal tract. In most cases where gastroparesis can be presumed or established, prokinetic therapy will be tried. A number of agents are available, with variable efficacy and tolerance. Rarely, in case of debilitating refractory symptoms, experimental or invasive therapies can be tried such as injection of botulinum toxin, enteral feeding tube insertion, gastric electrical stimulation or surgery.
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Affiliation(s)
- Jan Tack
- Department of Gastroenterology, University Hospital Gasthuisberg, Katholieke Universiteit Leuven, 3000 Leuven, Belgium.
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28
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Chaikomin R, Rayner CK, Jones KL, Horowitz M. Upper gastrointestinal function and glycemic control in diabetes mellitus. World J Gastroenterol 2006; 12:5611-5621. [PMID: 17007012 PMCID: PMC4088160 DOI: 10.3748/wjg.v12.i35.5611] [Citation(s) in RCA: 28] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/19/2006] [Revised: 06/06/2006] [Accepted: 06/16/2006] [Indexed: 02/06/2023] Open
Abstract
Recent evidence has highlighted the impact of glycemic control on the incidence and progression of diabetic micro- and macrovascular complications, and on cardiovascular risk in the non-diabetic population. Postprandial blood glucose concentrations make a major contribution to overall glycemic control, and are determined in part by upper gastrointestinal function. Conversely, poor glycemic control has an acute, reversible effect on gastrointestinal motility. Insights into the mechanisms by which the gut contributes to glycemia have given rise to a number of novel dietary and pharmacological strategies designed to lower postprandial blood glucose concentrations.
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Affiliation(s)
- Reawika Chaikomin
- Department of Medicine, Royal Adelaide Hospital, North Terrace, Adelaide, South Australia 5000, Australia
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29
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Friedenberg FK, Parkman HP. Delayed gastric emptying: Whom to test, how to test, and what to do. ACTA ACUST UNITED AC 2006; 9:295-304. [PMID: 16836948 DOI: 10.1007/s11938-006-0011-x] [Citation(s) in RCA: 23] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/27/2022]
Abstract
Gastroparesis, or delayed gastric emptying, is a common cause of chronic nausea and vomiting as seen in a gastroenterology practice. Diabetic, postsurgical, and idiopathic causes remain the three most common forms of gastroparesis. In addition to nausea and vomiting, symptoms of gastroparesis may include early satiety, postprandial fullness, and abdominal pain. Physiologic changes that may explain symptoms in patients with gastroparesis, in addition to delayed gastric emptying, include impaired fundic accommodation, antral hypomotility, gastric dysrhythmias, pylorospasm, and perhaps visceral hypersensitivity. Diagnosis of gastroparesis is best determined using a radioisotope-labeled solid meal with scintigraphic imaging for at least 2 hours, and preferably 4 hours, postprandially. Most commonly, a 99mTc sulfur colloid-labeled egg sandwich with imaging at 0, 1, 2, and 4 hours is used. Extension of the gastric emptying test to 4 hours improves the accuracy of the test, but unfortunately, this is not commonly performed at many centers. Emptying of liquids remains normal until the late stages of gastroparesis and is less useful. The aims of treatment should be to control symptoms and maintain adequate nutrition and hydration. Patients should be advised to eat small meals and to limit their intake of fat and fiber. Additional dietary recommendations may include increasing caloric intake in the form of liquids. For diabetic patients, control of blood glucose levels is important, as symptom exacerbation is frequently associated with poor glycemic control. Specific treatment often begins with metoclopramide, 10 mg, up to four times daily, after a discussion of possible side effects with the patient. An antiemetic agent, such as prochlorperazine, 5 to 10 mg orally or 25 mg by suppository, can be added on an as-needed basis every 4 to 6 hours to control nausea. If these antiemetic medications are not effective, or if side effects develop, orally dissolving ondansetron, 8 mg every 8 to 12 hours, can be tried on an as-needed basis. If this regimen is unsuccessful, then alternative prokinetic agents--erythromycin, 125 mg, or tegaserod, 6 mg, prior to meals--can be tried. For cases refractory to these treatments, referral to a center with US Food and Drug Administration permission to use domperidone should be considered. Alternatively, symptom modulators such as low-dose tricyclic antidepressants can be tried to reduce symptoms, but these do not improve gastric emptying. In patients for whom all medical therapy fails, other options that are tried at experienced centers include the injection of botulinum toxin into the pylorus, placement of a feeding jejunostomy, and/or placement of a gastric electrical stimulator.
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Affiliation(s)
- Frank K Friedenberg
- Temple University School of Medicine, Gastroenterology Section, Parkinson Pavilion, 8th Floor, 3401 North Broad Street, Philadelphia, PA 19140, USA. henry.parkman@ temple.edu
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30
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Affiliation(s)
- M-F Kong
- Department of Diabetes & Endocrinology, Leicester General Hospital, Leicester, UK
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31
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Parkman HP, Hasler WL, Fisher RS. American Gastroenterological Association technical review on the diagnosis and treatment of gastroparesis. Gastroenterology 2004; 127:1592-622. [PMID: 15521026 DOI: 10.1053/j.gastro.2004.09.055] [Citation(s) in RCA: 508] [Impact Index Per Article: 24.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/23/2022]
Abstract
This literature review and the recommendations herein were prepared for the American Gastroenterological Association Clinical Practice Committee. The paper was approved by the Committee on May 16, 2004, and by the AGA Governing Board on September 23, 2004.
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Russo A, Stevens JE, Giles N, Krause G, O'Donovan DG, Horowitz M, Jones KL. Effect of the motilin agonist KC 11458 on gastric emptying in diabetic gastroparesis. Aliment Pharmacol Ther 2004; 20:333-338. [PMID: 15274670 DOI: 10.1111/j.1365-2036.2004.02066.x] [Citation(s) in RCA: 36] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
BACKGROUND KC 11458, a motilin agonist without antibiotic properties, accelerates gastric emptying in animals and healthy humans. AIM To evaluate the acute effects of KC 11458 on gastric emptying in diabetic gastroparesis. METHODS Twenty-nine patients (6 type 1 and 23 type 2) with gastroparesis underwent assessments of: (i) gastric emptying of a solid/liquid meal using scintigraphy, (ii) glycaemic control (blood glucose at 0, 30, 60, 90 and 120 min during the gastric emptying measurement) and (iii) upper gastrointestinal and 'meal-related' symptoms (questionnaire), at baseline and after treatment with KC 11458 in a dose of 8 mg t.d.s., or placebo for 8 days. RESULTS KC 11458 had no statistically significant or clinically relevant effect on gastric emptying of either the solid intragastric retention at 100 min (T100) (P = 0.87) or liquid 50% emptying time (T50) (P = 0.17) components of the meal. KC 11458 slightly worsened (P = 0.04) upper gastrointestinal symptoms when compared with placebo. The magnitude of the change in solid gastric emptying correlated with the change in the blood glucose concentration (r = 0.49; P < 0.05). CONCLUSIONS KC 11458, in a dose of 8 mg t.d.s. for 8 days, does not accelerate gastric emptying in patients with diabetic gastroparesis. The absence of efficacy may relate to an effect of hyperglycaemia.
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Affiliation(s)
- A Russo
- Department of Medicine, Royal Adelaide Hospital, University of Adelaide, Australia
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33
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O'Donovan D, Feinle-Bisset C, Jones K, Horowitz M. Idiopathic and Diabetic Gastroparesis. CURRENT TREATMENT OPTIONS IN GASTROENTEROLOGY 2003; 6:299-309. [PMID: 12846939 DOI: 10.1007/s11938-003-0022-9] [Citation(s) in RCA: 20] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
The management of both diabetic and idiopathic gastroparesis often represents a substantial clinical challenge. In formulating recommendations for therapy, it should be recognized that these are based on less than optimal evidence; in particular, there are substantial deficiencies in current knowledge relating to the pathophysiology of gastroparesis, as well as the natural history of gastrointestinal symptoms, and the majority of pharmacologic trials have been short term and associated with methodologic limitations. Although the etiologic factors differ, the overall management principles are similar in the two conditions. Maintenance of adequate nutrition is pivotal, and parenteral nutrition may be required in severe cases associated with malnutrition. In patients with diabetes, rigorous attempts should be made to optimize glycemic control--hyperglycemia slows gastric emptying and may exacerbate symptoms and attenuate the effects of prokinetic drugs. Despite the relatively poor predictive value of symptoms, it is reasonable to suggest a trial of prokinetic therapy for about 4 weeks, rather than initially establishing the diagnosis by measurement of gastric emptying. However, it should be recognized that there is a substantial placebo response, a lack of evidence to support the cost effectiveness of such an approach, and that most patients will require prolonged therapy. In type 1 diabetic patients, prokinetic therapy may potentially benefit glycemic control, and this forms an additional rationale (albeit not established) for therapy. Some patients with diabetes and idiopathic gastroparesis with severe vomiting are unable to tolerate oral medication; in such cases subcutaneous metoclopramide may prove useful. Patients with intractable symptoms should be hospitalized and given intravenous erythromycin. The repertoire of prokinetic agents available in the United States is limited and includes metoclopramide, erythromycin, and cisapride (available by special program from its manufacturer); all of these drugs are associated with side effects. The use of metoclopramide may represent the first choice for chronic oral therapy, although it has been studied less comprehensively than cisapride. Combination therapy may be potentially more efficacious than the use of single agents. Dehydration and metabolic derangements should be corrected. The choice of chronic medical therapy should be individualized, taking factors such as age, presence of diabetes, concurrent medications, and comorbidities into account. In a small number of patients in whom medical treatment fails, surgery should be considered, and, if performed, done in a specialized center. A number of novel therapies, including gastric electrical stimulation, are currently being evaluated.
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Affiliation(s)
- Deirdre O'Donovan
- Department of Medicine, University of Adelaide, Level 6, Eleanor Harrald Building, Frome Road, Adelaide, SA 5000, Australia.
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Ishiguchi T, Tada H, Nakagawa K, Yamamura T, Takahashi T. Hyperglycemia impairs antro-pyloric coordination and delays gastric emptying in conscious rats. Auton Neurosci 2002; 95:112-20. [PMID: 11871775 DOI: 10.1016/s1566-0702(01)00383-6] [Citation(s) in RCA: 57] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/15/2023]
Abstract
Delayed gastric emptying has been shown in diabetes. Although it has been proposed that hyperglycemia, and not only autonomic neuropathy, contributes to the pathogenesis of delayed gastric emptying, the inhibitory mechanism of hyperglycemia on gastric emptying remains unclear. We studied the effects of hyperglycemia per se on gastric emptying and postprandial gastric motility in conscious rats. Liquid and solid gastric emptying were compared between saline-infused rats and D-glucose-infused rats. Two strain gauge transducers were implanted on the antrum and pylorus and the postprandial antro-pyloric coordination was compared between euglycemia and hyperglycemia. D-glucose infusion for 30 min increased blood glucose level from 5.4 +/- 0.5 to 13.0 +/- 1.3 mM and significantly delayed gastric emptying. Forty minutes after the feeding, contractions with low frequency (<3 cycles min(-1)) and high amplitude (>15 g) of the antrum were observed. This period reflects the emptying process of the gastric content and the coordination between the antrum and pylorus was frequently observed. D-glucose infusion significantly reduced feeding-induced antral contractions and abolished the number of episodes of antro-pyloric coordination. Sham feeding-induced gastric contractions were also significantly reduced by hyperglycemia. Postprandial antro-pyloric coordination was not observed in vagotomized rats, suggesting a mediation of vagus nerve. It is concluded that hyperglycemia impairs antral contractions and antro-pyloric coordination in rats. The inhibitory effect of hyperglycemia on gastric emptying is mediated, at least in part, via impaired vagal activity.
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Horowitz M, Jones KL, Harding PE, Wishart JM. Relationship between the effects of cisapride on gastric emptying and plasma glucose concentrations in diabetic gastroparesis. Digestion 2002; 65:41-46. [PMID: 11961342 DOI: 10.1159/000051930] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
BACKGROUND/AIMS The effect of erythromycin on gastric emptying is attenuated during hyperglycaemia. The aim of this study was to determine in patients with diabetic gastroparesis whether the effect of cisapride on gastric emptying of solids and liquids is influenced by the plasma glucose concentration. METHODS Nineteen patients with type 1 diabetes mellitus, who had delayed gastric emptying of solids and/or liquids, were studied. On 2 separate days, each patient received cisapride (20 mg) or placebo orally 60 min before scintigraphic measurement of gastric emptying of a mixed solid (ground beef) and liquid (dextrose) meal. The plasma glucose concentrations were measured at -5, 30, 60, 90, and 120 min during each gastric emptying measurement. RESULTS Cisapride accelerated both solid (retention at 100 min 43 +/- 4 vs. 69 +/- 4%, p < 0.001) and liquid (T50 27 +/- 2 vs. 39 +/- 2 min, p < 0.001) gastric emptying. The mean plasma glucose level was not significantly different after placebo when compared with cisapride (19.5 +/- 1.1 vs. 18.2 +/- 1.0 mmol/l). The change in the 50% emptying time (T50) for liquid, but not solid, emptying was related (r = 0.55, p = 0.01) to the change in the plasma glucose AUC from 0 to 30 min between the placebo and cisapride tests, i.e., the acceleration was greater if the plasma glucose concentration was relatively less during the gastric emptying test performed on cisapride. CONCLUSION The effect of cisapride on gastric emptying, at least that of liquids, in patients with diabetic gastroparesis appears to be dependent on the plasma glucose concentration.
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Affiliation(s)
- Michael Horowitz
- Department of Medicine, University of Adelaide, Royal Adelaide Hospital, Adelaide, Australia.
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Jones KL, Russo A, Stevens JE, Wishart JM, Berry MK, Horowitz M. Predictors of delayed gastric emptying in diabetes. Diabetes Care 2001; 24:1264-1269. [PMID: 11423513 DOI: 10.2337/diacare.24.7.1264] [Citation(s) in RCA: 217] [Impact Index Per Article: 9.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
OBJECTIVE To define the predictors of the rate of gastric emptying in patients with diabetes. RESEARCH DESIGN AND METHODS A total of 101 outpatients with diabetes (79 type 1 and 22 type 2) underwent measurements of gastric emptying of a solid/liquid meal (scintigraphy), upper gastrointestinal symptoms (questionnaire), glycemic control (blood glucose concentrations during gastric emptying measurement), and autonomic nerve function (cardiovascular reflexes). RESULTS The gastric emptying of solid and/or liquid was delayed in 66 (65%) patients. Solid (retention at 100 min 64 +/- 3.2 vs. 50.2 +/- 3.6%, P < 0.005) and liquid (retention at 100 min 22.7 +/- 1.7 vs. 16.0 +/- 1.8%, P < 0.001) gastric emptying was slower in women than in men. Of all upper gastrointestinal symptoms (including nausea and vomiting), only abdominal bloating/fullness was associated with slower gastric emptying (P < 0.005). A multiple regression analysis demonstrated that both abdominal bloating/fullness and female sex were predictors of slower gastric emptying of both solids and liquids. CONCLUSIONS We conclude that the presence of abdominal bloating/fullness but not any other upper gastrointestinal symptom is associated with diabetic gastroparesis and that gastric emptying is slower in diabetic women than in diabetic men.
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Affiliation(s)
- K L Jones
- Department of Medicine, University of Adelaide, Royal Adelaide Hospital, Adelaide, Australia.
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Yacyshyn BR, Thomson AB. Critical review of acid suppression in nonvariceal, acute, uppergastrointestinal bleeding. Dig Dis 2001; 18:117-28. [PMID: 11279330 DOI: 10.1159/000051385] [Citation(s) in RCA: 18] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/02/2023]
Abstract
Nonvariceal, upper gastrointestinal (GI) bleeding is a very common source of morbidity and mortality. The concept of ulcer clot dissolution being facilitated by a low gastric pH has allowed us to better understand the pathophysiology of nonvariceal upper GI bleeding. Placebo-controlled trials have shown the benefit of oral proton pump inhibitor administration in contrast to H(2) receptor antagonists. Furthermore, our recent experience with intravenous proton pump inhibitors has reinforced these observations.
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Affiliation(s)
- B R Yacyshyn
- Department of Medicine, Division of Gastroenterology, University of Alberta, Edmonton, Alta., Canada.
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Rayner CK, Samsom M, Jones KL, Horowitz M. Relationships of upper gastrointestinal motor and sensory function with glycemic control. Diabetes Care 2001; 24:371-381. [PMID: 11213895 DOI: 10.2337/diacare.24.2.371] [Citation(s) in RCA: 306] [Impact Index Per Article: 12.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
Acute changes in the blood glucose concentration have a major reversible effect on esophageal, gastric, intestinal, gallbladder, and anorectal motility in both healthy subjects and diabetic patients. For example, gastric emptying is slower during hyperglycemia than euglycemia and accelerated during hypoglycemia. Acute hyperglycemia also affects perceptions arising from the gastrointestinal tract and may accordingly, be important in the etiology of gastrointestinal symptoms in diabetes. Elevations in blood glucose that are within the normal postprandial range also affect gastrointestinal motor and sensory function. Upper gastrointestinal motor function is a critical determinant of postprandial blood glucose concentrations by influencing the absorption of ingested nutrients. Interventions that reduce postprandial hyperglycemia, by modulating the rate of gastric emptying, have the potential to become mainstream therapies in the treatment of diabetes.
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Affiliation(s)
- C K Rayner
- University of Adelaide Department of Medicine, Royal Adelaide Hospital, South Australia, Australia
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Rayner CK, Su YC, Doran SM, Jones KL, Malbert CH, Horowitz M. The stimulation of antral motility by erythromycin is attenuated by hyperglycemia. Am J Gastroenterol 2000; 95:2233-2241. [PMID: 11007223 DOI: 10.1111/j.1572-0241.2000.02250.x] [Citation(s) in RCA: 20] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
OBJECTIVE Diabetic gastroparesis is usually treated with prokinetic drugs, of which the most potent, when given intravenously during euglycemia, is erythromycin. Recent studies have demonstrated that the gastrokinetic effects of erythromycin are attenuated by hyperglycemia. The aim of this study was to determine whether the effects of erythromycin on antropyloroduodenal motility, including the organization of antral pressure waves, are modified by hyperglycemia. METHODS A total of eight healthy male volunteers (median age 24 yr) were studied on 2 days each in randomized order. A manometric assembly, incorporating six antral, two pyloric, and seven duodenal sideholes and a pyloric sleeve sensor, was positioned with the sleeve spanning the pylorus. The blood glucose concentration was stabilized at about 5 mmol/L (euglycemia) or 15 mmol/L (hyperglycemia). After 30 min (T = 0), an intraduodenal lipid infusion (1.5 kcal/min) was commenced and continued until the end of the study. At T = 20 minutes, erythromycin (200 mg) as the lactobionate was infused intravenously over 20 min, followed by 100 mg over the next 40 min. RESULTS Intravenous erythromycin increased the amplitude of antral waves during intraduodenal lipid infusion at both blood glucose concentrations (p < 0.01 for euglycemia and p < 0.05 for hyperglycemia). After erythromycin (T = 20 to T = 80), the frequency (p < 0.05) and amplitude (p < 0.01) of antral waves were less during hyperglycemia than euglycemia. Both propagated (p < 0.0005) and nonpropagated (p < 0.01) antral waves were decreased by hyperglycemia, but the suppression of propagated waves was greater (p < 0.05). Erythromycin reduced the frequency (p = 0.09) but increased the amplitude (p < 0.05) of phasic pyloric pressures, and decreased basal pyloric pressure (p < 0.0005). The frequency (p = 0.06) and amplitude (p < 0.05) of phasic pyloric waves during erythromycin infusion were slightly less during hyperglycemia than euglycemia, whereas there was no effect of the blood glucose concentration on basal pyloric pressure. Erythromycin increased the amplitude (p < 0.001) but not the frequency of duodenal waves; the frequency and amplitude of duodenal waves did not differ between the two blood glucose concentrations. CONCLUSIONS Hyperglycemia attenuates the stimulation of antral pressures and propagated antral sequences by erythromycin, but not the effects of erythromycin on pyloric or duodenal motility.
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Affiliation(s)
- C K Rayner
- University of Adelaide Department of Medicine, Royal Adelaide Hospital, Australia
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Jones KL, Wishart JM, Berry MK, Abitbol JL, Horowitz M. Effects of fedotozine on gastric emptying and upper gastrointestinal symptoms in diabetic gastroparesis. Aliment Pharmacol Ther 2000; 14:937-943. [PMID: 10886051 DOI: 10.1046/j.1365-2036.2000.00790.x] [Citation(s) in RCA: 22] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
BACKGROUND Delayed gastric emptying and upper gastrointestinal symptoms occur frequently in patients with diabetes mellitus. AIM To evaluate the effects of fedotozine on gastric emptying and gastrointestinal symptoms in diabetic gastroparesis. METHODS Thirty-one diabetic patients (20 type 1, 11 type 2) with gastroparesis were randomized to receive fedotozine (30 mg as the tartrate) or placebo t.d.s. Measurements of gastric emptying (100 g ground beef labelled with 20 MBq 99mTc-sulphur colloid chicken liver and 150 mL 10% dextrose labelled with 10 MBq 113mIn-DTPA) and gastrointestinal symptoms were performed before and after 12-16 days of treatment. Data are the mean +/- s.d. RESULTS Of the 31 patients enrolled, two were excluded from analysis. Data from the remaining 29 patients (18 type 1, 11 type 2; 22 female, seven male), aged 42.7 +/- 11.1 years (of whom 14 were randomized to fedotozine and 15 to placebo), were analysed. Fedotozine had no effect on either gastric emptying (solid retention at 100 min; fedotozine: baseline, 84 +/- 15%; treatment, 73 +/- 23% vs. placebo: baseline, 83 +/- 10%; treatment, 70 +/- 20%) or liquid 50% emptying time (fedotozine: baseline, 59 +/- 32 min; treatment, 58 +/- 38 min vs. placebo: baseline, 44 +/- 9 min; treatment, 43 +/- 21 min) or gastrointestinal symptoms (fedotozine: baseline, 4.4 +/- 2.9; treatment, 4.1 +/- 3.9 vs. placebo: baseline, 4.9 +/- 4.2; treatment, 4.8 +/- 3.9). CONCLUSIONS Fedotozine has no effect on gastric emptying in patients with diabetic gastroparesis.
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Affiliation(s)
- K L Jones
- Department of Medicine, University of Adelaide, Royal Adelaide Hospital, SA, Australia.
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Jenkins SA. Drug therapy for non-variceal upper gastrointestinal bleeding. Assessment of options. Digestion 1999; 60 Suppl 3:39-49. [PMID: 10567788 DOI: 10.1159/000051488] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/04/2023]
Abstract
The efficacy of somatostatin and octreotide have been widely studied in the control of bleeding from oesophageal varices. It has also been suggested that these drugs may be useful for the control of non-variceal upper gastrointestinal (UGI) bleeding, including that from peptic ulcers. In approximately 80% of patients presenting with non-variceal UGI bleeding, haemorrhage ceases spontaneously and does not recur. However, the remaining 20% of patients require active treatment. Results from recent studies have indicated that somatostatin is an effective treatment for the control of non-variceal UGI bleeding in high-risk patients, i.e. those in whom haemorrhage does not cease spontaneously or is likely to recur. In contrast there is no good evidence available at present to support a role for octreotide, histamine (H(2) antagonists) or proton pump inhibitors in this indication. The efficacy of somatostatin in controlling bleeding in patients with non-variceal UGI bleeding at high risk of mortality upon admission, or rebleeding following endoscopy, coupled with an excellent safety and tolerability profile, suggests it may be a valuable therapeutic option in the management of non-variceal bleeding.
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Affiliation(s)
- S A Jenkins
- Academic Department of Surgery, Morriston Hospital, Swansea, UK
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Quigley EM. Gastroduodenal motility. Curr Opin Gastroenterol 1999; 15:481-91. [PMID: 17023994 DOI: 10.1097/00001574-199911000-00005] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/10/2022]
Abstract
Several major themes emerged over the past year in the area of gastroduodenal motility. Mostly, these themes represented extensions of research areas discussed in prior reviews in this series rather than the emergence of completely new concepts. Thus, for example, considerable emphasis has again been placed on regional gastric motor function in dyspepsia and on the role of fundic relaxation and accommodation, in particular. Not surprisingly, basic physiologic research has also shown a keen interest in the regulation of fundic relaxation. One new and exciting development is the recognition of the stomach's role in satiety. The spectrum of gastric motor dysfunction in diabetes mellitus continues to be explored, and the important role of hyperglycemia in regulating gastric function has been further emphasized. More data have been provided on noninvasive alternatives to gastric motor function testing, and several studies have looked at factors that may influence variability in these various tests. There have been few innovations over the past year in the therapeutic arena; rather, the indications and limitations of current therapies have been further developed.
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Affiliation(s)
- E M Quigley
- Department of Medicine, National University of Ireland, Cork, Ireland.
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