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)

We reviewed the clinical records of 33 patients with Immunoblastic Sarcoma in order to further describe this disease clinically. Several common features were found. Thirty percent of the patients had a history of a prior immune disease or lymphoproliferative malignancy. Forty-four percent of the patients tested had a diffuse hypergammaglobulinemia. Lymphopenia (less than 1,000/mm3) was found in 45%, and anemia occurred in 73%. At initial presentation, 30% of the cases were clinically staged as either stage I or II, whereas 70% were found to be stage III or IV. Forty-nine percent of the patients had systemic symptoms at presentation. The median survival was 14 months. Advanced stage of disease, lymphopenia, and presence of systemic symptomatology were associated with significantly decreased survival times (p less than .05). We conclude that IBS is a clinical entity often associated with prior immune disease and/or diffuse hypergammaglobulinemia.
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PMID:Immunoblastic sarcoma: a clinical description. 36 72

To investigate whether the clinical history and basic laboratory test results can differentiate between an organic or functional cause of chronic diarrhea and thus avoid unnecessary hospital admissions and invasive procedures, we reviewed the charts of 58 adult patients admitted during 6 years because of chronic diarrhea who had normal stool and colonic examinations. The final diagnoses were irritable bowel syndrome in 34 patients, organic diarrhea in 21, and unknown cause in three. The following clinical data did not help in the differential diagnosis: age, sex, duration of diarrhea, presence of continuous diarrhea, abdominal pain, stool frequency or volume, and presence of stool mucus. Significant weight loss, nocturnal diarrhea, and the absence of tenesmus were associated with an organic cause. One or more laboratory alterations (increased erythrocyte sedimentation rate, anemia, hypokalemia, and low serum albumin level) were found in 62% of patients with organic diarrhea but in only 3% of those with functional disease; p less than 0.001. In 20 of 21 patients with organic diarrhea, an syndromic diagnosis (fat malabsorption, n = 13; inflammatory bowel disease, n = 4; and secretory diarrhea, n = 3) could be obtained with three simple tests (stool fat, rectal biopsy, and fecal water osmolality and electrolyte determination, respectively). Our study confirms that a detailed history and a few simple laboratory data can help to distinguish between functional and organic diarrhea and so avoid extensive investigation. The syndromic diagnosis of organic diarrhea can also be approximated with relatively easy tests.
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PMID:Chronic diarrhea with normal stool and colonic examinations: organic or functional? 174 88

A retrospective study on the syndrome of chronic diarrhea was carried out on 50 revised clinical histories. The patients were hospitalized at the E. Rebaglati M. Hospital between April 1983 and March 1988. The purpose of the study was to evaluate the signs and symptoms of the syndrome, as well as the etiological agents and the methodology used for diagnoses. The selection criteria involved patients diagnosed as suffering from "chronic diarrhea of undetermined causes" upon entry. Seven were excluded due to incomplete study whereas 2 were diagnosed as acute infections diarrhea. Forty one patients were definite cases of chronic diarrhea and they were divided between 2 groups: the first one or Chronic Organic Diarrhea (58.53%) and the second one or Chronic Functional Diarrhea (41.46%). Out of the 41 revised clinical histories with chronic diarrhea, the following were the foundings: (1) the syndrome affects the economically active populations mainly and the length of the disease was more than 3 weeks in all the patients; (2) anemia, fever, weight loss, nightime bowel movements and bloody stools suggest organic problems whereas psychiatric disorders, daytime bowel movements, abdominal pain, disease recurrence and absence of detectable organic pathology suggest functional problems; (3) the most common cause of chronic diarrhea is the Irritable Bowel Syndrome followed by infectious diseases, with parasitosis in the first place; and (4) bearing in mind the mainly colonic affection and the predominant infectious diseases, the methodology used for their diagnosis would bring out good results.
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PMID:[Chronic diarrhea: clinical aspects]. 213 Oct 3

Forty-nine acromegalics and 57 controls matched for age and sex underwent colonoscopy. The control group consisted of patients investigated because of atypical abdominal complaints compatible with irritable bowel syndrome or constipation. The exclusion criteria for both groups included: age over 75 years, previous colonic polyps or cancer, previous colonic surgery, rectal blood loss, anemia, previous abdominal radiation, sigmoidoscopy, colonoscopy or barium enema performed for any indication within 3 years prior to the present study. Colonoscopy was successful in reaching the cecum in 72 and 77% of the controls and acromegalics, respectively (p = NS). Eleven (22%) of 49 acromegalics had biopsy-proven colonic adenomas versus only five (9%) of the control group (p < or = 0.05). Multiple adenomas were found in three of the 11 acromegalics and in none of the controls. In five of these 11 patients and in only one of the controls, at least one adenoma was located in the right colon. In addition, acromegalics tended to have larger adenomas. The group of acromegalics with and without adenomas did not differ significantly in age or duration of active disease. In conclusion, the present study shows that acromegalic patients have an increased risk of developing colonic adenomas.
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PMID:Increased prevalence of colonic adenomas in patients with acromegaly. 792 Dec 6

If one reviews the literature with zeal, it is increasingly apparent that few organs escape recruitment when IBD is chronic or progressive. Insights into mucosal pathophysiology have helped with understanding the more frequent extraintestinal manifestations, but the mechanisms attendant to the development of less common events (e.g. acute pancreatitis, concurrent gluten sensitive enteropathy, or active pulmonary disease) remain either poorly studied or obscure. It is particularly interesting, however, to read reports of abnormal pulmonary function, generally of the obstructive type, correlated to measurements of abnormal intestinal permeability in patients with either active pulmonary sarcoid or pulmonary involvement in Crohn's disease. It has been further speculated that similarities in the mucosal immune system of the lung and intestine are responsible for evidence of bronchial hyperreactivity in patients with active IBD. Finally, it is important to recognize that extensions of the inflammatory process are not restricted to the development of organ-based events but may be responsible for some of the most frequent systemic abnormalities detected in IBD patients. It is now also well confirmed that the cytokine environment in IBD can support activated coagulation and, in some clinical situations, overt vascular thrombosis. The cerebrovascular complications of IBD are well recognized and range from peripheral venous thrombosis to central stroke syndromes and pseudotumor cerebri. Reports of focal white matter lesions in the brains of patients with IBD or an increased incidence of polyneuropathy may be other clinical examples of regional microvascular clotting. Microvascular injury appears to be more ubiquitously present, with reports ranging from a speculated primary causative role (e.g., granulomatous vasculitis in the mesenteric circulation) to the utility of nailbed vasospasm, in Crohn's disease, as a clinical marker for disease activity. It is also reported that IL-6 suppression of erythropoietin production is a major feature of the chronic anemia seen in active IBD. Moreover, the capacity of peripheral monocytes from active IBD patients to secrete TNF and IL-8 is reported predictive for the degree of therapeutic response from recombinant erythropoietin. These collected observations constitute another excellent example of the symmetry between basic science and clinical utility. It is from the context of applied basic science that many future therapies will arise. Empiricism will lose much of its appeal as clinical observations will be increasingly translated into cellular language. Already in animal models, elemental diets diminish IL-6-related acute inflammatory injury, and reductions in dietary lipid alter the antigenicity of bacteria. Provocatively, in humans, unconfirmed reports have even associated diet therapy with the resolution of uveitis and pyoderma gangrenosum. It is likely that efforts will also be made to induce oral tolerance if specific triggering proteins are discovered or to alter bowel flora if such an arcane area of investigation becomes resurgent.
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PMID:Extraintestinal considerations in inflammatory bowel disease. 880 40

A 17 year old male suffered from iron deficiency of undetermined cause for 2 years. Iron substitution was able to correct it for short periods. With the exception of fatigue and recurring abdominal pain attributed to oral iron therapy no further symptoms were present. The physical status on admission was unremarkable. The laboratory detected intestinal disorders, an anemia of the chronic type without evidence for malignancy or renal failure suggested an inflammatory gastro-intestinal disorder. In spite of a twice negative noninvasive test for gluten-intolerance the clinician favored in his differential diagnosis non tropical sprue over inflammatory bowel disease (IBD, Crohn's disease, Whipple's disease). Histopathology of small bowel specimens did not indicate sprue. An ileo-colonoscopy revealed severe ulcerating ileitis and mild chronic colitis. The histologic specimen revealed a severe ileal inflammation with cosinophilia and the colon specimens epitheloid microgranuloma. These findings are highly compatible with the diagnosis of Crohn's disease. Iron deficiency anemia is common in Crohn's disease. In the current case it is due to disturbed iron uptake. Iron deficiency anemia as sole symptom of Crohn's disease is extremely rare.
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PMID:[Severe chronic iron deficiency in a 17-year-old student]. 962 33

During the past decade relevant progress has been made in the understanding and treatment of IBD-associated anemia. Effective replacement of iron deficits has become safe by using novel intravenous iron preparations such as iron sucrose. The ability of erythropoietin to interfere with key mechanisms of myelosuppression in anemia of chronic diseases also benefits patients with IBD-associated anemia. Concerns about cost effectiveness have been raised and weighed against the potential improvement in quality of life. Gastroenterologists who are caring for IBD patients should be concerned with low hemoglobin levels, since the quality of life in these patients can be as low as in anemic patients with advanced cancer. Also provided is a structured approach to cost-effective therapy.
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PMID:Anemia in IBD: the overlooked villain. 1083 75

We examined the therapeutic effects of the inflammatory cell infiltration inhibitor IS-741 (N-(2-((ethylsulfonyl)amino)-5-(trifluoromethyl)-3-pyridinyl)-cyclohexanecarboxamide monosodium salt monohydrate) on a rat colitis model. As a result of its effects on leukocyte infiltration, IS-741 inhibits cell adhesion, alleviates symptoms and signs of pancreatitis and multiple organ failure and demonstrates a life-saving effect in a model of severe acute pancreatitis. A rat model was prepared by inducing colitis with 3% dextran sodium sulfate (DSS) and maintaining pathology with 1% DSS. Repeated oral administration of IS-741 at 1, 10 or 100 mg/kg per day was conducted for 2 weeks (during treatment with 1% DSS). IS-741 at each dose decreased the area of erosion in the large intestine, thickening of the wall of the large intestine and anemia caused by melena. Some effects of IS-741 were nearly equivalent to those of the control compound salazosulfapyridine. Furthermore, IS-741 markedly alleviated inflammatory cell infiltration into the intestinal wall. IS-741 improved lesions in a rat DSS model by inhibiting leukocyte infiltration, suggesting the possibility of clinical application of this drug for IBD.
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PMID:Efficacy of the inflammatory cell infiltration inhibitor IS-741 on colitis induced by dextran sulfate sodium in the rat. 1170 14

Some chronic diseases have a favourable course and are cured spontaneously. Allergic diseases such as eczema, hay fever and asthma have a good outcome in more than 75% of cases within 7 to 25 years, depending on the kind of allergy. Migraines have also a good evolution in children and after menopause. Many symptoms due to menstruation such as dysmenorrhea, premenstrual syndrome or anemia, disappear after menopause as well as diseases due to estrogens such as uterine leiomyoma, endometriosis and prolactinoma. The risk of epilepsy relapse after a first seizure is about 40% after 2 years. The risk is lower in children. Attention deficit disorder affects 3 to 5% of children but is present in only 30% of them in adult age. The prevalence of depression decreases in women between 30 and 60 years of age. Functional somatic syndromes such as fibromyalgia, irritable bowel syndrome or dyspepsia decrease in 2/3 of cases within 5 to 10 years if there is no history of anxio-depressive symptoms. However, prognosis is reserved when initial symptoms are severe or if they are connected to sexual abuse, domestic violence or depression. Other diseases have a spontaneous favourable course such as myopia, idiopathic infertility, polycystic ovary disease or ventricular arrhythmia. The knowledge of a good prognosis enables to avoid unnecessary treatments and to reassure many patients.
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PMID:[The benefits of aging. I. Patience and cure: spontaneous beneficial course of certain diseases]. 1172 11

The activity of nitric oxide synthase (NOS) was assayed in enterocytes isolated from human duodenal biopsies to determine its role in celiac disease. Patients were categorized into groups with irritable bowel syndrome, iron-deficiency anemia, B(12)/folate deficiency, and treated and untreated celiac disease. Enterocytes isolated from all groups showed 1400W-inhibitable Ca2+-independent NOS activity with a pH level and temperature optimum of 9.4 and 37 degrees C, respectively. Western blotting showed that enterocytes expressed the inducible NOS protein and proteins with nitrated tyrosine residues, the latter being indicative of nitric oxide-driven peroxynitrite and/or free-radical damage. Endothelial NOS was seen only in the lamina propria. Patients with celiac disease had higher NOS activity than other patient groups. Treatment of the condition led to a fall in activity. Enzyme-linked immunosorbent assay demonstrated cGMP production by the enterocyte fraction, but cGMP levels did not correlate with NOS activity. These results suggest that inducible NOS is constitutively expressed in human duodenal enterocytes, is increased in patients with untreated celiac disease, and is partially corrected when such patients are treated. We found no evidence to support a role for nitric oxide in the formation of cGMP within the small intestine. Furthermore, we were unable to demonstrate a role for peroxynitrite/free radical damage in the pathophysiology of celiac disease.
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PMID:Increased activity and expression of iNOS in human duodenal enterocytes from patients with celiac disease. 1212 78


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