Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eosinophilic gastroenteritis is a relatively uncommon disease of unknown etiology. Eosinophilic ascites resulting from significant serosal involvement is the rarest clinical subtype. The case reported here is of a 30-year-old male presenting with abdominal pain, diarrhea, and ascites. His personal history included childhood asthma, allergic rhinitis, and recurrent urticaria. The clinical picture was characterized by peripheral eosinophilia and eosinophilic infiltrates of the stomach and small bowel. Computed tomogram (CT) of the abdomen showed generalized thickening of the gastric and small bowel wall. Paracentesis revealed exudative ascites rich in eosinophils. The patient experienced an impressive response to steroid therapy.
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PMID:Eosinophilic gastroenteritis with eosinophilic ascites: report of a case. 198 80

Anaphylactic reactions to Crotalidae envenomation are extremely rare. The presentation of anaphylaxis after envenomation can be a confusing variable in the timely diagnosis of both problems. The therapy of this dual disorder involves combining treatment of the obvious shock from the allergic reaction with a standard approach to Crotalidae envenomation. We present the case of a 22-year-old man who presented to the emergency department with urticaria, hypotension, and bronchospasm that developed immediately after his second envenomation from a rattlesnake. His symptoms resolved after administration of 0.8 mg SQ epinephrine, 100 mg IV diphenhydramine, 2,000 mL normal saline IV, and 250 mg IV methylprednisolone. Only one previous case report of anaphylactic shock from a rattlesnake bite could be found in the medical literature.
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PMID:Anaphylactic shock secondary to rattlesnake bite. 238 65

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 report a patient who developed recurrent urticaria and angioedema at age 2 years, severe hypocomplementemic glomerulonephritis at 11 years, and end-stage renal disease at 14 years. His disease resembled the hypocomplementemic vasculitis syndrome but was atypical in its early age of presentation, severe hypocomplementemia, and progression to end-stage renal disease. Serum C1q levels were extremely low, and C4, C2, C3, and C5 levels were significantly reduced. Serum C1 inhibitor (C1INH) levels were slightly low, presumably from consumption. Circulating C1INH-C1r-C1s complexes were evidenced by reduced ratios of functional to antigenic C1INH and antigenic C1r to C1s. Family members had normal functional and antigenic levels of all complement components studied. The patient's serum, erythrocytes, platelets, and mononuclear cells did not activate complement when mixed with normal target serum. Absence of a circulating complement activator and the low serum C3 and C5 levels suggested the presence of a solid-phase complement activator, possibly related to renal or systemic vascular endothelium. As in patients with homozygous deficiencies of classical pathway components, a severe, prolonged, acquired C1q deficiency may have predisposed this patient to the development of glomerulonephritis.
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PMID:Atypical hypocomplementemic vasculitis syndrome in a child. 298 70

The patient was a 46-year-old man. His chief complaints were urinary frequency and pain on urination. They first appeared one year earlier. The patient had had a history of bronchial asthma and urticaria. Vesical capacity decreased and vesico-cutaneous developed. The urine sediment contained eosinophils and vesico ureteral reflux was observed. The bladder tissues contained a moderate amount of eosinophils, lymphocytes and plasma cells. The total IgE was 360 IU/ml. The IgE RAST score and immediate reaction to the skin tests were all negative. The Arthus and delayed-type reaction skin tests were positive to various Eumycetees and foods. Provocation tests by eating foods such as eggs, meats, and shellfish reproduced the above-mentioned bladder disorders. The patient was therefore put on a diet that restricted the amount of animal protein consumed except for white meat fishes, and a mast cell membrane stabilizer was administered. The interstitial cystitis improved but the asthma aggravated. The cystitis was found to develop alternately with asthma.
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PMID:[A case of interstitial cystitis that developed alternately with bronchial asthma]. 357 70

We describe a 39-year-old man who suffered from delayed pressure urticaria for 2 years. His severe symptoms did not respond to antihistamine (H1 and H2) treatment and corticosteroid therapy was given despite severe side-effects. A new, nonsedating antihistamine drug, cetirizine, relieved most of his symptoms, enabled him to be weaned from corticosteroid therapy, and restored his former quality of life.
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PMID:[Delayed pressure urticaria: therapeutic response to cetirizine]. 834 26

Primary systemic allergy to human insulin is rare. We report a case of recurrent immediate local reactions followed eventually by generalized urticaria to recombinant human insulin (Humulin) in an insulin-dependent diabetic. Skin test to Humulin R was positive, and the patient was successfully desensitized using a modified rapid desensitization protocol. Two weeks later, he had another episode of generalized urticaria after Humulin R injection. His treatment was resumed at a lower dose, and within a week he was able to tolerate his usual regimen of insulin. To our knowledge, this is the first report of a recurrence of systemic reaction after successful desensitization.
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PMID:Primary systemic allergy to human insulin: recurrence of generalized urticaria after successful desensitization. 883 29

A 47-year-old man with hepatocellular carcinoma (HCC) at anterior and medical segment in the liver was treated with hepatic arterial infusion of Zinostatin Stimalamer-lipiodol suspension (SMANCS). After the 2nd infusion of SMANCS, the accumulation of lipiodol in the tumor was not good (Grade II), so additional administration was undertaken at five-weeks intervals. His systolic blood pressure immediately decreased from 120 to 60 mmHg, and he had numbness of hands, shaking chills, sweating, chest pain and numerous urticaria-like red exanthema. In spite of treatment by anti-shock agents such as steroid and catecholamines, these symptoms did not disappear, but antihistaminics greatly improved them without any serious side effects. Because of the remarkable effects of the antihistaminics and possibility of antibody production (IgE) after repeated infusions of high molecular SMANCS, this patient may have suffered anaphylactic shock caused by massive histamine release from mast cells.
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PMID:[An anaphylactic shock case after hepatic arterial infusion of zinostatin stimalamer suspension improved by anti-histaminics]. 921 13

In the past 2 years, a 4 year-old boy has had an anaphylactic reaction whenever he contacted food prepared with fish. The symptoms included intense itching in the throat and eyes, which progressed to generalized urticaria and facial angioedema. This was accompanied by cough, wheezing and dyspnea. Many fish preparations caused these episodes including several different kinds of fish (cod, tuna, salmon, trout, eel...), fish soup, chopsticks contaminated with fish preparations and canned fish. Elevated levels of total serum IgE (224 IU/ml) and specific IgE for cod (93.1 IU/ml), tuna (> 100 IU/ml), salmon (> 100 IU/ml), trout (64.4 IU/ml), mackerel (41.2 IU/ml) and eel (28.1 IU/ml) were found by the Pharmacia CAP system RAST FEIA in our allergy clinic. A skin prick test for mixed fish extracts (contain flounder, cod and halibut) was positive. A fish challenge test for cod, tuna, salmon, trout and eel all showed anaphylactic reactions. His allergic symptoms stabilized gradually after strictly avoiding ingestion of fish and using drug treatment. He also had a similar anaphylactic reaction to frogs. The best treatment for fish allergy is avoidance. Avoidance of fish may need to include both ingestion and inhalation of cooking vapors.
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PMID:Fish induced anaphylactic reaction: report of one case. 968 28

We report a truck driver with severe soft tissue contusion of both legs who developed atypical heparin-induced thrombocytopenia (HIT) after a thrombosis prophylaxis with unfractionated heparin; despite a thrombosis the patient showed a systemic allergic reaction to heparin in combination with elevation of thrombocytes and positive heparin-dependent antibodies. Six days after the initial trauma deep vein thrombosis of the left lower leg was diagnosed and fasciotomy was performed, preventing an imminent compartment syndrome. Another 5 days later the patient developed exanthema of the trunk and upper extremities and urticaria on his face, as well as severe headache. His platelet count increased from 134,000/microliter to 258,000/microliter. After exclusion of other causes for these symptoms, a reaction to heparin-dependent antibodies (heparin-platelet-factor 4 complex) was demonstrated 2 days later. Thrombosis prophylaxis was changed to hirudin (Refludan) and elevation of thrombocytes to 445,000/microliter was noted. Shortly after rinsing of an intravenous line with less than 50 IE unfractionated heparin at day 36 after trauma the patient developed an anaphylactic shock, which could be managed with cortisone. We suggest that in HIT the thrombocytopenia may represent only one form of an allergic reaction to heparin. The cause of the thromboembolic event is an antigen-antibody reaction to heparin taking place on the surface of the thrombocyte. This is similar in all forms of systemic reaction to heparin application, even though the symptoms may vary. As thrombocytopenia may not be the main symptom of a heparin-induced antibody reaction--in our hospital only 5 of 10 patients with HIT--the disease should rather be named "heparin allergy". We suggest a new classification of different pattern of heparin allergy types I-IV. The new types I and II are similar to HIT types I and II. Type III is the reaction of antibodies without decrease of thrombocytes, and type IV the reaction of antibodies associated with systemic allergic symptoms.
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PMID:[Atypical heparin-induced thrombocytopenia (HIT)--"heparin allergy" with thrombocytosis]. 1041 4


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