Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.108 (lactase)
 2,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was made of the morphofunctional status and local defence of the gastrointestinal tract in 122 children aged 4 months to 6 years, suffering from food intolerance showed up by atopic dermatitis in 52 children and by chronic diarrhea in 70 children. Based on the allergological anamnesis, scarification cutaneous tests with food allergens, detection of antibodies to food antigens (RAST, HAIT) food allergy was revealed in all the children. Chronic gastroduodenitis was identified in all the children suffering from atopic dermatitis and in 95% of the children with chronic diarrhea. It should be mentioned that one-third of that group had a graver illness--diffuse duodenitis with sub-atrophy of the villi. The allergic genesis of the impairment of the gastroduodenal mucosa was confirmed. It was more remarkable in atopic dermatitis (tissue eosinophilia and high content of IgE-plasmacytes in the duodenal mucosa). The decrease of local immune defence of the mucous membrane, lactase deficiency, elevated growth of microorganisms in the duodenal contents promote the rise of intestinal barrier permeability for food antigens and enhancement of sensitization.
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PMID:[Immunological aspects of food intolerance in children during first years of life]. 151 44

Cow's milk allergy in the first year of life is one of the most common problems faced by pediatricians. Both over and under diagnosis is seen. Cow's milk allergy, which is IgE-mediated should be differentiated from milk intolerance due to lactase deficiency or other causes. Cow's milk allergy may effect the gastrointestinal tract, respiratory tract, skin or blood. Anaphylaxis may occur. Diagnosis is made primarily on clinical grounds but skin tests and/or RAST are of value. Elimination and subsequent challenge confirms the diagnosis but challenge is not always necessary. Challenge should not be performed if there is evidence of anaphylaxis. Avoidance is the mainstay of treatment and breastfeeding is the optimal choice. Since antigenically intact cow's milk protein can pass into the breast milk, the mother should avoid excessive intake of milk products herself while breast feeding. Alternatives to breast milk such as soy formulas or hydrolysed casein or whey formulas may be used. Twenty-five percent of milk-sensitive infants are also allergic to soy protein. Hydrolysed casein formulas are more hypoallergenic but are expensive and less palatable. Hydrolysed whey formula, which is comparable in expense to soy formulas but is less allergenic, may prove of value in the management of the milk-allergic infant as well as for prophylaxis in infants from susceptible parents. Parents of infants born to families with bilateral atopic histories may be able to prevent milk allergy by using dietary manipulations which include decreased prenatal maternal milk intake and while breast feeding as well as careful avoidance of milk products in the infant's diet during the first year of life.
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PMID:Allergy to cow's milk in the first year of life and its prevention. 305 24

Food sensitivity or intolerance is not necessarily based on the Type I allergic reaction. Non-IgE antibody reactions, complement-dependent reactions, enzyme deficiencies such as lactase and non-immunologic histamine release (such as with some sea foods) have been described. Even the detection of specific antibodies on their own does not necessarily indicate that a given symptom is due to that antibody. Food allergy nevertheless exists. It is important that those observers fortunate enough to see many cases document their observations carefully and eventually publish them for the education of their less fortunate colleagues. Is food allergy more common in infants and young children? What happens as they grow older? How often is atopic eczema due to food allergy? Why are some foods more likely to be implicated than others? Does a negative RAST result eliminate the diagnosis or a positive one confirm it? Until the answers to these and other questions are known, the mainstay of diagnosis will be the history, and that of treatment will be the elimination diet.
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PMID:Non-IgE antibody mediated mechanisms in food allergy. 309 10

It has been reported that nutritional stress, such as short-term fasting and long-term energy restriction, has a suppressive effect on allergic dermatitis in experimental animals. Furthermore, clinical study has demonstrated a positive association between weight loss by low-energy diet and improvement in patients with atopic dermatitis. In this report, a 23-year-old female with atopic dermatitis received a treatment of repeated short-term fasting. 24-hour fasting was conducted once a week for a period of 20 weeks. On the fasting day, the amount of energy intake was 200 kcal. No medication was administered during the trial period. Clinical symptoms were evaluated using the Scoring Atopic Dermatitis index, and IgE, lactase dehydrogenase-5, and number of eosinophils were measured. At the end of the trial, body weight was reduced and clinical symptoms improved, whereas no improvements in laboratory findings were shown. For sufficient evidence of the effects of fasting, additional controlled study is needed.
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PMID:An adult with atopic dermatitis and repeated short-term fasting. 1451 13

Enzymes are high-molecular-weight proteins and highly sensitizing occupational allergens used widely in industrial processes. Lactase has been described to cause work-related respiratory and conjunctival immunoglobulin (Ig)-E-mediated sensitizations in workers in the pharmaceutical industry. In these previous reports, allergic rhinoconjunctivitis or asthma was confirmed with prick tests but not by challenge tests. Lactase previously has not been described as a cause of immediate or delayed contact skin reaction. Furthermore, there are no previous reports of lactase-specific IgE. We report a case of protein contact dermatitis and allergic rhinoconjunctivitis from occupational exposure to lactase in a pharmaceutical worker. The patient exhibited strong positive responses to lactase in prick tests. In an open application test, lactase elicited whealing, and in patch testing, lactase elicited an eczematous reaction. Serum lactase-specific IgE antibodies were demonstrated in immunospot and radioallergosorbent test assays, and lactase-IgE-binding fractions and their specificities were examined in immunoblot and immunoblot inhibition assays. The chamber challenge test was performed to detect the association between lactase sensitization and rhinoconjunctival symptoms. Our results have confirmed the previous observations that lactase can induce occupational IgE-mediated respiratory and conjunctival sensitizations, but they show that contact skin reactions caused by lactase may also occur.
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PMID:Lactase-induced occupational protein contact dermatitis and allergic rhinoconjunctivitis. 1762 46

The term "food allergy" is widely misused for all sorts of symptoms and diseases caused by food. Food allergy (FA) is an adverse reaction to food (food hypersensitivity) occurring in susceptible individuals, which is mediated by a classical immune mechanism specific for the food itself. The best established mechanism in FA is due to the presence of IgE antibodies against the offending food. Food intolerance (FI) are all non-immune-mediated adverse reactions to food. The subgroups of FI are enzymatic (e.g. lactose intolerance due to lactase deficiency), pharmacological (reactions against biogenic amines, histamine intolerance), and undefined food intolerance (e.g. against some food additives). The diagnosis of an IgE-mediated FA is made by a carefully taken case history, supported by the demonstration of an IgE sensitization either by skin prick tests or by in vitro tests, and confirmed by positive oral provocation. For scientific purposes the only accepted test for the confirmation of FA/FI is a properly performed double-blind, placebo-controlled food challenge (DBPCFC). A panel of recombinant allergens, produced as single allergenic molecules, may in future improve the diagnosis of IgE-mediated FA. Due to a lack of causal treatment possibilities, the elimination of the culprit "food allergen" from the diet is the only therapeutic option for patients with real food allergy.
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PMID:[Food allergy, food intolerance or functional disorder?]. 1934 Jul 68