Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sulfites are usually added to food, beverages and pharmaceuticals as preservative antioxidants, bleaching agents, and dough conditioning agents. Ingestion of foods containing sulfites can cause abdominal pain, diarrhoea, seizures and death. Sulfite can react with cellular components and can cause toxicity. Changes in mucosal disaccharidases and phosphatase alkaline after sodium metabisulfite administration were investigated in the small intestine of rats. Female Wistar rats were given a diet supplemented with 0.25 or 2.5% sodium metabisulfite for 5 weeks. Sucrase, maltase, lactase and alkaline phosphatase were assayed in intestinal homogenates and in brush border membrane fractions. The intake of only 2.5% sulfite induced an increase in the specific activities of sucrase, maltase, and alkaline phosphatase compared to control levels (P < 0.05). Lactase levels were affected in a variable manner. The origin of such altered enzyme activities is still unknown.
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PMID:Effect of sulfite intake on intestinal enzyme activity in rats. 795 44

The prevalence of lactose maldigestion is lowest in Scandinavia and Northwest Europe (3-8%) and close to 100% in most of Southeast Asia. In Europe the frequency increases in the southern and eastern directions, reaching 70% in southern Italy and Turkey. There is also a high prevalence of lactose maldigestion in the people of Africa with the exception of cattle-raising nomads. Lactose maldigestion causes uncharacteristic abdominal symptoms such as bloating, borborygmus, colic, flatulence, and diarrhea. The degree of discomfort depends on the amount of lactose consumed, but also on an individual sensitivity to lactose. The symptoms of irritable bowel syndrome (IBS) and lactose maldigestion are similar. Consequently, most investigations indicate an increased frequency of lactose maldigestion in patients suffering from IBS. Recurrent abdominal pain (RAP) in children corresponds to IBS in adults. Lactose maldigestion is a frequent cause of RAP in regions with a high prevalence of lactose maldigestion in early childhood. Diffuse small-intestinal damage in celiac disease or kwashiorkor leads to a proportional decrease of all disaccharidase activities, with the most pronounced being decrease of lactase. The consumption of milk may then cause abdominal discomfort and increased diarrhea. Several investigations have indicated an increased frequency of lactose maldigestion in patients with osteoporosis. A connection between lactose maldigestion and decreased absorption of calcium has not been proven, however. The increased tendency toward osteoporosis is more likely caused by a lower calcium intake because of milk intolerance. Milk and dairy products with reduced lactose content are better tolerated by patients with lactose maldigestion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The clinical significance of disaccharide maldigestion. 811 58

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.
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PMID:[The predictive value of antigliadin antibodies (AGA) in the diagnosis of non-celiac gastrointestinal disease in children]. 834 Dec 33

We examined the small intestinal histology disaccharidase activities as well as the incorporation of [3H]thymidine into DNA of biopsies maintained in organ culture from seven children (ages 9 months to 5 years) receiving total parenteral nutrition (TPN). Three children suffered from inflammatory bowel disease and received TPN for one month (short term). Four required long-term TPN (> 9 months) for short-bowel syndrome. DNA was extracted from the samples following serial precipitation with perchloric acid. Results were compared to those from 22 age-matched children investigated for abdominal pain or chronic diarrhea. Short-term TPN resulted in slightly lower lactase, sucrase, and palatinase activities that were not statistically different from controls. Long-term TPN resulted in focal mild villus atrophy and a decrease in disaccharidase activity in two patients. Biopsies from long-term TPN patients incorporated less thymidine compared to those of controls (P < 0.001) when data was expressed per total biopsy (3.6 +/- 1.1 vs. 8.4 +/- 1.1 fmol) or per milligram of tissue (1.0 +/- 0.12 vs 2.7 +/- 0.7 fmol). The above data are in general agreement with the hypoplastic effect of TPN in animals. However, in children, much longer periods of TPN are required to realize the changes.
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PMID:Small intestinal mucosa changes, including epithelial cell proliferative activity, of children receiving total parenteral nutrition (TPN). 835 71

Recurrent abdominal pain (RAP) syndrome is described by Apley 40 years ago. The definition of condition, still generally accepted, is at least three episodes of abdominal pain over a period of three months, with pain of intensity which affects the behaviour of the child. The prevalence of condition among school children is 10-15%. Apley's classic studies demonstrated organic disease in only 10% of the children. Apley's conclusions have dominated pediatric writing through present era. In recent years, however, a number of reports have appeared in the medical literature that have suggested that careful investigation of children with RAP may reveal previously unsuspected functional or morphologic abnormalities of the gastrointestinal tract. These have included reports of peptic disease and Helicobacter Pylori infection, abnormal antro-duodenal motility, lactase malabsorption, gastro-esophageal reflux. Nevertheless these abnormalities cannot be correlated always with specific complaints. Therefore pathogenetic background is not clarified. Despite greater understanding of these disorders the enigme remains. There is a need for controlled studies in non selected patients.
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PMID:[Abdominal pain syndrome recurring after 40 years: critical revision]. 868 27

Patients who met International Congress of Gastroenterology criteria for irritable bowel syndrome (IBS) and had breath hydrogen lactose testing were interviewed to determine whether detection of lactose maldigestion (LM) had an impact on their symptoms. Of 199 patients initially evaluated, 161 (81%) were contacted and asked to rate their symptoms. At baseline, 47 (29%) of the IBS group had LM. Before testing, 23 (49%) were aware that ingestion of lactose-containing food was associated with their gastrointestinal symptoms. Lactose-maldigesting IBS subjects (IBSLM, n = 47) and those who had IBS and no LM (n = 114) were similar in terms of age, sex, and ethnic background. Interviews performed 41 +/- 1.1 (SEM) months after baseline evaluation revealed no significant differences in abdominal pain, altered bowel habits, bloating/distension, mucus, and relief with defecation among those with IBS or LMIBS. Overall symptoms resolved, improved, did not change, or worsened in a manner not statistically different between IBS and IBSLM groups. IBSLM subjects (a) felt that identifying LM helped them gain awareness of food-symptom relationships (78.7%), (b) experienced some improvement in symptoms (83%), (c) were avoiding lactose foods (87.2%), or (d) used lactase enzyme supplements (38.3%). Identifying LM did not significantly affect rated variables.
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PMID:Does lactose maldigestion really play a role in the irritable bowel? 883 92

Lactose intolerance is widespread, with adult-type hypolactasia being the predominant cause of lactose malabsorption. Daily ingestion of less than 240 mL of milk is well tolerated by most lactose-intolerant adults. Some persons with normal lactase activity may become symptomatic on consumption of products containing lactose. Lactose maldigestion may coexist in adults with irritable bowel syndrome and in children with recurrent abdominal pain. Management consists primarily of dietary changes. People who avoid dairy products should receive calcium supplementation and should be advised to read ingredient labels carefully. Several lactase replacement products are available, but their efficacy varies.
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PMID:When to suspect lactose intolerance. Symptomatic, ethnic, and laboratory clues. 974 7

Lactose malabsorption and lactase deficiency are chronic organic pathologic conditions characterized by abdominal pain and distention, flatulence, and the passage of loose, watery stools. Though malabsorption of the sugar lactose is determinable by breath hydrogen test or jejunal biopsy, intolerance can only be confirmed by challenge with lactose-containing food, the response to which may not be immediate. The difficulty of making a positive diagnosis of these conditions has led to a proportion of lactose-intolerant patients being misdiagnosed with irritable bowel syndrome (IBS), which has a remarkably similar symptom complex and for which there is no current pathophysiologic marker. The incidence of the two disorders is approximately equal, but the actual proportion of patients with IBS incorrectly diagnosed in this way varies as a function of the methodology used. Once correct diagnosis is established, introduction of a lactose-free dietary regime relieves symptoms in most patients. Symptom similarity and the resultant incorrect diagnosis of IBS may explain the refractory nature of some patients labeled as IBS who remain largely unaware of the relationship between food intake and symptoms.
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PMID:Lactose intolerance: problems in diagnosis and treatment. 1019 5

Food intolerance is a reproducible adverse reaction to a specific food ingredient that is not psychologically based. Food allergy is a form of food intolerance in which there is evidence that the response is caused by an immunological reaction to food. Other mechanisms of food intolerance include enzyme defects (e.g. lactase deficiency), pharmacological effects (e.g. histamine), toxic properties (e.g. haemagglutinating lectins) and irritants (e.g. spices). Food allergy in children is a highly contentious subject and there is often a striking lack of published evidence from which to base clinical decisions. The true prevalence of food allergy in children is unknown, although there is evidence of an increasing incidence of allergic reactions to some foods, especially peanuts. Our understanding of why some children are unable to tolerate certain foods (e.g. cow's milk, egg), or how they grow out of this intolerance, is very poor. Symptoms of food allergy in children are diverse and include vomiting, poor weight gain, abdominal pain, malabsorption, cough, wheeze, rhinitis, atopic eczema, urticaria and angioedema. Despite the lack of objective data to support the notion that food intolerance contributes to behaviour in children, this is a belief firmly held by many parents and some professionals. The gold standard for diagnosing food intolerance is the double-blind placebo-controlled food challenge (DBPCFC). There is often a poor correlation between the results of food provocation tests and those of skin prick tests of radioallergosorbent tests for specific food antibodies. For proven food allergy, elimination diets are the mainstay of management. In children these must be closely supervised to avoid nutritional deficiency and compromise of growth. Some children who have had severe (anaphylactic) reactions after food need to have a supply of self-injectable adrenaline made available to their parents and teachers and must also practice strict avoidance of the offending food.
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PMID:Food allergy and food intolerance in childhood. 1113 67

Carbohydrates are hydrolyzed in the intestinal lumen by specific enzymes to monosaccharides before transport across the brush border membrane of epithelial cells into the cell interior. The enzymes implicated in the digestion of carbohydrates in the intestinal lumen are membrane-bound glycoproteins that are expressed at the apical domain of the enterocytes. Absent or reduced activity of one of these enzymes is the cause of disaccharide intolerance and malabsorption, the symptoms of which are abdominal pain, cramps or distention, flatulence, nausea and osmotic diarrhea. Lactose intolerance is the most common intestinal disorder that is associated with an absence or drastically reduced levels of an intestinal enzyme, in this case lactase-phlorizin hydrolase (LPH). The pattern of reduction of activity has been termed late onset of lactase deficiency or adult type hypolactasia. It was thought that the regulation of LPH was post-translational and was associated with altered structural features of the enzyme. Recent studies, however, suggest that the major mechanism of regulation of LPH is transcriptional. Other forms of lactose intolerance include the rare congenital lactase deficiency and secondary forms, such as those caused by mucosal injury, due to infectious gastroenteritis, celiac disease, parasitic infection, drug-induced enteritis and Crohn's disease. This review will shed light on important strucural and biosynthetic aspects of LPH, the role played by particular regions of the LPH protein in its transport, polarized sorting, and function, as well as on the gene expession and regulation of the activity of the enzyme.
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PMID:Molecular and cellular aspects and regulation of intestinal lactase-phlorizin hydrolase. 1133 11


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