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)

A 10-year-old boy with severe familial lactose intolerance in infancy (vomiting, failure to thrive, lactosuria (5.25 g/l), sucrosuria (12 g/l), and aminoaciduria. Intestinal disaccharidases (including lactase and sucrase) normal at age 6 and 20 weeks. Oral lactose tolerance test at this age resulted in lactosuria (4.6 g/l); sucrose tolerance test, in sucrosuria (18.5 g/l). In contrast, intraduodenal lactose tolerance test gave only low lactose excretion in urine (0.28 g/l). He improved rapidly and had no lactosuria on intraduodenal feeding with citric acid milk. The lactosuria diminished as age increased, but was still higher at age 6 years than that of controls. He tolerated normal disaccharide containing food after 1.5 years of age. At 5.5 to 6 years, he had symptoms of lactose malabsorption, and an isolated lactase deficiency was proved. At 10 years, he still tolerates only limited amounts of milk. The defect in severe familial infantile lactose intolerance seems to be localized in the gastric mucosa. Acquired lactase deficiency can appear later in childhood in this syndrome.
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PMID:A boy with severe infantile gastrogen lactose intolerance and acquired lactase deficiency. 52 43

Diarrhea is one of the most common causes of morbidity and mortality in infants and children less than 5 years old in developing countries. Diarrheal diseases are a major cause of childhood malnutrition. Toxin-producing bacteria are responsible for many acute diarrheas. Oral rehydration solution (ORS) treats dehydration caused by acute diarrheal episodes. WHO promotes the use of a single oral rehydration formula which contains 3.5 g sodium chloride, 2.5 g sodium bicarbonate or 2.9 g trisodium citrate dihydrate, 1.5 g potassium chloride, and 20 g glucose to 1 liter of water. This ORS formula can safely be used for all age groups and all etiologies of diarrhea. ORS replaces the lost fluid and electrolytes and maintains fluid and electrolytes. Pediatricians in most developed countries do not accept this ORS formula in cases of rotavirus-caused diarrhea because rotavirus blunts some absorptive villi and reduces the activity of lactase and other disaccharidase, resulting in reduced absorption. Yet, the unaffected villus cells may absorb enough water and electrolytes to be effective. In cases of vomiting, ORS should be administered in small amounts and slowly. Some health workers are concerned that 90 mmol/l sodium in the WHO formula causes hypernatremia in neonates and young infants who have low sodium levels in their stools. Specialists suggest ORS with 30-60 mmol/l or additional water administered in a 2:1 ratio for these young infants. Hypernatremia is also a concern for malnourished children, but studies show that WHO's ORS is safe and effective in treating malnourished children. Bottle fed children are more vulnerable to hypernatremia than breast fed children. Hypernatremia has neurological effects. Hyponatremia is more common in developing countries than developed countries. It also has neurological effects. In severe dehydration cases, intravenous fluid or ORS delivered via a nasogastric tube should be given immediately.
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PMID:Usefulness of ORT in certain special situations of diarrhoeal diseases. 783 95

Among 228 relatives of 101 gluten-sensitive patients, 13 anti-endomysium antibody (EmA) positive persons (7 children and 6 adults) were identified. In 12/13 cases jejunal biopsy confirmed severe villous atrophy consistent with celiac disease. In the single EmA positive sibling without villous atrophy the histology is thought to be influenced by a steroid treatment because of pulmonary disease. By routine EmA-testing 12 unexpected EmA positive patients were found out of 756 children with complaints and laboratory results otherwise not justifying jejunal biopsy at the first evaluation. Their initial diagnoses were: proteinuria, colitis, Crohn's disease, rickets, recurrent vomiting, resolved postinfectious lactase deficiency, "previously excluded" celiac disease. Severe villous atrophy could be demonstrated in all EmA positive patients subsequently. In further 204 EmA negative children the biopsy showed no atrophy. EmA positivity may reveal clinically not apparent severe villous atrophy emphasizing the role of a new non invasive and highly specific serological screening method for celiac disease.
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PMID:[New cases of celiac disease detected by anti-endomysial antibody test in families of gluten-sensitive patients and among children examined for non-specific gastrointestinal complaints]. 841 43

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

Although the American Academy of Pediatrics and the American Academy of Family Physicians recommend breast milk for optimal infant nutrition, many parents still choose formula as an acceptable alternative. The wide variety of available formulas is confusing to parents and physicians, but formulas can be classified according to three basic criteria: caloric density, carbohydrate source, and protein composition. Most infants require a term formula with iron. There is insufficient evidence to recommend supplementation with docosahexaenoic acid or arachidonic acid. Soy formulas are indicated for congenital lactase deficiency and galactosemia, but are not recommended for colic because of insufficient evidence of benefit. Hypoallergenic formulas with extensively hydrolyzed protein are effective for the treatment of milk protein allergy and the prevention of atopic disease in high-risk infants. Antireflux formulas decrease emesis and regurgitation, but have not been shown to affect growth or development. Most infants with reflux require no treatment. Family physicians can use these guidelines to counsel parents about infant formula, countering consumer advertising that is not evidence-based.
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PMID:Infant formula. 2038 68

Lactose malabsorption and milk products intolerance symptoms are the most common alimentary tract disorders. Lactose intolerance is a result of lactase deficiency or lack of lactase and lactose malabsorption. Three types of lactase deficiency were distinguished: congenital, late-onset lactase deficiency and secondary lactase deficiency. Lactose intolerance means the appearance of clinical gastrointestinal symptoms after ingestion of lactose. To the clinical symptoms of lactose intolerance belongs: nausea, vomiting, abdominal distension, cramps, flatulence, flatus, diarrhea and abdominal pain. The diagnosis of lactose intolerance is based on the breath hydrogen test and analysis of lactase activity in the small intestine mucosa. Dietary treatment eliminates clinical symptoms.
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PMID:[Lactose intolerance: pathophysiology, clinical symptoms, diagnosis and treatment]. 1938 23

Various positively selected adaptations to new nutrients have been identified. Lactase persistence is among the best known, conferring the ability for drinking milk at post weaning age. An augmented number of amylase gene (AMY1) copies, giving rise to higher salivary amylase activity, has been implicated in the consumption of starch-rich foods. Higher AMY1 copy numbers have been demonstrated in populations with recent histories of starchy-rich diets. It is however questionable whether the resulting polymorphisms have exerted positive selection only by providing easily available sources of macro and micronutrients. Humans have explored new environments more than any other animal. Novel environments challenge the host, but especially its immune system with new climatic conditions, food and especially pathogens. With the advent of the agricultural revolution and the concurrent domestication of cattle came new pathogens. We contend that specific new food ingredients (e.g., gluten) and novel pathogens drove selection for lactase persistence and higher AMY gene copy numbers. Both adaptations provide ample glucose for activating the sodium glucose-dependent co-transporter 1 (SGLT1), which is the principal glucose, sodium and water transporter in the gastro-intestinal tract. Their rapid uptake confers protection against potentially lethal dehydration, hyponatremia and ultimately multiple organ failure. Oral rehydration therapy aims at SGLT1 activity and is the current treatment of choice for chronic diarrhoea and vomiting. We hypothesize that lifelong lactase activity and rapid starch digestion should be looked at as the evolutionary covalent of oral rehydration therapy.
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PMID:Lactase persistence and augmented salivary alpha-amylase gene copy numbers might have been selected by the combined toxic effects of gluten and (food born) pathogens. 2447 65