Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022104 (irritable bowel syndrome)
 8,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fibromyalgia is a chronic functional illness that presents with widespread musculoskeletal pain as well as a constellation of symptoms including fatigue, cognitive dysfunction, sleep difficulties, stiffness, anxiety, and depressed mood. The diagnosis of fibromyalgia, similar to other functional disorders, requires that organic diseases are not causing the symptoms. Systemic and rheumatic diseases can be ruled out by a patient history, physical examination, and laboratory investigations. Because there are no specific laboratory tests for fibromyalgia, the 1990 American College of Rheumatology (ACR) classification criteria have been used in clinical settings; however, they are not ideal for individual patient diagnosis. Clinicians should be aware of limitations inherent in using tender points in the diagnosis of fibromyalgia. The multiple symptoms of fibromyalgia often overlap with those of related disorders and may further complicate the diagnosis. One of the most challenging diagnostic dilemmas that clinicians face is distinguishing fibromyalgia from other central pain disorders (e.g., irritable bowel syndrome, chronic fatigue syndrome, migraine). Screening questions based on published criteria can be used as a first approach in diagnosing functional illnesses. Numerous studies report a higher prevalence of psychiatric disorders in patients with fibromyalgia. Therefore, a careful history and evaluation should be taken for the presence of primary mood disturbances. To date, there is no "gold standard" for diagnosing fibromyalgia. Until a better clinical case definition of fibromyalgia exists, all diagnostic criteria should be interpreted with caution, considered rudimentary, and subject to modification.
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PMID:Diagnosis and differential diagnosis of fibromyalgia. 1996 92

The presentation of fibromyalgia is heterogeneous, and the treatment approach should be individualized for each patient, depending on the severity of the patient's pain, the presence of other symptoms or comorbidities, and the degree of functional impairment. The management of fibromyalgia includes the identification and treatment of all pain sources that may be present in addition to fibromyalgia, such as peripheral pain generators (e.g., comorbid osteoarthritis or neuropathic pain) or visceral pain (e.g., comorbid irritable bowel syndrome). It is also important to address other symptoms or disorders that commonly occur in patients with fibromyalgia, such as fatigue, sleep disturbances, cognitive impairment, stiffness, and mood or anxiety disorders. Finally, the treatment should strive to improve the patient's function and global health status. In most cases, the management of fibromyalgia involves both pharmacologic and nonpharmacologic treatments. This report provides an in-depth review of randomized, controlled trials for pharmacologic and nonpharmacologic approaches to fibromyalgia therapy.
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PMID:Strategies for managing fibromyalgia. 1996 95

Fibromyalgia and associated conditions such as irritable bowel syndrome and temporomandibular disorder involve dysfunctions in central sensitization and pain modulation. Central nervous system dysfunction may also contribute to other symptoms characteristic of fibromyalgia, such as fatigue and sleep disturbance. Two key neurotransmitters in the pain modulation pathway are serotonin and norepinephrine. Preclinical studies using animal models of chronic pain have shown that pharmacologic agents that combine serotonergic and noradrenergic reuptake inhibition, thus augmenting the function of these neurotransmitters, have stronger analgesic effects than agents that inhibit reuptake of either neurotransmitter alone. Although tricyclic antidepressants (TCAs) inhibit reuptake of both serotonin and norepinephrine and have shown efficacy for the treatment of fibromyalgia, long-term use of these drugs is limited owing to poor tolerability. Unlike TCAs, the newer dual reuptake inhibitors of serotonin and norepinephrine, such as the drugs approved by the US Food and Drug Administration (FDA) for fibromyalgia, milnacipran and duloxetine, do not possess significant affinity for other neurotransmitter systems, resulting in diminished side effects and enhanced tolerability. Both duloxetine and milnacipran have shown efficacy in clinical trials by improving pain and other symptoms associated with fibromyalgia. Both compounds inhibit the serotonin and norepinephrine transporters; however, there is a difference in their affinities and selectivity for these transporters. Although duloxetine has affinity for both receptors, it is somewhat more selective for the serotonin transporter. In contrast, milnacipran is somewhat more selective for norepinephrine than serotonin reuptake inhibition. Pharmacologic agents that specifically target serotonin and norepinephrine reuptake may prove to be valuable tools in the treatment of fibromyalgia.
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PMID:Further strategies for treating fibromyalgia: the role of serotonin and norepinephrine reuptake inhibitors. 1996 96

The aims of this study are to determine the frequency of fibromyalgia syndrome (FMS) in patients with chronic cervical myofascial pain (CMP) and to investigate the FMS characteristics in CMP patients. Ninty-three patients with CMP and 30 age-matched healthy women were included in this study. Main outcome measures included visual analog scale (VAS), Beck Depression Inventory (BDI), and pain pressure thresholds. CMP patients were evaluated for the existence of FMS. The severity of FMS was assessed with total myalgic score (TMS) and control point score (CPS). Most common clinical characteristics of FMS were noted. Of the 93 CMP subjects, 22 (23.6%) patients fulfilled the classification criteria for FMS. Number of tender points were higher (p=0.0), while TMS (p=0.0) and CPS (p=0.0) values were lower in comorbid CMP and FMS patients than regional CMP group. There were statistically significant differences between regional CMP patients and comorbid CMP and FMS patients regarding presence of fatigue (p=0.0) and irritable bowel syndrome (p=0.022). There was no statistically significant difference between patient groups regarding VAS values (p>0.05). BDI values of the regional CMP were significantly lower than comorbid CMP and FMS patients (p=0.011). In conclusion, we found that nearly a quarter of CMP patients were comorbid with FMS, and psychological and comorbid symptoms were more prominent in comorbid patients. We thought that, these two syndromes might be overlapping conditions and as a peripheral pain generator or inducer of central sensitisation, MPS might lead to FMS or precipitate and worsen the FMS symptoms.
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PMID:Comorbidity of fibromyalgia and cervical myofascial pain syndrome. 2006 49

Drugs used for treating inflammatory bowel disease are known to have a number of gastrointestinal and liver adverse effects. 5-ASA products are relatively safe and have few adverse events. In contrast sulfasalazine has side effects in 11-40% of treated patients including fatigue, nausea, abdominal pain and diarrhoea. Glucocorticoids can induce or propagate peptic ulcers and upper GI bleeding especially in combination with NSAIDs. Thioguanins may have severe gastrointestinal side effects including gastrointestinal complaints (in up to 12%), hepatotoxicity (up to 4%) and pancreatitis (1%). Nodular regenerative hyperplasia (NRH) is an important potential side effect of thiopurine therapy especially in men with Crohn's disease after ileocecal resection. NRH may ultimately lead to portal hypertension. A major concern of methotrexate therapy in IBD besides myelosuppression and pulmonary fibrosis is hepatotoxicity. 5mg of folic acid substitution per week potentially decreases gastrointestinal side effects by 80% without interfering with the efficacy of methotrexate. Besides renal dysfunction, tremor, hirsutism, hypertension and gum hyperplasia cyclosporine is known to have a number of gastrointestinal side effects that occur with less frequency such as diarrhoea (up to 8%) nausea and vomiting (up to 10%) and hepatotoxicity in 1-4%. Rare gastrointestinal adverse events are gastritis and peptic ulcers. Paying attention to these potential deleterious side effects is mandatory for physicians treating IBD patients.
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PMID:Gastrointestinal and liver adverse effects of drugs used for treating IBD. 2022 29

Due to the cross-sectional nature of previous studies, whether mechanical factors predict the onset of Chronic oro-facial pain remains unclear. Aims of the current study were to test the hypotheses that self-reported mechanical factors would predict onset of Chronic oro-facial pain and that any observed relationship would be independent of the confounding effects of psychosocial factors and reporting of other unexplained symptoms. About 1735 subjects who had completed a baseline questionnaire were assessed at 2year follow-up for the presence of Chronic oro-facial pain, psychosocial factors (anxiety and depression, illness behaviour, life stressors and reporting of somatic symptoms), mechanical dysfunction (facial trauma, grinding, phantom bite and missing teeth) and reporting of other unexplained symptoms (chronic widespread pain, irritable bowel syndrome and chronic fatigue). About 1329 subjects returned completed questionnaires (adjusted response rate 87%). About 56 (5%) reported new episodes of Chronic oro-facial pain at follow-up. Univariate analyses showed that age, gender, reporting of other unexplained symptoms, psychosocial factors and two self-report mechanical factors predicted the onset of Chronic oro-facial pain. However multivariate analysis showed that mechanical factors did not independently predict onset. The strongest predictors were health anxiety (Relative Risk (RR) 2.8, 95% CI 1.3-6.2), chronic widespread pain (RR 4.0 95% C.I. 2.2-7.4) and age (RR 0.2, 95% CI 0.1-0.7). The findings from this prospective study support the hypothesis that psychosocial factors are markers for onset of Chronic oro-facial pain. The efficacy of early psychological management of Chronic oro-facial pain to address these factors should be a priority for future investigations.
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PMID:Risk factors for onset of chronic oro-facial pain--results of the North Cheshire oro-facial pain prospective population study. 2030 56

Fibromyalgia is a complex condition that is characterized by chronic widespread pain and multiple other symptoms, including fatigue, sleep disturbances, cognitive dysfunction, stiffness, and depressive episodes. Fibromyalgia may coexist and/or overlap with other conditions that may involve central sensitivity, including chronic fatigue syndrome, irritable bowel syndrome, irritable bladder syndrome or interstitial cystitis, and temporomandibular disorder. The pathophysiology of fibromyalgia remains uncertain but is believed to be partly the result of central systems affecting afferent processing as well as impaired endogenous pain-inhibitory systems. Abnormal central nociceptive processing may contribute to fibromyalgia, producing heightened responses to various noxious stimuli with resulting mechanical hyperalgesia. Fibromyalgia remains a clinical diagnosis. There has been a recent paradigm shift away from requiring 11 or more out of 18 tender points and instead focusing on the presence of chronic widespread pain as well as symptoms of fatigue, unrefreshed sleep, and other somatic complaints. Although there is no known cure for fibromyalgia, multidisciplinary team efforts using combined treatment approaches, including patient education, aerobic exercise, cognitive behavioral therapy, and pharmacologic therapies (serotonin norepinephrine reuptake inhibitors [eg, duloxetine, milnacipran] and alpha 2-delta receptor ligands [eg, pregabalin]) may improve symptoms as well as function of patients with fibromyalgia.
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PMID:Fibromyalgia syndrome: a discussion of the syndrome and pharmacotherapy. 2056 96

Fatigue is a symptom whose causes are protean and whose phenotype includes physical, mood, and behavioral components. Chronic fatigue syndrome (CFS) is an illness that has strong biological underpinnings and no definite etiology. Diagnostic criteria established by the Centers for Disease Control and Prevention have helped classify CFS as an overlap of mood, behavioral, and biological components. These include the presence of fatigue for more than 6 months associated with a diminution of functional activity and somatic symptoms, and pain not attributable to a specific diagnosis or disease. Four of the following criteria need to be present: sore throat, impaired memory or cognition, unrefreshing sleep, postexertional fatigue, tender glands, aching stiff muscles, joint pain, and headaches. Many researchers have observed that CFS shares features in common with other somatic syndromes, including irritable bowel syndrome, fibromyalgia, and temporomandibular joint dysfunction. Correlations between inflammation and infection, augmented sensory processing, abnormalities of neurotransmitters, nerve growth factors, low levels of serotonin and norepinephrine, abnormalities of homeostasis of the stress system, and autonomic dysfunction may be hallmarks of CFS. The relative contributions of each of these abnormalities to the profound fatigue associated with CFS need to be explored further to better evaluate and treat the syndrome.
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PMID:Perspectives on fatigue from the study of chronic fatigue syndrome and related conditions. 2065 23

Lactose and food intolerance cause a wide range of gut and systemic symptoms, including gas, gut pain, diarrhoea or constipation, severe headaches, severe fatigue, loss of cognitive functions such as concentration, memory and reasoning, muscle and joint pain, heart palpitations, and a variety of allergies (Matthews and Campbell, 2000; Matthews et al., 2005; Waud et al., 2008). These can be explained by the production of toxic metabolites from gut bacteria, as a result of anaerobic digestion of carbohydrates and other foods, not absorbed in the small intestine. These metabolites include alcohols, diols such as butan 2,3 diol, ketones, acids, and aldehydes such as methylglyoxal (Campbell et al., 2005, 2009). These 'toxins' induce calcium signals in bacteria and affect their growth, thereby acting to modify the balance of microflora in the gut (Campbell et al., 2004, 2007a,b). These bacterial 'toxins' also affect signalling mechanisms in cells around the body, thereby explaining the wide range of symptoms in people with food intolerance. This new mechanism also explains the most common referral to gastroenterologists, irritable bowel syndrome (IBS), and the illness that afflicted Charles Darwin for 50 years (Campbell and Matthews, 2005a,b). We propose it will lead to a new understanding of the molecular mechanism of type 2 diabetes and some cancers.
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PMID:Bacterial metabolic 'toxins': a new mechanism for lactose and food intolerance, and irritable bowel syndrome. 2085 32

Chronic fatigue syndrome (CFS) is a debilitating disease characterized by unexplained disabling fatigue and a combination of accompanying symptoms the pathology of which is incompletely understood. Many CFS patients complain of gut dysfunction. In fact, patients with CFS are more likely to report a previous diagnosis of irritable bowel syndrome (IBS), a common functional disorder of the gut, and experience IBS-related symptoms. Recently, evidence for interactions between the intestinal microbiota, mucosal barrier function, and the immune system have been shown to play a role in the disorder's pathogenesis.Studies examining the microecology of the gastrointestinal (GI) tract have identified specific microorganisms whose presence appears related to disease; in CFS, a role for altered intestinal microbiota in the pathogenesis of the disease has recently been suggested. Mucosal barrier dysfunction promoting bacterial translocation has also been observed. Finally, an altered mucosal immune system has been associated with the disease. In this article, we discuss the interplay between these factors in CFS and how they could play a significant role in GI dysfunction by modulating the activity of the enteric nervous system, the intrinsic innervation of the gut.If an altered intestinal microbiota, mucosal barrier dysfunction, and aberrant intestinal immunity contribute to the pathogenesis of CFS, therapeutic efforts to modify gut microbiota could be a means to modulate the development and/or progression of this disorder. For example, the administration of probiotics could alter the gut microbiota, improve mucosal barrier function, decrease pro-inflammatory cytokines, and have the potential to positively influence mood in patients where both emotional symptoms and inflammatory immune signals are elevated. Probiotics also have the potential to improve gut motility, which is dysfunctional in many CFS patients.
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PMID:Gut inflammation in chronic fatigue syndrome. 2093 23


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