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 generalized allergic reaction to or anaphylaxis from honeybee sting may involve the skin with erythema, puritus, urticaria, or angioedema; the respiratory tract with laryngeal edema, and brochospasm; the cardiovascular system with myocardial depression, hypotension, and shock; and the gastrointestinal system with nausea, vomiting, and incontinence. Acute pulmonary hemorrhage following a honeybee sting has never been reported. We describe a previously healthy 14-year-old girl who developed acute pulmonary hemorrhage, hypotension, and generalized skin rash after a single honeybee sting on her right fourth finger. Her serum immunoglobulin E (IgE) was high (360 IU/mL). Chest X-ray revealed perihilar alveolar infiltrative lesions. Metabolic acidosis and hypoxemia were also found. After treatment with antihistamines, dopamine, corticosteroids, bronchodilaters, fluid replacement, and mechanical ventilation, her condition improved dramatically. A hypersensitivity reaction to honeybee venom is the most likely explanation for this unusual case of acute pulmonary hemorrhage.
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PMID:Acute pulmonary hemorrhage following a honeybee sting: a case report. 1059 91

A forty-four-year-old Japanese female, who had persistant rhinorrhea, was administered Benza block tablets orally along with two other medicines. Immediately after ingestion, the patient displayed itching of the right upper eyelid, followed by coughing, sneezing, nasal discharge, nasal obstruction, nausea, vomiting, swelling of the face, and dyspnea. She had edema, a wheal extending from the face to the neck, and swelling of the eyelids and lips. Her symptoms subsided after treatment. Her reaction to ibuprofen, which was contained in the Benza Block tablets, was confirmed by a positive reaction to prick testing. From the results of these examinations, our patient was diagnosed as having anaphylaxis due to the ibuprofen in the Benza Block tablets. A review of the literature revealed no previous reports of anaphylaxis due to ibuprofen, although a few cases of ibuprofen urticaria have been reported.
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PMID:A case of anaphylaxis due to ibuprofen. 1087 2

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

Adverse reactions to food may be toxic or non toxic, depending on the susceptibility to a certain food; non toxic reactions that involve immune mechanisms are termed allergy if they are IgE-mediated. If no immunological mechanism is responsible, it is termed intolerance. The following disorders are considered a consequence of food allergy: gastrointestinal reactions (oral allergy syndrome, vomiting, diarrhea, protein-induced enterocolitic syndrome, eosinophilic gastroenteritis); respiratory reactions (rhinitis, asthma, laryngeal edema); cutaneous reactions (urticaria-angioedema, atopic dermatitis); anaphylaxis. There is much recent evidence to consider celiac disease an immunological disorder. Food allergy diagnosis is based on history, SPT, specific IgE, food challenges. DBPCFC is fundamental for diagnosing true food allergy; patients who have had anaphylaxis to food must not undergo DBPCFC. Rapidly progressive respiratory reactions and anaphylactic shock are life-threatening reactions that can be caused by food allergy. The doses of food inducing anaphylaxis can be very low, therefore commercial cross-contamination with an unsuspected food during food processing can be risky for the food allergic patient. The prevention of severe anaphylactic food reactions may lie in interdisciplinary collaboration among allergologists, chemists, food technologists, and experts in food industry research.
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PMID:Introducing chemists to food allergy. 1129 97

We report a case of a patient who suffered generalized urticaria, chest tightness, wheezing, nausea, vomiting, hypotension, and loss of consciousness. Two hours earlier she had taken Eulitop Retard following lunch. She had tolerated all the implicated food after the reaction. Allergy evaluation revealed intense positive responses to intradermal tests with bezafibrate active component and Eulitop Retard (skin tests in control subjects were negative). Specific IgE tests (RAST) to Eulitop Retard were negative. An IgE mechanism is suggested to be responsible for this adverse reaction on the basis of the positive skin tets. The delayed onset (two hours) of this anaphylactic shock is unusual. Although infrequent, it may be caused by the specific pharmacokinetic characteristics of this drug, which is a slow releasing agent, mainly absorbed in the gut. The drug was taken just after lunch, and this concomitant food ingestion could also have produced a delay in gastric drainage and a retarded drug absorption. An IgE-mediated accelerated type reaction could also explain this delay. Apparently the patient reacted after the first contact to the drug, and the absence of a sensitization period is not usual in this type of immune reponse. Finally, we recommend the performance of prick and intradermal skin tests prior to any systemic challenge when allergic reactions to fibric acid derivatives are suspected.
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PMID:Bezafibrate-induced anaphylactic shock: unusual clinical presentation. 1143 73

CAMPATH-1H (CP-1H) is a humanized monoclonal antibody directed against the CD52 antigen with promising therapeutic effects in patients with small cell lymphocytic non-Hodgkin's lymphomas (NHL) of B- and T-cell type. We report about the response and toxicity of CP-1H in 18 patients with B-cell NHL who were treated in four clinical centers in Germany. Sixteen patients suffered from a low-grade and two from a high-grade NHL. All patients had received chemotherapy before and had either relapsed or were refractory to conventional therapy. Two patients received CP-1H in a dose-range finding trial once weekly and 16 patients as a fixed dose of 30 mg three times weekly. Of 18 patients, 8 (44%) achieved a clinical response, 2 (11%) had stable disease, and 5 (28%) had progressive disease. Four patients could not be evaluated for response because of death (two patients) and serious adverse events (two patients). All patients with response to CP-1H had a low-grade NHL. Nonhematological toxicity was severe in two patients who suffered from WHO grade III/IV bronchospasm. Common acute adverse events (WHO grade I-III) included fever, chills, rigor, urticaria, nausea, and vomiting. Eleven patients suffered from bacterial or viral infections; some had recurrent infections. A total of 12 different infections were reported. The most frequent infections were caused by herpesvirus (seven patients). Hematological toxicity included thrombocytopenia in four and lymphocytopenia in seven patients. Although the antibody is humanized, the nonhematological toxicity was substantial and probably due to a cytokine release syndrome. Prophylactic treatment of the side effects is strongly recommended for patients treated either with CP-1H alone or in combination with chemotherapy.
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PMID:Monoclonal antibody therapy with CAMPATH-1H in patients with relapsed high- and low-grade non-Hodgkin's lymphomas: a multicenter phase I/II study. 1180 32

Proton pump inhibitors (PPI) are widely used for the treatment of peptic ulcer, but cases of anaphylactic reactions have rarely been described. We present a patient who experienced an episode of urticaria 30 minutes after oral intake of an omeprazole capsule. Skin prick tests to omeprazole, pantoprazole and lansoprazole were positive. Challenge test with lansoprazole was carried out and within 45 minutes the patient developed urticaria, facial edema, vomiting, and hypotension. Oral challenge with other imidazole derivatives (ketoconazole, cimetidine, metronidazole) were carried out with good tolerance. Serum tryptase levels determined 3 hours after the adverse reaction to lansoprazole were elevated. Specific IgE to PPI were not detected by an enzyme-linked immunosorbent assay technique. The clinical findings, positive skin prick test to PPI and elevated serum tryptase levels suggest that an IgE-mediated mechanism was implicated in the reactions to both omeprazole and lansoprazole. Skin prick tests may be a useful tool for detecting patients sensitized to PPI. An experimental protocol was used to detect specific IgE antibodies against PPI, which may explain RAST negativity. The previous findings suggest that cross-reactivity between PPI exists, but not with other imidazoles.
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PMID:Anaphylaxis to proton pump inhibitors. 1246 68

A human nasopharyngeal linguatuliasis was reported for the second time in Egypt. The patient (20 years old male) was presented with main conspicuous complaints, fever, urticaria (face and neck), coughing, vomiting and passage of small (less than 1 cm. in length) worm-like structures in his nasal discharge and vomitus. Symptomatic treatment was given followed by a single dose of praziquantel after identification of the causative parasite. Human linguatuliasis (pentastomiasis) was discussed.
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PMID:Human nasopharyngeal linguatuliasis (Pentasomida) caused by Linguatula serrata. 1256 18

This was a great save. The crew could easily have missed the presentation of anaphylaxis and let the window for treatment with epinephrine slip away. This patient was in anaphylactic shock. There were no signs that supported a traumatic injury, and that, combined with diaphoresis, urticaria and tachycardic central pulse, contributed to the suspicion of anaphylaxis. Anaphylaxis is classified as distributive shock. This type of shock is caused by profound systemic vasodilation, and the heart is unable to increase output enough to maintain blood pressure. Other causes of distributive shock include sepsis and spinal cord injury. It is rare to have both hypotension and wheezing in such cases. In an anaphylactic reaction, an allergen, such as a food protein, medication, insect venom or latex, is introduced into the body. The mast cells of the immune system have a protein on their surface called IgE antibodies (Immunoglobulin E). The mast cells are filled with histamines [table: see text] and leukotrienes, which are chemical mediators. These are released when the allergen reacts with the IgE antibodies. When these mediators are released, they cause smooth-muscle constriction in the respiratory and gastrointestinal tracts, resulting in wheezing, stridor, nausea, vomiting and diarrhea. They also cause vascular dilation, leading to edema and urticaria. Most patients will present with either profound vascular effect (shock) or wheezing; this is a rather rare presentation of a patient having both. The medication best suited to counteract the effects of these medicators is epinephrine. Epinephrine is an alpha- and beta-agonist, acting to constrict the vasculature and dilate the smooth muscles in the bronchial tree. Antihistamines can alleviate symptoms of anaphylaxis, but should only be used in addition to epinephrine, not as a substitute. In life-threatening reactions, epinephrine must be given quickly and in a form that the body can distribute. Use of the subcutaneous route with a solution mixed at 1:1,000 dilution is appropriate in most patients, but if the patient is in profound shock and not perfusing the skin (pale, cold, clammy skin), then a more diluted concentration must be given i.v. at a slow rate (1 cc every minute of the 1:1,000 dilution) until the patient recovers. If i.v. access is delayed or not available, give the 1:1,000 dilution intramuscularly, in the tongue or down the endotracheal tube. Refer to your local protocols for dosage, but the usual dose of epinephrine is 0.3-0.5 mg, or 0.01 mg/kg in a child. There are more than 40 million people in the U.S. with allergic histories that place them at risk for developing anaphylaxis. Each year over 5,000 deaths are attributed to anaphylaxis. The risk of death from anaphylaxis increases with a more rapid onset of signs and symptoms. Up to 25% of patients will experience a biphasic reaction. This means there is a recurrence of symptoms several hours after the initial reaction, and it is prudent to observe patients for a period of time following their initial treatment.
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PMID:Bugged. 1277 12

Scombroid fish poisoning is a clinical syndrome attributed to the ingestion of contaminated fish. A toxin or toxins, known as scombrotoxin, result from decomposition by endogenous flora of the amino acid histidine liberating bioactive amines, predominantly histamine. The presentation has features of histamine toxicity, typically with urticaria, flushing, headache, abdominal cramps, diarrhoea and vomiting. The course is usually mild and self-limiting. The author describes six cases of scombroid poisoning after ingestion of fish from the same Canberra restaurant. One case resulted in significant hypotension necessitating a prolonged stay in the ED.
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PMID:Something fishy: six patients with an unusual cause of food poisoning! 1278 52


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