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)

Anisakis simplex IgE may bring on allergic responses such as angioedema, vomiting, and urticaria from eating seafood, but it is not the only etiology. Induced cholinergic hyperreactivity or adrenergic blockade in the target tissue can cause these diseases nonimmunologically also. Here we studied the effects on normal intestinal motility of brief A. simplex infections and in vitro exposures to the parasite's extract (CE). Each approach was evaluated according to its ability to induce cholinergic hyperreactivity or adrenergic blockade in rat duodenum (RD), jejunum (RJ), and ileum (RI) in vitro. Additionally, bolus propulsion in RD, RJ, and RI was evaluated with time in vivo utilizing animals infected 4 h previously with A. simplex larvae (L3) vs sham animals. Tissues, after inoculation of 1, 5, 10, and 20 L3, exhibited time- and dose-dependent motility changes after carbachol (Ch) and noradrenaline (NA), justifying our using herein rats from the fourth hour of infection with 20 L3. We observed a persistent, yet differential effect of the infection on RD, RJ, and RI responses to Ch or NA. It caused cholinergic (muscarinic) hyperreactivity in RD only, and adrenergic blockade in all other parts, and consequently increased the transit index in RD, not in RJ or RI. In contrast, exposing RD, RJ, and RI to CE persistently increased both parameters, amplitude of twitches and muscular tone, in all, albeit that, here also, responses to Ch and NA were CE dose dependent. Interestingly, sensitivity to CE was in the order RI > RJ > RD, the reverse situation of that observed during active infection. Thus, previously viable A. simplex L3, after digestion, can exert bystander disturbance in autonomic control in the whole intestine. Our findings demonstrate that A. simplex L3, alive or dead, can induce cholinergic hyperactivity and adrenergic blockade in the whole small intestine and, as a consequence, gastrointestinal symptoms. Significantly, they may do so long before parasite-specific IgE is detectably induced or despite the occurrence of such IgE.
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PMID:Altered autonomic control in rat intestine due to both infection with Anisakis simplex and incubation with the parasite's crude extract. 1471 23

Malarial infection during pregnancy increases the risks of severe sequelae for the pregnant woman and the risk of delivering a low birthweight baby. The aim of this intervention study was to reduce significantly the prevalence of malaria parasitaemia in adolescent parturients in Matola and Boane in Mozambique. The study was focused upon the most malaria-vulnerable group, adolescent nulliparous and primiparous women. After completing the usual antenatal clinic and giving informed consent, 600 pregnant women were randomly chosen in a double blind manner to one of two regimens comparing the prevailing routine (placebo) for malaria prevention with a two dose regimen of sulphadoxine-pyrimethamine (SP). The first dose was given at enrollment with a second dose at the beginning of the third trimester. At delivery maternal and placental malaria parasitaemia as well as birthweight and gestational duration were analysed. At booking the prevalence of malaria parasitaemia was 35.3% in the placebo group and 30.6% in the SP group. At the second dose, the prevalence of malaria parasitaemia in the placebo group and SP group was 19.7% and 8.7%, respectively. This implies a relative risk (RR) of 2.24 with 95% CI (1.34, 3.75). The corresponding figures at delivery were 13.6% and 6.3% with an RR of 2.22 (1.07, 4.60) and in placenta 13.3% and 2.4% with an RR of 4.87 (1.58, 15.0). Newborns with malaria within 7 days were significantly more frequent in the placebo group, 6.4% and 0.7% respectively, with an RR of 6.55 (1.20, 35.7). Almost all (approximately 98%) of the women studied had Plasmodium falciparum, the remainder had P. malariae and P. ovale. The mean birthweight in the SP group was 3077 g and in the placebo group 2926 g. The estimated mean difference between the two groups was 151 g with 95% CI (51, 252). The mean placental weight in the placebo group was 596 and 645 g in the SP group, implying a difference of 49 g with a 95% CI (11, 88). The mean gestational duration was 6.1 days longer in the SP group, 95% CI (1.5, 10.6). In the placebo group there were two cases of urticaria and one case of nausea; in the SP group there was one case of vomiting. No newborn showed any sign of serious SP side-effect. Two doses of SP were enough to significantly reduce the prevalence of peripheral and placental malaria parasitaemia among young nulliparous and primiparous pregnant women in Matola and Boane.
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PMID:Impact of a double dose of sulphadoxine-pyrimethamine to reduce prevalence of pregnancy malaria in southern Mozambique. 1548 98

Atopic conditions include allergic rhinitis, atopic eczema, allergic conjunctivitis and asthma. Doctors and patients can choose from a variety of antiallergy medications, testifying that no one medication will suffice to treat all symptoms and that each has a different side-effect profile. Antiallergy medications target histamine receptors, as histamine release contributes to the unpleasant symptoms of itching, tearing, runny nose and skin urticaria. The ideal antihistamine would control the symptoms of atopic disease but cause very few side effects. Traditionally, unwanted effects include drowsiness and somnolence due to CNS depression, and digestive tract problems such as loss of appetite, nausea, vomiting and constipation or diarrhea. Some antihistamines also have anticholinergic effects that are mediated by muscarinic receptors. These atropine-like actions, which can affect the cardiovascular system, are sufficiently prominent in some drugs to be manifest during clinical usage. Epinastine hydrochloride minimally penetrates the blood/brain barrier and has almost no effect on the muscarinic receptors. This drug is marketed as having very few CNS-depressant side effects, few drug interactions and gastrointestinal side effects, and a low risk of cardiotoxicity.
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PMID:Epinastine hydrochloride for atopic disease. 1551 Feb 39

The only venomous reptile that naturally occurs in Poland is the adder or common viper (Vipera berus). Its bites are not of great epidemiological importance, but in some cases serious life-threatening symptoms may appear. The most common symptoms of adder envenomation are: local edema, reddening and pain of the bitten site and also the general symptoms coming from the alimentary tract (vomiting, diarrhoea, abdominal pain), the circulatory system (hypotension, shock, ECG abnormalities), the central nervous system (sleepiness, vertigo, disorientation, loss of consciousness), hematological symptoms (leukocytosis, hemolysis, coagulopathy) and allergic symptoms (fever, urticaria, angio-oedema). In the present study we described the case of a twenty-year-old patient hospitalized at the Toxicology Department of the Collegium Medicum UJ after a viper bite. Except for some above-mentioned symptoms he also developed ocular symptoms like ptosis and blurred vision. Such symptoms after the common viper bite have not been described in the literature till now. The cause of them seems to be an intense allergic reaction in the region of the orbit and eyelids all the more so because the patient had the positive allergy history. However, taking into account the latest reports from the literature, a neurotoxic action of some components of the Vipera berus venom may also play a role. Because of the developing general symptoms a specific equine antivenom was administered to the patient, apart from the supportive care, without any serious side effects that usually are observed after the use of such a kind of sera. It is thought that the sheep antivenom is better than the equine one considering a lack of allergic side effects. As a result of applied treatment the local and general symptoms including ocular symptoms subsided.
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PMID:[Envenoming by common viper (Vipera berus)--subject still exists...]. 1552 21

Foods that account for 90% of allergic reactions in children are cow's milk protein, eggs, peanut, soy, tree nuts, fish, and wheat. Food allergy can manifest as urticaria/angioedema, anaphylaxis, atopic dermatitis, respiratory symptoms, or a gastrointestinal (GI) disorder. GI allergic manifestations can be classified as immunoglobulin E (IgE) mediated (immediate GI hypersensitivity and oral allergy syndrome); "mixed" GI allergy syndromes (involving some IgE components and some non-IgE or T-cell-mediated components) include eosinophilic esophagitis and eosinophilic gastroenteritis. Non-IgE-mediated or T-cell-mediated allergic GI disorders include dietary protein enteropathy, protein-induced enterocolitis, and proctitis. All these conditions share a common denominator: the response of the immune system to a specific protein leading to pathologic inflammatory changes in the GI tract. This immunological response can elicit symptoms such as diarrhea, vomiting, dysphagia, constipation, or GI blood loss, symptoms consistent with a GI disorder. The detection of food allergies can be accomplished by the use of radioallergosorbent (RAST) testing and skin prick tests in helping to assess the IgE-mediated disorders. Patch tests may help evaluate delayed hypersensitivity reactions. Treatment of GI allergic disorders ranges from strict dietary elimination of offending food(s), use of protein hydrolysates, and use of L-amino acid-based formula when protein hydrolysates fail. Treatment with topical (for eosinophilic esophagitis) or systemic steroids is used if all dietary measures are unsuccessful. Maternal breast feeding or the use from birth of hydrolysate formulas (extensive or partial hydrolysates) may be efficacious in the prevention of atopic disease in "high-risk" families (with at least 1 parent or sibling with a history of atopic disease).
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PMID:Gastrointestinal manifestations of food allergies in pediatric patients. 1620 93

Reactions after bee or wasp sting are similar to anaphylaxis. Symptoms such as weakness, fatigue, vomiting, diarrhea, urticaria, and hypotension may occur. Serious toxic reactions usually occur after numerous stings. Massive bee envenomations can result in immediate onset of shock, hemolysis, rhabdomyolysis, disseminated intravascular coagulation (DIC), coma, and renal failure. In milder cases, patients may only have isolated prolonged activated partial thromboplastin time (aPTT) and normal prothrombin time (PT), clinically without a tendency to bleed. As a rule, they recover spontaneously without any complication. We report three cases of wasp stings; they all manifested prolongation of aPTT and finally recovered completely. Isolated prolongation of aPTT in cases of wasp stings may be related to an extract from the venom inhibiting the coagulation pathway.
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PMID:Isolated prolongation of activated partial thromboplastin time following wasp sting. 1623 65

While 6% of children under three years of age suffer from a food allergy, the figure for adults varies between 1.5 and 3%. Leading allergens in foodstuffs are glycoproteins having a molecular weight of between 10,000 and 60,000. The symptoms of an immediate type nutrient allergy mediated by IgE usually manifest within a matter of a few minutes to two hours after ingestion of the offending nutrient and take the form, for example, of tingling and itching, tissue swelling in the mouth, hoarseness, asthma, gastrointestinal complaints or acute urticaria; in severe cases anaphylactic shock may even occur. In contrast, no IgE antibodies are to be found in nutrient-induced enterocolitis, which is associated with diarrhea and vomiting occurring after a delay of one to six hours. Differential diagnostic considerations must include intolerance for certain foodstuffs, such as lactose intolerance, or pseudoallergic reactions.
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PMID:[Food allergies are often an unrecognized cause of clinical complaints]. 1630 89

Allergy is caused by an immune reaction that is out of all proportion to the antigenic stimuli. Classical allergy is a type I hypersensitivity reaction mediated by the interaction of mast cells (and eosinophils) coated with allergen-specific IgE and a cross-linking allergen. The physiological outcome is inflammation commonly displayed by urticaria, rhinitis, vomiting and diarrhoea, depending on the route of allergen entry. In extreme reactions anaphylactic shock can result that may lead to death. Chronic allergic responses most commonly present themselves as asthma and eczema. All these symptoms are the consequence of an imbalanced immune system making an unsuitable response to an environmental or food antigen. On bacterial colonisation of the colon after birth the appropriate microbiological stimuli is essential to redress the balance of the skewed T-helper 2 immune response present in the newborn. This normal interaction between baby and microbes is thought to be compromised in the Western world, with a reduction in bifidobacteria and an increase in clostridial species, particularly in bottle-fed infants. The use of probiotic therapy to prevent allergic disease has been demonstrated in two studies using a probiotic Lactobacillus rhamnosus GG in neonates. A long-term reduction in allergy has been shown in the test group, with lactobacillus reducing the incidence of atopic eczema. Management of allergy through probiotics has also been demonstrated in infants, using lactobacilli to control atopic eczema and cow's milk allergy. Unfortunately, these positive results have not been repeated in studies with older children and young adults.
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PMID:Probiotics and allergy. 1631 88

Cow milk protein intolerance (CMPI) affects 3% of infants under the age of 12 months and is often misdiagnosed as GERD or colic, risking dangerous exposure to antigens. Most infants out grow CMPI by 12 months; however, those with IgE-mediated reactions usually continue to be intolerant to cow's milk proteins and also develop other allergens including environmental allergens that cause asthmatic symptoms. Clinical manifestations of CMPI include diarrhea, bloody stools, vomiting, feeding refusal, eczema, atopic dermatitis, urticaria, angioedema, allergic rhinitis, coughing, wheezing, failure to thrive, and anaphylaxis. The research and literature showed that CMPI is easily missed in the primary care setting and needs to be considered as a cause of infant distress and clinical symptoms. This article focuses on correctly diagnosing CMPI and managing it in the primary care setting.
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PMID:The diagnosis and management of cow milk protein intolerance in the primary care setting. 1641 42

Adverse reactions to foods are frequent in everyday life. They are divided into toxic and immunologic food reactions. The awareness of toxic food reactions among adverse reactions to food is essential for correct diagnosis. Enzymatic food intolerance, adverse reactions to food or food additives, pharmacologic food intolerance, psychosomatic factors, food allergy with classic symptoms (anaphylaxis, urticaria-angioedema), atopic dermatitis, contact dermatitis (protein), upper and lower respiratory symptoms like rhinitis or asthma, and gastrointestinal disorders (oral allergy syndrome, colic, nausea, vomiting, diarrhea, abdominal pain) are discussed. Target organs throughout the body-ear, eye, pharynx, skin, lung, joints, and muscles-can be involved. The gold standard in diagnosis is a double-blind, placebo-controlled food challenge test. The diagnostic tools available for most food-related disorders are the skin-prick test and radioallergosorbent test. The treatment of food-induced urticaria consists of elimination of the offending food or substance from the diet, use of antihistamines, and immunotherapy.
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PMID:Adverse reactions to food and clinical expressions of food allergy. 1668 80


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