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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Non-specific abdominal complaints are a very frequent cause of discomfort. Even if only comparatively few are brought to the attention of the physician, they account for a considerable portion of the reasons for seeking medical care, both in acute and chronic conditions. On the other hand, few drugs are free of the suspicion of causing abdominal complaints, which make up between one-tenth and one-third of reported adverse reactions. A wide variety of possible alternative or concomitant causes makes a clear causative attribution to suspected drugs very difficult. This holds especially true for the ill-defined conditions of indigestion and anorexia. For nausea and vomiting, specific scales have been developed which facilitate differentiation between drugs causing these effects most frequently and most intensively. They have been applied in cytostatic therapy, where this is one of the most frequently encountered problems, but nausea and vomiting can seriously affect compliance in many other treatments. Somatic abdominal pain results in most instances from the irritation of the parietal peritoneum and is usually the effect of a lesion. This may or may not be caused by a drug, but this cause should be the first consideration. Visceral pain may result from functional disturbance of secretory glands or of the muscular coat, from drug action on bowel content or from irritation of the mucosa, all of which are frequently interrelated. Most frequently suspected pharmacological causes are drugs with anticholinergic action, antibiotics, potassium supplements and non-steroidal, anti-inflammatory agents. Drug-induced hyperinsulinism and porphyria are rare cases. Abuse of laxatives should always be considered because of its prevalence. A great number of other untoward drug effects have been described in the literature, but rarely merit first consideration. With the exception of promptly occurring or persistent emesis, gastrointestinal symptoms usually are not pathognomonic for drug effects and are the result of several factors. The usual approach to identifying an adverse drug effect is to delineate the functional or structural disorder, and to associate this diagnosis with possible pharmacodynamic aetiologies.
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PMID:Abdominal pain, indigestion, anorexia, nausea and vomiting. 304 63

Physiology of pain is a manifold and very complex phenomenon that is far from being understood. It cannot be explained without reference to psychosocial conditions. Pain has the function of a warning system, but the system is far from perfect, because a number of chronic diseases (e.g., arterial hypertension or malignant neoplasms) begin slowly and nearly painless. The role of pain in internal medicine will be exemplified by thoracic and abdominal pain. With regard to diagnoses both types of pain represent ambiguous symptoms. Their anatomic and physiologic substrates often cannot be ascertained completely by anamnestic means (according to localization, quality, trigger factors, time structure, and concomitant symptoms of pain). Visceral pain is regularly characterized by the phenomenon of the so-called "transferred pain": that means that the perception of pain is not restricted to the place of its origin but is also found in distant regions of the body, primarily in well defined dermatomes ("Head's areas"). This makes the differential diagnosis of internal diseases very difficult because of the parallel connection of nociceptive afferences from the skin and deeper-seated strata on identical spinal segments. Statements according to the pharmacotherapeutic aspects of pain primarily focus on the causal therapy of the prethoracic pain. In this regard differential-therapeutic aspects of angina pectoris, pericarditis, pleurisy, gastro-esophageal reflux, and vertebragenic, myogenic, and neurogenic disturbances are well to the fore.
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PMID:[Pain--from the physiological and internal medicine viewpoint]. 852 23

Peritoneal irritation in rats induced by i.p. administration of acetic acid produces abdominal contractions reflecting visceral pain, and gastrointestinal ileus characterized by inhibition of gastric emptying and small intestine transit. In this study, gastric emptying (GE) and intestinal transit, calculated by the geometric center (GC) method, were estimated using a test meal labeled with 51Cr-EDTA. Visceral pain was assessed by counting abdominal contractions. Acetic acid produced abdominal contractions (80.8 +/- 3.3) and inhibition of GE (-54%) and GC (-63%) during the test-period. The kappa-opioid receptor agonists, CI-977 (+/-)-U-50,488H, (+/-)-bremazocine, PD-117,302, (-)-cyclazocine, and U-69,583, reversed abdominal contractions and inhibitions of gastrointestinal transit in a dose-related manner. The mu-opioid receptor agonists and potent analgesics, morphine and fentanyl did not restore normal gastric emptying and intestinal transit. These data suggest that selective kappa-opioid receptor agonists might be used to treat abdominal pain associated with motility and transit impairment during postoperative ileus.
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PMID:Reversal by kappa-agonists of peritoneal irritation-induced ileus and visceral pain in rats. 904 65

This study investigates the contribution of prostaglandins (PG) and calcitonin gene-related peptide (CGRP) pathways in visceral pain induced by peritoneal irritation in rats. Peritoneal irritation was produced by i.p. administration of acetic acid (AA: 0.06-1.0%, 10 ml/kg). Visceral pain was scored by counting abdominal contractions. The effect of CGRP (3-100 microg/kg, i.p.) was also evaluated. Like AA, CGRP induced abdominal pain. Neonatal pretreatment with capsaicin reduced abdominal contractions produced by AA (0.6%) and CGRP (20 microg/kg) with 64.6% and 45.6%, respectively. Abdominal contractions induced by AA and CGRP were blocked by two antinociceptive drugs, mu-and kappa-opioid agonists, morphine and (+/-)-U-50,488H, respectively. Indomethacin (3 mg/kg, s.c.) reduced the number of abdominal contractions produced by AA by 78.1%+/-6.4% but did not inhibit abdominal contractions produced by CGRP. The CGRP, receptor antagonist, hCGRP(8-37) (300 microg/kg, i.v.) inhibited AA- and CGRP-induced abdominal contractions with 57.5%+/-12.4% and 51.6%+/-11.3%, respectively. Concomitant i.p. administration of PGE1 and PGE2 (0.3 mg/kg of each) produced abdominal contractions which were inhibited 45.6%+/-9.3% by hCGRP(8-37) (300 microg/kg i.v.). Taken together, these results suggest that peritoneal irritation is likely to trigger the release of prostaglandins, which in turn produces a release of CGRP from primary sensory afferents.
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PMID:Involvement of prostaglandins and CGRP-dependent sensory afferents in peritoneal irritation-induced visceral pain. 925 May 75

Irritable bowel syndrome (IBS) is characterized by abdominal pain associated with disordered defecation, which may include urgency and altered stool frequency. Visceral pain syndromes, including IBS, may be effectively treated by a variety of therapies that modulate the interactions between the central and enteric nervous systems. Clinical observations and preliminary data suggest that antidepressants may be efficacious for the treatment of these syndromes. The tricyclic antidepressants (TCAs) have been utilized most extensively in this area, but there is a need for more rigorous efficacy data. Serotonin, an important neurotransmitter in both the central and enteric nervous systems, modifies both motility and sensation in the gut. Recognition of the importance of serotonin in digestive motility and sensation has sparked interest in the use of agents that modify serotonergic transmission in visceral pain syndromes. Pharmacological therapeutics that modulate the biological amines (serotonin, norepinephrine, dopamine and catecholamines) both peripherally and within the central nervous system may offer more effective therapies for these disorders. The selective serotonin reuptake inhibitors are commonly used in clinical practice, but more rigorous, controlled studies are needed to determine their effects beyond the treatment of psychiatric comorbidity. The newer generation antidepressants may provide additional insight into the pathophysiology of the brain-gut interactions and their relationship to functional bowel disorders, providing new therapeutic interventions.
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PMID:Antidepressants in the treatment of irritable bowel syndrome and visceral pain syndromes. 1529 70

Models of stress-induced hyperalgesia state that exposure to stress can exaggerate subsequent pain experiences. Studies using both animal and human subjects have shown evidence for hyperalgesia as a function of stress [e.g., Jorum E. Analgesia or hyperalgesia following stress correlates with emotional behavior in rats. Pain 1988;32:341-48; Peckerman A, Hurwitz BE, Saab PG, Llabre MM, McCabe PM, Schneiderman N. Stimulus dimensions of the cold pressor test and the associated patterns of cardiovascular response. Psychophysiology 1994;31:282-90; Gameiro et al. Nociception and anxiety-like behavior in rats submitted to different periods of restraint stress. Physiol. Behav. 2006;87:643-49; Lucas et al. Visceral pain and public speaking stress: neuroendocrine and immune cell responses in healthy subjects. Brain Behav. Immun. 2006;20:49-56]. However, the role of stress in pediatric pain is not well understood. This study examined stress reactivity and pain tolerance and sensitivity in a population of children with Recurrent abdominal pain (RAP). Forty-nine children meeting criteria for RAP (28 female; mean age 13years; range 9-17years) were randomly assigned to either a condition in which they completed an experimental stressor paradigm (stress interview, serial subtraction task) followed by a pain task (cold pressor) or a condition in which they received the pain task prior to the stress tasks. Children who underwent the stress tasks before the pain task exhibited lower levels of pain tolerance than those who received the pain task first (p<.01); no differences were found between the two groups in pain threshold or pain intensity ratings. Further, pain tolerance was not related to individual differences in physiological reactivity (heart rate change) to the stressor. The present research demonstrates the first evidence of the occurrence of stress-induced hyperalgesia in a pediatric pain population.
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PMID:Effects of stress on pain threshold and tolerance in children with recurrent abdominal pain. 1771 18

Abdominal pain is a major reason patients seek medical attention yet relatively little is known about neuronal pathways relaying visceral pain. We have previously characterized pathways transmitting information to the brain about visceral pain. Visceral pain arises from second order neurons in lamina X surrounding the spinal cord central canal. Some of the brain regions of interest receiving axonal terminations directly from lamina X were examined in the present study using enhanced functional magnetic resonance imaging (fMRI) before and one week after induction of a rat pancreatitis model with persistent inflammation and behavioral signs of increased nociception. Analysis of imaging data demonstrates an increase in MRI signal for all the regions of interest selected including the rostral ventromedial medulla, dorsal raphe, periaqueductal grey, medial thalamus, and central amygdala as predicted by the anatomical data, as well as increases in the lateral thalamus, cingulate/retrosplenial and parietal cortex. Occipital cortex was not activated above threshold in any condition and served as a negative control. Morphine attenuated the MRI signal, and the morphine effect was antagonized by naloxone in lower brainstem sites. These data confirm activation of these specific regions of interest known as integration sites for nociceptive information important in behavioral, affective, emotional and autonomic responses to ongoing noxious visceral activation.
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PMID:fMRI of supraspinal areas after morphine and one week pancreatic inflammation in rats. 1872 38

Recent advances in brain science have shown that the brain function encoding emotion depends on interoceptive signals such as visceral pain. Visceral pain arose early in our evolutionary history. Bottom-up processing from gut-to-brain and top-down autonomic/neuroendocrine mechanisms in brain-to-gut signaling constitute a circuit. Brain imaging techniques have enabled us to depict the visceral pain pathway as well as the related emotional circuit. Irritable bowel syndrome (IBS) is characterized by chronic recurrent abdominal pain or abdominal discomfort associated with bowel dysfunction. It is also thought to be a disorder of the brain-gut link associated with an exaggerated response to stress. Corticotropin-releasing hormone (CRH), a major mediator of the stress response in the brain-gut axis, is an obvious candidate in the pathophysiology of IBS. Indeed, administration of CRH has been shown to aggravate the visceral sensorimotor response in IBS patients, and the administration of peptidergic CRH antagonists seems to alleviate IBS pathophysiology. Serotonin (5-HT) is another likely candidate associated with brain-gut function in IBS, as 5-HT3 antagonists, 5-HT4 agonists, and antidepressants were demonstrated to regulate 5-HT neurotransmission in IBS patients. Autonomic nervous system function, the neuroimmune axis, and the brain-gut-microbiota axis show specific profiles in IBS patients. Further studies on stress and visceral pain neuropathways in IBS patients are warranted.
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PMID:Stress and visceral pain: focusing on irritable bowel syndrome. 2402 63

Visceral pain and intestinal dysbiosis are associated with Irritable Bowel Syndrome (IBS), a common functional gastrointestinal disorder without available efficient therapies. In this study, a decrease of Faecalibacterium prausnitzii presence has been observed in an IBS-like rodent model induced by a neonatal maternal separation (NMS) stress. Moreover, it was investigated whether F. prausnitzii may have an impact on colonic sensitivity. The A2-165 reference strain, but not its supernatant, significantly decreased colonic hypersensitivity induced by either NMS in mice or partial restraint stress in rats. This effect was associated with a reinforcement of intestinal epithelial barrier. Thus, F. prausnitzii exhibits anti-nociceptive properties, indicating its potential to treat abdominal pain in IBS patients.
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PMID:Anti-nociceptive effect of Faecalibacterium prausnitzii in non-inflammatory IBS-like models. 2677 47

Fibromyalgia syndrome (FMS) is a central sensitization syndrome; however, peripheral pain sources potentially exacerbate its symptoms of chronic diffuse musculoskeletal pain and hyperalgesia. This prospective study evaluated visceral pain as a possible triggering factor for FMS pain and hyperalgesia in comorbid patients. Women with (1) FMS + irritable bowel syndrome (IBS); (2) FMS + primary dysmenorrhea (Dys); (3) FMS + Dys secondary to endometriosis (Endo); (4) FMS + colon diverticulosis (Div) were compared with FMS-only women, for fibromyalgia pain (number and intensity of episodes and analgesic consumption) over comparable periods and for somatic hyperalgesia (electrical and pressure pain thresholds) in painful (tender points) and control areas (trapezius, deltoid, quadriceps muscles, and overlying subcutis and skin). In comorbid subgroups, FMS symptoms were also reassessed after treatment of the visceral condition or no treatment. All comorbid groups vs FMS-only had significantly higher FMS pain (number/intensity of episodes and analgesic consumption) and hyperalgesia in deep somatic tissues (subcutis and muscle) at all sites (0.05 < P < 0.0001). Visceral pain (number of IBS days, painful menstrual cycles, and abdominal pain episodes from diverticulitis) correlated directly with all parameters of FMS pain and inversely with muscle pain thresholds at all sites (0.03 < P < 0.0001). Fibromyalgia syndrome pain and hyperalgesia in all tissues and all sites significantly decreased in patients after visceral comorbidity treatment (dietary for 6 months [IBS], hormonal for 6 months [dysmenorrhea], laser [endometriosis], and surgery [diverticulosis]) (0.05 < P < 0.0001) vs no change in untreated patients. Visceral pain enhances FMS symptoms, probably augmenting the level of central sensitization typical of the syndrome. Systematic assessment and treatment of visceral pain comorbidities should be a part of FMS management strategy.
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PMID:Visceral pain as a triggering factor for fibromyalgia symptoms in comorbid patients. 2868 25


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