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)

The aim of this study was to determine serum retinol levels in patients with inflammatory bowel disease and to attempt to elucidate the mechanism of changes in vitamin A metabolism in these disorders. It was found that in 15 patients with active ulcerative colitis, 14 patients with active Crohn's disease and in 3 operated patients with recurrent Crohn's disease serum retinol levels and retinol-binding protein were significantly lower than in controls. Concentrations of vitamin A did not depend on the localization of inflammatory bowel disease, previous ileal resections, duration of the disease or age and sex of the patients. During successful treatment of active ulcerative colitis normalization of serum retinol levels without substitution of vitamin A was observed. Repeated determinations in patients with Crohn's disease who had low serum retinol levels in an active phase of disease revealed normal vitamin A levels in an inactive phase. The absorption of vitamins A and E in patients with inflammatory bowel disease was normal. The normal serum retinol concentrations in patients with diarrhea due to irritable bowel syndrome, and in those with anorexia nervosa exclude the influence of diarrhea and body weight itself on vitamin A levels. The results of this study indicate that serum retinol levels in patients with active inflammatory bowel disease are secondary to the decreased serum retinol-binding protein concentrations, and probably depend on the increased protein catabolism in these disorders.
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PMID:Metabolism of vitamin A in inflammatory bowel disease. 176 54

Gastrointestinal functions such as food intake, propulsive peristalsis, inhibition of reflux, secretion, digestion and defecation are controlled by a complex autonomous neurohumoral system, which is influenced by higher cortical impulses. Life stress may modulate these impulses and in this way cause two types of gastrointestinal reactions. Psychophysiological reactions involve accentuations, inhibition or distortion of the pattern of function of gastrointestinal organs without changes in their structure. Examples of this type of reaction are often painful accentuation of bowel movements in patients with the irritable bowel syndrome, and increased gastric secretion elicited by emotional stress. Psychosomatic reactions lead to morphological changes in the end organ, e.g. activation of peptic ulcer or ulcerative colitis. Psychophysiological reactions may be important in the onset of symptoms in some functional diseases, e.g. in the irritable bowel syndrome. These patients need support from the physician, but specific psychiatric therapy is required only in cases with severe psychopathology, e.g. in patients with anorexia nervosa. The role of psychosomatic reactions in the development of organic gastrointestinal diseases is still unclear, as is the value of specific psychiatric therapy in the treatment of diseases such as peptic ulcer or ulcerative colitis. If this kind of therapy has some effect, it may be directed mainly towards subjective symptoms.
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PMID:Psychosomatic factors in gastrointestinal disorders. 347 93

Ulcerative colitis and Crohn's disease are significant childhood illnesses. With their many extraintestinal manifestations, they may masquerade as fever of unknown etiology, arthritis, anorexia nervosa, growth hormone deficiency, collagen-vascular disease, idiopathic growth retardation and even irritable bowel syndrome of childhood. In any child who presents with growth failure and/or chronic abdominal pain with fever or weight loss, the diagnosis of inflammatory bowel disease must be considered. As in any other chronic disease of childhood, long-term management will often challenge the physician emotionally and intellectually. As the etiology is yet unknown and a definitive cure is lacking, proper treatment depends on optimal medical and surgical management and supportive care.
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PMID:Inflammatory bowel disease in children and adolescents. 737 73

Ten to 25% of healthy persons have bloating at some time or other. It is very common in those with the irritable bowel syndrome, constipation, or anorexia nervosa. Although the cause of functional bloating remains unknown, old explanations such as a low diaphragm, exaggerated lumbar lordosis, and psychiatric problems have been disproved. New suggestions on its etiology include recent weight gain, weak abdominal muscles, and retained fluid in loops of small intestine. No treatment is of proven benefit, but treatment by weight loss, exercise, and prokinetics should be studied.
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PMID:Functional abdominal bloating. 793 Apr 28

Among the numerous positive effects of probiotic microorganisms and prebiotic carbohydrates observed in clinical studies--the majority of which, however, does not fulfil the criteria of pharmaceutical verification--some are of specific relevance to female health. The present review addresses--besides some notes concerning the potential microbiota-hormone interactions--the first line with preventive and/or therapeutic applications of probiotic bacteria in order to maintain a balanced intestinal and urogenital flora, as well as in the case of irritable bowel syndrome, constipation (idiopathic slow-transit) and urogenital tract infections. Further aspects are the promotion of bone health and osteoporosis prevention brought about by inulin, oligofructose and galactooligosaccharides. Some further conditions, namely anorexia nervosa, the premenstrual syndrome as well as prevention or alleviation of climacteric and menopausal disorders, for which the use of probiotics is rather hypothetical or is largely studied by alternative medicine practising physicians, are addressed briefly.
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PMID:Health benefits of probiotics and prebiotics in women. 1923 21

The two most clinically serious eating disorders are anorexia nervosa and bulimia nervosa. A drive for thinness and fear of fatness lead patients with anorexia nervosa either to restrict their food intake or binge-eat then purge (through self-induced vomiting and/or laxative abuse) to reduce their body weight to much less than the normal range. A drive for thinness leads patients with bulimia nervosa to binge-eat then purge but fail to reduce their body weight. Patients with eating disorders present with various gastrointestinal disturbances such as postprandial fullness, abdominal distention, abdominal pain, gastric distension, and early satiety, with altered esophageal motility sometimes seen in patients with anorexia nervosa. Other common conditions noted in patients with eating disorders are postprandial distress syndrome, superior mesenteric artery syndrome, irritable bowel syndrome, and functional constipation. Binge eating may cause acute gastric dilatation and gastric perforation, while self-induced vomiting can lead to dental caries, salivary gland enlargement, gastroesophageal reflux disease, and electrolyte imbalance. Laxative abuse can cause dehydration and electrolyte imbalance. Vomiting and/or laxative abuse can cause hypokalemia, which carries a risk of fatal arrhythmia. Careful assessment and intensive treatment of patients with eating disorders is needed because gastrointestinal symptoms/disorders can progress to a critical condition.
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PMID:Gastrointestinal symptoms and disorders in patients with eating disorders. 2649 70

The hypothesis proposed is that functional disorders, such as irritable bowel syndrome, chronic fatigue syndrome and anorexia nervosa are caused by auto-antibodies to neuronal proteins induced by molecular mimicry with microbial antigens. The age incidence of these conditions, the marked female excess, increase with economic and technological advance, precipitation by infection, and the paucity of histological changes are all consistent with the hypothesis. It can be tested directly using human sera to search for cross reaction with brain proteins in model systems such as Drosophila melanogaster. The conditions might be amenable to treatment using pooled immunoglobulin. Identification and elimination from the microbial flora of the bacteria that express the cross reacting antigens should be possible.
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PMID:Microbes, molecular mimicry and molecules of mood and motivation. 2682 39

Patients with anorexia nervosa often voice a multitude of symptoms in regards to their gastrointestinal tract. These complaints can complicate the treatment of their eating disorder as they distract attention from the important goal of weight restoration. Moreover, the restricting of certain food groups also makes the task of weight restoration substantially more difficult, or may result in binging. Therefore a working knowledge of common gastrointestinal comorbidities, such as celiac disease, irritable bowel syndrome, inflammatory bowel disease, and gastroparesis, is useful when treating a patient who has anorexia nervosa.
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PMID:Gastrointestinal comorbidities which complicate the treatment of anorexia nervosa. 2786 66

HIV infection progressively destroys CD4+ mononuclear cells, leading to profound cellular immune deficiency that manifests as life-threatening opportunistic infections and malignancies (i.e., AIDS). Gut microbiota plays key roles in the modulation of host metabolism and gene expression, maintenance of epithelial integrity, and mediation of inflammatory and immunity. Hence, the normal intestinal microbiota plays a major role in the maintenance of health and disease prevention. In fact, a large number of studies have shown that the alteration of the gut microbiota contributes to the pathogenesis of several diseases, such as inflammatory bowel diseases, irritable bowel syndrome, metabolic diseases, anorexia nervosa, autoimmune diseases, multiple sclerosis, cancer, neuropsychiatric disorders, and cardiovascular diseases. Recently, accumulating evidence has shed light on the association of dysbiosis of gut microbiota with HIV infection. Hence, the modification of gut microbiota may be a potential therapeutic tool. Fecal microbiota transplantation may improve the conditions of patients with HIV infection by manipulating the human intestinal bacteria. However, the relevant research is very limited, and a large amount of scientific research work needs to be done in the near future.
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PMID:Altered Gut Microbiota in HIV Infection: Future Perspective of Fecal Microbiota Transplantation Therapy. 2987 92

We have reviewed the scientific literature related to four diseases in which to serotonin (5-HT) is involved in the etiology, herein named 5-HT-linked diseases, and whose prevalence is influenced by estrogenic status: depression, migraine, irritable bowel syndrome and eating disorders. These diseases all have in common a sex-dimorphic prevalence, with women more frequently affected than men. The co-occurrence between these 5-HT-linked diseases suggests that they have common physiopathological mechanisms. In most 5-HT-linked diseases (except for anorexia nervosa and irritable bowel syndrome), a decrease in the serotonergic tone is observed and estrogens are thought to contribute to the improvement of symptoms by stimulating the serotonergic system. Human pregnancy is characterized by a unique 5-HT and estrogen synthesis by the placenta. Pregnancy-specific disorders, such as hyperemesis gravidarum, gestational diabetes mellitus and pre-eclampsia, are associated with a hyperserotonergic state and decreased estrogen levels. Fetal programming of 5-HT-linked diseases is a complex phenomenon that involves notably fetal-sex differences, which suggest the implication of sex steroids. From a mechanistic point of view, we hypothesize that estrogens regulate the serotonergic system, resulting in a protective effect against 5-HT-linked diseases, but that, in turn, 5-HT affects estrogen synthesis in an attempt to retrieve homeostasis. These two processes (5-HT and estrogen biosynthesis) are crucial for successful pregnancy outcomes, and thus, a disruption of this 5-HT-estrogen relationship may explain pregnancy-specific pathologies or pregnancy complications associated with 5-HT-linked diseases.
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PMID:Serotonin-estrogen interactions: What can we learn from pregnancy? 3094 49


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