Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The time taken for a solid meal to pass through the stomach, small intestine, and colon was measured in 61 patients with irritable bowel syndrome, subdivided according to their presenting symptoms, and in 53 healthy volunteers. Small bowel transit times were significantly shorter in patients who complained predominantly of diarrhoea (3.3 +/- 0.3 vs 4.2 +/- 0.2 h; p = 0.01; n = 21) and significantly longer in patients who complained predominantly of constipation (5.4 +/- 0.3 vs 4.2 +/- 0.2 h; p less than 0.01; n = 23) or pain and distension (5.4 +/- 0.4 vs 4.2 +/- 0.2 h; p less than 0.01; n = 17) compared with controls. Whole gut transit times were shorter in patients who complained of diarrhoea (35 +/- 5 vs 53 +/- 4 h; p less than 0.01), and longer in patients with constipation (87 +/- 13 vs 53 +/- 4 h; p less than 0.05) compared with controls. No significant differences in gastric emptying rates were shown between any of the patient groups and normal controls. Thirty-four patients reported pain, particularly in the right iliac fossa, during the meal transit test, and in 25 of these (74%), the onset of the pain was associated with the arrival of residues of the test meal in the caecum. Our results indicate that irritable bowel syndrome should be considered a disease of the small intestine as well as the colon.
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PMID:Irritable bowel syndrome: relationship of disorders in the transit of a single solid meal to symptom patterns. 684 Jun 14

In patients suffering from the irritable bowel syndrome no morphological substrate for this disease can be found; thus quantitation of functional parameters might be desirable. In the colon these patients exhibit myoelectrical waves of increased frequency, e.g. 3 per minute, as well as an exaggerated retropulsion and a prolonged motor response after food intake, indicating an abnormal motility pattern. In the small gut transit is either accelerated, causing diarrhea, or slowed down, causing constipation; in addition, there is an increased retrograde movement of intestinal gas. The pain threshold is decreased in the small and large bowel; inflation of a balloon or insufflation of gas may reproduce the clinical symptoms of the patients. In the terminal ileum there is net fluid secretion instead of net absorption, as normal. Even the esophagus may be affected, since manometry has demonstrated disturbed peristalsis and a reduced pressure of the lower esophageal sphincter. Such quantification of intestinal function is not a substitute for careful clinical work-up. It has however contributed to a better understanding of the underlying functional disturbances in irritable bowel syndrome.
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PMID:[Measurable parameters in the irritable bowel syndrome (author's transl)]. 707 Jan 90

In reviewing the records of almost 1000 infants and children with intussusception in two children's hospitals over the last 25 yr, there have been seven bowel perforations during attempted hydrostatic barium enema reduction of an intussusception. Except for one instance, these have all occurred during the last 6 yr. The infants were all 6 mo old or less and most had a preceeding viral illness. Only 4 of the 7 had pain, all vomited, in only 2 was a mass felt and all but 1 had rectal bleeding. The duration of these signs and symptoms was longer than 36 hr with most ill for 3 or 4 days. All seven infants had abdominal x-rays that showed complete small bowel obstruction. Once the intussusception was suspected, barium enema reduction was attempted without excessive hydrostatic pressure and not for a prolonged time; all the ileocolic intussusceptions were met in the transverse colon with only a minimal reduction produced. It was at this time that a perforation was suddenly noted. All infants required immediate right hemicolectomy for the area (s) of colonic necrosis. Postoperatively, there were two wound infections, a volvulus which left the child with a short gut and another infant suffered severe brain damage. These babies seem to fit a pattern in which they are younger and sicker longer than the average infant with an intussusception, and have a complete small bowel obstruction. These facts may be a warning that such infants are at increased risk for a barium enema bowel perforation.
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PMID:Colon perforation during attempted barium enema reduction of intussusception. 725 34

It is hypothesized that chronic gastritis and ulcerative colitis both are induced by viral infection, and that such chronic infection of the mucosa may lead to ulceration and occasionally cancer. Duodenal ulcer disease and Crohn's disease may on the other hand, be due to activation of latent viral infection of the corresponding neural ganglions, with subsequent migration of virus along the nerves to the gut wall. The gastric acid hypersecretion often occurring in patients with duodenal ulcer disease might be a consequence of viral interference with the efferent nerve function of vagal ganglions. Correspondingly, non-ulcer dyspepsia as well as irritable colon may reflect viral infection of afferent nerve function leading to pain and discomfort.
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PMID:Gastritis, peptic ulcer disease, inflammatory bowel disease, and stomach and colon cancers- are they all caused by viral infections? 732 19

Hypersensitivity to pain is a common component of functional bowel disorders. Hyperalgesia may be induced by various stimuli which produce a cocktail of inflammatory mediators that decrease the pain threshold. Drugs able to block these peripheral events within the gut may offer a new pharmacological approach for treating functional bowel disorders. Kappa opioids have been shown to inhibit somatic pain through a peripheral mechanism of action, acting directly on receptors located on peripheral sensory endings. They can block both the nociceptive messages as well as the release of sensory peptides. This paper reviews the effects of opioid agonists on gut visceral pain and motility anomalies induced by visceral pain. Kappa opioids have strong effects on all models tested, with a peripheral mechanism of action allowing the design of drugs acting only in the periphery and having no central nervous system side-effects. This contrasts with mu agonists which are centrally active on pain and worsen the subsequent transit and motility anomalies.
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PMID:Review article: the hypersensitive gut--peripheral kappa agonists as a new pharmacological approach. 760 51

Excessive release of kinin (BK) in the synovial fluid can produce oedema, pain and loss of functions due to activation of B1 and B2 kinin receptors. Activation of the kinin forming system could be mediated via injury, trauma, coagulation pathways (Hageman factor and thrombin) and immune complexes. The activated B1 and B2 receptors might cause release of other powerful non-cytokine and cytokine mediators of inflammation, e.g., PGE2, PGI2, LTs, histamine, PAF, IL-1 and TNF, derived mainly from polymorphonuclear leukocytes, macrophages, endothelial cells and synovial tissue. These mediators are capable of inducing bone and cartilage damage, hypertrophic synovitis, vessel proliferation, inflammatory cell migration and, possibly, angiogenesis in pannus formation. These pathological changes, however, are not yet defined in the human model of chronic inflammation. The role of kinins and their interacting inflammatory mediators would soon start to clarify the detailed questions they revealed in clinical and experimental models of chronic inflammatory diseases. Several B1 and B2 receptor antagonists are being synthesized in an attempt to study the molecular functions of kinins in inflammatory processes, such as rheumatoid arthritis, periodontitis, inflammatory diseases of the gut and osteomyelitis. Future development of specific potent and stable B1 and B2 receptor antagonists or combined B1 and B2 antagonists with y-IFN might serve as a pharmacological basis for more effective treatment of joint inflammatory and related diseases.
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PMID:Pathogenic responses of bradykinin system in chronic inflammatory rheumatoid disease. 770 72

We wished to determine if visceral perception in the rectum and stomach is altered in patients with irritable bowel syndrome and to evaluate the effects on visceral sensation of 5-HT3 receptor blockade. Twelve community patients with diarrhea-predominant irritable bowel syndrome and 10 healthy controls were studied in a double-blind, randomized, placebo-controlled study. Using two barostats, the stomach and rectum were distended, with pressure increments of 4 mm Hg, from 10 to 26 mm Hg; visceral perception was measured on an ordinal scale of 0-10. Personality traits were measured using standard psychological methods, and somatic pain was evaluated by immersion of the nondominant hand in cold water. The effect of 5-HT3 antagonism was tested with a single intravenous dose of ondansetron at 0.15 mg/kg. Gastric perception was higher in irritable bowel syndrome, but rectal distension was perceived similarly in irritable bowel syndrome and controls. Pain tolerance to cold water was also similar in irritable bowel syndrome and controls. Ondansetron induced rectal relaxation and increased rectal compliance but did not significantly alter gastric compliance or visceral perception. Psychological test scores were similar in patients and controls. We conclude that in this group of psychologically normal patients with irritable bowel syndrome, who were not chronic health-care seekers, visceral perception was normal. Ondansetron did not alter gut perception in health or in irritable bowel syndrome.
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PMID:Visceral perception in irritable bowel syndrome. Rectal and gastric responses to distension and serotonin type 3 antagonism. 772 Apr 76

Since the first comprehensive description of the symptoms of FMS by Yunus et al (1981), numerous investigations have confirmed that FMS is a clinical entity. However, the aetiology of the syndrome is still not fully elucidated. It seems, however, logical to place the origin of the disorder in the muscle. Muscle pain, especially at the muscle-tendon junctions, fatigue and stiffness are the first symptoms. A malfunction of energy metabolism has been detected in part of the muscle fibres. However, it has to be considered that the muscle is not an isolated entity. Its activity is controlled by segmentally arranged motor units of the ventral horn of the spinal cord in response to proprioceptive afferent signals arising in the muscle spindles or in other sensory elements including nociceptors. Together with supraspinal descending inputs, the spinal motor neurone pool is the common final pathway for segmental and suprasegmental inputs, making the motor system extremely powerful for adaptive adjustments but also vulnerable if deficits occur in either of these input levels. A second, recently discovered abnormality seen in FMS is a lowered serotonin level in peripheral and most likely also central structures. The underlying mechanism seems to be defective absorption of the precursor amino acid tryptophan from the gut. Serotonin is involved centrally in the regulation of the sleep pattern, and at the spinal level it acts as a 'gain setter' of motoneurone excitability and suppresses signal transmission of noxious stimuli in dorsal horn neurones. Either of these two disturbances, muscle energy depletion or serotonin deficiency, could by itself evoke many of the symptoms of FMS, and their combined appearance will perpetuate the disease. Depressed levels of somatomedin C, caused by a deficit of stage 4 sleep-dependent release of GH, might represent an additional factor in preventing proper development or repair of myoskeletal structures. Malabsorption of certain amino acids, possibly due to a genetic disorder of gut transport mechanisms, may constitute an additional deleterious factor. The abnormalities found in the HPA and HPT axis may be seen as an attempt of the organism to restore homeostasis. The stimulus eliciting this counter-regulatory reaction may be pain or other afferent signals which normally do not reach the central nervous system. It is doubtful whether the unspecific activation of the HPA axis in a non-inflammatory disease is beneficial.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neuromediator and hormonal perturbations in fibromyalgia syndrome: results of chronic stress? 785 Aug 79

Liquid esophageal transit and gastric emptying, mouth-to-cecum transit, and whole gut transit of a solid-liquid meal were measured in 14 patients with PSS, 16 control subjects (esophageal transit), and 20 control subjects (gastrointestinal transit), respectively, by using scintigraphic techniques, the hydrogen breath test, and stool markers. In patients with PSS, the glucose hydrogen breath test for detection of small intestinal overgrowth was performed and various gastrointestinal symptoms were determined. Esophageal transit and gastric emptying were significantly prolonged in PSS patients with 11 of 14 PSS patients (79%) disclosing delayed esophageal transit and eight of 14 PSS patients (57%) disclosing delayed gastric emptying. All PSS patients with prolonged gastric emptying also had delayed esophageal transit and there was a significant positive correlation between esophageal transit and gastric emptying (r = 0.696, P < 0.01). No significant differences between PSS patients and controls were detected concerning mouth-to-cecum transit and whole gut transit, but abnormally delayed mouth-to-cecum transit was found in four of 10 PSS patients (40%) and abnormally prolonged whole gut transit was detected in three of 13 PSS patients (23%). Small bacterial overgrowth was diagnosed in three of 14 PSS patients (21%). Delayed esophageal transit and gastric emptying were associated with dysphagia, retrosternal pain, and epigastric fullness, while prolonged whole gut transit was associated with constipation. It is concluded that delayed gastric emptying is frequently associated with esophageal transit disorders in PSS patients and may be one important factor for the development of gastroesophageal reflux disease in these patients.
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PMID:Gastrointestinal transit through esophagus, stomach, small and large intestine in patients with progressive systemic sclerosis. 792 44

This chapter reviews the therapeutic use of octreotide in a variety of pancreatic disorders, including acute pancreatitis, in the prevention of postoperative and post-ERCP pancreatitis, in the control of postoperative pancreatic fistulae, and in chronic pancreatitis for the control of pain and of pseudocysts and ascites. The review also discusses the use of octreotide in intestinal disorders of motility, gastrointestinal bleeding, intestinal fistulae and refractory diarrhoea, including the diarrhoeas of AIDS, diabetes, short gut, chemotherapy, ileostomy and gastric surgery. The use of octreotide in neuroendocrine tumours, both for therapy and diagnostic imaging, is reviewed briefly. The paucity of adequately controlled studies in many of these situations is indicated and the potential usefulness of octreotide estimated.
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PMID:Expanding uses of octreotide. 794 61


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