Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously reported impressive results in using a gonadotropin-releasing hormone analog, leuprolide acetate (Lupron), in the treatment of moderate to severe symptoms (especially abdominal pain and nausea) in patients with functional bowel disease (FBD). Pain is the hallmark of patients with FBD, and there is no consistent therapy for the treatment of these patients. The purpose of the present study was to expand the investigation to study similar patients (menstruating females) in a multicenter, double-blind, placebo-controlled, randomized study using Lupron Depot (which delivers a continuous dose of drug for one month), 3.75 mg (N = 32) or 7.5 mg (N = 33), or placebo (N = 35) given intramuscularly every four weeks for 16 weeks. Symptoms were assessed using daily diary cards to record abdominal pain, nausea, vomiting, early satiety, anorexia, bloating, and altered bowel habits. Additional assessment tools were quality of life questionnaires, psychological profile, oral-to-cecal transit using the hydrogen breath test, antroduodenal manometry, reproductive hormone levels, and global evaluations by both patient and investigator. Patients in both Lupron Depot-treated groups showed consistent improvement in symptoms; however, only the Lupron Depot 7.5 mg group showed a significant improvement for abdominal pain and nausea compared to placebo (P < 0.001). Patient quality of life assessments and global evaluations completed by both patient and investigators were highly significant compared to placebo (P < 0.001). All reproductive hormone levels significantly decreased for both Lupron Depot-treated groups by week 4 and were significantly different compared to placebo at week 16 (P < 0.001). This study shows that leuprolide acetate is effective in controlling the debilitating symptoms of abdominal pain and nausea in patients with FBD.
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PMID:Effect of leuprolide acetate in treatment of abdominal pain and nausea in premenopausal women with functional bowel disease: a double-blind, placebo-controlled, randomized study. 963 30

We report herein the case of a 70-year-old woman with enteropathy accompanied by protein loss, the cause of which was found to be thrombophlebitis of the mesenteric vein. The patient was admitted to our hospital for investigations to determine the cause of hypoproteinemia. She had suffered an episode of left abdominal pain with high fever and vomiting lasting 10 days, 8 months prior to her admission. She also had a 6-year history of uncontrolled diabetes. The alpha1-antitrypsin clearance was 85.7 ml/day, suggesting protein-losing enteropathy. A scintigraphy with 99m-technetium-human serum albumin disclosed protein leakage into the intestine. X-Rays and computed tomography showed a stenotic and thickened area of small intestine 50 cm in length. Thus, a laparotomy was performed to resect this part of the intestine which was found to have undergone past thrombophlebitic changes. Following the operation, the alpha1-antitrypsin clearance decreased to within the normal range and the patient gained 5 kg in weight.
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PMID:Protein-losing enteropathy due to thrombophlebitis of the mesenteric vein: report of a case. 974 3

Bone marrow transplantation is often associated with multiple organ failure which is usually reversible. Oral mucositis and dysphagia, vomiting, diarrhoea, protein losing enteropathy, transient exocrine pancreatic impairment, hypoalbuminaemia, biochemical trace element and mineral deficiencies are all common following transplantation and have profound nutritional consequences. Malnutrition affects negatively the clinical outcome. Nutritional support is provided to malnourished patients and those who suffer deterioration in nutritional status despite the provision of dietetic counselling. Only a few randomised studies comparing enteral with parenteral nutrition after transplant exist. Both enteral tube feeding (in the absence of mucositis) and parenteral nutrition are effective in maintaining nutritional status. However, enteral nutrition is associated with a better nutritional response and fewer complications than parenteral. With existing enteral and parenteral nutrition regimens close monitoring of trace element and mineral status is required.
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PMID:Nutritional considerations in children undergoing bone marrow transplantation. 988 80

Coeliac disease is a gluten-sensitive enteropathy which results in a permanent malabsorption of nutrients in that portion of the small intestine (the jejunum) that is damaged. A genetic, inheritable disease, it is directly related to ingestion of certain wheat proteins especially found in rye secalins, barley hordeins and, in a much lower amount, oat avenins. A fundamental role in the pathological response is played by grain prolamins (gliadins). The actual damage to intestinal mucosa is almost certainly mediated by the immune system but its mechanism has not been so far clarified. Coeliac disease incidence rate is ever increasing among children and adolescents and it is rather frequently reported as relapsing in the third and fourth decade. The most distressing problems of malabsorption syndrome are diarrhea, weight loss, meteorism, abdominal pain, vomiting and asthenia; nonetheless, not all patients report symptoms. Both diagnosis and differential diagnosis--intestinal lymphoma, refractory sprue--prove difficult: a diagnosis of gluten intolerance can be made through careful consideration of a series of laboratory findings which are being improved by researchers in order to avoid delays for patients with probable gluten-sensitive enteropathy with non-specific symptoms. Although there may be many clinical signs and laboratory tests indicating probable malabsorption, the likely gold standard of diagnosing coeliac disease remains to be the jejunal biopsy.
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PMID:[Celiac disease. Recent findings on its pathogenesis, diagnosis and clinical presentation]. 1019 64

We report the case of a patient with carbohydrate-deficient glycoprotein syndrome type Ib who developed normally until 3 months of age, when she was referred to the hospital for evaluation of hypoglycemia that was found to be related to hyperinsulinism. She also had vomiting episodes, hepatomegaly, and intractable diarrhea, which evoked the diagnosis of carbohydrate-deficient glycoprotein syndrome. Oral mannose treatment at a dose of 0.17 g/kg body weight 6 times/d was followed by a clinical improvement and normalization of blood glucose, aminotransferases, and coagulation factor levels. Hyperinsulinemic hypoglycemia should be considered as a leading sign of carbohydrate-deficient glycoprotein syndrome type Ib, especially when it is associated with enteropathy and abnormal liver tests.
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PMID:Hyperinsulinemic hypoglycemia as a presenting sign in phosphomannose isomerase deficiency: A new manifestation of carbohydrate-deficient glycoprotein syndrome treatable with mannose. 1048 8

A syndrome of chronic diarrhea, vomiting, and failure to thrive was described 35 years ago. The syndrome was caused by damage in the jejunum after ingestion of cow's milk. Symptoms appeared in young infants shortly after introduction of cow's milk formula. Patients had moderate steatorrhea, decreased absorption of D-xylose, and, often, iron-deficiency anemia and hypoproteinemia. They had strong IgA and IgG antibodies to cow's milk. IgE antibodies to cow's milk were negative, as a rule. Indicators of cell-mediated immune reaction to cow's milk proteins were often positive. Patients were tolerant to cow's milk by the age of 3 years. Malabsorption was due to damage to the jejunal mucosa: Varying villus atrophy was associated with inflammation in surface epithelium and lamina propria. The epithelial cell renewal rate increased. Surface epithelial cells decreased in height, with short, furry microvilli and large aggregates of lysozymes. The number of intraepithelial lymphocytes was markedly increased, but normalized during cow's milk elimination. Most of these lymphocytes had alpha/beta T-cell receptors, and many were cytotoxic. Some specimens had an increase in gamma/delta T-cell receptor-bearing cells. In the lamina propria, CD4+ cells predominated, and some of them were activated. IgA- and IgM-containing cells were markedly increased during cow's milk exposure, but IgE cells were not abnormal. The density of eosinophils was moderately increased. Secretion of interferon-gamma by cells isolated from patients' intestines was markedly increased. Morphologic and immunologic findings suggest that T-cell-mediated reaction to proteins in cow's milk is present in the small intestines of patients with this syndrome and causes this enteropathy.
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PMID:Food-induced malabsorption syndromes. 1063 1

There have frequently been doubts as to the relevance of food allergy, in particular as far as the involvement of the intestinal tract is concerned. Several studies, however, have confirmed the existence of allergic reactions in the gut, with an estimated prevalence of about 1-2% in adults. Clinical symptoms are unspecific and include nausea, vomiting, abdominal pain, cramping and diarrhea. Intestinal mast cells, as well as intestinal eosinophils, have been shown to be involved in the pathogenesis of food-allergy-related enteropathy. In addition to classical IgE-dependent degranulation, further agonists have been demonstrated for mast cell activation, for example IL-4. The methods used to confirm the diagnosis of intestinal allergy are still insufficient. Until now, blinded oral challenge procedures with food antigens have been accepted as the 'gold standard' in diagnosing food allergy, although these tests have practical problems. Therefore, new test systems have been developed, such as endoscopic provocation tests, that may improve diagnostic procedures. Elimination diet still presents the main basis of therapy. Aspects to be focused on in the future are the role fo IgE-independent allergic mechanisms in intestinal allergy, the impact of cross-reactivity with other allergens and the relationship to other inflammatory bowel diseases such as Crohn's disease, ulcerative colitis, celiac disease and irritable bowel syndrome.
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PMID:Allergy and the gut. 1082 17

Dietary protein enterocolitis generally presents in the 1st year of life with diarrhea, emesis, and irritability. When there is a delay in diagnosis, persistent exposure to the offending dietary antigen leads to increasing enteric inflammation manifesting as bloody diarrhea, anemia, dehydration, and failure to sustain normal patterns of weight gain and growth. The extent of enteric inflammation may be limited to mild proctitis, pancolitis, or true enterocolitis with esophagitis, gastritis, enteropathy, and colitis. The offending antigen is usually cow's milk protein or soy protein. A significant number of the infants are exclusively breast fed, especially those with proctitis. In older children, a wide variety of dietary proteins have been implicated. The inconsistency between allergists and gastroenterologists in the clinical definition of the syndrome remains a significant problem. To the allergist, the definition is based on clinical criteria, allergy testing, and response to double-blind food challenge, whereas to the gastroenterologist, it is defined by histologic criteria and the response of clinical and histologic manifestations to elimination diets. To further complicate the issue, European studies have emphasized the alterations in enteric permeability noted in both enteropathy and enterocolitis. In an effort to establish a unified approach, the International Life Sciences Institute sponsored a workshop in late 1998, which resulted in a document entitled "Classification of Gastrointestinal Disease of Infants and Children Due to Adverse Immunologic Reactions."
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PMID:Dietary protein enterocolitis. 1189 89

We report the clinical and laboratory features of a 19-year-old man with findings of both eosinophilic gastroenteritis and gluten-sensitive enteropathy. Before the onset of clinical symptoms, the patient had received a series of hepatitis B vaccinations but had not developed a measurable antibody response or any allergic reaction. Radioallergosorbent test results were positive to several foods, and the total serum immunoglobulin E (IgE) level was elevated. Adherence to a gluten-free diet caused a normalization in the endomysial antibody titer; however, the total serum IgE level continued to increase, and the total eosinophil count remained elevated. Symptoms of recurrent vomiting and abdominal pain necessitated prednisone burst therapy. The simultaneous occurrence of eosinophilic gastroenteritis and gluten-sensitive enteropathy is rare; therapy should be directed to each disorder individually.
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PMID:Eosinophilic gastroenteritis and gluten-sensitive enteropathy in the same patient. 1196 68

In adults untreated coeliac disease (CD) is associated with a wide variety of malignant complications. The overall mortality in CD is approximately twice that of the general population. The excess deaths are due mainly to intestinal lymphoma. In Europe, only 26 cases of CD and cancer in children have been published. There is evidence that cancer and CD in children are underreported. We report a case of Wilms tumour in a child who developed CD. As a neonate the boy had been successfully operated for congenital mesoblastic nephroma. Gluten was introduced in his diet at age of 12 months. He developed vomiting, abdominal distention ad hypertransaminosaemia. Up to the age of 16 months he had lost 1500 g and coeliac crisis was diagnosed (IgAEMA titre 1:50 and in the duodenal biopsy specimen there was crypt hyperplastic total villous atrophy). Symptoms improved rapidly when gluten-free diet was initiated, and 4 years later, clinical and serological findings were normal. Wilms tumour accounts for 6% to 7% of all childhood malignancies. There are no reports in MEDLINE about coeliac disease in patients who have been operated for the tumour. This seemed intriguing because prevalence of gluten-sensitive enteropathy calculated for Europe varies between 1/100 and 1/300.
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PMID:[Cancer in children with celiac disease. Gluten-sensitive enteropathy in a boy operated for Wilms tumour]. 1263 77


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