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

Diarrhea and malabsorption due to intestinal dysfunction are common symptoms in HIV infection. The pathophysiologic mechanisms of these alterations are often not known, and the role of HIV per se is still controversially discussed. We measured the epithelial transport and barrier function by means of a miniaturized Ussing chamber system in the duodenum of HIV-infected patients in different disease stages, determined by the CD4 cell count in the serum as well as symptoms in patients with and without diarrhea. We could show that diarrhea induced by HIV per se is caused by a leak flux mechanism due to impaired epithelial barrier function. Antisecretory therapy does not seem to be useful in these patients, because we did not find increased active ion secretion. Along the course of the HIV infection, the epithelial transport and barrier function varies with HIV disease stage (expressed by CD4 cell status). In addition, an in vitro model was studied to characterize the effect of HIV-infected human immune cells on the epithelial barrier function using the human colonic epithelial cell line HT-29/B6. HIV infection of human immune cells induced an increase in cytokine release--for example, TNF-alpha, IL-1 beta, IFN-alpha, and IFN-gamma--downregulating the epithelial barrier function of the human colonic epithelial cell line HT-29/B6. Taken together we postulate a specific stage-dependent cytokine pattern released from HIV-infected immune cells in the mucosa, which, corresponding to the HIV disease stage, is responsible for the variation in epithelial function.
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PMID:Mechanisms of epithelial barrier impairment in HIV infection. 1119 91

Patients with chronic liver disease exhibit a progressive loss of fat and muscle mass leading to mixed protein-energy malnutrition. The severe loss of muscle mass and body cell mass have convincingly been shown to carry a grave prognosis. Cachexia is likely to progress due to increased requirements as a consequence of hypermetabolism on the one hand and reduced volitional food intake and malabsorption on the other. Hypermetabolism may be mediated by factors such as frequent episodes of endotoxinemia, an activation of the inflammatory cytokine and/or the beta-adrenergic system. Some of these factors may also be responsible for reduced appetite. Obviously, these mechanisms may also be operative in other disease entities but clearly, portal hypertension and portosystemic shunting pose the cirrhotic patient at a particular risk for such disturbances including that of malabsorption. Apart from the established value of providing sufficient nutritious substrate to meet requirements the use of beta-adrenergic blocking agents and endotoxinemia lowering strategies seem worthwhile options that merit further clinical evaluation.
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PMID:Cachexia in liver cirrhosis. 1216 12

Chronic fatigue syndrome (CFS) is complex illness with unknown aetiology. Recent research shows that patients with CFS have marked alterations in microbial flora, including lowered levels of bifidobacteria and small intestinal bacterial overgrowth (SIBO). Research also indicates that CFS patients are under increased oxidative stress, have a type 2 helper cell dominate cytokine profile, frequently report allergies, have altered essential fatty acid (EFA) status and may have malabsorption of certain micronutrients. Lactic acid bacteria (LAB) have the potential to influence the immune system in CFS patients by supporting T helper cell 1 driven cellular immunity and may decrease allergies. In addition LAB are strong antioxidants, may improve EFA status, can enhance absorption of micronutrients by protecting the intestinal epithelial barrier, and have been used to treat SIBO. It is our contention that LAB may have a therapeutic role in the treatment of CFS.
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PMID:Chronic fatigue syndrome: lactic acid bacteria may be of therapeutic value. 1269 26

Multiple growth hormones (GHs) and factors are relevant to inflammatory bowel disease (IBD) due to their trophic effects on epithelial cells to promote mucosal integrity, renewal, and repair, on mesenchymal cells to promote wound healing, and on intestinal immune cells to modulate inflammation. The anabolic effects of GHs and factors outside the intestine are relevant to minimizing nutritional insufficiency, catabolic state, and the inability to maintain body weight due to inflammation-induced malabsorption. GHs and factors can, however, have a dual role, whereby trophic effects can be beneficial but, if excessive, can promote complications including the increased risk of intestinal tumors/adenocarcinoma and fibrosis. This review focuses on GH and insulin-like growth factor (IGF-I), for which evidence suggests such a dual role may exist. The actions of GH and IGF-I on the healthy intestine are compared with effects during intestinal inflammation or associated complications. Interactions between these growth factors and others relevant to IBD are considered. The role of the newly discovered suppressors of cytokine signaling proteins, which may dictate the balance between beneficial and excessive actions of GH and IGF-I, is also addressed.
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PMID:Growth factors in inflammatory bowel disease: the actions and interactions of growth hormone and insulin-like growth factor-I. 1562 5

Osteoporosis is a frequent finding in patients with Crohn's disease and ulcerative colitis. The prevalence of vertebral fractures in those patients with significantly reduced bone mineral density is up to 22%. Factors contributing to osteoporosis in inflammatory bowel disease (IBD) patients are treatment with glucocorticoids, increased cytokine production by the inflammation itself, malabsorption and possibly hypogonadism. Therefore, consequent treatment of the underlying IBD and minimising therapy with systemic glucocorticoids, as well as the adequate intake of calcium and vitamin D, may be very important measures to prevent bone loss in IBD. In patients with osteoporosis associated with Crohn's disease or ulcerative colitis, various treatment strategies, such as sodium fluoride and aminobisphosphonates, are discussed. Unfortunately, interventional studies in secondary osteoporosis are often limited by the small study population. The efficacy in prevention of vertebral fractures is not proven in any of the described treatment modalities in these patients. Therefore, guidelines are based on data using bone density as the most accepted surrogate marker and treatment guidelines are based on data from patients with postmenopausal and steroid-induced osteoporosis.
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PMID:Diagnosis and management of osteoporosis in inflammatory bowel disease. 1578 33

Celiac disease is manifested by an enteropathy caused by intolerance to gluten, a family of proteins found in wheat and other cereals. Following intestinal T-cell activation in predisposed individuals, different inflammatory mechanisms are triggered under the control of the cytokine balance including those with a pro-inflammatory Th1 pattern such as IFNgamma, TNFalpha, IL-15 and IL-18; and regulatory cytokines such as TGFbeta and IL-10. These cytokines, besides increasing the intensity of the activation and the number of immune cells within the intestinal mucosa, regulate the activity of epithelial growth factors and metalloproteinases, a group of molecules involved in the maintenance and turnover of the intestinal mucosa structure; in inflammatory conditions, they also induce the intestinal lesion responsible for malabsorption syndrome.
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PMID:[Cytokines in the pathogeny of celiac disease]. 1623 30

1. Based on earlier studies it was hypothesised that there is an immunological basis for the differences in susceptibility to malabsorption syndrome (MAS). A study was conducted to investigate base-line and MAS-induced cytokine levels in the intestine of broilers that differ in MAS susceptibility. 2. The transcription of cytokine mRNA in the intestine was quantified using a real-time polymerase chain reaction (PCR) method. At different time points after disease induction the intestines of broilers were investigated for expression of interleukin (IL)-2, IL-6, IL-8, IL-18 and interferon (IFN)-gamma. Age-matched non-MAS-induced chickens served as controls. 3. Control chickens from a MAS-resistant line had higher concentrations of mRNA for IL-2, IL-6, IL-18 and IFN-gamma in the small intestine while no difference between the lines was found for IL-8. After induction of MAS the relative amounts of IL-2, IL-6, IL-8 and IFN-gamma mRNA increased more in the intestines of the susceptible line than in the gut of the resistant line. 4. We suggest that differences in cytokine mRNA in the base-line situation and in MAS-induced conditions indicate a difference in immune response regulation in the two broiler lines. This difference in response could lead to the difference in susceptibility to MAS.
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PMID:Cytokine responses in broiler lines that differ in susceptibility to malabsorption syndrome. 1642 10

Patients with Crohn's disease are at increased risk of developing disturbances in bone and mineral metabolism because of several factors, including the cytokine-mediated nature of the inflammatory bowel disease, the intestinal malabsorption resulting from disease activity or from extensive intestinal resection and the use of glucucorticoids to control disease activity. Inability to achieve peak bone mass when the disease starts in childhood, malnutrition, immobilization, low BMI, smoking and hypogonadism may also play a contributing role in the pathogenesis of bone loss. The relationship between long-term use of glucocorticoids for any disease indication and increased risk for osteoporosis and fractures is well established. However, the relationship between Crohn's disease and ulcerative colitis and bone loss remains controversial. Depending on the population studied the prevalence of osteoporosis has thus been variably reported to range from 12 to 42% in patients with inflammatory bowel disease (IBD). In IBD most studies demonstrate a negative correlation between bone mineral density (BMD) and glucocorticoid use, but not all authors agree on the relationship between long-term glucocorticoid use and continuing bone loss. Whereas prospective studies do suggest sustained bone loss at both trabecular and cortical sites in long-term glucocorticoid users with inflammatory bowel disease, a decrease in bone mass is also observed in patients with active Crohn's disease not using glucocorticoids, and bone loss is not universally observed in patients with Crohn's disease using orally or rectally administered glucocorticoids. Data on vertebral fractures are scarce and there is no agreement about the risk of non-vertebral fractures in patients with Crohn's disease, although it has been suggested that non-vertebral fracture risk may be increased by up to 60% in patients with IBD. A recent publication reports an increased risk of hip fractures in Crohn's disease related to current and cumulative corticosteroid use and use of opiates, although these fractures could not be related to the severity of osteoporosis. The issue of the magnitude of the problem of osteoporosis has become particularly relevant in Crohn's disease, since the ability of therapeutic interventions to beneficially influence skeletal morbidity has been clearly established in patients with osteoporosis, whether post-menopausal women, men or glucocorticoid users. The main question that arises is whether all patients with Crohn's disease should be treated with bone protective agents on the assumption that they all have the potential to develop osteoporosis or whether the use of these agents should be restricted to patients clearly at risk of osteoporosis and fractures, providing these can be identified. We recommend, based on the available literature and our own experience, that all patients with Crohn's disease should be screened for osteoporosis by means of a bone mineral density measurement in addition to full correction of any potential calcium and vitamin D deficiency, to allow timely therapeutic intervention of the patient at risk while sparing the vast majority unnecessary medical treatment.
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PMID:Skeletal morbidity in inflammatory bowel disease. 1678 23

The neuropeptide Y (NPY), peptide YY (PYY) and pancreatic polypeptide (PP) family of hormones exhibit a wide variety of biological actions on the mammalian gastrointestinal tract through known G-protein coupled receptor pathways. At least four receptor subtypes, denoted as Y(1), Y(2), Y(4) an Y(5), each with specific affinities to NPY ligands, serve as regulators of mucosal function, gastrointestinal motility and secretion. Investigations to date, however, have implicated the NPY peptides as mediators in the pathogenesis of numerous gastrointestinal disorders, including malabsorption, short gut, inflammatory bowel diseases, and forms of pancreatitis. Our understanding of these diseases and the interactions of NPY peptides have been advanced by the development of receptor agonists and antagonists that can be used experimentally in animal models. Potent selective PYY agonists have been developed that exhibit clinical potential as proabsorptive agents. NPY receptor agonists and antagonists as well as mice harboring null mutations in the Y(1) and Y(4) receptors have provided novel approaches in preventing intestinal inflammation and diarrhea. The use of competitive antagonists and Y(2) receptor knockouts have also aided in understanding secretory tone and electrogenic ion transport in the colon. In the pancreas, PYY suppresses amylase and cytokine release, which would be desirable in the clinical therapy of pancreatitis. Protein/DNA array analysis has revealed that PYY reduces transcription factor binding activity and disrupts signal transduction pathways activated by TNF-alpha in acinar cells. The present review gives an overview of NPY research in gastrointestinal disease and discusses its clinical relevance and potential use as therapy.
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PMID:NPY family of hormones: clinical relevance and potential use in gastrointestinal disease. 1797 80

The availability of osteodensitometry has contributed significantly to increase the awareness of inflammatory bowel disease (IBD)-associated bone disease. Reported osteoporosis prevalence in patients with IBD range from 2% to 30%. The fractures risk varies between studies, influenced by demographic, clinical and genetic factors. The main pathogenetic factors involved are malabsorption, treatment with glucocorticoids, inflammation (increased cytokine production) and hypogonadism. A screening should be considered for all patients with small bowel Crohn's disease and especially for those with extensive disease, multiple resections, and malnutrition. Supplementation with both calcium and vitamin D is frequently the first step taken, but is insufficient to inhibit bone loss in many patients requiring use of glucocorticoids. Among available therapies, only biphosphonates are effective for treatment of glucocorticoid-induced osteoporosis.
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PMID:A 2008 panorama on osteoporosis and inflammatory bowel disease. 1829 97


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