[Somatostatin and octreotide in therapy of gastrointestinal diseases].
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Recent antigliadin antibody (AGA) determination has become an important diagnostic tool in coeliac disease (CD). Although this test has high sensibility for the disease, it is less specific, especially for IgG class, because of its having been found in some acute and chronic common intestinal childhood diseases. We studied the behaviour of AGA, IgA and IgG, in 234 children affected by various gastrointestinal diseases, comparing the results with those obtained in 125 coeliac children and 788 normal children. The intestinal diseases were as follows: irritable bowel syndrome, cow's milk protein intolerance, acute infectious diarrhoea, parasitosis, lactase deficiency, recurrent abdominal pain, cystic fibrosis, chronic constipation, gastroesophageal reflux, intestinal lymphangiectasia, chronic intractable diarrhoea and nodular lymphoid hyperplasia. Our results showed that while AGA-IgA were absent in all children studied, with the exception of 3 cases of acute diarrhoea, a moderate percentage of AGA-IgG was observed in subjects with cow's milk protein intolerance, acute diarrhoea, irritable bowel syndrome, lactase deficiency, chronic intractable diarrhoea and in a low percentage of children with parasitosis, intestinal lymphangiectasia and nodular lymphoid hyperplasia. There was no antibody movement in subjects with cystic fibrosis, gastroesophageal reflux, recurrent abdominal pains and chronic constipation. The different behaviour of the two antibody classes could be explained by the fact that AGA-IgG were detected in diseases where scattered areas of mucosal damage could allow the permeability of the macromolecules inducing passage of gliadin through the mucosal barrier and immune system-induced antibody stimulation.
Tumor-associated trypsin inhibitor (TATI) is a 6 K dalton protease inhibitor, that was isolated from urine of a patient with ovarian cancer. In our experience, mean serum level of TATI in healthy subjects (n. 120), is 13 micrograms/l (range 5.1-42 micrograms/l). The cut-off point is established in 32 micrograms/l (mean +/- 3 SD). We have examined 357 patients with gastrointestinal diseases: 98 gastric cancer, 50 colon cancers, 52 pancreatic cancers, 32 chronic pancreatitis, 38 IBD, 28 colon polyps, 40 gastric ulcers and 25 non-neoplastic biliary tree diseases. TATI may be a good tumor marker only in gastric cancer. Elevated levels of TATI also occur in obstructive hepatobiliary disease and active pancreatitis or IBD.
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Polydipsia, defined as a water intake of over 100 ml/kg/day, is a common presenting medical complaint in dogs. Polydipsia can be secondary (eg, to central or nephrogenic diabetes insipidus) or primary in origin, where increased water intake cannot be explained as a response to obligatory water loss. Primary polydipsia is confirmed by ruling out other known causes of polydipsia and demonstrating that renal concentrating ability is intact. The causes and associations of primary polydipsia in dogs are poorly defined. This report describes three dogs presented with signs of gastrointestinal disease with concurrent polydipsia. Investigations (including water deprivation testing) showed normal renal urinary concentrating ability and indicated primary polydipsia. Treatment of the gastrointestinal signs resulted in resolution of the polydipsia in each case. This is the first description of a possible association between gastrointestinal disease and primary polydipsia in the dog, the pathophysiology of which remains obscure.
BACKGROUND: There are considerable variations in estimates of the number of emergency upper gastrointestinal admissions per annum which are attributable to nonsteroidal anti-inflammatory drug (NSAID) use. AIM: To obtain a more accurate estimate of the number of these emergency admissions per annum in UK. METHODS: A retrospective survey of the case notes of all emergency admissions for upper gastrointestinal disease ('Cases') to two English District General Hospitals with a combined catchment population of 550,000. Records of all community deaths attributed to upper gastrointestinal diagnoses (with the same ICD codes) were also surveyed. Matched controls were identified from emergency admissions not caused by upper gastrointestinal diagnoses. The proportions of patients taking NSAIDs on admission to hospital (or at the time of death at home) and the outcome following admission to hospital were analysed. RESULTS: 620 emergency upper gastrointestinal admissions were identified and matched with 460 controls. Cases were more likely to be NSAID users than Controls (31% vs. 16%, OR 2.4, 95% CI: 1.8, 3.3: P < 0.001). Case NSAID use was higher in females and with increasing age. As severity of mode of presentation worsened, the probability of NSAID use increased (e.g. OR relative to controls for peptic pain 1.9, for perforation 5.9). Blood transfusion requirements were significantly higher (P < 0.0001) in Cases taking NSAIDs, although NSAID use did not influence mortality. Extrapolation from these data indicate that there are 65,000 emergency upper gastrointestinal admissions per annum in UK; 12,000 of these admissions (including 2230 deaths) are attributable to NSAID use. A further 330 attributable deaths occur in the community. CONCLUSIONS: There is a strong association between NSAID use and propensity for upper gastrointestinal emergency admission; NSAID use is associated with significant morbidity and mortality each year in UK.
Activated T cells can be visualized in the intestinal lamina propria in a number of gastrointestinal diseases including food-sensitive enteropathy (coeliac disease), inflammatory bowel disease and intractable diarrhoea of infancy. Experimental studies have shown that T-cell activation in human intestinal lamina propria in vitro produces an increase in crypt cell proliferation, villous atrophy, increased HLA-DR expression on enterocytes, increased intra-epithelial lymphocyte numbers, and phenotypically, macrophage activation. All of these features are seen in human gastrointestinal disorders and it is proposed that T-cell activation to wheat (in coeliac disease), milk (cows' milk-sensitive enteropathy), and unidentified luminal antigens (Crohn's disease) plays a primary role in the pathogenesis of these disorders.
Determination of carbon or hydrogen markers in breath has allowed closer investigation of the pathogenic mechanisms of several gastrointestinal diseases. Thus, the 13C-urea breath test is a nonaggressive, simple and safe test with excellent accuracy both in the initial diagnosis of Helicobacter pylori infection and in confirmation of its eradication following treatment. Moreover, because of the simplicity, reproducibility and safety of these types of procedure, they have tended to substitute more uncomfortable and expensive techniques that were traditionally used in gastroenterology. Several breath tests have been developed that allow reliable evaluation of liver or exocrine pancreatic function, gastrointestinal motility, as related to gastric emptying or orocecal transit time, and a diagnostic approach to clinical problems that could be due to bacterial overgrowth or malabsorption of various sugars.
Recurrent aphthae is rather often disease during infantjuvenile age. The aphthous alterations on mucosa of the oral cavity could be of various etiology. They could be symptoms of a general aphthosis (recurrent aphthous stomatitis, Behçet's disease, Turen disease), an individual manifestation of allergic states, manifestation of immuno-deficiency states as well as secondary stomatitis during some general diseases. The present study presents information of the incidence of recurrent aphthae during various gastrointestinal diseases which progress with often alterations of oral cavity mucosa.
BACKGROUND AND AIMS: Diagnosis of irritable bowel syndrome (IBS) is based on arbitrary criteria due to the lack of an accurate diagnostic test. The aim of this study was to evaluate whether rectosigmoid tone modification after a meal represents an accurate diagnostic approach. METHODS: In a secondary care setting, 32 constipation predominant and 24 diarrhoea predominant IBS patients, 10 functional diarrhoea and 10 functional constipation patients, 29 organic gastrointestinal disease patients, and 10 healthy volunteers underwent a rectal barostat test to measure fasting and postprandial rectosigmoid tone. Rectosigmoid response was assessed following three meals containing different amounts of calories: 200 kcal, 400 kcal and 1000 kcal. RESULTS: After 200 kcal, healthy volunteers and patients with organic diseases showed a reduction in rectosigmoid volume of at least 28% of fasting volume, indicating a meal induced increase in muscle tone. In contrast, patients with diarrhoea predominant IBS showed dilation of the rectosigmoid colon, indicative of reduced tone, and patients with constipation predominant IBS showed a mild volume reduction or no modification. Functional diarrhoea and constipation patients showed rectosigmoid tone modification resembling that of the corresponding IBS subtype. A 400 kcal meal normalised rectosigmoid tone in more than half of the constipation predominant IBS patients but none of the diarrhoea predominant IBS patients. In contrast, a 1000 kcal meal normalised tone response in all IBS patients. Sensitivity of the test was 100%, specificity 93%, positive predictive value 96%, and negative predictive value 100%. CONCLUSION: A postprandial reduction in rectosigmoid tone of at least 28% of fasting value after a low caloric meal accurately separates organic and functional gastrointestinal disease patients. This parameter may therefore be used in the positive diagnosis of IBS.
The amount of free and acetylated norsulfazol in the urine of patients with gastrointestinal diseases was analysed 3 hours after peroral administration of the drug (20 mg/kg). The acetylation rate of norsulfazol in patients of 21--30 years of age was significantly lower than that in heathy subjects of the same age. In groups of 31--40, 41--50 and 51--60 years of age the acetylation rate was 47, 42 and 43%, respectively. In patients with chronic cholecystitis excretion with urine of free norsulfazol was 2-fold as increased whereas in chronic gastritis there was a 2.7-fold increase as compared to controls. The acetylation rate of norsulfazole was 1.6, 1.4 and 1.5-fold reduced in duodenal ulcer, cholecystitis and gastritis, respectively.
OBJECTIVE: To determine whether health services use by patients with selected acid-related gastrointestinal disorders (peptic ulcer disease, gastroesophageal reflux disease, and gastritis or dyspepsia) is lower after initial treatment with proton pump inhibitors (PPIs) than with histamine2 receptor antagonists (H2RAs). STUDY DESIGN: Retrospective, 2-year longitudinal study. PATIENTS AND METHODS: Among continuous enrollees from December 1, 1996, to June 1, 2002, in a group model health maintenance organization, 13,971 members were electronically selected who began receiving antisecretory therapy during that period and who had no previous drug therapy, endoscopy, or hospitalization for gastrointestinal disease. Adjusted medical costs and healthcare use related to gastrointestinal disease (measured by office visits, endoscopy, or imaging and hospital admissions) and factors associated with initial and subsequent drug therapy were analyzed using a 2-stage model. This method adjusted for unobservable confounders, primarily drug selection bias, an inherent limitation of retrospective database studies. RESULTS: Drug costs were more than 4-fold higher (P < .001) when PPIs rather than H2RAs were prescribed initially, but non-drug costs and health services use showed no decrease. A history of physicians' prescribing PPIs in the prior 12 months was associated with prescribing PPIs as initial therapy (odds ratio, 4.29; 95% confidence interval, 3.74-4.90) and with step-up therapy (change from H2RAs to PPIs). A history of physicians' prescribing H2RAs in the prior 12 months was associated with step-down therapy (change from PPIs to H2RAs). CONCLUSION: Prescribing PPI compared with H2RA therapy as initial therapy for acid-related gastrointestinal disease produced no decrease in nondrug costs or health services use.
Whether patients with mitral prolapse (MP) have specific features in the course of their gastrointestinal diseases (GD) was studied in 420 MP patients with various GD. Echocardiography and examination of the vegetative status were conducted in all the patients. On demand, esophagogastroduodenoscopy, ultrasonic investigation of the abdominal organs, multistage fraction duodenal intubation were made. The findings evidence of more severe course of GD in MP patients. This manifests in early onset, severe pain and dispeptic syndromes, marked mucosal inflammation and is explained by dysfunction of the vegetative nervous system and generalized dysplasia of the connective tissue.
BACKGROUND: Our aim was to determine the diagnostic value of electron microscopy in evaluating the etiology of gastrointestinal disease in patients infected with the human immunodeficiency virus (HIV). METHODS: A retrospective review of electron microscopic and light microscopic results of all HIV-positive patients with gastrointestinal and liver diseases was made during a 3-year period from June 1995 to June 1998. RESULTS: A total of 145 HIV-positive patients had their electron microscopy specimens reviewed. Of these, 136 were investigated for diarrhea, and the other 9 for increased liver enzymes. Twenty-seven of the 145 (18.6%) HIV-positive patients had a pathogen identified by electron microscopy, compared with only 13 of 145 (9%) identified by light microscopy (P < 0.005). The sensitivity of light microscopy for detecting opportunistic pathogens was 68%. Twenty-one of the 27 (77.8%) patients diagnosed by electron microscopy had microsporidiosis, and the most commonly diagnosed species was Enterocytozoon bieneusi. Light microscopy failed to identify 12 cases of microsporidiosis and 2 cases of leishmaniasis. CONCLUSIONS: Electron microscopy contributes substantially to the identification of pathogens in HIV-positive patients. Light microscopy failed to identify one of every two pathogens diagnosed by electron microscopy.
The gastrointestinal tract is a rich source of mast cells with an enormous surface area that permits a high degree of interaction between the mast cell and intestinal luminal contents. The active metabolic products of the mast cell influence gastrointestinal secretion, absorption, and motility through paracrine effects of local mast cell degranulation and also cause systemic effects through the release of cellular products into the blood stream. Systemic mastocytosis influences physiologic function through the systemic effects of mast cell products released from focal (e.g., bone marrow) or wide spread increases in mast cell number. Local gastrointestinal proliferation of mast cells in response to recognized (e.g., gluten in celiac sprue) or obscure stimuli can alter gastrointestinal function and induce systemic symptoms. Celiac sprue, inflammatory bowel disease, and non-ulcer dyspepsia are three examples of gastrointestinal diseases in which mast cells can be implicated in the pathophysiology of the symptoms.
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