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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Solid organ transplant recipients can experience serious disease and death from infection due to the parasitic roundworm Strongyloides stercoralis. This parasite lives in soil contaminated with human feces. Domestic dogs and cats may be another reservoir. Larvae can penetrate the skin, are carried hematogenously to the lungs, migrate up the bronchial tree, and then can be passed to the upper small intestine. Autoinfection occurs in the setting of immunosuppression when invasive larvae penetrate the gut wall and cause disseminated infection. Polymicrobial sepsis is sometimes seen due to enteric organisms adhering to the parasite. Transplant recipients are at highest risk during the first 3 months posttransplant. Many organ systems may be affected. Pulmonary symptoms include cough, wheezing, sputum production, dyspnea, hemoptysis, tachypneas, and pleuritic pain. Hyperinfection, an augmentation of the normal skin-lung-intestine life cycle, occurs in roughly two-thirds of infected transplant recipients, with dissemination in the remainder. Diagnosis is made primarily by examination of the stool or intestinal secretions for ova and parasites. Occasionally, parasites are noted in the sputum. New serologic tests show promise. The parasite may remain in the host for over 25 years before immunosuppression causes either dissemination or hyperinfection. Thiabendazole given for 3 to 7 days is the treatment of choice for organ transplant recipients. Repeat courses may be needed to eradicate infection.
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PMID:Strongyloides infections in transplant recipients. 234 6

In a series of 18 patients with angina pectoris, in whom treatment over at least 3 years with nitroderivatives and Ca-antagonists had become partially ineffective on chest pain, and in 18 patients with angina-like non-cardiac chest pain, the following examinations were carried out: upper gut x-ray and endoscopy, acid perfusion test, esophageal manometry, 24-hour esophageal pH monitoring associated with Holter recording. The presence or absence of coronary insufficiency was established by means of scintigraphic and ECG tests, Holter monitoring and coronary arteriography. In both groups the majority of patients had abnormal esophageal function, but in patients with angina pectoris treated for a long period of time the motility changes were prevalently reflux-related. With respect to the origin of chest pain, the esophagus was found to be the likely cause in 4 patients with angina pectoris, and the probable cause in another 10 of the same group; it was the likely cause in 7 patients without angina pectoris, and the probable cause in another 7 of the same group. As nitroderivatives and Ca-antagonists decrease the LES tone and the amplitude of esophageal pressure waves, long-term treatment with these drugs may be taken into account in the genesis of gastro-esophageal reflux and related changes, including esophageal pain.
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PMID:The esophagus as a possible cause of chest pain in patients with and without angina pectoris. 237 62

In this study, gut functioning and the prevalence of functional bowel disorders among a Wellington community sample of 285 apparently healthy people was estimated using a standardised questionnaire. When asked for their opinion of their bowel functioning generally, 37% of respondents were satisfied that it was always normal, 57.2% regarded it as not always normal, and 5.6% felt it was normal less than half the time or not normal at all. However, only 11.6% had actually consulted a physician about a stomach or bowel disorder in the past year. Average bowel frequency was 8.4 movements per week (SD = 3.9) for the total sample. Approximately three quarters of the total sample had experienced diarrhoea at least occasionally, but only 2.5% half the movements or more often. Constipation was reported by 8.1% for half the time or more, and 1.8% for most bowel movements. Abdominal distension was experienced by 7.2% on half of days or more, and 3.6% on most days or daily. Abdominal pain occuring on six or more separate days in the previous year was reported by 26.4% of men and 31.9% of women. Pain not due to organic disorders that was colonic in nature and of the irritable bowel syndrome type was reported by 15.9% of men and 17.2% of women.
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PMID:Functional gastrointestinal symptoms in a Wellington community sample. 239 67

Cimetropium bromide is a new antimuscarinic compound with strong antispasmodic activity. The aim of this study was to evaluate the effects of oral cimetropium bromide on total gut transit time in patients with irritable bowel syndrome. Forty patients, divided according to their initial total gastrointestinal transit times and presenting symptoms, were treated with cimetropium bromide 50 mg t.d.s. or placebo for 1 month according to a double-blind, parallel group design. Before and after treatment all subjects ingested 24 radio-opaque markers. The total intestinal transit time was determined by evaluating the rate of disappearance of markers from plain X-ray films of the abdomen taken every 24 h for 4 days. Pain and bowel habits were also monitored. Seven patients did not complete the study. Cimetropium bromide significantly (P less than 0.01) shortened the whole gut transit time in patients with prolonged transit time (80.8 +/- 4.0 h before vs 60.8 +/- 6.7 h after treatment) and improved the global clinical condition significantly compared with placebo (P = 0.029). In patients with a short total intestinal transit time, cimetropium bromide had no effect on whole gut transit time and did not significantly improve symptoms. The results of this study indicate that oral cimetropium bromide is effective both objectively and subjectively in a subgroup of irritable bowel syndrome patients with constipation.
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PMID:Effects of cimetropium bromide on gastrointestinal transit time in patients with irritable bowel syndrome. 252 Jun 22

Medical records of 210 horses that survived ventral midline celiotomy for at least 4 months were examined and owners were queried to determine factors contributing to incisional hernia formation. The incidence rate of incisional hernias within 4 months was 16%. Factors significantly associated with occurrence of incisional hernias were incisional drainage, closure of the linea alba with chromic gut suture material, previous midline celiotomy, excessive incisional edema, castrated male sex, postoperative leukopenia, and postoperative pain (colic). Factors not significantly associated with occurrence of incisional hernias were suture pattern used for linea alba closure, concurrent enterotomy or intestinal resection, postoperative bandage or stent, postoperative fever, hypoproteinemia, diarrhea, respiratory disease (coughing), and peritonitis. Hernias developed in horses within 12 weeks of surgery, with the earliest hernia recognized at week 2. Of 30 horses for which information was available, only one hernia developed in 24 (80%) and two or more hernias developed in 6 (20%) along the incision. Multiple hernias tended to be smaller than single hernias.
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PMID:Incisional hernias in the horse. Incidence and predisposing factors. 253 Jun 84

Bradykinin and its active metabolites, produced by kallikreins at their sites of action, potently elicit a variety of biological effects: hypotension, bronchoconstriction, gut and uterine contraction, epithelial secretion in airway, gut, and exocrine glands, vascular permeability, pain, connective tissue proliferation, cytokine release, and eicosanoid formation. These effects are mediated by at least two broad classes of receptors. The most common is the B2 subtype. The availability of competitive antagonists of B2 receptors has provided powerful tools for the study of bradykinin's actions. The significance of kinins in certain human diseases is being explored by using these agents as potential therapeutic agents. Human clinical trials are under way to test the usefulness of bradykinin receptor antagonists to treat symptoms of the common cold and the pain associated with severe burns. Trials are also being comtemplated for use in treatment of asthma.
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PMID:Antagonists of B2 bradykinin receptors. 254 96

The control mechanisms of gastrointestinal motility are complex. Extrinsic neurohormonal effects modulate an intrinsic system, often called the "gut brain," composed of nervous and neuropeptide components. To exert pharmacologic influence on GI motility, use is made of agents that mimic the external control system. Agents that stimulate opioid receptors, block adrenoceptors, block or facilitate acetylcholine action, or antagonize the action of prostaglandins are used to effect changes in GI motility. The major indications for pharmacologic intervention are to increase motility in constipation, to reduce it in most cases of diarrhea, and to restore propulsive coordination in postoperative ileus. In cases of clinical colic the primary requirement is control of pain. Agents used for this purpose may adversely affect motility, and choice requires knowledge of their actions in this respect. In addition, drugs used for other purposes, anthelmintics for instance, may also influence gut motility. A synopsis of the actions of the agents commonly employed in GI motility control and some associated drugs are displayed in Table 3. Recent advances in the understanding of drug action on the gut should help in the selection of drugs for clinical use.
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PMID:Effects of pharmacological agents on gastrointestinal motility. 267 Jan 8

We conducted a survey on functional gut disorders and health care seeking behavior in a large non-patient population of an Italian region (Umbria). 533 subjects were interviewed by means of a specific questionnaire. 44 (8.5%) reported symptoms compatible with the irritable bowel syndrome, 30 (5.8%) had non-colonic pain, 48 (9.2%) chronic constipation, and 20 (3.8%) dyspepsia. It is concluded that in our region there is a relatively high percentage of subjects that do not commonly seek health care, although affected by functional gut disorders.
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PMID:Functional gut disorders and health care seeking behavior in an Italian non-patient population. 276 61

Acidosis in gastric mucosa (pHi less than 7.32) was evaluated as a diagnostic test for gastric ischemia, using 80 asymptomatic subjects as controls. Mucosal acidosis was found in 6 patients with abdominal pain and 1 with gastrointestinal bleeding. Three had occlusive disease of 2 or more visceral arteries, 3 had occlusive disease of the celiac axis alone, and 1 had an occluded portal vein. One patient had infarcted gut. The abnormal pHi (7.10 +/- 0.11, mean +/- SD) in those with pain was returned to normal levels (7.43 +/- 0.08, p = 0.0003) and the symptoms relieved by revascularization. The abnormal pHi (6.84 +/- .04) in the patient who bled was restored to normal levels (7.48 +/- .03, t = 9.69, p less than .0001) and the bleeding stopped by a central splenorenal shunt. Measurements of pHi in gastrointestinal mucosa may be used as an objective test for evaluating patients suspected of having chronic gastrointestinal ischemia.
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PMID:Chronic gastric ischemia. A cause of abdominal pain or bleeding identified from the presence of gastric mucosal acidosis. 280 10

The only non-general sensation that can be evoked from the gastrointestinal (GI) tract is that of pain ranging from mild discomfort to intense pain. However, in certain regions of the gut, such as the rectum and gastro-oesophagus, the feeling of pain can be preceded by non-painful sensations of distension at lower stimulus intensities. GI pain is often dull, aching, ill-defined and badly localized. In some cases, GI pain is projected to areas of the body away from the originating viscus ('referred' pain). These properties indicate that the representation of internal organs within the central nervous system is very imprecise. Behavioural, neurophysiological and clinical evidence shows that most forms of GI pain are mediated by activity in visceral afferent fibres running in sympathetic nerves and that the afferent innervation of the gut mediated by parasympathetic nerves is not primarily concerned with the signalling and transmission of GI pain. As for the encoding mechanism of the peripheral sensory receptor in the gut, there is evidence for the existence of specific visceral nociceptors in some locations (e.g. the biliary system) and for the existence of non-specific 'intensity' type receptors in other locations (e.g. the colon). In any case, the actual number of nociceptive afferent fibres in the gut is very small and this explains why large areas of the GI tract appear to be insensitive or require considerable stimulation before giving rise to painful sensations. The few nociceptive afferents contained in sympathetic nerves can excite many second order neurones in the spinal cord which in turn generate extensive divergence within the spinal cord and brain stem, sometimes involving long supraspinal loops. Such a divergent input can activate many different systems, motor and autonomic as well as sensory, and thus trigger the general reactions that are characteristic of visceral nociception: a diffuse and ill-localized pain sometimes referred to somatic areas, and autonomic and somatic reflexes that result in prolonged motor activity.
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PMID:Neurophysiology of gastrointestinal pain. 283 8


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