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V Memeo - One of the best experts on this subject based on the ideXlab platform.
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slow transit constipation solitary symptom of a systemic gastrointestinal disease
Diseases of The Colon & Rectum, 1999Co-Authors: D F Altomare, Piero Portincasa, M Rinaldi, Agostino Di Ciaula, E Martinelli, Annacinzia Amoruso, Giuseppe Palasciano, V MemeoAbstract:INTRODUCTION: Autonomic neuropathy is thought to play a role in the pathogenesis of slow-transit constipation, but other gastrointestinal organs may also be involved, even if they are symptom-free. We investigated whether motility in gastrointestinal organs other than the colon was impaired in patients with slow-transit constipation and whether the autonomic nervous system was involved. METHODS: Twenty-one consecutive patients (18 females; median age, 46 years) with severe chronic constipation (≤2 defecations/week and delayed colonic transit time) were studied. Autonomic neuropathy function was tested with esophageal manometry, gastric and Gallbladder emptying (fasting and postprandial motility) by ultrasonography, orocecal transit time (H2-breath test), colonic transit time (radiopaque markers), and anorectal volumetric manometry. The integrity of the autonomic nervous system was assessed by a quantitative sweat-spot test for preganglionic and postganglionic fibers, tilt-table test, and Valsalva electrocardiogram R-R ratio. RESULTS: Esophageal manometry showed gastroesophageal reflux or absence of peristalsis in five of the seven patients examined. Gallbladder Dysmotility (i.e., increased fasting, postprandial residual volume, or both) was observed in 6 of 14 (43 percent) patients. Gastric emptying was decreased in 13 of 17 (76 percent) patients. Orocecal transit time was delayed in 18 of 20 (90 percent) patients; median transit time was 160 (range, 90–200) minutes. Median colonic transit time was 97 (range, 64–140) hours. Anorectal function showed abnormal rectoanal inhibitory reflex and decreased rectal sensitivity in 11 of 19 (58 percent) patients. Signs of autonomic neuropathy of the sympathetic cholinergic system were found in 14 of 18 (78 percent) patients. Only one of nine patients had vagal abnormalities detected with the Valsalva test and four of five patients with a history of orthostatic hypotension had a positive tilt-table test. CONCLUSIONS: Slow-transit constipation may be associated with impaired function of other gastrointestinal organs. More than 70 percent of patients with slow-transit constipation present some degree of autonomic neuropathy. Severe constipation may be the main complaint in patients with a systemic disease involving several organs and possibly involving the autonomic nervous system. This should be considered in the management of such cases.
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Slow-transit constipation
Diseases of the Colon & Rectum, 1999Co-Authors: D F Altomare, Piero Portincasa, M Rinaldi, Agostino Di Ciaula, E Martinelli, Annacinzia Amoruso, Giuseppe Palasciano, V MemeoAbstract:INTRODUCTION: Autonomic neuropathy is thought to play a role in the pathogenesis of slow-transit constipation, but other gastrointestinal organs may also be involved, even if they are symptom-free. We investigated whether motility in gastrointestinal organs other than the colon was impaired in patients with slow-transit constipation and whether the autonomic nervous system was involved. METHODS: Twenty-one consecutive patients (18 females; median age, 46 years) with severe chronic constipation (≤2 defecations/week and delayed colonic transit time) were studied. Autonomic neuropathy function was tested with esophageal manometry, gastric and Gallbladder emptying (fasting and postprandial motility) by ultrasonography, orocecal transit time (H_2-breath test), colonic transit time (radiopaque markers), and anorectal volumetric manometry. The integrity of the autonomic nervous system was assessed by a quantitative sweat-spot test for preganglionic and postganglionic fibers, tilt-table test, and Valsalva electrocardiogram R-R ratio. RESULTS: Esophageal manometry showed gastroesophageal reflux or absence of peristalsis in five of the seven patients examined. Gallbladder Dysmotility ( i.e. , increased fasting, postprandial residual volume, or both) was observed in 6 of 14 (43 percent) patients. Gastric emptying was decreased in 13 of 17 (76 percent) patients. Orocecal transit time was delayed in 18 of 20 (90 percent) patients; median transit time was 160 (range, 90–200) minutes. Median colonic transit time was 97 (range, 64–140) hours. Anorectal function showed abnormal rectoanal inhibitory reflex and decreased rectal sensitivity in 11 of 19 (58 percent) patients. Signs of autonomic neuropathy of the sympathetic cholinergic system were found in 14 of 18 (78 percent) patients. Only one of nine patients had vagal abnormalities detected with the Valsalva test and four of five patients with a history of orthostatic hypotension had a positive tilt-table test. CONCLUSIONS: Slow-transit constipation may be associated with impaired function of other gastrointestinal organs. More than 70 percent of patients with slow-transit constipation present some degree of autonomic neuropathy. Severe constipation may be the main complaint in patients with a systemic disease involving several organs and possibly involving the autonomic nervous system. This should be considered in the management of such cases.
Henry A Pitt - One of the best experts on this subject based on the ideXlab platform.
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Resistin-Like Molecule Alpha Reduces Gallbladder Optimal Tension
Journal of Gastrointestinal Surgery, 2007Co-Authors: Hayder H. Al-azzawi, Attila Nakeeb, Abhishek Mathur, Deborah A. Swartz-basile, Henry A PittAbstract:Introduction Insulin resistance is associated with increased Gallbladder volume and impaired Gallbladder emptying. Resistin and resistin-like molecule alpha (RELM-α) are adipose-derived hormones that are believed to mediate insulin resistance. Therefore, we tested the hypothesis that administration of resistin or RELM-α would cause insulin resistance and diminish Gallbladder contractility. Methods In two sequential studies 40 eight-week-old nondiabetic lean mice were fed a chow diet for 4 weeks. In Study A, 10 mice received 20 μg of resistin IP, while in Study B 10 mice received 20 μg of RELM-α IP for seven days. In each study, 10 control mice received an equal volume of saline IP for seven days. At 12 weeks animals were fasted and underwent cholecystectomy, and in vitro Gallbladder response to neurotransmitters was determined. Serum resistin, RELM-α, glucose, and insulin levels were measured. HOMA index, a measure of insulin resistance, was calculated. Results RELM-α significantly increased HOMA index. RELM-α decreased Gallbladder optimal tension, but did not alter responses to neurotransmitters. Resistin had no effect on HOMA index or on Gallbladder optimal tension or response. Conclusion These data suggest that in nondiabetic lean mice: 1) resistin does not alter insulin resistance or Gallbladder optimal tension, but 2) RELM-α increases insulin resistance and reduces Gallbladder optimal tension. Therefore, we concluded that RELM-α may play a role in insulin-resistance mediated Gallbladder Dysmotility.
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insulin resistance causes human Gallbladder Dysmotility
Journal of Gastrointestinal Surgery, 2006Co-Authors: Attila Nakeeb, Anthony G Comuzzie, Hayder H Alazzawi, Gabriele E Sonnenberg, Ahmed H Kissebah, Henry A PittAbstract:Obesity, diabetes, and hyperlipidemia are known risk factors for the development of gallstones. A growing body of animal and human data has correlated insulin resistance with organ dysfunction. The relationship among obesity, diabetes, hyperlipidemia, and abnormal Gallbladder motility remains unclear. Therefore, we designed a study to investigate the association among obesity, insulin resistance, hyperlipidemia, and Gallbladder Dysmotility. One hundred ninety-two healthy adult nondiabetic volunteers were studied. Gallbladder ultrasounds were performed before and after a standardized fatty meal. A Gallbladder ejection fraction (EF) was calculated, and an EF of 25% (109±20 mg/dl versus 78±2 mg/dl, P 25% (3.3±1.2 versus 2.0±0.2, P<0.05). In obese subjects (n=66), fasting glucose, insulin, and insulin resistance were not associated with a Gallbladder EF <25%. These data suggest that in lean, nondiabetic volunteers without gallstones, Gallbladder Dysmotility is associated with an elevated fasting glucose as well as a high index of insulin resistance. We conclude that insulin resistance alone may be responsible for Gallbladder Dysmotility that may result in acalculous cholecystitis or gallstone formation.
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Insulin resistance causes human Gallbladder Dysmotility
Journal of Gastrointestinal Surgery, 2006Co-Authors: Attila Nakeeb, Anthony G Comuzzie, Gabriele E Sonnenberg, Ahmed H Kissebah, Hayder Al-azzawi, Henry A PittAbstract:Obesity, diabetes, and hyperlipidemia are known risk factors for the development of gallstones. A growing body of animal and human data has correlated insulin resistance with organ dysfunction. The relationship among obesity, diabetes, hyperlipidemia, and abnormal Gallbladder motility remains unclear. Therefore, we designed a study to investigate the association among obesity, insulin resistance, hyperlipidemia, and Gallbladder Dysmotility. One hundred ninety-two healthy adult nondiabetic volunteers were studied. Gallbladder ultrasounds were performed before and after a standardized fatty meal. A Gallbladder ejection fraction (EF) was calculated, and an EF of
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Insulin resistance causes human Gallbladder Dysmotility.
Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract, 2006Co-Authors: Attila Nakeeb, Anthony G Comuzzie, Gabriele E Sonnenberg, Ahmed H Kissebah, Hayder H. Al-azzawi, Henry A PittAbstract:Obesity, diabetes, and hyperlipidemia are known risk factors for the development of gallstones. A growing body of animal and human data has correlated insulin resistance with organ dysfunction. The relationship among obesity, diabetes, hyperlipidemia, and abnormal Gallbladder motility remains unclear. Therefore, we designed a study to investigate the association among obesity, insulin resistance, hyperlipidemia, and Gallbladder Dysmotility. One hundred ninety-two healthy adult nondiabetic volunteers were studied. Gallbladder ultrasounds were performed before and after a standardized fatty meal. A Gallbladder ejection fraction (EF) was calculated, and an EF of 25% (109±20 mg/dl versus 78±2 mg/dl, P 25% (3.3±1.2 versus 2.0±0.2, P
D F Altomare - One of the best experts on this subject based on the ideXlab platform.
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slow transit constipation solitary symptom of a systemic gastrointestinal disease
Diseases of The Colon & Rectum, 1999Co-Authors: D F Altomare, Piero Portincasa, M Rinaldi, Agostino Di Ciaula, E Martinelli, Annacinzia Amoruso, Giuseppe Palasciano, V MemeoAbstract:INTRODUCTION: Autonomic neuropathy is thought to play a role in the pathogenesis of slow-transit constipation, but other gastrointestinal organs may also be involved, even if they are symptom-free. We investigated whether motility in gastrointestinal organs other than the colon was impaired in patients with slow-transit constipation and whether the autonomic nervous system was involved. METHODS: Twenty-one consecutive patients (18 females; median age, 46 years) with severe chronic constipation (≤2 defecations/week and delayed colonic transit time) were studied. Autonomic neuropathy function was tested with esophageal manometry, gastric and Gallbladder emptying (fasting and postprandial motility) by ultrasonography, orocecal transit time (H2-breath test), colonic transit time (radiopaque markers), and anorectal volumetric manometry. The integrity of the autonomic nervous system was assessed by a quantitative sweat-spot test for preganglionic and postganglionic fibers, tilt-table test, and Valsalva electrocardiogram R-R ratio. RESULTS: Esophageal manometry showed gastroesophageal reflux or absence of peristalsis in five of the seven patients examined. Gallbladder Dysmotility (i.e., increased fasting, postprandial residual volume, or both) was observed in 6 of 14 (43 percent) patients. Gastric emptying was decreased in 13 of 17 (76 percent) patients. Orocecal transit time was delayed in 18 of 20 (90 percent) patients; median transit time was 160 (range, 90–200) minutes. Median colonic transit time was 97 (range, 64–140) hours. Anorectal function showed abnormal rectoanal inhibitory reflex and decreased rectal sensitivity in 11 of 19 (58 percent) patients. Signs of autonomic neuropathy of the sympathetic cholinergic system were found in 14 of 18 (78 percent) patients. Only one of nine patients had vagal abnormalities detected with the Valsalva test and four of five patients with a history of orthostatic hypotension had a positive tilt-table test. CONCLUSIONS: Slow-transit constipation may be associated with impaired function of other gastrointestinal organs. More than 70 percent of patients with slow-transit constipation present some degree of autonomic neuropathy. Severe constipation may be the main complaint in patients with a systemic disease involving several organs and possibly involving the autonomic nervous system. This should be considered in the management of such cases.
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Slow-transit constipation
Diseases of the Colon & Rectum, 1999Co-Authors: D F Altomare, Piero Portincasa, M Rinaldi, Agostino Di Ciaula, E Martinelli, Annacinzia Amoruso, Giuseppe Palasciano, V MemeoAbstract:INTRODUCTION: Autonomic neuropathy is thought to play a role in the pathogenesis of slow-transit constipation, but other gastrointestinal organs may also be involved, even if they are symptom-free. We investigated whether motility in gastrointestinal organs other than the colon was impaired in patients with slow-transit constipation and whether the autonomic nervous system was involved. METHODS: Twenty-one consecutive patients (18 females; median age, 46 years) with severe chronic constipation (≤2 defecations/week and delayed colonic transit time) were studied. Autonomic neuropathy function was tested with esophageal manometry, gastric and Gallbladder emptying (fasting and postprandial motility) by ultrasonography, orocecal transit time (H_2-breath test), colonic transit time (radiopaque markers), and anorectal volumetric manometry. The integrity of the autonomic nervous system was assessed by a quantitative sweat-spot test for preganglionic and postganglionic fibers, tilt-table test, and Valsalva electrocardiogram R-R ratio. RESULTS: Esophageal manometry showed gastroesophageal reflux or absence of peristalsis in five of the seven patients examined. Gallbladder Dysmotility ( i.e. , increased fasting, postprandial residual volume, or both) was observed in 6 of 14 (43 percent) patients. Gastric emptying was decreased in 13 of 17 (76 percent) patients. Orocecal transit time was delayed in 18 of 20 (90 percent) patients; median transit time was 160 (range, 90–200) minutes. Median colonic transit time was 97 (range, 64–140) hours. Anorectal function showed abnormal rectoanal inhibitory reflex and decreased rectal sensitivity in 11 of 19 (58 percent) patients. Signs of autonomic neuropathy of the sympathetic cholinergic system were found in 14 of 18 (78 percent) patients. Only one of nine patients had vagal abnormalities detected with the Valsalva test and four of five patients with a history of orthostatic hypotension had a positive tilt-table test. CONCLUSIONS: Slow-transit constipation may be associated with impaired function of other gastrointestinal organs. More than 70 percent of patients with slow-transit constipation present some degree of autonomic neuropathy. Severe constipation may be the main complaint in patients with a systemic disease involving several organs and possibly involving the autonomic nervous system. This should be considered in the management of such cases.
Walter J Hogan - One of the best experts on this subject based on the ideXlab platform.
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sphincter of oddi dysfunction and other functional biliary disorders evaluation and treatment
Gastroenterology Clinics of North America, 2003Co-Authors: Devang Prajapati, Walter J HoganAbstract:Functional biliary disorders are complex conditions that originate from aberrant biliary motility or visceral hyperalgesia. Traditionally two conditions have been identified as functional biliary disorders: sphincter of Oddi dysfunction (SOD) and Gallbladder Dysmotility. The prevalence of these conditions is difficult to estimate because many studies have had inherent bias related to nonuniform investigation of control and study patients and varied diagnostic gold standards. Frequently these patients require invasive investigations available only at tertiary medical centers, making diagnosis and treatment of these conditions difficult. This article presents methodologies for evaluation and treatment of these conditions. Anatomy and physiology The sphincter of Oddi (SO), named after Ruggero Oddi [1], is a segment of circular and longitudinal smooth muscle that incorporates the distal common bile duct and pancreatic duct. The length of the sphincter is approximately 6 to 10 mm [2] and is contained in the duodenal wall. The SO in most clinical situations is treated as a single sphincter, but is in fact composed of the biliary sphincter (sphincter choledochus) and pancreatic sphincter (sphincter pancreaticus), which encircle the distal biliary and pancreatic ducts and the ampullary sphincter, which encompasses both in the
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Sphincter of Oddi dysfunction and other functional biliary disorders: evaluation and treatment.
Gastroenterology clinics of North America, 2003Co-Authors: Devang Prajapati, Walter J HoganAbstract:Functional biliary disorders encompass the conditions of SOD and Gallbladder Dysmotility, both of which result in clinical pain syndromes. Obtaining objective diagnostic and outcomes data for both disorders has been an ongoing challenge over the last two decades. SOD, although initially believed to be strictly a biliary disorder, has now been implicated in recurrent pancreatitis. The biliary-type classification allows a clinician to stratify patients who would benefit from SOM and endoscopic sphincterotomy. Further study into the impact of endoscopic therapy for recurrent pancreatitis is needed. By the same token, the dilemma of postcholecystectomy abdominal pain, whether classified as biliary or pancreatic type III, remains challenging. The current limitations of knowledge highlight the need for prospective randomized studies to evaluate the clinical significance of SOM abnormalities to facilitate treatment of these patients.
Attila Nakeeb - One of the best experts on this subject based on the ideXlab platform.
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Resistin-Like Molecule Alpha Reduces Gallbladder Optimal Tension
Journal of Gastrointestinal Surgery, 2007Co-Authors: Hayder H. Al-azzawi, Attila Nakeeb, Abhishek Mathur, Deborah A. Swartz-basile, Henry A PittAbstract:Introduction Insulin resistance is associated with increased Gallbladder volume and impaired Gallbladder emptying. Resistin and resistin-like molecule alpha (RELM-α) are adipose-derived hormones that are believed to mediate insulin resistance. Therefore, we tested the hypothesis that administration of resistin or RELM-α would cause insulin resistance and diminish Gallbladder contractility. Methods In two sequential studies 40 eight-week-old nondiabetic lean mice were fed a chow diet for 4 weeks. In Study A, 10 mice received 20 μg of resistin IP, while in Study B 10 mice received 20 μg of RELM-α IP for seven days. In each study, 10 control mice received an equal volume of saline IP for seven days. At 12 weeks animals were fasted and underwent cholecystectomy, and in vitro Gallbladder response to neurotransmitters was determined. Serum resistin, RELM-α, glucose, and insulin levels were measured. HOMA index, a measure of insulin resistance, was calculated. Results RELM-α significantly increased HOMA index. RELM-α decreased Gallbladder optimal tension, but did not alter responses to neurotransmitters. Resistin had no effect on HOMA index or on Gallbladder optimal tension or response. Conclusion These data suggest that in nondiabetic lean mice: 1) resistin does not alter insulin resistance or Gallbladder optimal tension, but 2) RELM-α increases insulin resistance and reduces Gallbladder optimal tension. Therefore, we concluded that RELM-α may play a role in insulin-resistance mediated Gallbladder Dysmotility.
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insulin resistance causes human Gallbladder Dysmotility
Journal of Gastrointestinal Surgery, 2006Co-Authors: Attila Nakeeb, Anthony G Comuzzie, Hayder H Alazzawi, Gabriele E Sonnenberg, Ahmed H Kissebah, Henry A PittAbstract:Obesity, diabetes, and hyperlipidemia are known risk factors for the development of gallstones. A growing body of animal and human data has correlated insulin resistance with organ dysfunction. The relationship among obesity, diabetes, hyperlipidemia, and abnormal Gallbladder motility remains unclear. Therefore, we designed a study to investigate the association among obesity, insulin resistance, hyperlipidemia, and Gallbladder Dysmotility. One hundred ninety-two healthy adult nondiabetic volunteers were studied. Gallbladder ultrasounds were performed before and after a standardized fatty meal. A Gallbladder ejection fraction (EF) was calculated, and an EF of 25% (109±20 mg/dl versus 78±2 mg/dl, P 25% (3.3±1.2 versus 2.0±0.2, P<0.05). In obese subjects (n=66), fasting glucose, insulin, and insulin resistance were not associated with a Gallbladder EF <25%. These data suggest that in lean, nondiabetic volunteers without gallstones, Gallbladder Dysmotility is associated with an elevated fasting glucose as well as a high index of insulin resistance. We conclude that insulin resistance alone may be responsible for Gallbladder Dysmotility that may result in acalculous cholecystitis or gallstone formation.
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Insulin resistance causes human Gallbladder Dysmotility
Journal of Gastrointestinal Surgery, 2006Co-Authors: Attila Nakeeb, Anthony G Comuzzie, Gabriele E Sonnenberg, Ahmed H Kissebah, Hayder Al-azzawi, Henry A PittAbstract:Obesity, diabetes, and hyperlipidemia are known risk factors for the development of gallstones. A growing body of animal and human data has correlated insulin resistance with organ dysfunction. The relationship among obesity, diabetes, hyperlipidemia, and abnormal Gallbladder motility remains unclear. Therefore, we designed a study to investigate the association among obesity, insulin resistance, hyperlipidemia, and Gallbladder Dysmotility. One hundred ninety-two healthy adult nondiabetic volunteers were studied. Gallbladder ultrasounds were performed before and after a standardized fatty meal. A Gallbladder ejection fraction (EF) was calculated, and an EF of
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Insulin resistance causes human Gallbladder Dysmotility.
Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract, 2006Co-Authors: Attila Nakeeb, Anthony G Comuzzie, Gabriele E Sonnenberg, Ahmed H Kissebah, Hayder H. Al-azzawi, Henry A PittAbstract:Obesity, diabetes, and hyperlipidemia are known risk factors for the development of gallstones. A growing body of animal and human data has correlated insulin resistance with organ dysfunction. The relationship among obesity, diabetes, hyperlipidemia, and abnormal Gallbladder motility remains unclear. Therefore, we designed a study to investigate the association among obesity, insulin resistance, hyperlipidemia, and Gallbladder Dysmotility. One hundred ninety-two healthy adult nondiabetic volunteers were studied. Gallbladder ultrasounds were performed before and after a standardized fatty meal. A Gallbladder ejection fraction (EF) was calculated, and an EF of 25% (109±20 mg/dl versus 78±2 mg/dl, P 25% (3.3±1.2 versus 2.0±0.2, P
