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

Every physician managing patients with inflammatory bowel disease should be alert to the possibility of the development of hepatobiliary disorders, especially in patients with extensive colonic involvement. There is the question concerning type of follow-up study to be instituted in patients with IBD. Elevation of the level of serum alkaline phosphatase appears to be the most useful and consistent biochemical indicator of hepatic dysfunction (101). This should be estimated at six monthly intervals. A persistent elevation of the level of serum alkaline phosphatase or more overt clinical manifestations, such as pain in the right upper quadrant, hepatomegaly, obstructive jaundice or weight loss, would all indicate the need for further investigations. This would normally take the form of roentgenologic investigation of the biliary tree and biopsy of the liver. Once a patient with IBD has been diagnosed as having one or more hepatobiliary disorders, what is the appropriate management? Each instance should be treated individually according to the nature of the disorder. In general, most of these conditions are histologic abnormalities and are of little clinical importance. There is the question of whether or not there is a role for prophylactic colectomy. There has been conflicting evidence to both support and refute the rationale that colectomy will prevent the development of, or arrest, existing disease of the liver. In the view of the authors, based upon a large experience with the management of these patients, the indication for colectomy should be based upon the severity and extent of colonic disease and almost never upon the existence of associated hepatobiliary disorders.
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PMID:Hepatobiliary disorders in inflammatory bowel disease. 388 36

The chronic, unpredictability of inflammatory bowel disease makes it difficult for patients to cope. In fact several studies quoted by Cox (1995) found that the Majority of IBD patients, even the one's who considered themselves "well," experienced some impairment in quality of life. Early detection of IBD is essential in developing patient confidence and providing motivation for cooperation in treatment. Irvine (1997) conducted a study dealing with the quality of life issues with IBD and concluded that despite impairments, most patients with IBD overcame the obstacles imposed by their illness and managed to remain productive members of society. Similar management (with anti-inflammatory drugs) makes differentiating between Crohn's disease and ulcerative colitis during the early stages of the disease, unnecessary. Situations that require differentiation include: right sided pain or tenderness, steatorrhea, nutritional deficiencies, or a palpable mass (Macrae & Bhathal, 1997). Although IBD continues to be of unknown etiology, recent advances and further study in the areas of the immune system, genetics and environmental influences may provide helpful treatment options in the future. For now, the clinician/patient goal must be to maintain adequate nutrition, promote healing, treat complications, and maintain an optimal lifestyle.
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PMID:Diagnosis and management of inflammatory bowel disease. 1050 19

Similar to in the upper gastrointestinal tract, prostaglandins represent one of the most important components of mucosal defense in the small intestine and colon. The effects of prostaglandins in this context are widespread, ranging from maintenance of blood flow to stimulation of mucus secretion to modulation of the mucosal immune system. There is little doubt that the ability of NSAIDs to cause injury throughout the gastrointestinal tract and to exacerbate IBD is due in large part to the ability of these agents to suppress prostaglandin synthesis. With the advent of selective COX-2 inhibitors, it has become possible to dissect further the roles of prostaglandins in mucosal defense. The weight of evidence collected so far suggests that prostaglandins derived from COX-2 are important in promoting the healing of mucosal injury, in protecting against bacterial invasion, and in down-regulating the mucosal immune system. Suppression of COX-2 in a setting of gastrointestinal inflammation and ulceration has been shown in experimental models to result in impairment of healing and exacerbation of inflammation-mediated injury. In the near future, pharmacologic probes will be available that will permit clinicians to identify better the specific prostaglandin receptors that mediate the effects of this group of mediators on the various aspects of mucosal defense. This identification should permit the development of therapeutic agents that specifically can modulate some aspects of mucosal defense without having undesired effects on other aspects of mucosal function. Such agents may permit clinicians to enhance mucosal repair selectively and to block selectively any contribution of prostaglandins to the pain associated with IBD.
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PMID:Prostaglandin biology in inflammatory bowel disease. 1176 38

Irritable Bowel Syndrome (IBS) may be diagnosed on the presence of symptoms, according to Rome II criteria, [corrected] and some studies have shown that abnormal colonic fermentation may be an important factor in the development of symptoms in some patients with IBS. Since the fermentation [corrected] of substrates by the intestinal flora may play a key role in the use of probiotics in the treatment of IBS, seventy [corrected] patients (31 [corrected] males, 39 [corrected] females), mean age 40 years (range = 26-64 years) with IBS, according to Rome II criteria, were enrolled into the study after informed consensus. Patients were randomly assigned to receive for 4 weeks [corrected] either the active preparation containing Lactobacillus plantarum LP 01 [corrected] and Bifidobacterium breve BR 03 [corrected] or Lactobacillus plantarum LP 01 and Lactobacillus acidophilus LA 02, all strains at concentrations of 5 x 10(9) CFU/g) [corrected] or placebo powder containing starch identical to the study product [corrected] To evaluate treatment efficacy two different scores were considered [corrected] Pain score in different abdominal locations after treatment decreased in probiotics groups A and B 42% and 49% versus 25% [corrected] (P < 0.05) in [corrected] placebo group after 14 days and 45% and 49% versus 29.5% [corrected] (P < 0.001) after 28 days. The severity score of characteristic IBD symptoms significantly decreased in probiotic groups A and B [corrected] versus placebo group after 14 days, 49.3% and 55.6% [corrected] versus 8% [corrected] (P < 0.001), and these data were confirmed after 28 days (56% and 55.6% versus 14.4% [corrected] P < 0.001). In conclusion, short-term therapy with Lactobacillus plantarum LP 01 and Bifidobacterium breve BR 03 or Lactobacillus plantarum LP 01 and Lactobacillus acidophilus LA 02 [corrected] may be considered a promising approach for IBS therapy [corrected]
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PMID:Probiotics in the treatment of irritable bowel syndrome. 1522 Jun 71

Sleep is vital to health and quality of life while sleep abnormalities are associated with adverse health consequences. Nevertheless, sleep problems are not generally considered by clinicians in the management of chronic inflammatory conditions (CIC) such as asthma, RA, SLE and IBD. To determine whether this practice is justified, we reviewed the literature on sleep and chronic inflammatory diseases, including effects of sleep on immune system and inflammation. We found that a change in the sleep-wake cycle is often one of the first responses to acute inflammation and infection and that the reciprocal effect of sleep on the immune system in acute states is often protective and restorative. For example, slow wave sleep can attenuate proinflammatory immune responses while sleep deprivation can aggravate those responses. The role of sleep in CIC is not well explored. We found a substantial body of published evidence that sleep disturbances can worsen the course of CIC, aggravate disease symptoms such as pain and fatigue, and increase disease activity and lower quality of life. The mechanism underlying these effects probably involves dysregulation of the immune system. All this suggests that managing sleep disturbances should be considered as an important factor in the overall management of CIC.
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PMID:The relevance of sleep abnormalities to chronic inflammatory conditions. 1743 41

Gastroenterologists often encounter situations when the clinical and pathophysiological features that typically distinguish functional from organic disorders overlap. This "blurring of boundaries" can occur with post-infectious irritable bowel syndrome (PI-IBS), a subset of IBS and a newly described entity IBD-IBS. The key associating features include pain and usually diarrheal symptoms that are disproportionate to the observed pathology, microscopic inflammation, and often a co-association with psychological distress. A previous initiating gastrointestinal infection is required for PI-IBS and assumed for IBD-IBS. Using this perspective we discuss the clinical and pathophysiological features of PI-IBS and IBD-IBS and the growing evidence for the overlapping features of these two disorders in terms of alteration of gut flora, immune dysregulation, and role of stress. A unifying model of PI-IBS and IBD-IBS is proposed that may have important clinical and research implications. It obligates us to reframe our understanding of illness and disease from the dualistic biomedical model into a more integrated biopsychosocial (BPS) perspective.
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PMID:The functional-organic dichotomy: postinfectious irritable bowel syndrome and inflammatory bowel disease-irritable bowel syndrome. 1884 9

Abdominal pain is a common symptom of inflammatory bowel disease (IBD: Crohn's disease, ulcerative colitis). Pain may arise from different mechanisms, which can include partial blockage and gut distention as well as severe intestinal inflammation. A majority of patients suffering from acute flares of IBD will experience pain, which will typically improve as disease activity decreases. However, a significant percentage of IBD patients continue experiencing symptoms of pain despite resolving inflammation and achieving what appears to be clinical remission. Current evidence suggests that sensory pathways sensitize during inflammation, leading to persistent changes in afferent neurons and central nervous system pain processing. Such persistent pain is not only a simple result of sensory input. Pain processing and even the activation of sensory pathways is modulated by arousal, emotion, and cognitive factors. Considering the high prevalence of iatrogenic as well as essential neuropsychiatric comorbidities including anxiety and depression in IBD patients, these central modulating factors may significantly contribute to the clinical manifestation of chronic pain. The improved understanding of peripheral and central pain mechanisms is leading to new treatment strategies that view pain as a biopsychosocial problem. Thus, improving the underlying inflammation, decreasing the excitability of sensitized afferent pathways, and altering emotional and/or cognitive functions may be required to more effectively address the difficult and disabling disease manifestations.
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PMID:Pain and inflammatory bowel disease. 1910 73

Elevated colonic luminal serine-protease (Ser-P) activity of diarrhea-predominant IBS (IBS-D) patients evokes a proteinase-activated receptor (PAR)-2-mediated colonic hypersensitivity in mice. Despite similarly elevated Ser-P levels in feces, patients with IBD exhibit visceral hypo- or normosensitivity to rectal distension, as opposed to IBS-D. To explain these discrepancies we studied the effect of colonic infusion of fecal supernatants from ulcerative colitis (UC) patients to colorectal mechanical sensitivity of mice and explored the involvement of PAR-4 and its activator Cathepsin-G (Cat-G). Fecal protease activities were assayed in healthy subjects, IBS-D and UC patients in presence or not of antiproteases or Cat-G inhibitor. Following intracolonic infusion of fecal supernatants from healthy subjects, IBS-D and UC patients or PAR-4 activating peptide (PAR-4-AP) or Cat-G, EMG response to colorectal balloon distension was recorded in mice. This nociceptive response was also determined after treatment with pepducin (PAR-4 antagonist) on UC supernatant or after a preincubation with antiproteases or Cat-G inhibitor. In contrast to IBS-D supernatant, UC supernatant promoted colonic hyposensitivity to distension, an effect mimicked by PAR-4-AP or Cat-G. UC supernatant-induced hypoalgesia was inhibited by a cocktail of antiproteases. However, blockade of PAR-4 or Cat-G inhibition resulted in colonic hypersensitivity similar to that observed after IBS-D supernatant infusion. Despite similarly elevated Ser-P activities, IBS-D and UC fecal supernatant display visceral pro- and antinociceptive effects in mice, respectively. Visceral hyposensitivity induced by fecal supernatant from UC patients results from PAR-4 activation by cathepsin-G, counterbalancing the pronociceptive effect of simultaneous PAR-2 activation.
Pain 2009 Jul
PMID:Fecal proteases from diarrheic-IBS and ulcerative colitis patients exert opposite effect on visceral sensitivity in mice. 1945 Sep 26

The antinociceptive mechanism underlying protease-activated receptor-4 (PAR(4)) activation was studied in Fast Blue-labelled dorsal root ganglia (DRG) neurons from mouse colon which expressed transcript for PAR(4). Whole cell perforated patch clamp recordings were obtained from these neurons and the effects on neuronal excitability of PAR(4) activating peptides (AP) and reverse peptides (RP) were examined. A 3-min application of PAR(4)-AP (100 micromol L(-1)) markedly suppressed the number of action potential discharged at twice rheobase for up to 60 min. PAR(4)-RP had no effect. PAR(4) application suppresses the excitatory effects of PAR(2). These findings demonstrated that activation of PAR(4) on colonic DRG neurons suppresses their excitability, suggesting these receptors could provide important targets for modifying pain in colonic GI disorders such as IBS and IBD.
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PMID:Activation of protease-activated receptor-4 inhibits the intrinsic excitability of colonic dorsal root ganglia neurons. 1956 87

Cases of immigrant families affected by IBD have rarely been reported and seem to be of exceptional interest towards a better understanding of disease aetiopathogenesis. The first case of Crohn's disease in a family of immigrants from Albania to Greece with three offspring is described herein. A family with three children, one 22 year-old male and two 18-year-old twin females immigrated from southern Albania to northwest Greece ten years ago. The whole family lived in the same house and had no previous history of bowel or other chronic diseases. Two years ago the boy complained of diarrhoea, perianal pain and loss of weight. Subsequent investigation revealed ileal and perianal Crohn's disease. One year after Crohn's disease was diagnosed in the boy, one of the twins was diagnosed with ileal Crohn's disease. Six months afterwards, the second twin underwent emergency appendectomy due to acute appendicitis; four months later she was diagnosed with ileal Crohn's disease. Genetically predisposed individuals seem to be vulnerable to a continuous pressure of a still unknown environmental factor(s). In addition, lifestyle modification seems to represent a predisposing factor toward inflammatory bowel disease in immigrants.
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PMID:A family report of Crohn's disease in three children immigrating from Albania to Greece and review of the literature. 2112 63


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