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)

Histamine poisoning results from the consumption of foods, typically certain types of fish and cheeses, that contain unusually high levels of histamine. Spoiled fish of the families, Scombridae and Scomberesocidae (e.g. tuna, mackerel, bonito), are commonly implicated in incidents of histamine poisoning, which leads to the common usage of the term, "scombroid fish poisoning", to describe this illness. However, certain non-scombroid fish, most notably mahi-mahi, bluefish, and sardines, when spoiled are also commonly implicated in histamine poisoning. Also, on rare occasions, cheeses especially Swiss cheese, can be implicated in histamine poisoning. The symptoms of histamine poisoning generally resemble the symptoms encountered with IgE-mediated food allergies. The symptoms include nausea, vomiting, diarrhea, an oral burning sensation or peppery taste, hives, itching, red rash, and hypotension. The onset of the symptoms usually occurs within a few minutes after ingestion of the implicated food, and the duration of symptoms ranges from a few hours to 24 h. Antihistamines can be used effectively to treat this intoxication. Histamine is formed in foods by certain bacteria that are able to decarboxylate the amino acid, histidine. However, foods containing unusually high levels of histamine may not appear to be outwardly spoiled. Foods with histamine concentrations exceeding 50 mg per 100 g of food are generally considered to be hazardous. Histamine formation in fish can be prevented by proper handling and refrigerated storage while the control of histamine formation in cheese seems dependent on insuring that histamine-producing bacteria are not present in significant numbers in the raw milk.
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PMID:Histamine poisoning (scombroid fish poisoning): an allergy-like intoxication. 268 58

We assessed the relationships of clinical symptoms and serum antibody levels during follow-up of 47 patients, aged 3 to 66 months, who were shown by formal milk challenge to have cow milk allergy. Three groups of patients were identified. Group 1 patients (n = 15) were sensitized to IgE and responded rapidly to small volumes of milk with urticaria, an exacerbation of eczema, wheeze, or vomiting. In the second group (n = 24), symptoms of milk enteropathy (vomiting and diarrhea) developed between 1 and 20 hours after milk ingestion. In the group 3 patients (n = 8), coughing, diarrhea, eczematoid rashes, or a combination of these developed more than 20 hours after normal volumes of milk were given. Serum levels of IgG, IgA, IgM, and IgE and of milk-specific anti-cow milk antibodies of these isotypes were measured initially and then at a median follow-up time of 16 months (range 6 to 39 months). In this investigation, changes in these immunologic measures during the study period were related to whether or not clinical tolerance to cow milk was achieved. At follow-up, six patients from group 1, ten from group 2, and two from group 3 were milk tolerant. No consistent change in any of the immunologic measurements was associated with remission of the disease. These findings raise the question of whether acquisition of clinical tolerance to cow milk in cow milk allergy can be attributed solely to immunologic events.
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PMID:Recovery from milk allergy in early childhood: antibody studies. 271 89

We present a case of hypersensitivity to kiwi in a 26 year-old patient with no previous atopic history. The first reaction episode occurred a few minutes after kiwi ingestion, presenting with a localized pruritic reaction. This symptomatology repeated itself a few months later, again immediately after eating kiwi and was accompanied by dysphagia, vomiting and urticaria. In the complementary laboratory analyses a total IgE of 187 IU/ml was appreciated. The skin test to inhalant and food antigens were negative, while the kiwi extract produced a + + + + reaction. The histamine release test was positive (20%). Specific IgE levels (Kallestad) demonstrated results of 0.35 AEU/ml (class I). Specific IgG4 levels were normal and the hemagglutination test was negative. With the above results, we concluded that we were dealing with a case of monosensitivity to kiwi which was probably IgE mediated.
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PMID:A rare case of food allergy: monosensitivity to kiwi (Actinidia chinensis). 281 64

Angioedema is characterized by a well-demarcated swelling on the skin, oropharyngolaryngeal tissue, or the gastrointestinal wall. Underlying mechanisms may include IgE-mediated reactions, complement activation, inhibition of the cyclo-oxygenase pathway of arachidonic acid metabolism, direct release of mediators from mast cells, and activation of the kinin-forming system. Foods, drugs, inhalants, insect bites, blood transfusion, collagen vascular disease, infections, physical factors, neoplasms, and hereditary factors can cause angioedema through one or more of these mechanisms. Chronic angioedema lasts more than 6 weeks or recurs during this period. Acute angioedema is a self-limited disorder and resolves spontaneously, or with simple therapy, in several days; the patient rarely requires a complete work-up. Chronic angioedema may necessitate a detailed history, physical examination, and limited clinical or laboratory tests to exclude serious underlying illnesses. The H1 antihistamines are used for the treatment of both acute and chronic angioedema. An H2 antihistamine, a second H1 antihistamine, or rarely even a low dose of corticosteroid may be added to the regimen if H1 antihistamine alone fails to control chronic angioedema. Hereditary angioedema is an autosomal dominant disease that is caused by C1INH deficiency. In patients with this disorder, swelling of the lip, pharynx, and extremities may follow trauma to soft tissue. Other clinical manifestations include abdominal pain, nausea, vomiting, and suffocation because of laryngeal swelling. Diagnosis can be confirmed by the finding of low levels of C4 and C2 and the absence of nonfunction of C1INH. Androgens reverse the biochemical defects.
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PMID:Angioedema. 286 18

This investigation studied 487 babies for symptoms of allergic disease during their first year of life. Because of their positive family histories all the babies are at high risk of becoming allergic. The babies were randomly divided such that cows' milk was deliberately withheld from one group; infants in this group were fed with a soya substitute where required. No benefit resulted from withholding cows' milk, indeed symptoms were more usually associated with this group. Breast feeding, even for a short period, was clearly associated with a lower incidence of wheeze, prolonged colds, diarrhoea, and vomiting. It seemed that the duration of breast feeding was less important than whether or not the child had been breast-fed at all. Wheezing was both more common among boys than girls (P less than .05) and if the mother was a smoker. Other environmental features related to wheezing were social class, month of birth, lack of breast feeding, exposure to dampness, mould and coal fires, but not to domestic pets nor to the numbers of mites found in bedding and carpets. Mite exposure was, however, associated with prolonged colds. Eczema was the only allergic symptom not positively associated with any environmental factor; moreover, it was neither associated with a lack of breast feeding nor with inclusion of cows' milk in the diet. Eczema was associated with the incidence of positive skin prick tests and IgE antibodies to egg white. IgE and IgG4 antibodies were estimated at birth (mothers' and cord bloods) and 3 and 12 months later.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Infant feeding and allergy: 12-month prospective study of 500 babies born into allergic families. 306 16

The diagnosis of Cow's Milk Protein Allergy was considered in 303 infants aged less than 1 year, who presented with one or more of the following symptoms: acute reaction related to cow's milk proteins (CMP) ingestion, severe colics, persisting vomiting, protracted diarrhea with or without blood and mucus, failure to thrive, eczema, respiratory symptoms, such as chronic rhinitis and wheezing. A diagnosis of CMPA was confirmed in 148 cases (60%): 125 relapsed on milk challenge, 23 were not challenged because of acute reactions at onset, presence of specific IgE (RAST and prick), and improvement on milk free diet. Familial atopy, familial history of CMPA and previous acute gastroenteritis were significantly more frequent in cases than in 191 age matched controls. Breast feeding was not more common or of longer duration in controls, compared to cases. Mean IgE serum levels were higher (46.3 U/ml) in cases than in controls (17 U/ml), while specific Cow's Milk Protein IgE were found in 71/148 cases (48%). 15 infants entered the study while on breast milk, because of the confirmed relation between their symptoms and CMP on the maternal diet. These infants had a higher prevalence of IgE mediated problems. All cases improved on a milk free diet but in 26 (17.8%) a further modification of the diet was required after the first prescription. Milk challenge was monitored by simple laboratory tests: all cases who had symptoms on challenge showed at least one test modification. Six infants, with no history of acute reaction, showed severe self-limited clinical symptoms at challenge. Key words: cow's milk allergy, milk, allergy, prick test, eczema, diarrhea.
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PMID:Cow's milk allergy in the first year of life. An Italian Collaborative Study. 307 Oct 78

The diagnosis of cow's milk proteins allergy can only be established if the symptoms disappear with an elimination diet and if a later controlled challenge leads either to a recurrence of symptoms or to some other clearly identified changes. At the moment there is not a specific immunological test surely effective in all cases. Anyway the three Gooldmann's tests are not necessary. In fact a single challenge with a cow's milk meal will be sufficient when clinical observation is accompanied by monitoring some simple laboratory tests (serum and nasal eosinophils, steathorrea, coproleucocytes, hemoccult, xylosemia and leucocytes PMN). The challenge must be tested in a double-blind trial only in patients with non specific symptoms (such as tension fatigue syndrome, hyperactivity, ecc...). The double-blind challenge is not necessary generally for the diagnosis of cow's milk proteins allergy in childhood, because at this time of life not only the symptoms are very clear (diarrhea, vomiting, skin symptoms) but also there is a prevalence of non reaginic reactions: this kind of reactions are usually delayed and they generally occur after a relatively high dose of food allergens. In the group of patients with specific anti-cow's milk IgE (RAST and prick tests) and severe reactions (anaphylaxis), the challenge is not necessary to confirm the diagnosis, but is usefully to verify the acquired tolerance, generally after the first year of life.
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PMID:[Diagnosis of allergy to cow's milk proteins]. 332 Sep 92

A patient with an immediate type hypersensitivity reaction against poppy seed is reported. Clinical symptoms consisted of swelling of the oral mucosa, vomiting, respiratory distress, and urticaria. Specific IgE antibodies were demonstrable by RAST.
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PMID:[Poppy seed allergy]. 338 34

In 47 infants and children aged 4-66 months with clinically proven cow's milk allergy and in a group of age-matched controls, serum IgG, IgA and IgM cow's milk-specific antibodies were determined with ELISA assays while IgE cow's milk-specific antibodies were measured with Pharmacia RAST. The patients were divided into three separate groups according to the time of clinical response to a standardized cow's milk challenge protocol. Immediate reactions (less than 45 min after challenge), which were mainly accompanied by urticarial skin eruptions, were associated with elevated IgE milk-specific antibody levels, indicating the involvement of an immediate hypersensitivity mechanism. Alternatively, intermediate reactions (1-20 h after challenge), which were mainly accompanied by vomiting and diarrhea, were not IgE-mediated. In the late reactions (greater than 20 h after challenge) both eczematous and gastrointestinal reactions were seen. Patients with eczematous eruptions also showed elevated IgE milk-specific antibody levels. IgG milk-specific antibody levels were similar in each of the patient groups but all groups were significantly lower than in the controls. Levels of IgA and IgM milk-specific antibodies were similar in patients and controls. The results indicate that different immunopathogenic mechanisms are operative in these subgroups of patients with cow's milk allergy.
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PMID:Humoral immune response to cow's milk in children with cow's milk allergy. Relationship to the time of clinical response to cow's milk challenge. 365 3

In a study of the manifestations of cow milk allergy in 100 young children (mean age 16 months), 30 items of historical data and information relating to the effects of a standardized milk challenge were entered into a computer data base. Three clusters of patients were derived using a K-means algorithm. In group 1 were 27 patients with predominantly urticarial and angioedematous eruptions, which developed within 45 minutes of ingesting cow milk. They had positive skin test reactions to milk and elevated total and milk specific IgE serum antibody levels. In group 2, 53 patients had pallor, vomiting, or diarrhea between 45 minutes and 20 hours after milk ingestion. These children were relatively IgA deficient. The 20 patients in group 3 had eczematous or bronchitic or diarrheal symptoms; in 17 symptoms developed more than 20 hours after commencing milk ingestion. Of the patients in group 3, only those with eczema had a positive skin test reaction and elevated IgE antibodies to milk. The patients in group 3 were the most difficult to identify clinically; they had a history of chronic ill health, and symptoms developed many hours or days after commencing milk ingestion in the challenge situation. In view of the heterogeneous clinical and immunologic findings in our patients, it is unlikely that a single laboratory test will identify cow milk allergy in all susceptible patients.
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PMID:Manifestations of milk allergy in infancy: clinical and immunologic findings. 373 64


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