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)

In this investigation 98 children (median age 24 months) with cows' milk allergy (CMA) were studied over a median period of 2 years to see whether acquisition of clinical tolerance to cows' milk was associated with the changes in levels of IgG and IgE anti-cows' milk antibodies, and skin test reactivity to a cows' milk extract. Two groups of CMA patients were examined. The first were IgE sensitized and responded rapidly to small volumes of cows' milk with urticaria, and/or exacerbations of eczema, and/or wheeze, and/or vomiting (n = 69). The second, a late reacting group (n = 29) demonstrated coughing, diarrhoea, eczematoid rashes, and/or a combination of these which developed more than 20 hr after commencing normal volumes of cows' milk. Significant immunological changes were confined to the 69 IgE sensitized immediate-reacting-group of patients. Of these, there were 15 children who achieved clinical tolerance to cows' milk and they showed a significant fall in the levels of skin test reactivity to cows' milk over the study period (P < 0.01). In addition, these 15 children had lower serum IgE antibodies to cows' milk proteins both at the outset and the final follow-up compared with the 54 patients whose CMA persisted. No consistent change in the IgG antibody responses to cows' milk proteins was seen in either group of patients over the study period. The findings suggest patients with immediate type hypersensitivity to cows' milk proteins whose disease persists for more than 2 years have a more severe dysregulation of IgE synthesis to cows' milk proteins from the outset.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Natural history of cows' milk allergy in children: immunological outcome over 2 years. 844 85

Inhalation or ingestion of very small amounts of buckwheat allergen can initiate severe symptoms including wheezing, rhinorrhea, urticaria, vomiting and anaphylactic shock in patients with hypersensitivity against buckwheat. However, few studies of the immunological properties of buckwheat allergen have been made. The aim of the present investigation was to analyze the allergen in buckwheat antigen using the immunoblotting method, radioallergosorbent test (RAST) and RAST inhibition assay. Buckwheat 24 kilodalton protein (BW24KD) was shown by immunoblotting analysis to be the most frequently recognized allergenic component, binding to IgE antibodies from 100% of the patients' sera. There was a significant positive correlation (p < 0.001) between % bindings for BW24KD and buckwheat. In the RAST inhibition assay using patients' sera which showed positive IgE antibodies to buckwheat and BW24KD, there was effective inhibition in a dose-dependent manner between inhibition in a dose-dependent manner between BW24KD and buckwheat. These data indicated that BW24KD was a major allergen in buckwheat antigens. The experiments of SDS-PAGE using digestion buffer with or without 2-mercaptoethanol suggested that BW24KD was a component of heterodimer and the paired components had different molecular weights.
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PMID:[Allergen analysis of buckwheat by the immunoblotting method]. 850 55

Numerous undesirable reactions to alcoholic beverages, foods, drugs and other substances are characterized by allergy-like signs and symptoms and yet show unambiguously negative allergy test results. Such persons should be assessed for evidence of histamine intolerance caused by histamine overload and/or diamine oxidase deficiency. Diamine oxidase is the main histamine degrading enzyme with a predominantly gut activity. This would explain why nutritional allergies are often primarily suspected. The clinical evidence for histamine intolerance is based on chronic headache, diarrhoea, vomiting, flush, urticaria, asthma-like symptoms, rhinitis and others. Histamine restricted food, supported if necessary by H1 antihistamine blockade are simple but highly efficacious measures as shown by us in large patient groups. Intolerance to red wine probably is the most outstanding clinical characteristic and a directed question must be included into any allergy history in order to avoid missing a very major diagnostic spectrum with good therapeutic maneuverability.
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PMID:[Pseudo-allergies are due to histamine intolerance]. 901 5

We have studied, as part of a group of international multicenter phase II clinical trials, the toxicity and effectiveness of CAMPATH1H administered intravenously three times a week in an outpatient setting to patients with recurrent or progressive low grade lymphoma. We report here on the toxicity and therapeutic results of the first seven patients treated before the study was closed prematurely because of unacceptable toxicity. Classical complete or partial responses of treatment were seen in three of seven patients. One complete response lasted 8.5 months and the other complete response is ongoing at 1 year. Responses occurred in nodal sites as well as in skin and peripheral blood. The first three or four antibody infusions in each patient was associated with grade 1 or 2 side-effects including rigor, fever, facial flushing, nausea, vomiting, hives, wheezes, hypotension, and/or diarrhea but these subsequently decreased or disappeared. The most significant toxicity was profound lymphopenia and associated infection, usually viral. Six of seven patients had culture or serologically documented infections and four patients had two or more such episodes. All infections responded to temporary discontinuation of antibody therapy and appropriate antiviral or antibiotic agents. We conclude that CAMPATH1H monoclonal antibody has therapeutic activity against low grade non-Hodgkin's lymphoma but that this activity is limited by marked lymphopenia and an unacceptably high frequency of serious infection at the dose and schedule used in this trial.
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PMID:Immunosuppressive toxicity of CAMPATH1H monoclonal antibody in the treatment of patients with recurrent low grade lymphoma. 904 65

To investigate whether there are differences in the frequency of ADRs (adverse drug reactions) to parenteral iron preparations, we compared the results of 4 different data collections which contain observations in particular on i.m. or i.v. iron dextran and i.v. iron hydroxide sucrose complex, primarily in relation to anaphylactic/anaphylactoid reactions and common exanthemas. 1. In 206 patients of the department of general internal medicine in a city/teaching hospital (in association with the Swiss Foundation for Comprehensive Hospital Drug Monitoring--CHDM), 4 probably allergic reactions to i.m. iron dextran were found, one with acute severe dyspnea, cyanosis and flush, 3 with slight generalized, probably allergic reactions. Data from the USA on i.v. iron dextran do not show marked differences in the frequency of ADRs as compared with our data with i.m. administration. 2. A group of 400 otherwise healthy patients of the obstetric department of Zurich University Hospital were treated with i.v. iron sucrose for anemia due to iron loss during pregnancy or following childbirth. Seven generalized skin reactions, 4 in the form of flush and 3 of common exanthema, occurred. 3. In a retrospective study on patients on maintenance hemodialysis with chronic renal insufficiency and anemia, a questionnaire was answered by the medical heads of 17 selected hemodialysis units in Switzerland. Response was 100%. During around 8100 patient-years with approximately 160,000 ampoules of iron sucrose (with 100 mg elementary iron), not a single life threatening reaction was observed; only 5-7 situations of rapidly reversible blood pressure fall occurred, some 10 with flush, and one each with urticaria and vomiting/diarrhea. 4. The relatively good tolerance of i.v. iron sucrose in patients with chronic renal failure may be due either to reduced immune competence in patients with chronic renal insufficiency and/or to the use of the preparation itself, or probably both. 5. In ADRs of allergic appearance to iron sucrose, the 7 generalized skin reactions occurred on the first day of the injections, as did those under iron dextran. Preexisting hypersensitivity must be taken into consideration. 6. If our experience is confirmed, preventive measures with i.v. iron sucrose, mainly in patients with chronic renal insufficiency, could be reduced.
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PMID:[Parenteral iron therapy: problems and possible solutions]. 959 94

During a 4-month period, 34 dogs with tumors received a total of 60 doses of a single generic formulation of doxorubicin; 13 acute drug reactions were observed in these 34 dogs, and no acute reactions were observed after replacing the product with the proprietary brand. These reactions were characterized by one or more of the following signs: pruritus; head-shaking; urticaria; erythema of the pinnal, axillary, or inguinal regions; vocalization; vomiting; hyperemic or pale mucous membranes; high heart rate; and high respiratory rate. We propose that a component unique to generic doxorubicin was responsible for the unusually high number of acute drug reactions observed.
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PMID:Acute reactions in dogs treated with doxorubicin: increased frequency with the use of a generic formulation. 959 78

Azithromycin (AZM), a new oral macrolide antibiotic, in 10% fine granules or 100 mg capsules was given to pediatric patients to treat various infections. The following results were obtained in our studies of AZM for its antibacterial activities against clinical isolates, its pharmacokinetics, its efficacy, and its safety. 1. MICs of AZM, erythromycin (EM) and clarithromycin (CAM) were determined against a total of 57 strains all at 10(6) cfu/ml. Among Gram-positive cocci, MICs of AZM ranged from 0.78 to > 100 micrograms/ml against Staphylococcus aureus (20 strains), from 0.05 to 0.1 microgram/ml against Streptococcus pyogenes (11 strains), and from 0.0125 to 3.13 micrograms/ml against Streptococcus pneumoniae (10 strains). These MICs were similar to those of the other macrolides. Among Gram-negative bacilli, MICs of AZM were 0.05 micrograms/ml against Moraxella subgenus Branhamella catarrhalis (1 strain), from 0.78 to 3.13 micrograms/ml against Haemophilus influenzae (9 strains), 0.78 micrograms/ml against Haemophilus parainfluenzae (1 strain) and 6.25 micrograms/ml against salmonella sp. (1 strain). These values were similar to or lower than those of the other macrolides. Against Mycoplasma pneumoniae, MICs of AZM were < or = 0.0008 micrograms/ml in three strains. One strain of M. pneumoniae showed tolerance to AZM at MIC 25 micrograms/ml. The other agents exhibited higher MIC than AZM against this organism. 2. Plasma samples were collected from five patients receiving fine granules and four patients receiving capsules for drug level determination. The patients received AZM at 10.0 approximately 16.3 mg/kg body weight once daily for 3 days. Drug concentrations in plasma at two hours after Day 3 dosing were in a range between 0.02 and 0.19 micrograms/ml for fine granules and were in a range between 0.11 and 0.42 micrograms/ml for capsules. 3. Urine samples were collected from four patients receiving fine granules and four patients receiving capsules. Drug levels were determined to be 3 micrograms/ml at post-treatment 48 hours for fine granules and post-treatment 72 hours for capsules. Urinary excretion rates of AZM in three patients on capsules lied in a range between 4.69 and 10.17%. 4. Effectiveness of AZM in fine granules was evaluated in 128 patients having a total of 19 different infections. AZM was rated "excellent" in 51 patients, "good" in 63, "fair" in 8, "poor" in 6, resulting in an efficacy rate of 89.1%. Effectiveness of AZM in capsular form was evaluated in 23 patients with five different infections. AZM was found "excellent" in 13 patients and "good" in 10, resulting in an efficacy rate of 100%. 5. AZM in fine granules eradicated 45 strains of 54 in 8 different bacteria. AZM in capsules eradicated 9 strains of 10 strains in 6 different bacteria. 6. As for adverse reactions, one patient complained of eruption, one vomiting, one loose stool, five diarrhea, when administered with fine granular form of AZM. One patient on AZM capsules experienced urticaria and vomiting. 7. As for abnormal laboratory changes, three patients were found with decreased WBC, seven with increased eosinophil, two with increased GOT and GPT, one with increased GPT. They were all on fine granular form of AZM. As far as abnormalities found in patients administered with AZM in capsular form, two showed decreased WBC, one decreased WBC along with increased eosinophil, and three increased eosinophil.
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PMID:[Clinical study on azithromycin in 10% fine granules and 100mg capsules in the field of pediatrics]. 963 60

Assessment of activation of immune mechanisms is valuable in the early diagnosis of cow's milk allergy (CMA). The purpose of this study was to evaluate peripheral blood lymphocyte subclasses in children suspected of having CMA and healthy infants in order to detect an early marker for food allergy. Altogether 47 breast-fed infants, aged from 0.4 to 10 months were followed-up prospectively from birth because of atopic heredity. Twenty-three of the infants were healthy and 24 infants had a strong suspicion of and later challenge-proven cow's milk allergy. Leucocyte subsets were determined from peripheral blood mononuclear cells by flow cytometry. In response to a clinical cow's milk challenge, seven infants developed urticaria, 11 infants had eczema, three patients had loose stools, diarrhoea or vomiting and three infants had eczema and diarrhoea, loose stools or vomiting. The total percentage of B cells and also the proportion of B cells bearing a low-affinity IgE receptor as a marker for activation were significantly higher, whereas the percentage of CD8+ T cells was significantly lower in infants with challenge-proven CMA than in healthy controls. These results imply that infants with active CMA have a defect in regulation of B-cell function. Further, they suggest that imbalance of the ratio of suppressor and helper T cells might be an important factor in the etiopathogenesis of CMA. Our results show that large numbers of activated CD19+ B cells and low numbers of CD8+ T cells could be considered as early markers for food allergy since they are already detectable in peripheral blood during the earliest symptoms of CMA.
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PMID:Large number of CD19+/CD23+ B cells and small number of CD8+ T cells as early markers for cow's milk allergy (CMA). 981 28

There have been reports of increased prevalence of certain food allergies in patients with Type I latex allergy (LA). A detailed food allergy history was obtained from 137 patients with LA. Latex allergy was defined by positive history of IgE mediated reactions to contact with latex and positive skin prick test to latex and/or positive in vitro test (AlaSTAT and/or Pharmacia CAP). Food allergy was diagnosed by a convincing history of possible IgE mediated symptoms occurring within 60 minutes of ingestion. We identified 49 potential allergic reactions to foods in 29 (21.1%) patients. Foods responsible for these reactions include banana 9 (18.3%), avocado 8 (16.3%), shellfish 6 (12.2%), fish 4 (8.1%), kiwi 6 (12.2%), tomato 3 (6.1%), watermelon, peach, carrot 2 (4.1%) each, and apple, chestnut, cherry, coconut, apricot, strawberry, loquat, one (2.0%) each. Reactions to foods included local mouth irritation, angioedema, urticaria, asthma, nausea, vomiting, diarrhea, rhinitis, or anaphylaxis. Our study confirms the earlier reports of increased prevalence of food allergies in patients with LA. We also report increased prevalence of shellfish and fish allergy not previously reported. The nature of cross reacting epitopes or independent sensitization between latex and these foods is not clear.
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PMID:Prevalence of food allergy in 137 latex-allergic patients. 1020 85

Confirmed adverse reactions to foods may be caused by toxic, enzymatic, pharmacological, "pseudoallergic" or allergic mechanisms. True food allergies are mostly IgE-mediated and directed against one or only a few food proteins. They appear typically as eczema and gastrointestinal symptoms (vomiting, diarrhoea, abdominal cramps) among infants and as oral allergy syndrome, urticaria/angioedema, rhinoconjunctivitis or anaphylaxis among adults. The majority of food allergies among adults is caused by cross-reactivity of IgE against inhalative allergens also reacting with food proteins. This must be considered in investigations by skin-prick testing and/or specific IgE measurement, since the sensitivity of these tests for inhalative allergens is higher than for food proteins. The most frequent differential diagnoses of true allergies are pseudoallergic reactions to food additives or pharmacological reactions to biogenic amines. The diagnosis of these reactions can usually be based on the history and course under a corresponding diet. In clinical practice additional investigations by double-blind placebo-controlled food challenges are rarely required. A positive challenge test demonstrates only the cause-and-effect relationship of the foods and the patient's symptoms but does not demonstrate the underlying mechanism. The therapy of food intolerance is a corresponding diet. This requires a careful diagnosis and identification of the causative foods.
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PMID:[Food intolerance and food allergy]. 1041 28


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