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)

Radioisotopes allow accurate quantitation of the pattern and effectiveness of the transit of chyme through the small and large intestines. Abnormalities of small bowel transit can be demonstrated in patients with the irritable bowel syndrome, and patients with chronic idiopathic intestinal pseudo-obstruction due to either a visceral myopathy or neuropathy. In the colon, radioisotopic studies of transit have demonstrated the site of delayed transit in some severely constipated patients. In patients with these disorders of transit, functional studies may influence the choice of medical or surgical therapy although there are few prospective studies which have established their worth in this context. Radioisotope studies can also be utilised to study the effectiveness of delivery of drugs to the small and large bowel, and to study the adequacy of rectal evacuation in patients with a defaecatory disturbance. The low radiation dose and possibility of frequent observations make radioisotope studies valuable for clinical and research studies in functional gastrointestinal disorders.
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PMID:The small intestine and colon: scintigraphic quantitation of motility in health and disease. 849 Dec 32

First, it is important to find out whether the patient is complaining of infrequent defaecation, excessive straining at defaecation, abdominal pain or bloating, a general sense of malaise attributed to constipation, soiling, or a combination of more than one symptom. Second, one must decide if there is a definable abnormality as a cause of the symptom(s). Is the colon apparently normal or is its lumen widened (megacolon)? Is the upper gut normal or is there evidence of neuropathy or myopathy? Is the ano-rectum normal or is there evidence of a weak pelvic floor, mucosal prolapse, major rectocele, an internal intussusception or solitary rectal ulcer? Is there any systemic component such as hypothyroidism, hypercalcaemia, neurological or psychiatric disorder or relevant drug therapy? Choice of treatment will depend on this clinical evaluation. The range of treatments available is: Reassurance and stop current treatment: Patients with a bowel obsession may take laxatives or rectal preparations regularly without need. Increase dietary fibre: Most cases of 'simple' constipation respond to increased dietary fibre, possibly with an added supplement of natural bran. Toilet training and altered routine of life: Young people particularly may need to recognise the call to stool and alter their daily routine to permit and encourage regular defaecation. Medicinal bulking agent: Ispaghula, methyl cellulose, concentrated wheat germ or bran, and similar preparations are useful when patients with a normal colon find it difficult to take adequate dietary fibre. These preparations increase the bulk of stool and soften its consistency. They may be useful for those patients with the constipated form of irritable bowel syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical management of constipation. 823 32

A study was undertaken to assess the evaluation and treatment of chronic intractable rectal pain. Sixty consecutive patients, 23 males and 37 females with a mean age of 69 (range, 29-87) years and a mean length of symptoms of 4.5 years, were evaluated by questionnaire, office examination, anal manometry, electromyography, cinedefecography, and pudendal nerve study. In all cases, organic abdominopelvic and anorectal etiologies for the pain were excluded by extensive radiologic and endoscopic evaluation. All patients had failed conservative and medical therapy. Ninety-five percent of patients had one or more associated factors: constipation or dyschezia (57 percent), prior pelvic surgery (43 percent), prior anal surgery (32 percent), prior spinal surgery (8 percent), irritable bowel syndrome (10 percent), or psychiatric disorders (depression or anxiety; 25 percent). Possible etiologies for the pain included levator spasm or anismus in 62 percent, coccygodynia in 8 percent, and pudendal neuropathy in 24 percent of patients. Therapy for pain control included electrogalvanic stimulation (EGS) in 29, biofeedback (BF) in 14, and steroid caudal block (SCB) in 11 patients. Pain control was assessed by an independent observer at a mean of 15 (range, 2-36) months after completion of therapy. Continued successful pain relief was classified by patients as good or excellent after EGS in 38 percent, after BF in 43 percent, and after SCB in 18 percent; overall success was reported by 47 percent of patients. The presence of levator spasm, coccygodynia, or pudendal neuropathy did not influence outcome. The routine use of physiologic investigation of rectal pain may not be justifiable. Moreover, more than half of the patients were refractory to all three therapeutic options used in this study.
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PMID:Evaluation and treatment of chronic intractable rectal pain--a frustrating endeavor. 1185 48

* The enteric nervous system has sensory neurons, interneurons and motor neurons and functions as a brain-in-the-gut. * Smooth muscles of the digestive tract are autogenic in the absence of neural control. * Enteric inhibitory motor neurons control excitability of the autogenic musculature. * The neuropathic form of chronic intestinal pseudo-obstruction is a form of disinhibitory motor disease linked with neuropathic degeneration in the enteric nervous system. * Patients with inflammatory degenerative neuropathy may progress from irritable bowel syndrome (IBS)-like symptoms to chronic pseudo-obstruction. * Detection of anti-enteric neuronal antibodies may be a useful diagnostic test for early stages of inflammatory degenerative neuropathy in patients with symptoms of a functional gastrointestinal disorder. Awareness is increasing that autoimmune attack targeted to neuronal elements of the enteric nervous system may underlie irritable bowel-like symptoms that progress to chronic pseudo-obstruction. The inflammatory neuropathy disrupts the integrative functions of the brain-in-the-gut, including reduction in the population of inhibitory motor neurons to the musculature. Extreme loss of inhibitory motor neurons is manifest as disinhibitory motor disease characterized by achalasia in smooth muscle sphincters and hyperactive, disorganized contractile behaviour of intestinal circular muscle which results in pseudo-obstruction. Detection of anti-enteric neuronal antibodies in the serum of patients with early symptoms of a functional gastrointestinal motility disorder may prove to be a useful diagnostic test for inflammatory enteric neuropathy.
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PMID:Neuropathy in the brain-in-the-gut. 1091 73

At the outset of the research programme into irritable bowel syndrome (IBS) it was perceived that there was a need to develop a symptom-based classification for the patients. Four groups of patients were identified, those with spastic colon syndrome, diarrhoea-predominant spastic colon syndrome, functional diarrhoea and midgut dysmotility. While working with outpatients with IBS it was noted how some of them had suffered symptoms for many years; specifically, a group of patients satisfying the criteria for midgut dysmotility had also suffered from particularly severe and intractable intestinal symptoms. These patients underwent 24 h ambulatory studies of small intestinal motility and the majority were found to have manometric features of chronic idiopathic intestinal pseudo-obstruction (CIIP). To characterise the cause, laparoscopic full-thickness small intestine and colonic biopsies have been obtained in forty-five of the latter group of patients. Of these patients 58% have been found to have complete or partial deficiency of alpha-actin epitope staining in the inner circular layer of small intestinal smooth muscle. This deficiency is believed to represent an important biomarker rather than the cause of CIIP, since alpha-actin epitope deficiency has been observed in association with enteric neuropathy and myopathies. In relation to the management of CIIP patients, a multidisciplinary model is proposed incorporating management of co-morbid psychological and psychiatric pathology, abdominal and musculoskeletal pain, fatigue, urological symptoms and nutrition. A six-stage nutritional management plan for these patients is presented.
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PMID:Chronic idiopathic intestinal pseudo-obstruction: the need for a multidisciplinary approach to management. 1537 60

Neuroplastic changes in the enteric nervous system (ENS) may be observed in physiological states, such as development and aging, or occur as a consequence of different pathological conditions, ranging from enteric neuropathies (e.g., Hirschsprung's disease) to intestinal (e.g., inflammatory bowel disease) or extra-intestinal diseases (e.g., Parkinson's disease). Studying ENS plasticity may help to elucidate the pathophysiology of several diseases and have a bearing on the development of new pharmacological interventions. In the present review, we would like to focus on neuronal plasticity evoked by gastrointestinal inflammation occurring in inflammatory bowel disease and in a subset of patients with severe derangement of gut motility due to an enteric neuropathy characterized by an inflammatory infiltrate of the enteric plexuses. Major features of neuroplasticity within the enteric microenvironment encompass structural abnormalities ranging from nerve re-arrangement (e.g., hypertrophy and hyperplasia) to degeneration and loss of enteric ganglion cells; altered synthesis, content and release of neurotransmitters as well as up- or down-regulation of receptor systems; gastrointestinal dysfunction characterized by sensory-motor and secretory impairment of the gut. Interestingly, neuronal changes may also occur in segments of the gastrointestinal tract remote from the site of the original inflammation, e.g. the ileum may show neuroplastic changes during colitis. Sometimes, the inflamed site may even be outside the gut. Among potential mechanisms underlying ENS plasticity, neurotrophins and enteric glia deserve special attention. A better comprehension of ENS plasticity during inflammation could be instrumental to develop new therapeutic options for patients with IBD and inflammatory enteric neuropathies.
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PMID:Enteric neuroplasticity evoked by inflammation. 1662 34

The gastrointestinal tract is a highly innervated organ and enteric neuropathy is emerging as a central feature of a wide range of gut diseases. Although most considerations of the enteric nervous system have focused on neuronal dysfunction, a large population of astrocyte-like glia populates gut muscle layers and the intestinal mucosa, and mounting new evidence points toward enteric glia as active participants in gut pathology. Similarly, in the central nervous system increasing evidence suggests that dysfunctions of astrocytes play central roles in disease mechanisms. On the basis of the premise that gut-brain disease paradigms may exist, we explore the possibility that enteric glia constitute a previously unrecognized disease target in pathologies associated with intestinal barrier dysfunction, notably inflammatory bowel disease, necrotizing enterocolitis, irritable bowel syndrome, diabetes, autoimmune disease and neurotrophic virus infection of the gut.
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PMID:Starring roles for astroglia in barrier pathologies of gut and brain. 1760 1

Many patients with diabetes mellitus suffer from upper and lower GI symptoms. The reported prevalence of these symptoms varies among different ethnic groups/populations. The natural history of GI symptoms as well as their pathogenesis in patients with diabetes remains poorly understood, although it is known that gastric emptying is influenced by hyperglycemia, euglycemia, and hypoglycemia. Poor glycemic control over a long period of time can lead to neuropathy and damage the vagus nerve, resulting in diabetic gastroparesis whose signs and symptoms vary in the individual patient. Gastroparesis can further worsen glycemic control by adversely altering the pharmacokinetics of orally administered hypoglycemic agents as well as by altering the delivery of diet-derived calories to intestines from which absorption, subsequently, determines incipient blood glucose, and thus effectiveness of various injectable antidiabetics including various insulins and related insulin analogs. As GI symptoms may overlap with other disorders, including functional dyspepsia, irritable bowel syndrome, and depression, it is important to have such patients/patients with diabetes undergo standardized testing for measuring gastric emptying. Certain medications including metformin, amylin analogues (i.e. pramlintide), glucagon-like peptide 1 analogs (i.e. exenatide, liraglutide), anticholinergic agents, antidepressants, calcium-channel blockers, and others may contribute to GI symptoms observed in patients with diabetes. Given the global diabetes pandemic, it is of utmost importance to not only diagnose and treat present patients with diabetes mellitus and its comorbidities, but also to help prevent the development of further disease burden by educating children and adolescents about healthy lifestyle modifications (avoidance of overeating, portion control, healthy food choices, increased physical and reduced sedentary activity), as changing behavior in adulthood has proven to be notoriously difficult.
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PMID:Are gastrointestinal symptoms related to diabetes mellitus and glycemic control? 1879 3

We report two patients manifesting with involvement of central and peripheral nervous system with brain magnetic resonance imaging (MRI) changes and pathological features of neuropathy possibly due to harmful and chronic use of various nitroimidazole group of medications for recurrent diarrheal illness. Patient 1, a 21-year-old man with obsessive-compulsive disorder, impulsive behavior and harmful use of substance (tinidazole), had developed encephalopathy and biopsy-proven neuropathy with partial remission. The MRI of brain showed involvement of bilateral caudate, lentiform and dentate nuclei, and splenium, with contrast enhancement of the caudate and putaminal lesions and restricted diffusion of the splenial lesion. Patient 2 was a 50-year-old woman with irritable bowel syndrome and was on harmful use of tinidazole and metronidazole. She manifested with encephalopathy, ataxia, and neuropathy. Her MRI of brain revealed involvement of bilateral putamen, dentate nuclei and periventricular white matter with restricted diffusion. Sural nerve biopsy revealed evidence of vasculitic neuropathy. At follow-up, there was definite, though incomplete, recovery in both the patients. The MRI alterations improved completely in patient 2 and substantially in patient 1. Increasing awareness among the physicians may enable early recognition of potentially reversible neurotoxicity and avoid unwarranted prescription of such medications.
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PMID:Clinical, neuroimaging and pathological features of 5-nitroimidazole-induced encephalo-neuropathy in two patients: Insights into possible pathogenesis. 2201 62

This narrative review covers the mechanisms of actions of trendy drugs approved for or proposed for calming the irritable bowel. Many drugs that target functional gastrointestinal disorders (FGIDS), which includes IBS, have their actions in the enteric nervous system (i.e., the brain-in-the-gut). The in-depth insight into fundamental neurophysiology, which is essential for understanding how the drugs act to achieve their effects, is covered from a neurogastroenterological view point. Pharmacotherapeutic research in FGIDS, which is now lagging, is focused mainly on symptom control. Major progress will require a change to orientation on the malfunction underlying each of the symptoms that constitute Manning, Rome I and Rome II symptom-based criteria for FIGD diagnoses. A high incidence of autoimmune degenerative neuropathy in the enteric nervous system occurs in IBS and is postulated to be the cause of symptoms emerging from failure of normal neural control of motility, blood flow and secretory glands, in concert with sensitization of spinal and vagal sensory mechanisms.
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PMID:Taming the irritable bowel. 2295 Apr 98


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