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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Small intestinal bacterial overgrowth (SIBO) is characterized by nutrient malabsorption, associated with an excessive number of bacteria in the proximal small intestine. Unfortunately, the diagnosis of bacterial overgrowth presents several difficulties and limitations, and as yet there is not a widespread agreement on the best diagnostic test. SIBO occurs when there are alterations in intestinal anatomy, gastrointestinal motility, or a lack of gastric acid secretion. The true association between SIBO and irritable bowel syndrome and celiac disease remains uncertain. The treatment usually consists in the eradication of bacterial overgrowth with repeated courses of antimicrobials, nutritional support and when it is possible, the correction of underlying predisposing conditions.
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PMID:[Small intestinal bacterial overgrowth. An update]. 1644 61

Hydrogen breath tests are widely used to explore the pathophysiology of functional gastrointestinal disorders. Small intestinal bacterial overgrowth and carbohydrate malabsorption are disorders detected by these tests that have been proposed to be of great importance for symptoms in, for instance, irritable bowel syndrome. However, conclusions drawn from these studies are highly controversial and divergent results exist. There is also an extensive use of these tests in clinical practice with difficulties regarding interpretation of the tests and sometimes erroneous conclusions. The limitations and pitfalls of these tests will be reviewed in this article, and hopefully the occasional abuse of these tests can be turned into proper clinical and scientific use instead in the future.
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PMID:Use and abuse of hydrogen breath tests. 1647

Because of the wide variations in the clinical presentation of celiac disease and because treatment exists that is effective in most cases, screening of the general population for celiac disease has been considered. There is still no evidence that patients who have symptom-free celiac disease are at increased risk of small intestinal lymphoma or other complications. Prevention of osteoporosis seems to be the strongest indicator for widespread screening today [22]. The major cause of failure to respond to a gluten-free diet is continuing ingestion of gluten, but other underlying diseases must be considered. Many different drugs (eg, anti-tumor necrosis factor [TNF]-alpha) have been used in patients who have RCD [23]. Steroid treatment has been reported to be effective even in patients who have underlying early EATL. Histologic recovery in patients who have celiac disease usually takes several months but can take up to 1 year, even if the patient remains on a strict gluten-free diet. Some patients report celiac-related symptoms for months after a single gluten intake. The definitions for RCD in literature vary. The authors consider the definition give by Daum and colleagues [24] suitable. They defined true RCD as villous atrophy with crypt hyperplasia and increased IELs persisting for more than 12 months in spite of a strict gluten-free diet. If a patient is not responding well to a gluten-free diet, three considerations are necessary: (1) the initial diagnosis of celiac disease must be reassessed;(2) the patient should be sent to a dietician to check for errors in diet or compliance problems, because problems with the gluten-free diet are the most important cause for persisting symptoms; (3) other reasons for persisting symptoms (eg, pancreatic insufficiency, irritable bowel syndrome, bacterial overgrowth, lymphocytic colitis, collagenous colitis, ulcerative jejunitis, protein-losing enteropathy,T-cell lymphoma, fructose intolerance, cavitating lymphadenopathy, and tropical sprue) should be considered. Other causes for villous atrophy are Crohn's disease, collagenous sprue, and autoimmune enteropathy. Abdulkarim and colleagues [25] examined 55 patients who had a diagnosis of nonresponsive celiac disease. He found that 6 did not have celiac disease, and25 still had some gluten ingestion.Tursi and colleagues [26] reported 15 patients who had celiac disease with persisting symptoms. Because histology improved in all patients after several months, RCD was excluded. Of the 15 patients, 10 had small intestinal bacterial overgrowth, 2 showed lactose malabsorption causing the described symptoms, 1 had mistakenly taken an antibiotic containing gluten, and 1 patient each had Giardia lamblia and Ascaris lumbricoides. Thus, other entities must be considered in patients who have celiac disease and ongoing symptoms. In a follow-up clinical trial, 158 patients who had celiac disease underwent follow-up small intestine biopsies within 2 years after starting a gluten-free diet. Eleven patients (7.0%) with persisting (partial) villous atrophy were considered to have RCD; 5 of them developed EATL [27].RCD type I is characterized by normal expression of T-cell antigens and polyclonal TCR gene rearrangement.RCD type II is characterized by an abnormal IEL phenotype with the expression of intracytoplasmic CD3e, surface CD103, and the lack of classic surface T-cell markers such as CD8, CD4, and TCR-alpha/beta. This clonal IEL population can be considered crypt IEL [24]. RCD II has a poor prognosis, which is a problem for therapy. Clonal TCR gene rearrangements and loss of T-cell antigens such as CD8 and TCR-beta in IELs may indicate the development of an EATL in patients who have RCD. The markers for an overt EATL are a positive stool blood test, increased lactate dehydrogenase, or beta2-microglobulin [24]. If an overt lymphoma is suspected, upper and lower endoscopy, an ear, nose, and throat work-up, CT scan, capsule endoscopy, and possibly double-balloon enteroscopy should be performed. Most reports of the difficulties in treating patients who have true RCE are casereports. Turner and colleagues [28] reported on an induction of remission by useof the anti-TNF-alpha antibody infliximab and maintenance with prednisoloneand azathioprine. Olaussen and colleagues [29] and Mandal and colleagues [30]tried a nonimmunogenic elemental diet. Gillet and colleagues [31] reported successful treatment of a patient who hadRCD using anti-TNF-alpha antibodies (infliximab) for induction and azathioprinefor maintenance. Maurino and colleagues [32] studied seven consecutive patients diagnosed ashaving refractory sprue and no response to oral or parenteral steroids. Aftertreatment with azathioprine (2 mg/kg/d) and oral prednisone (1 mg/kg/d), fivepatients had a complete clinical remission. Two patients who did not respond totreatment at any time died. Goerres and colleagues [33] described 18 patients who had RCD, 10 of whomhad type I RCD, and 8 of whom had type II RCD. Treatment consisted ofazathioprine combined with prednisone for 1 year. Consistent with reports byother investigators, the response rates in the two groups differed. Eight of the10 patients who had type I RCD had a histologic response. Seven of the eightpatients who had type II RCD died, and six of the eight developed a lymphoma. At present there is no effective treatment for type II RCD.Fig. 3 presents a proposed algorithm for monitoring patients who have ce-liac disease.
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PMID:Monitoring nonresponsive patients who have celiac disease. 1687 29

Functional diarrhea (FD), one of the functional gastrointestinal disorders, is characterized by chronic or recurrent diarrhea not explained by structural or biochemical abnormalities. The treatment of FD is intimately associated with establishing the correct diagnosis. First, FD needs to be distinguished from diarrhea-predominant irritable bowel syndrome (IBS), in which, unlike in FD, abdominal pain is a primary diagnostic criterion. Next, FD must be differentiated from the myriad organic causes of chronic diarrhea. Unlike IBS, in which a positive diagnosis can be made with an acceptable level of confidence using symptom-based criteria and minimal testing, the diagnosis of FD is still primarily a diagnosis of exclusion. Thus, the onus is on the physician to eliminate potential underlying causes, both common and uncommon, in the proper clinical setting. Once the diagnosis has been established, the clinician and patient should first focus on identifying, eliminating, and/or treating aggravating factors. These may include physiologic factors (eg, small bowel bacterial overgrowth), psychological factors (eg, stress and anxiety), and dietary factors (eg, carbohydrate malabsorption). Thereafter, appropriate treatment for functional diarrhea may be instituted. Treatment options include dietary and lifestyle modification, pharmacologic therapies, and alternative modalities. Although many of these strategies have been studied in IBS, almost none of them has been examined specifically in FD. Furthermore, given the poorly understood pathophysiologic basis of FD, these treatments primarily target a patient's symptoms and presumed altered physiology rather than underlying etiologic mechanisms. Therefore, we stress that treatment must be approached in an individualized manner and that dietary and pharmacologic therapies should be part of a comprehensive therapeutic approach in which education and reassurance form the foundation. In general, we attempt to remove dietary triggers and recommend increased fiber intake. We then add anticholinergic, antispasmodic, antimotility, and antidiarrheal agents as the first line of pharmacotherapy. Should a patient not respond to these, and for patients who have a significant degree of psychological dysfunction, central acting agents, including antidepressants and/or anxiolytics, may be beneficial. During the treatment period, we also recommend that physicians keep an open mind. If signs or symptoms that suggest an ongoing or previously unrecognized organic process develop, then a re-evaluation of the clinical picture is indicated.
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PMID:Treatment of functional diarrhea. 1683 52

The redox homeostasis of patients with inflammatory bowel disease is not balanced because of malnutrition and malabsorption. The seriousness of this illness often hinders the intake and use of bioactive agents. We have just a small amount of knowledge about how patients can get access to these important materials. The authors' aim was to edit a questionnaire, which can estimate, with large precision, the amount of fruit and vegetable consumption among a random-chosen group of IBD patients. We also thought that the measuring of tea, fruit-juice and wine consumption is also important in order to see whether the intake of these can help the intake of natural polyphenol, vitamin and trace elements. For this study 50 IBD patients (25 male, 25 female, 35-67 years) and 50 healthy people (35 male, 15 female, 25-47 years) were asked. During the completion of the questionnaire in 8 cases (5 male, 3 female) the provided data could not be accepted, because of inaccuracy. During this study, it became obvious that the intake of polyphenols was not enough if we focus on the average daily consumption of fruits and vegetables. Red wine cannot be considered efficient for replacing polyphenols, because more than the half of patients doesn't drink it at all, or drink it once or twice a month. From the aspect of drinking tea or eating fruits, the situation is much better. The participants' (92 people) consumption of vegetables and fruits is reduced to a small variety, which is not beneficial. Mostly used plants often caused different disorders, and that is why a controlled recommendation of polyphenol, vitamin, trace element and fiber would be favorable.
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PMID:[Surveys of the consumption of nutritional antioxidants in inflammatory bowel diseases]. 1685 10

Dietary fructose induces abdominal symptoms in patients with fructose malabsorption, but there are no published guidelines on its dietary management. The objective was to retrospectively evaluate a potentially successful diet therapy in patients with irritable bowel syndrome and fructose malabsorption. Tables detailing the content of fructose and fructans in foods were constructed. A dietary strategy comprising avoidance of foods containing substantial free fructose and short-chain fructans, limitation of the total dietary fructose load, encouragement of foods in which glucose was balanced with fructose, and co-ingestion of free glucose to balance excess free fructose was devised. Sixty-two consecutively referred patients with irritable bowel syndrome and fructose malabsorption on breath hydrogen testing underwent dietary instruction. Dietary adherence and effect on abdominal symptoms were evaluated via telephone interview 2 to 40 months (median 14 months) later. Response to the diet was defined as improvement of all symptoms by at least 5 points on a -10- to 10-point scale. Forty-eight patients (77%) adhered to the diet always or frequently. Forty-six (74%) of all patients responded positively in all abdominal symptoms. Positive response overall was significantly better in those adherent than nonadherent (85% vs 36%; P<0.01), as was improvement in individual symptoms (P<0.01 for all symptoms). This comprehensive fructose malabsorption dietary therapy achieves a high level of sustained adherence and good symptomatic response.
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PMID:Fructose malabsorption and symptoms of irritable bowel syndrome: guidelines for effective dietary management. 1700 Jan 96

Patients complaining of 'chronic diarrhoea' usually mean the passage of loose, urgent stools. Chronic diarrhoea is a feature of malabsorption; it may also be seen in the 'dumping syndrome' which follows gastric surgery, small intestinal bacterial overgrowth, bile salt malabsorption and in malabsorption of simple sugars including most commonly lactose, fructose and sorbitol. Excessively rapid entry of chyme into the small or large intestine generates propulsive motor patterns leading to accelerated transit. Inflammation is associated with decreased normal mixing motor patterns but increased propulsive motility including high amplitude propagated contractions (HAPCs). Evidence for abnormal small intestinal motility in the diarrhoea associated with irritable bowel syndrome (IBS) is conflicting and any difference appears small. Increased colonic HAPCs with increased propulsion is seen in IBS with diarrhoea (IBS-D). Stress-induced colonic motility is increased in IBS-D with hyper-responsiveness to corticotrophin releasing factor (CRF). Long-lasting increases in mucosal serotonin availability may contribute to the chronic diarrhoea seen in IBS-D and coeliac disease. Treatments for abnormal motility in chronic diarrhoea include those designed to correct specific underlying abnormalities including octreotide, antibiotics, colestyramine, specific food avoidance and anti-inflammatory agents. There are also treatments aimed primarily at altering motility directly including opiates, 5HT3 receptor antagonists and amitriptyline.
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PMID:Role of motility in chronic diarrhoea. 1710 87

Small intestinal bacterial overgrowth (SIBO) is a clinical condition characterized by a malabsorption syndrome due to an increase in microorganisms within the small intestine. The main mechanisms restricting bacterial colonization in the upper gut are the gastric acid barrier, mucosal and systemic immunity and intestinal clearance. When these mechanisms fail, bacterial overgrowth develops. Diarrhea, steatorrhea, chronic abdominal pain, bloating and flatulence are common symptoms and are similar to those observed in irritable bowel syndrome. Breath tests (glucose and/or lactulose breath tests) have been proposed as a sensitive and simple tool for the diagnosis of bacterial overgrowth, being non-invasive and inexpensive compared to the gold standard represented by the culture of intestinal aspirates. Antibiotic therapy is the cornerstone of SIBO treatment. Current SIBO treatment is based on empirical courses of broad-spectrum antibiotics since few controlled studies concerning the choice and duration of antibiotic therapy are available at present.
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PMID:Small intestinal bacterial overgrowth: diagnosis and treatment. 1782 47

Small bowel bacterial overgrowth historically has been associated with malabsorption syndrome attributed to deconjugation of bile acids in the upper small intestine. Recent reports raise the possibility that bacterial overgrowth may be a cause of watery diarrhea or irritable bowel syndrome. Quantitative culture of jejunal contents has been the gold standard for diagnosis, but a variety of indirect tests have been developed (and mostly discarded) over the years in an attempt to facilitate the diagnosis of small bowel bacterial overgrowth. These include breath tests and biochemical tests based on bacterial metabolism of various substrates. Problems with these indirect tests include rapid transit, which may cause substrate to reach the luxuriant bacterial flora in the colon, producing false positives and vagaries of the tests themselves, which may produce falsely negative results. The perfect test for small bowel bacterial overgrowth is yet to be devised.
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PMID:Evaluation of small bowel bacterial overgrowth. 1799 37

Histopathologic data demonstrate low-grade mucosal inflammation in a subset of patients with irritable bowel syndrome (IBS). This inflammatory infiltrate is mainly represented by increased numbers of T lymphocytes and mast cells lying in the lamina propria. The close apposition of immunocytes to gut nerves supplying the mucosa provides a basis for neuroimmune cross-talk, which may explain gut sensorimotor dysfunction and related symptoms in patients with IBS. A previous gastroenteritis (due to Campylobacter jejuni, Salmonella, Shigella, Escherichia coli, and, likely, viruses) is now an established etiologic factor for IBS (hence, postinfectious IBS). Other putative causes, such as undiagnosed food allergies, genetic abnormalities, stress, or bile acid malabsorption, may also promote and maintain a low-grade mucosal inflammation in IBS. The identification of mucosal inflammation in IBS has pathophysiologic implications and paves the way for novel therapeutic options.
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PMID:Is irritable bowel syndrome an inflammatory disorder? 1862 50


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