Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diarrhea continues to be a prevalent symptom in patients with inflammatory bowel disease (IBD), requiring a wide differential diagnosis to define the pathophysiologic mechanisms in individual patients. It is essential that physicians properly evaluate complaints of diarrhea by assessing both patient symptoms and potential physiologic impacts on fluid and electrolyte status. Underlying mechanisms of diarrhea with IBD are the location, extent, and severity of inflammation; malabsorption; altered motility; and iatrogenic causes such as medications, diet, and antibiotic-associated colitis (eg, Clostridium difficile). When treating diarrhea, physicians need to control inflammatory activity using appropriate treatment algorithms. Therapies include aminosalicylates, corticosteroids, immune modifiers, and, most recently, biologic treatment. Other medications, including loperamide, diphenoxylate, codeine sulfate, and tinctures of opium, slow motility and increase the absorption of fluids and nutrients. For iatrogenic issues, medications that cause diarrhea should be withdrawn and individual diets modified. Not all diarrheas in the IBD patient are the same; therefore, it is essential to tailor therapies according to presumed etiologies. Antidiarrheal agents are not recommended in extremely ill patients and those with known hypersensitivity or evidence of obstruction or colonic dilation, fever, or abdominal tenderness. Concomitant use of loperamide with diphenoxylate and atropine should be avoided in early pregnancy.
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PMID:Treatment of diarrhea in patients with inflammatory bowel disease: concepts and cautions. 1819 64

Celiac disease is a gluten-dependent small intestinal mucosal disorder that causes malabsorption, often with diarrhea and weight loss. Diagnosis is based on detection of typical biopsy changes in the proximal small bowel, followed by evidence for an unequivocal response to a gluten-free diet. Refractoriness in celiac disease may be due to poor diet compliance, sometimes intentional, or consumption of ubiquitious sources of gluten. Alternatively, the original diagnosis may not be correct (eg., duodenal Crohn's disease), or a second cause for symptoms may be present (eg., collagenous colitis, functional bowel disorder). In some with recurrent symptoms, a complication may be present (eg., collagenous sprue, small bowel carcinoma, lymphoma). In some, a response to a gluten-free diet can not be unequivocally defined, and more precise historical terms have been used including "sprue-like intestinal disease" or "unclassified sprue". Although a "wastebasket diagnosis", these likely represent a heterogeneous group, and some, but not all, may develop lymphoma. Precise definition will be critical in the future as an array of new treatments, including biological agents, may emerge.
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PMID:Refractory celiac disease and sprue-like intestinal disease. 1824 Mar 39

Diarrhea is a frequent adverse event involving the most frequently antibiotics, laxatives and NSAI. Drug induced diarrhea may be acute or chronic. It may be due to expected, dose dependant properties of the drug, to immuno-allergic or bio-genomic mechanisms. Several pathophysiological mechanisms have been described resulting in osmotic, secretory or inflammatory diarrhea, shortened transit time, or malabsorption. Histopathological lesions sometimes associated with drug induced diarrhea are usually non specific and include ulcerations, inflammatory or ischemic lesions, fibrous diaphragms, microscopic colitis and apoptosis. The diagnosis of drug induced diarrhea, sometimes difficult to assess, relies on the absence of other obvious causes and on the rapid disappearance of the symptoms after withdrawal of the suspected drug.
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PMID:[Drug induced diarrhea]. 1883 7

Systemic mastocytosis is an uncommon condition characterized by abnormal proliferation of mast cells in one or more organ. The specific D816V KIT mutation is present in most cases. Gastrointestinal symptoms occur commonly but histologic characterization of gastrointestinal involvement is incomplete. The purpose of this study was (1) to describe the clinicopathologic features in five patients with systemic mastocytosis involving the gastrointestinal tract and (2) to determine whether gastrointestinal involvement is associated with the usual D816V mutation or a different mutation. Clinical details were obtained from the hospital of origin or referring pathologist. Histologic features were documented in slides stained with hematoxylin and eosin, mast cell tryptase and CD117. Molecular analysis for the D816V KIT mutation was performed on formalin-fixed paraffin-embedded sections. Symptoms included diarrhea/loose stools (n=5), abdominal pain (n=4), vomiting (n=3) and weight loss (n=3). Other findings included cutaneous lesions of mastocytosis (n=4), malabsorption (n=2), hypoalbuminemia (n=2) and constitutional growth delay (n=1). Sites of gastrointestinal involvement included the colon (n=5), duodenum (n=3) and terminal ileum (n=3). Endoscopic/gross findings included mucosal nodularity (n=4), erosions (n=2) and loss of mucosal folds (n=2). In three patients the endoscopic appearance was considered consistent with inflammatory bowel disease. All cases showed increased mast cell infiltration of the lamina propria, confirmed by immunohistochemistry for mast cell tryptase and CD117. In two cases, mast cells had abundant clear cytoplasmic resembling histiocytes. Marked eosinophil infiltrates were present in four patients, in one patient leading to confusion with eosinophilic colitis. Architectural distortion was noted in three cases. The D816V KIT mutation was present in all four cases tested. In conclusion, gastrointestinal involvement by systemic mastocytosis is characterized by a spectrum of morphologic features that can be mistaken for inflammatory bowel disease, eosinophilic colitis or histiocytic infiltrates. Systemic mastocytosis involving the gastrointestinal tract is associated with the usual D816V KIT mutation.
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PMID:Systemic mastocytosis involving the gastrointestinal tract: clinicopathologic and molecular study of five cases. 1893 52

Phosphate homeostasis is critical for many physiological functions. Up to 85% of phosphate is stored in bone and teeth. The remaining 15% is distributed in cells. Phosphate absorption across the brush-border membrane (BBM) of enterocytes occurs mainly via a sodium-dependent pathway, which is mediated by type IIb sodium-phosphate cotransporters (NaPi-IIb). Patients of inflammatory bowel diseases (IBDs) suffer not only from diarrhea and nutrient malabsorption but also from bone loss. About 31-59% of patients with IBD develop bone disorders. Since the intestine is a primary location for dietary phosphate absorption, it is logical to postulate that there is an inverse relationship between gastrointestinal disorders and phosphate transport, which, in turn, contributes to bone disorders observed in patients with IBD. Phosphate absorption and NaPi-IIb expression was studied with BBM vesicles isolated from trinitrobenzene sulphonic acid (TNBS) animals as well as in Caco-2 cells. The mechanism of TNF-alpha downregulation of NaPi-IIb expression was investigated by luciferase assay, gel mobility shift assay (GMSA), and coimmunoprecipitation. Intestinal phosphate absorption mediated by NaPi-IIb was reduced both in TNBS colitis and in TNF-alpha-treated cells. Transient transfection indicated that TNF-alpha inhibits NaPi-IIb expression by reducing NaPi-IIb basal promoter activity. GMSAs identified NF1 protein as an important factor in TNF-alpha-mediated NaPi-IIb downregulation. Signaling transduction study and coimmunoprecipitation suggested that TNF-alpha interacts with EGF receptor to activate ERK1/2 pathway. Intestinal phosphate absorption mediated by NaPi-IIb protein is reduced in colitis. This inhibition is mediated by the proinflammatory cytokine TNF-alpha through a novel molecular mechanism involving TNF-alpha/EGF receptor interaction.
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PMID:Tumor necrosis factor-alpha impairs intestinal phosphate absorption in colitis. 1919 48

Nutrition plays a role in inflammatory bowel disease (IBD) primarily in prevention and treatment of malnutrition and growth failure. Furthermore, in Crohn disease (CD), nutrition can induce remission, maintain remission, and prevent relapse. Malnutrition is common in IBD and the mechanisms involved include decreased food intake, malabsorption, increased nutrient loss, increased energy requirements, and drug-nutrient interactions. At the time of diagnosis, up to 85% of pediatric patients with CD and 65% of those with ulcerative colitis (UC) have weight loss. Growth failure occurs in 15% to 40% of children with IBD and is less common in UC compared with CD, both at diagnosis and during follow-up. In CD, nutritional therapy with enteral formulas induces remission at a rate comparable with that achieved with steroids. In adults with CD, limited information suggests that enteral nutrition (EN) may play a role in maintenance of remission. In children with CD colitis, one study suggested that children without colitis respond better to EN than children with colitis, and another study found no such difference but reported a trend toward earlier relapse in those with isolated colonic involvement. Finally, nutrition may play a role in IBD via the possible protective effect of breastfeeding against UC and CD. In summary, although only CD may benefit from nutrition as primary therapy for remission induction and possibly maintenance of remission, nutrition plays an important role in the prevention and treatment of malnutrition in IBD, and may have a protective role, via the effect of breast-feeding on disease occurrence.
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PMID:Nutritional aspects in inflammatory bowel disease. 1930 Jan 35

Collagenous sprue is a rare form of small bowel enteropathy characterized by chronic diarrhea and progressive malabsorption with little data available on its natural history. The pathologic lesion consists of subepithelial collagen deposition associated with variable alterations in villous architecture. The small bowel biopsies of 12 cases were reviewed. Clinical details, celiac serology, and T-cell receptor gene rearrangement study results, when available, were collated. There were 8 females and 4 males (age ranged from 41 to 84 y) who presented with chronic diarrhea and weight loss. Small intestinal biopsies showed subepithelial collagen deposition with varying degrees of villous atrophy and varying numbers of intraepithelial lymphocytes. Four patients had previous biopsies showing enteropathic changes without collagen deposition. Seven cases were associated with collagenous colitis and 1 also had features of lymphocytic colitis. Three patients also had collagen deposition in gastric biopsies. One case was associated with lymphocytic gastritis. Celiac disease (CD, gluten-sensitive enteropathy) was documented in 4 patients. Five patients made a clinical improvement with combinations of a gluten-free diet and immunosuppressive therapy. Two patients died of complications of malnutrition and 1 of another illness. Clonal T-cell populations were identified in 5 of 6 cases tested. Four of these patients improved clinically after treatment but 1 has died. Collagenous sprue evolved on a background of CD in 4 cases. There was no history of CD in others and these cases may be the result of a biologic insult other than gluten sensitivity. None has developed clinical evidence of lymphoma to date.
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PMID:Collagenous sprue: a clinicopathologic study of 12 cases. 1964 52

Colitis can occur from viral or bacterial infections, ischemic insult, or autoimmune disorders; most notably Ulcerative Colitis and the colonic variant of Crohn's Disease - Crohn's Colitis. Acute colitis may present with abdominal pain and distention, malabsorption, diarrhea, hematochezia and mucus in the stool. We are beginning to understand the complex interactions between the environment, genetics, and epithelial barrier dysfunction in Inflammatory Bowel Disease and animal models of colitis have been essential in advancing our understanding of this disease. One popular model involves supplementing the drinking water of mice with low-molecular weight Dextran Sodium Sulfate (DSS), resulting in epithelial damage and a robust inflammatory response in the colon lasting several days.Variations of this approach can be used to model acute injury, acute injury followed by repair, and repeated cycles of DSS interspersed with recovery modeling chronic inflammatory diseases. After a single four-day treatment of 3% DSS in drinking water, mice show signs of acute colitis including weight loss, bloody stools, and diarrhea. Mice are euthanized at the conclusion of the treatment course and at necropsy dissected colons are processed and can be 'Swiss rolled" to allow microscopic analysis of the entire colon or infused with formalin as "sausages" to allow macroscopic analysis. Tissue is then embedded in paraffin, sectioned, and stained for histologic review.
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PMID:Murine Colitis modeling using Dextran Sulfate Sodium (DSS). 2008 13

Celiac disease may be initially detected in either children or adults, even in the elderly. This small intestinal mucosal disorder is gluten-dependent and causes nutrient malabsorption, often with diarrhea and weight loss. Diagnosis depends on detection of typical biopsy changes in the proximal small bowel along with an unequivocal response to a gluten-free diet. Recurrent changes usually result from poor adherence to the gluten-free diet, sometimes intentional, or from consumption of unsuspected gluten sources. In others, the original diagnosis may not be correct (e.g., duodenal involvement with Crohn's disease) or another cause for symptoms may have supervened (e.g., collagenous colitis, functional bowel disease). Rarely, a complication may occur (e.g., collagenous sprue, lymphoma). In some, the gluten-dependent nature of the small bowel disorder was not initially documented and biopsy changes continued despite a gluten-free diet. These have a sprue-like intestinal disorder, also labeled unclassified sprue. This represents a small, but likely, heterogeneous group, and in these, intractable symptoms may be present and, in some, lymphoma is eventually diagnosed.
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PMID:Celiac disease (gluten-sensitive enteropathy). 2048 60

Chronic diarrhea, defined as a decrease in stool consistency for more than four weeks, is a common but challenging clinical scenario. It can be divided into three basic categories: watery, fatty (malabsorption), and inflammatory. Watery diarrhea may be subdivided into osmotic, secretory, and functional types. Watery diarrhea includes irritable bowel syndrome, which is the most common cause of functional diarrhea. Another example of watery diarrhea is microscopic colitis, which is a secretory diarrhea affecting older persons. Laxative-induced diarrhea is often osmotic. Malabsorptive diarrhea is characterized by excess gas, steatorrhea, or weight loss; giardiasis is a classic infectious example. Celiac disease (gluten-sensitive enteropathy) is also malabsorptive, and typically results in weight loss and iron deficiency anemia. Inflammatory diarrhea, such as ulcerative colitis or Crohn disease, is characterized by blood and pus in the stool and an elevated fecal calprotectin level. Invasive bacteria and parasites also produce inflammation. Infections caused by Clostridium difficile subsequent to antibiotic use have become increasingly common and virulent. Not all chronic diarrhea is strictly watery, malabsorptive, or inflammatory, because some categories overlap. Still, the most practical diagnostic approach is to attempt to categorize the diarrhea by type before testing and treating. This narrows the list of diagnostic possibilities and reduces unnecessary testing. Empiric therapy is justified when a specific diagnosis is strongly suspected and follow-up is available.
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PMID:Evaluation of chronic diarrhea. 2208 67


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