Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with biliary dyskinesia have biliary colic, a normal gallbladder ultrasound, and a gallbladder ejection fraction typically less than 35%. We report a retrospective review of 70 patients with biliary dyskinesia who underwent cholecystectomy. Seventy-seven percent of the patients were women. Average age was 40. The most common symptoms were right upper quadrant pain, nausea, vomiting, and fatty food intolerance. All patients underwent a cholecystokinin-hepatobiliary scan or cholecystokinin-oral cholecystogram. Average ejection fractions were 20.2% and 28.4% respectively. Average post-operation follow-up was 10.9 months. Eighty-four percent of patients (59 of 70) reported improvement at follow-up. Eight patients had ejection fractions greater than 35%; seven of them reported improvement after cholecystectomy. Eleven patients did not improve after cholecystectomy; their average ejection fraction was 25%. These patients also had atypical symptoms (mid-epigastric pain and reflux symptoms). We believe cholecystectomy is effective therapy for biliary dyskinesia. Surgical outcomes could be improved by careful histories distinguishing biliary colic from other complaints. Less reliance should be placed on the ejection fraction when the patient has biliary colic without another etiology of abdominal pain.
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PMID:Outcomes of surgical therapy for biliary dyskinesia. 1450 24

We report our experience of cholecystectomy for treating symptoms suggestive of biliary disease in association with a decreased gallbladder ejection fraction (GBEF) but without evidence of cholelithiasis. Five children with normal biliary ultrasounds were evaluated between January 1990 and December 2000 for recurrent upper abdominal pain. Based on a cholecystokinin (CCK)-provoked GBEF of less than 50% and the absence of any other gastrointestinal pathology, patients underwent cholecystectomy with operative cholangiography for presumed biliary dyskinesia. Pathological examination demonstrated chronic inflammation in all cases. Two patients had complete resolution of their symptoms, but three had persistent pain following surgery. Biliary dyskinesia seems an uncommon cause of persistent abdominal pain in childhood. Cholecystectomy was not always effective in relieving symptoms. Biliary scintigraphy with CCK provocation should not be used as the sole criterion for cholecystectomy. Sphincteric manometry may be valuable in the assessment of this small group of patients to avoid inappropriate intervention. The future perhaps lies in better understanding of the physiological action and pharmacological control of the sphincter of Oddi.
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PMID:Biliary dyskinesia: is the problem with Oddi? 1477 Mar 23

Cholecystokinin (CCK) is a brain-gut peptide; it functions both as a neuropeptide and as a gut hormone. Although the pancreas and the gallbladder were long thought to be the principal peripheral targets of CCK, CCK receptors are found throughout the gut. It is likely that CCK has a physiological role not only in the stimulation of pancreatic and biliary secretions but also in the regulation of gastrointestinal motility. The motor effects of CCK include postprandial inhibition of gastric emptying and inhibition of colonic transit. It is now evident that at least two different receptors, CCK(1) and CCK(2) (formerly CCK-A and CCK-B, respectively), mediate the actions of CCK. Both localization and functional studies suggest that the motor effects of CCK are mediated by CCK(1) receptors in humans. Since CCK is involved in sensory and motor responses to distension in the intestinal tract, it may contribute to the symptoms of constipation, bloating and abdominal pain that are often characteristic of functional gastrointestinal disorders in general and irritable bowel syndrome (IBS), in particular. CCK(1) receptor antagonists are therefore currently under development for the treatment of constipation-predominant IBS. Clinical studies suggest that CCK(1) receptor antagonists are effective facilitators of gastric emptying and inhibitors of gallbladder contraction and can accelerate colonic transit time in healthy volunteers and patients with IBS. These drugs are therefore potentially of great value in the treatment of motility disorders such as constipation and constipation-predominant IBS.
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PMID:Involvement of endogenous CCK and CCK1 receptors in colonic motor function. 1510 Jan 63

Biliary dyskinesia is defined as symptomatic biliary colic without cholelithiasis, and is diagnosed during cholescintigraphy by assessing gallbladder emptying with cholecystokinin (CCK) stimulation. Unfortunately, gallbladder emptying is not routinely assessed during cholescintigraphy in pediatric patients. The purpose of this review is to assess the effectiveness of cholecystectomy in patients with chronic abdominal pain and delayed gallbladder emptying and to assess whether these findings correlate with the histologic evidence of chronic cholecystitis. We retrospectively reviewed the medical records of all patients ( n=16) at our institution from October 1997 to August 2001 who underwent quantitative cholescintigraphy with CCK stimulation that demonstrated delayed gallbladder emptying (< 35% at 60 min) and who subsequently underwent cholecystectomy. Laparoscopic cholecystectomy was performed in 16 patients with chronic abdominal pain. All 16 patients had delayed gallbladder emptying (mean ejection fraction: 15+/-8%, range: 3-32%). The mean age was 12+/-2 years (range: 8-17 years). Presenting symptoms included abdominal pain (86%), fatty food intolerance (27%), emesis (13%), and diarrhea (13%). Mean duration of abdominal pain before operation was 11+/-19 months (range: 2 weeks-6 years). One patient's symptoms persisted postoperatively, but abdominal pain resolved in all other patients. Histologic evidence of chronic cholecystitis was demonstrated in 86% of surgical specimens. Five patients underwent concurrent appendectomy, and all had normal appendiceal histology. Our experience suggests that children with chronic abdominal pain and delayed gallbladder emptying on CCK-stimulated cholescintigraphy are likely to benefit from cholecystectomy and to have histologic evidence of chronic cholecystitis.
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PMID:Biliary dyskinesia: a potentially unrecognized cause of abdominal pain in children. 1532 41

Acalculous biliary-type abdominal pain is a commonly encountered clinical problem whose pathophysiology is unclear and evaluation and management are controversial. Cholecystokinin cholescintigraphy to measure the gallbladder ejection fraction (GEF) has been advocated as a criterion for cholecystectomy. However, there is no consensus regarding the dose and rate of infusion of cholecystokinin, both of which can alter the GEF, and the definition of an abnormal ejection fraction varies among studies. Many but not all studies have concluded that a low GEF predicts good outcomes after cholecystectomy, but most studies suffer from poor methodology and there is only one prospective randomized controlled trial. Also, some patients with a normal GEF have responded to cholecystectomy. Another controversial area has been the role of sphincter of Oddi dysfunction (SOD) in patients with biliary-type pain and gallbladder in situ. Some reports suggest an overlap between SOD and low GEF, although a causal relationship has not been established. Yet another subject of interest is the role of visceral hyperalgesia in patients with acalculous biliary-type pain. We have reviewed the relevant literature relating to these issues and have highlighted the controversial aspects. In the absence of high-quality studies, an evidence-based treatment algorithm is difficult to design but will be proposed. More prospective controlled trials are warranted to better define the appropriate evaluation and management of patients with this syndrome.
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PMID:Controversies concerning pathophysiology and management of acalculous biliary-type abdominal pain. 1790 73

Biliary dyskinesia is a potential cause for acalculous biliary colic in pediatric patients. A triad of symptoms and signs, consisting of abdominal pain (with or without associated nausea or fatty food intolerance), absence of gallstones, and an abnormally low cholecystokinin-stimulated gallbladder ejection fraction is used to diagnose the disorder. In several small pediatric case series, cholecystectomy resulted in symptomatic improvement in a majority of patients with biliary dyskinesia. However, the diagnosis of biliary dyskinesia and appropriate management remain controversial. This review discusses the purported pathophysiology of biliary dyskinesia and the data available regarding diagnosis and treatment of this entity in the pediatric population.
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PMID:Biliary dyskinesia in pediatrics. 1653 82

Women often complain gut symptoms during pregnancy and the luteal phase of the menstrual cycle. To investigate the relationship between ovarian steroids and the abnormal gut motility and sensitivity, the expressions of cholecystokinin (CCK), calcitonin gene-related peptide (CGRP) and their receptors in stomach were studied in ovariectomized rats. Blood samples were collected for estradiol (E(2)), progesterone (P(4)), CCK and CGRP radioimmunoassay. Expression of CCK(A) receptor in fundus was assessed by Western blot and CGRP receptor was determined by (125)I-CGRP radioligand binding assay (RBA). The replacement therapy with estradiol benzoate (EB) could dose-dependently increase the plasma CCK level and the expression of gastric CCK(A) receptor (P<0.05 respectively). P(4) replacement therapy could stimulate the release of CGRP and increase the binding sites of CGRP receptors in stomach (P<0.05 respectively). The combined effect of EB and P(4) was to stimulate the release of CCK and CGRP, and to increase the expressions of gastric CCK(A) and CGRP receptors. These results indicate that EB could inhibit gastric emptying by increasing CCK secretion and CCK(A) receptor expression in ovariectomized rats. P(4) could increase gut sensitivity by up-regulating the release of CGRP and the activity of CGRP receptor. It could be deduced from these observations that CCK(A) and CGRP receptor antagonists could be used for female patients who suffer from gastrointestinal dysfunction closely related with the menstrual cycle, such as distension, satiety, bloating and abdominal pain.
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PMID:Regulative effects of ovarian steroids on rat gastric motility and sensitivity. 1678 13

Irritable bowel syndrome (IBS) is a highly prevalent functional gastrointestinal disorder affecting up to 3-15% of the general population in Western countries. It is characterised by unexplained abdominal pain, discomfort and bloating in association with altered bowel habits. The pathophysiology of IBS is considered to be multifactorial, involving disturbances of the brain-gut-axis: IBS has been associated with abnormal gastrointestinal motor functions, visceral hypersensitivity, psychosocial factors, autonomic dysfunction and mucosal inflammation. Traditional IBS therapy is mainly symptom oriented and often unsatisfactory. Hence, there is a need for new treatment strategies. Increasing knowledge of brain-gut physiology, mechanisms, and neurotransmitters and receptors involved in gastrointestinal motor and sensory function have led to the development of several new therapeutic approaches. This article provides a systematic overview of recently approved or novel medications that show promise for the treatment of IBS; classification is based on the physiological systems targeted by the medication. The article includes agents acting on the serotonin receptor or serotonin transporter system, novel selective anticholinergics, alpha-adrenergic agonists, opioid agents, cholecystokinin antagonists, neurokinin antagonists, somatostatin receptor agonists, neurotrophin-3, corticotropin releasing factor antagonists, chloride channel activators, guanylate cyclase-c agonists, melatonin and atypical benzodiazepines. Finally, the role of probiotics and antibacterials in the treatment of IBS is summarised.
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PMID:Irritable bowel syndrome: recent and novel therapeutic approaches. 1678 93

Narcotic bowel syndrome (NBS) is a subset of opioid bowel dysfunction that is characterized by chronic or frequently recurring abdominal pain that worsens with continued or escalating dosages of narcotics. This syndrome is underrecognized and may be becoming more prevalent. In the United States this may be the result of increases in using narcotics for chronic nonmalignant painful disorders, and the development of maladaptive therapeutic interactions around its use. NBS can occur in patients with no prior gastrointestinal disorder who receive high dosages of narcotics after surgery or acute painful problems, and among patients with functional gastrointestinal disorders or other chronic gastrointestinal diseases who are managed by physicians who are unaware of the hyperalgesic effects of chronic opioids. The evidence for the enhanced pain perception is based on the following: (1) activation of excitatory antianalgesic pathways within a bimodal opioid regulation system, (2) descending facilitation of pain at the rostral ventral medulla and pain facilitation via dynorphin and cholecystokinin activation, and (3) glial cell activation that produces morphine tolerance and enhances opioid-induced pain. Treatment involves early recognition of the syndrome, an effective physician-patient relationship, graded withdrawal of the narcotic according to a specified withdrawal program, and the institution of medications to reduce withdrawal effects.
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PMID:The narcotic bowel syndrome: clinical features, pathophysiology, and management. 1791 40

Irritable bowel syndrome is a functional gastrointestinal disorder affecting up to 3-15% of the general population in western countries. It is characterised by unexplained abdominal pain, discomfort, and bloating in association with altered bowel habits. The pathophysiology of irritable bowel syndrome is multifactorial involving disturbances of the brain-gut axis. The pathophysiology provides the rationale for pharmacotherapy: abnormal gastrointestinal motor functions, visceral hypersensitivity, psychosocial factors, autonomic dysfunction, and mucosal immune activation. Understanding the mechanisms, and their mediators or modulators including neurotransmitters and receptors have led to several therapeutic approaches including agents acting on the serotonin receptor or serotonin transporter system, antidepressants, novel selective anticholinergics, alpha-adrenergic agonists, opioid agents, cholecystokinin-antagonists, neurokinin-antagonists, somatostatin receptor agonists, corticotropin releasing factor antagonists, chloride channel activators, guanylate cyclase-c agonists, melatonin, atypical benzodiazepines, antibiotics, immune modulators and probiotics. The mechanisms and current evidence regarding efficacy of these agents are reviewed.
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PMID:Current and novel therapeutic options for irritable bowel syndrome management. 1966 53


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