The Experts below are selected from a list of 1416 Experts worldwide ranked by ideXlab platform
Edy E Soffer - One of the best experts on this subject based on the ideXlab platform.
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Intestinal Dysmotility and its relationship to sphincter of Oddi dysfunction
Current Gastroenterology Reports, 2004Co-Authors: Claudia P. Sanmiguel, Edy E SofferAbstract:Sphincter of Oddi dysfunction (SOD) is a clinical entity that presents with pain as the predominant symptom, and patients may require invasive procedures for its proper diagnosis. Those with abnormal sphincter of Oddi manometry (SOM) are commonly treated with endoscopic ablation of the sphincter. The results of such therapy vary and depend on the type of SOD. In the past several years, evidence has emerged of an association between SOD, Intestinal Dysmotility, and visceral hyperalgesia. This article reviews the evidence supporting such an association.
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Small bowel motility: Ready for prime time?
Current Gastroenterology Reports, 2000Co-Authors: Edy E SofferAbstract:The primary function of the small bowel is the absorption of nutrients, and the motor patterns of the healthy bowel are intended to promote that function. The motor patterns of the small bowel are the result of close interaction between the enteric nervous system, extrinsic nerves, regulatory peptides, and the Intestinal smooth muscle. The basic electrical rhythm governing Intestinal contractions is determined by specialized pacemaker cells called the interstitial cells of Cajal. Diseases affecting any of these components may result in Intestinal Dysmotility and its associated symptoms. Although transit studies and Intestinal manometry are helpful in the diagnosis of Dysmotility, our understanding of pathophysiology is hampered by the difficulties involved in obtaining and analyzing Intestinal tissue. Treatment of Intestinal Dysmotility relies on dietary manipulations and nutritional support (enteral or parenteral) because there is no drug therapy that can effectively enhance the propulsive function of the small bowel. Small bowel transplantation remains a life-saving intervention for patients who fail to respond to other therapies.
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Small Bowel Dysmotility.
Current treatment options in gastroenterology, 1998Co-Authors: Edy E SofferAbstract:The most important initial step in treating patients with Intestinal Dysmotility is to exclud reversible causes, in particular mechanical obstruction. The presence or absence of bacterial overgrowth should be determined by small bowel aspirate or breath test, although an empiric trial with antibiotics is an appropriate alternative. Physicians should use agents effective against gram-negative organisms, such as broad-spectrum penicillins or tetracycline, particularly those that provide coverage of anaerobes, such as metronidazole.
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Gastric and Intestinal Dysmotility syndromes.
Cleveland Clinic journal of medicine, 1997Co-Authors: Edy E SofferAbstract:Disorders of motility of the stomach and small intestine are quite common, and patients often present with a variety of nonspecific symptoms.
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Intestinal Dysmotility in patients with sphincter of oddi dysfunction
Digestive Diseases and Sciences, 1994Co-Authors: Edy E Soffer, Frederick C. JohlinAbstract:Sphincter of Oddi dysfunction (SOD) is associated with abdominal pain and is treated by sphincterotomy. Of 215 patients who underwent biliary sphincterotomy for SOD in our institution, 26 reported no improvement and 25 of those were found to have pancreatic sphincter dysfunction and subsequently underwent pancreatic septotomy. Nine patients remained symptomatic after the second intervention. Six of those nine patients, and seven of the 16 patients who improved after the septotomy, agreed to undergo an ambulatory duodenojejunal (DJ) manometry. DJ manometry was abnormal in four of the six symptomatic patients but only in one of seven patients who became asymptomatic after endoscopic treatment. We conclude that the persistence of symptoms after endoscopic ablation of the biliary and pancreatic sphincters is associated with abnormal Intestinal motility, which may explain in part the lack of response to the endoscopic treatment.
Marcel Jiménez - One of the best experts on this subject based on the ideXlab platform.
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Functional neuromuscular impairment in severe Intestinal Dysmotility.
Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society, 2018Co-Authors: D Gallego, Carolina Malagelada, Anna Accarino, Fernando Azpiroz, Juan R. Malagelada, Alessandra Gori, Roberto De Giorgio, Marcel JiménezAbstract:BACKGROUND Chronic Intestinal pseudo-obstruction (CIPO) and enteric Dysmotility (ED) are severe Intestinal motility disorders usually associated with underlying neuromuscular abnormalities. OBJECTIVE To evaluate the in vitro neuromuscular function of patients with severe Intestinal motility disorders. METHODS Full-thickness Intestinal biopsies (16 jejunum and 3 ileum) obtained from patients with CIPO (n = 10) and ED (n = 9) were studied using muscle bath and microelectrode techniques. Control samples (n = 6 ileum and n = 6 jejunum) were used to establish the range of normality. KEY RESULTS Fourteen parameters were defined to assess muscle contractility and nerve-muscle interaction: five to evaluate smooth muscle and interstitial cells of Cajal (ICC) and nine to evaluate inhibitory neuromuscular transmission. For each sample, a parameter was scored 0 if the value was inside the normal range or a value of 1 if it was outside. Patients' samples (CIPO/ED) had more abnormal parameters than controls (P
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morphofunctional changes underlying Intestinal Dysmotility in diabetic rip i hifnβ transgenic mice
International Journal of Experimental Pathology, 2011Co-Authors: Anna Domènech, Alessandra Gori, Gianandrea Pasquinelli, Roberto De Giorgio, Fatima Bosch, Martí Pumarola, Marcel JiménezAbstract:The pathogenetic mechanisms underlying gastroIntestinal Dysmotility in diabetic patients remain poorly understood, although enteric neuropathy, damage to interstitial cells of Cajal (ICC) and smooth muscle cell injury are believed to play a role. The aim of this study was to investigate the morphological and functional changes underlying Intestinal Dysmotility in RIP-I/hIFNβ transgenic mice treated with multiple very low doses of streptozotocin (20 mg/kg, i.p., 5 days). Compared with vehicle-treated mice, streptozotocin-treated animals developed type 1 diabetes mellitus, with sustained hyperglycaemia for 3.5 months, polyphagia, polydipsia and increased faecal output without changes in faecal water content (metabolic cages). Diabetic mice had a longer intestine, longer ileal villi and wider colonic crypts (conventional microscopy) and displayed faster gastric emptying and Intestinal transit. Contractility studies showed selective impaired neurotransmission in the ileum and mid-colon of diabetic mice. Compared with controls, the ileal and colonic myenteric plexus of diabetic mice revealed ultrastructural features of neuronal degeneration and HuD immunohistochemistry on whole-mount preparations showed 15% reduction in neuronal numbers. However, no immunohistochemical changes in apoptosis-related markers were noted. Lower absolute numbers of neuronal nitric oxide synthase- and choline acetyltransferase-immunopositive neurons and enhanced vasoactive Intestinal polypeptide and substance P immunopositivity were observed. Ultrastructural and immunohistochemical analyses did not reveal changes in the enteric glial or ICC networks. In conclusion, this model of diabetic enteropathy shows enhanced Intestinal transit associated with Intestinal remodelling, including neuroplastic changes, and overt myenteric neuropathy. Such abnormalities are likely to reflect neuroadaptive and neuropathological changes occurring in this diabetic model.
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Morphofunctional changes underlying Intestinal Dysmotility in diabetic RIP‐I/hIFNβ transgenic mice
International journal of experimental pathology, 2011Co-Authors: Anna Domènech, Alessandra Gori, Gianandrea Pasquinelli, Roberto De Giorgio, Fatima Bosch, Martí Pumarola, Marcel JiménezAbstract:The pathogenetic mechanisms underlying gastroIntestinal Dysmotility in diabetic patients remain poorly understood, although enteric neuropathy, damage to interstitial cells of Cajal (ICC) and smooth muscle cell injury are believed to play a role. The aim of this study was to investigate the morphological and functional changes underlying Intestinal Dysmotility in RIP-I/hIFNβ transgenic mice treated with multiple very low doses of streptozotocin (20 mg/kg, i.p., 5 days). Compared with vehicle-treated mice, streptozotocin-treated animals developed type 1 diabetes mellitus, with sustained hyperglycaemia for 3.5 months, polyphagia, polydipsia and increased faecal output without changes in faecal water content (metabolic cages). Diabetic mice had a longer intestine, longer ileal villi and wider colonic crypts (conventional microscopy) and displayed faster gastric emptying and Intestinal transit. Contractility studies showed selective impaired neurotransmission in the ileum and mid-colon of diabetic mice. Compared with controls, the ileal and colonic myenteric plexus of diabetic mice revealed ultrastructural features of neuronal degeneration and HuD immunohistochemistry on whole-mount preparations showed 15% reduction in neuronal numbers. However, no immunohistochemical changes in apoptosis-related markers were noted. Lower absolute numbers of neuronal nitric oxide synthase- and choline acetyltransferase-immunopositive neurons and enhanced vasoactive Intestinal polypeptide and substance P immunopositivity were observed. Ultrastructural and immunohistochemical analyses did not reveal changes in the enteric glial or ICC networks. In conclusion, this model of diabetic enteropathy shows enhanced Intestinal transit associated with Intestinal remodelling, including neuroplastic changes, and overt myenteric neuropathy. Such abnormalities are likely to reflect neuroadaptive and neuropathological changes occurring in this diabetic model.
Satish S C Rao - One of the best experts on this subject based on the ideXlab platform.
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Dysmotility and proton pump inhibitor use are independent risk factors for small Intestinal bacterial and or fungal overgrowth
Alimentary Pharmacology & Therapeutics, 2013Co-Authors: Carolyn Jacobs, Coss E Adame, Ashok Attaluri, Jessica Valestin, Satish S C RaoAbstract:Introduction Whether Intestinal Dysmotility and proton pump inhibitor (PPI) use either independently or together contributes to small Intestinal bacterial overgrowth (SIBO), and/or small Intestinal fungal overgrowth (SIFO) is not known.
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Dysmotility and proton pump inhibitor use are independent risk factors for small Intestinal bacterial and/or fungal overgrowth.
Alimentary pharmacology & therapeutics, 2013Co-Authors: Carolyn Jacobs, Ashok Attaluri, Jessica Valestin, E. Coss Adame, Satish S C RaoAbstract:Introduction Whether Intestinal Dysmotility and proton pump inhibitor (PPI) use either independently or together contributes to small Intestinal bacterial overgrowth (SIBO), and/or small Intestinal fungal overgrowth (SIFO) is not known.
William L Hasler - One of the best experts on this subject based on the ideXlab platform.
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Generalized Transit Delay on Wireless Motility Capsule Testing in Patients with Clinical Suspicion of Gastroparesis, Small Intestinal Dysmotility, or Slow Transit Constipation
Digestive Diseases and Sciences, 2011Co-Authors: Monthira Maneerattanaporn, Stephen M Wiener, William D Chey, Gregory E Wilding, Jason R. Baker, William L HaslerAbstract:Background The prevalence of generalized transit delay and relation to symptoms in suspected gastroparesis, Intestinal Dysmotility, or slow transit constipation are unknown. Aims The aims of this study were (1) to define prevalence of generalized Dysmotility using wireless motility capsules (WMC), (2) to relate to symptoms in suspected regional delay, (3) to compare results of WMC testing to conventional transit studies to quantify new diagnoses, and (4) to assess the impact of results of WMC testing on clinical decisions. Methods WMC transits were analyzed in 83 patients with suspected gastroparesis, Intestinal Dysmotility, or slow transit constipation. Results Isolated regional delays were observed in 32% (9% stomach, 5% small bowel, 18% colon). Transits were normal in 32% and showed generalized delays in 35%. Symptom profiles were similar with normal transit, isolated delayed gastric, small Intestinal, and colonic transit, and generalized delay ( P = NS). Compared to conventional tests, WMC showed discordance in 38% and provided new diagnoses in 53%. WMC testing influenced management in 67% (new medications 60%; modified nutritional regimens 14%; surgical referrals 6%) and eliminated needs for testing not already done including gastric scintigraphy (17%), small bowel barium transit (54%), and radioopaque colon marker tests (68%). Conclusions WMC testing defines localized and generalized transit delays with suspected gastroparesis, Intestinal Dysmotility, or slow transit constipation. Symptoms do not predict the results of WMC testing. WMC findings provide new diagnoses in >50%, may be discordant with conventional tests, and can influence management by changing treatments and eliminating needs for other tests. These findings suggest potential benefits of this method in suspected Dysmotility syndromes and mandate prospective investigation to further define its clinical role.
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generalized transit delay on wireless motility capsule testing in patients with clinical suspicion of gastroparesis small Intestinal Dysmotility or slow transit constipation
Digestive Diseases and Sciences, 2011Co-Authors: Braden Kuo, Monthira Maneerattanaporn, Allen Lee, Jason Baker, Stephen M Wiener, William D Chey, Gregory E Wilding, William L HaslerAbstract:Background The prevalence of generalized transit delay and relation to symptoms in suspected gastroparesis, Intestinal Dysmotility, or slow transit constipation are unknown.
Monthira Maneerattanaporn - One of the best experts on this subject based on the ideXlab platform.
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Generalized Transit Delay on Wireless Motility Capsule Testing in Patients with Clinical Suspicion of Gastroparesis, Small Intestinal Dysmotility, or Slow Transit Constipation
Digestive Diseases and Sciences, 2011Co-Authors: Monthira Maneerattanaporn, Stephen M Wiener, William D Chey, Gregory E Wilding, Jason R. Baker, William L HaslerAbstract:Background The prevalence of generalized transit delay and relation to symptoms in suspected gastroparesis, Intestinal Dysmotility, or slow transit constipation are unknown. Aims The aims of this study were (1) to define prevalence of generalized Dysmotility using wireless motility capsules (WMC), (2) to relate to symptoms in suspected regional delay, (3) to compare results of WMC testing to conventional transit studies to quantify new diagnoses, and (4) to assess the impact of results of WMC testing on clinical decisions. Methods WMC transits were analyzed in 83 patients with suspected gastroparesis, Intestinal Dysmotility, or slow transit constipation. Results Isolated regional delays were observed in 32% (9% stomach, 5% small bowel, 18% colon). Transits were normal in 32% and showed generalized delays in 35%. Symptom profiles were similar with normal transit, isolated delayed gastric, small Intestinal, and colonic transit, and generalized delay ( P = NS). Compared to conventional tests, WMC showed discordance in 38% and provided new diagnoses in 53%. WMC testing influenced management in 67% (new medications 60%; modified nutritional regimens 14%; surgical referrals 6%) and eliminated needs for testing not already done including gastric scintigraphy (17%), small bowel barium transit (54%), and radioopaque colon marker tests (68%). Conclusions WMC testing defines localized and generalized transit delays with suspected gastroparesis, Intestinal Dysmotility, or slow transit constipation. Symptoms do not predict the results of WMC testing. WMC findings provide new diagnoses in >50%, may be discordant with conventional tests, and can influence management by changing treatments and eliminating needs for other tests. These findings suggest potential benefits of this method in suspected Dysmotility syndromes and mandate prospective investigation to further define its clinical role.
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generalized transit delay on wireless motility capsule testing in patients with clinical suspicion of gastroparesis small Intestinal Dysmotility or slow transit constipation
Digestive Diseases and Sciences, 2011Co-Authors: Braden Kuo, Monthira Maneerattanaporn, Allen Lee, Jason Baker, Stephen M Wiener, William D Chey, Gregory E Wilding, William L HaslerAbstract:Background The prevalence of generalized transit delay and relation to symptoms in suspected gastroparesis, Intestinal Dysmotility, or slow transit constipation are unknown.
