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)

Plasma cholecystokinin levels were measured in children with recurrent abdominal pain to investigate the relationship of plasma cholecystokinin levels with colonic transit patterns and clinical symptoms. Subjects consisted of 120 children (mean age 9.6 +/- 2.6 years) for whom colonic transit study had also been done. Plasma cholecystokinin levels were 79.2 +/- 58.7 pg/mL in children with colonic inertia, 70.7 +/- 47.0 pg/mL in hindgut dysfunction, 57.4 +/- 53.1 pg/mL in pelvic outlet obstruction, and 67.6 +/- 47.9 pg/mL in normal colonic transit. These data showed that there was a tendency of increasing plasma cholecystokinin levels in children with proximal colon transit delay, although there was no significant difference among four groups. Plasma cholecystokinin levels in children of 10 years of age and under (54.5 +/- 40.4 pg/mL) were significantly lower (p = 0.01) than in children over 10 years (79.1 +/- 59.8 pg/mL). Plasma cholecystokinin levels based on colonic transit patterns, however, were not significantly different between the two age groups. There was no significant difference in plasma cholecystokinin levels between groups based on defecation frequency per week, presence of defecation pain, symptoms of milk intolerance, or the presence of emotional stress. These results suggested that there was a tendency of increasing plasma cholecystokinin levels in the younger age group and in children with delay in proximal colonic transit, but further study is required in relation to plasma cholecystokinin levels based on colonic transit patterns in a large number of patients.
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PMID:Colonic transit patterns and plasma cholecystokinin levels in children with recurrent abdominal pain. 1048 38

Cholecystokinin (CCK) is a major gastrointestinal hormone that plays an important role in stimulation of pancreatic secretion and gall-bladder contraction, regulation of gastrointestinal motility and induction of satiety. Ingestion of fat and protein induces significant increases in plasma CCK. Intraluminal mediators of CCK secretion, luminal CCK releasing factor and diazepam-binding inhibitor, were purified from rat intestinal secretion. These CCK-releasing factors (RF) are secreted tonically by the small intestine and stimulate CCK release. Another kind of CCK-RF named 'monitor peptide' was purified from the rat pancreatic juice that stimulates CCK secretion when introduced into rat intestine. Bile exclusion from the duodenum causes an increase in basal CCK and enhances stimulated plasma CCK release, and bile salt replacement reverses these effects. Thus, the CCK-RF are spontaneously secreted into the intestinal lumen in humans, while the CCK-producing cells are under constant suppression by intraduodenal bile acids. In acute pancreatitis, plasma CCK levels are high in patients with gallstone pancreatitis, but not in patients with pancreatitis from other causes, such as alcoholic and idiopathic pancreatitis. A transient disturbance of bile flow into the duodenum by stones or oedema of the pancreas together with impairment of pancreatic exocrine function might cause the increase in plasma CCK release in gallstone pancreatitis. Patients with chronic pancreatitis with mild to moderate impairment of exocrine function and abdominal pain, had significantly higher plasma CCK concentrations, whereas patients with pancreatic insufficiency had a significantly lower plasma CCK response to a test meal than the healthy subjects. The increased CCK may further aggravate pancreatitis and worsen the prognosis of pancreatitis by stimulating the injured pancreas, resulting in the vicious circle via endogenous CCK release. The CCK-A receptor antagonist might be therapeutically useful in acute pancreatitis by stopping the vicious circle.
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PMID:Pathophysiological role of cholecystokinin in humans. 1075 24

Abdominal pain/discomfort, bloating, need to rush to the toilet, straining, feeling of incomplete bowel emptying and alternating periods of diarrhea and constipation is the clinical definition of the irritable bowel syndrome. The internationally used syndrome definition is based on expert opinions and answers to patient questionnaires. When symptoms are registered prospectively, abdominal pain starts or worsens after meals and is not relieved by defecation. As in the general population patients with the syndrome define diarrhea as loose stools and constipation as hard stools regardless of stool frequencies. Variation in defecatory symptoms and discrepancies between these symptoms and stool consistency are the hallmarks of the syndrome, and the degree of variation per fortnight is relatively stable in the individual patient. Fermentation of carbohydrates by colonic bacteria, increased sensitivity to bowel distention by gas, gas-producing food, increased secretion of cholecystokinin after fatty meals and/or increased sympathetic nerve tone at stress can give rise to symptoms. Symptoms can start after a single period of bacterial gastroenteritis. Although patients seeking medical care for the syndrome are more often anxious, the syndrome itself is not psychosomatic. Symptoms are possibly mediated through partial degranulation of mast cells in bowel mucosa, but this does not make it an allergic disease. If bowel dysmotility can be measured, early stage or a mild case of intestinal pseudoobstruction should be considered. Hyperreactivity in the enteric nervous system and/or in the brain is the likely main cause of the symptoms. More widespread activity in the brain after exposure to stimuli originating from bowel nerves or less inhibition of this stimulation in the brain are possible mechanisms.
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PMID:[Irritable bowel syndrome. Survey of definitions, differential diagnosis and pathogenesis]. 1147 55

Because treatment of irritable bowel syndrome (IBS) patients can be frustrating to the clinician and patient as well, the physician should strive to gain the patient's confidence with a concise, appropriate work-up and by offering reassurance and education that IBS is a functional disorder without significant long-term health risks. First-line treatment should be aimed at treating the most bothersome symptom. Tricyclic antidepressants are superior to placebo in reducing abdominal pain scores, as well as improving global symptom severity. Loperamide is superior to placebo in managing IBS-associated diarrhea. Whereas fiber has a role in treating constipation, its value for IBS or, specifically, in the relief of abdominal pain or diarrhea associated with IBS is controversial. Although certain antispasmodics have demonstrated superiority over placebo in managing abdominal pain, none of these agents are available in the United States. Probiotic therapy using Lactobacillus plantarum has demonstrated superiority to placebo in improving pain, regulating bowel habits, and decreasing flatulence. As studied in a recent placebo-controlled prospective study, Chinese herbal medicines significantly improved bowel symptom scores and global symptom profile, and reduced IBS-related quality of life impairment. Some of the most promising emerging therapies in IBS revolve around targeted pharmacotherapeutic modulation of serotonin receptors (ie, 5-HT3 and 5-HT4 subtypes), which are involved in sensory and motor functions of the gut. Other investigational agents that are also being explored include cholecystokinin antagonists, alpha2-adrenergic agonists (eg, clonidine), serotonin reuptake inhibitors (eg, citalopram), and neurokinin antagonists. IBS is best understood through the biopsychosocial paradigm, and therefore, its effective management requires a comprehensive multidisciplinary approach based on patient education and reassurance, enhanced by diet recommendations and lifestyle modifications, and complemented by pharmacotherapy and psychosocial intervention in more severe cases.
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PMID:Irritable Bowel Syndrome. 1209 74

Anticholinergics and prokinetics are mainstays of therapy for Irritable Bowel Syndrome (IBS) patients despite their limited efficacy and troublesome side-effect profile. The clinical limitations of these drugs are a result of their relative broad and nonspecific pharmacologic interaction with various receptors. Recent advances in gut physiology have led to the identification of various receptor targets that may play a pivotal role in the pathogenesis of IBS. Medicinal chemists searching for safe and effective IBS therapies are now developing compounds targeting many of these specific receptors. The latest generation of anticholinergics, such as zamifenacin, darifenacin, and YM-905, provide selective antagonism of the muscarinic type-3 receptor. Tegaserod, a selective 5-HT4 partial agonist, tested in multiple clinical trials, is effective in reducing the symptoms of abdominal pain, bloating, and constipation. Ezlopitant and nepadudant, selective antagonists for neurokinin receptors type 1 and type 2, respectively, show promise in reducing gut motility and pain. Loperamide, a mu (mu) opioid receptor agonist, is safe and effective for IBS patients with diarrhea (IBS-D) as the predominant bowel syndrome. Fedotozine, a kappa (kappa) opioid receptor agonist, has been tried as a visccral analgesic in various clinical trials with conflicting results. Alosetron, a 5-HT3 receptor antagonist, has demonstrated efficacy in IBS-D patients but incidents of ischemic colitis seen in post-marketing follow-up resulted its removal from the market. Compounds that target cholecystokinin. A, N-methyl-D-aspartate, alpha 2-adrenergic, and corticotropin-releasing factor receptors are also examined in this review.
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PMID:Irritable bowel syndrome neuropharmacology. A review of approved and investigational compounds. 1218 41

Biliary dyskinesia (BD) is a well-recognized cause of chronic abdominal pain in adults, but is less common in children. We reviewed our experience with the diagnosis, treatment, and follow-up in a group of children treated with cholecystectomy from March 1995 to October 2000. We identified children with chronic upper abdominal pain, normal ultrasonography (US), and delayed cholecystokinin (CCK)-stimulated gallbladder emptying (<35%). All other diagnostic tests for their abdominal pain were reviewed. Their treatment, surgical intervention, and outcome were recorded. During the study period, 74 cholecystectomies were performed in our institution, 10 (13.5%) of them for BD. The duration of symptoms ranged between 1 and 60 months (mean 22). All patients had a normal plain abdominal radiograph, normal US, and delayed gallbladder ejection fraction (EF). All were treated by elective laparoscopic cholecystectomy. Symptoms were completely relieved in all patients during the follow-up period, which ranged between 9 and 24 months (mean 12.8). Cholecystectom should be considered in children with chronic upper-abdominal pain and delayed EF on CCK-HIDA scintigraphy. Laparoscopic cholecystectomy is the procedure of choice in these patients.
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PMID:Biliary dyskinesia in children. 1241 55

The effects of evodiamine on gastric emptying, gastrointestinal transit, and plasma levels of cholecystokinin (CCK) were studied in male rats. Evodiamine, isolated from the dry unripened fruit of Evodia rutaecarpa Bentham (a Chinese medicine named Wu-chu-yu), has been recommended for abdominal pain, acid regurgitation, nausea, diarrhea, and dysmenorrhea. Gastrointestinal motility was assessed in rats 15 min after intragastric instillation of a test meal containing charcoal and Na(2)51CrO(4). Gastric emptying was determined by measuring the amount of radiolabeled chromium contained in the small intestine as a percentage of the initial amount received. Gastrointestinal transit was evaluated by calculating the geometric center of distribution of the radiolabeled marker. Blood samples were collected for CCK radioimmunoassay (RIA). After administration of evodiamine (0.67-6.00 mg/kg), both gastric emptying and gastrointestinal transit were inhibited, whereas the plasma concentration of CCK was increased in a dose-dependent manner. The selective CCK(1) receptor antagonists, devazepide and lorglumide, effectively attenuated the evodiamine-induced inhibition of gastric emptying and gastrointestinal transit. L-365,260 (3R-(+)-N-(2,3-dihydro-1-methyl-2-oxo-5-phenyl-1H-1,4-benzodiazepine-3-yl)-N'-(3-methylphenyl)-urea), a selective CCK(2) receptor antagonist, did not alter the evodiamine-induced inhibition of gastric emptying and gastrointestinal transit. These results suggest that evodiamine inhibits both gastric emptying and gastrointestinal transit in male rats via a mechanism involving CCK release and CCK(1) receptor activation.
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PMID:Effects of evodiamine on gastrointestinal motility in male rats. 1246 63

Chronic pancreatitis should be considered in all patients with unexplained abdominal pain. Management of abdominal pain in these patients continues to pose a formidable challenge. The importance of small duct disease without radiographic abnormalities is now a well-established concept. It is meaningful to determine whether patients with chronic pancreatitis have small duct or large duct disease because this distinction has therapeutic implications. Diagnostic evaluation should begin with simple noninvasive and inexpensive tests like serum trypsinogen and fecal elastase, to be followed where appropriate by more complicated measures such as the secretin hormone stimulation test, especially in patients with suspected small duct disease. No universal causal treatment is available. Non-enteric-coated enzyme preparations are useful for treatment of pain, whereas enteric-coated enzyme preparations are preferred for steatorrhea. Octreotide is used increasingly for abdominal pain that is unresponsive to pancreatic enzyme therapy. When medical therapy for chronic pancreatitis pain has failed, endoscopic therapy, endoscopic ultrasound-guided celiac plexus block, and thoracoscopic splanchnicectomy, performed by experts, may be considered for a highly selected patient population. Surgical ductal decompression is appropriate in patients with considerable pancreatic ductal dilation. The role and efficacy of cholecystokinin-receptor antagonists, antioxidants, and antidepressant drugs remain to be defined.
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PMID:Medical therapy for chronic pancreatitis pain. 1263 50

The management of the irritable bowel syndrome (IBS) remains unsatisfactory. For abdominal pain, antispasmodics are, at best, of only modest efficacy. Tricyclic antidepressants in low dose are useful (with the number needed to treat being three), but side effects and patient concerns regarding use of a centrally acting agent for depression remain limitations. Selective serotonin reuptake inhibitors are of uncertain efficacy in IBS. Opioid agonists, especially loperamide, are useful for diarrhea but not for pain in IBS; rebound constipation also remains a problem. Bile salt sequestering agents are not of established value in IBS but seem to be useful clinically in a small group of IBS patients with diarrhea. Aloestron, a 5HT(3) antagonist, should be reserved, if available, for women with severe diarrhea predominant IBS who have failed to respond to conventional therapy, and started at a low dose. Fiber and bulking agents may help constipation in some trials, but the evidence that they are efficacious in IBS is equivocal; they are frequently prescribed as first-line drugs for IBS regardless of the primary bowel disturbance but often increase bloating, gas, and pain. Laxatives are not of established value in IBS but are often taken by patients with constipation predominant IBS. Tegaserod, a partial 5HT(4) agonist, is now available in the United States and other countries for use in women with IBS whose primary bowel symptom is constipation; its efficacy in men and in those with alternating bowel habits is unknown. Probiotics are of uncertain efficacy. Chinese herbal medicine data are insufficient. Other new drugs in development include the cholecystokinin antagonists and novel visceral analgesics. Both current and potential therapies for IBS are reviewed in this article.
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PMID:Pharmacologic therapy for the irritable bowel syndrome. 1273 51

Patients with acalculous biliary-like pain present a difficult clinical challenge. Our aim was to evaluate the outcome of patients with recurrent biliary-like pain without gallstones who underwent testing of gallbladder ejection fraction (GBEF) by cholecystokinin-cholescintigraphy (CCK-CS) in order to determine clinical factors that may predict symptom resolution. We reviewed the records of patients with recurrent acalculous biliary-like pain who underwent CCK-CS from January 1995 to December 1999. For comparison, we also studied an age- and sex-matched group of patients who underwent cholecystectomy for symptomatic cholelithiasis. Outcome was obtained by telephone interview, using a scale from 0 to 3 where 0 = no improvement and 3 = clinical remission. Patient demographics, predominant symptom(s), method of management, gallbladder pathology, and response to treatment were recorded. One hundred twenty-nine patients underwent CCK-CS. Of 69 with an abnormal GBEF, 48 (70%) were available for interview. Forty patients underwent cholecystectomy. Twenty-seven patients reported symptom resolution after surgery while 4 nonsurgical patients reported the same (P = NS). Univariate analysis revealed no association between symptom outcome and presence of gastrointestinal symptom(s), severity and duration of abdominal pain, management, or gallbladder pathology. In addition, no GBEF cutoff level predicted symptom outcome. Of the remaining 60 patients with a normal GBEF, 30 (50%) were available for interview. Twenty-eight patients in this group were managed medically and 2 patients underwent cholecystectomy. Eighteen patients managed medically were asymptomatic, as were the 2 who underwent cholecystectomy. There was no difference in symptom outcome between patients who had GBEF >35% vs <35%. In conclusion, in a group of patients with recurrent acalculous biliary-like pain who underwent CCK-CS, we found a high rate of symptom resolution following cholecystectomy; however, this was not statistically different from a smaller cohort who did not undergo surgery. We were unable to determine any variable predictive of symptom resolution.
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PMID:Gallbladder ejection fraction and symptom outcome in patients with acalculous biliary-like pain. 1277 85


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