Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the case of an atopic male, 76 years old, with post-myocardial infarction ischaemic cardiopathy, arterial hypertension and a history of insect-sting induced large local reactions who died because of a biphasic anaphylaxis subsequent to multiple Vespid stings (about 15). Within approximately ten minutes after the stings he developed urticaria, extended erythema and hypotension (90/60 mmHg), measured by a family member. The objective physical examination by the emergency doctor at the patient's home revealed an orticarioid reaction and erythema of the back and neck, an unaffected respiratory apparatus and CNS, normal pupils, a pulse rate of 74, normal blood pressure ranging from 120/70 to 130/60 mmHg. The patient was administered antihistamine and corticosteroid through parenteral route. During the 45' observation period at the patient's home the urticaria subsided but not to completion. Approximately 40 minutes after the emergency doctor left, the urticaria reoccurred, angioedema of the neck and worsening asthenia developed. The patient died, despite attempts to resuscitate him by the emergency doctor that had been called out again. A post-mortem examination revealed generalised eodema of the lungs, brain, glottis, and bowels due to the severe characteristic systemic compromise of anaphylaxis. The Authors discuss whether an early use of adrenalin and/or a longer observation time could have saved the patient.
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PMID:A case of fatal biphasic anaphylaxis secondary to multiple stings: adrenalin and/or a longer observation time could have saved the patient? 1645 66

Fullerenes are a class of novel carbon allotropes that may have practical applications in biotechnology and medicine. Human mast cells (MC) and peripheral blood basophils are critical cells involved in the initiation and propagation of several inflammatory conditions, mainly type I hypersensitivity. We report an unanticipated role of fullerenes as a negative regulator of allergic mediator release that suppresses Ag-driven type I hypersensitivity. Human MC and peripheral blood basophils exhibited a significant inhibition of IgE dependent mediator release when preincubated with C(60) fullerenes. Protein microarray demonstrated that inhibition of mediator release involves profound reductions in the activation of signaling molecules involved in mediator release and oxidative stress. Follow-up studies demonstrated that the tyrosine phosphorylation of Syk was dramatically inhibited in Ag-challenged cells first incubated with fullerenes. In addition, fullerene preincubation significantly inhibited IgE-induced elevation in cytoplasmic reactive oxygen species levels. Furthermore, fullerenes prevented the in vivo release of histamine and drop in core body temperature in vivo using a MC-dependent model of anaphylaxis. These findings identify a new biological function for fullerenes and may represent a novel way to control MC-dependent diseases including asthma, inflammatory arthritis, heart disease, and multiple sclerosis.
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PMID:Fullerene nanomaterials inhibit the allergic response. 1757 89

Working in the Brazilian backland, Chagas described a new disease. He discovered the etiologic agent, the vector, the reservoir, the acute stage, the several clinical aspects of the chronic stage (particularly the heart disease), role of autoimmunity in its pathogenesis, and anticipated the social impact of the disease. Chagas was nominated to Nobel Prize twice: in 1913, and in 1921. In 1913, Richet won the prize because his work on anaphylaxis. In 1921, no one received the Nobel Prize. It is believed that detraction of Chagas' work at the National Academy of Medicine, made by jealousy, mediocrity, and political rivalries can be maculated the image of the scientist. Furthermore, misperception of Chagas' work may also have led the Nobel Committee not to award him. One-hundred years after the discovery, we can appreciate the greatness of the discovery of Carlos Chagas, never seem in the realm of biological research. Time to make justice, therefore, has finally come.
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PMID:Justice where justice is due: A posthumous Nobel Prize to Carlos Chagas (1879-1934), the discoverer of American Trypanosomiasis (Chagas' disease). 1918 67

Between 1995 and 2008, a case-control study was conducted to determine the role of drugs as risk factors for severe food anaphylaxis in adults. Data including exercise, alcohol intake, and use of aspirin, non steroidal anti-inflammatory drugs, beta-blockers, and angiotensin-converting-enzyme inhibitors (ACEI) were prospectively recorded. Multivariate analysis was used to compare 76 cases of severe anaphylaxis (SA) with 235 cases of mild to moderate food allergy (mmFA). The M/F sex ratio was 54.6% in SA and 36% in mmFA (p < .003). SA represented 17.3% of all food allergies below 45 years and 54.6% over this age. Drug intake did not differ between the two age categories. Drug use was noted in 40.8% of SA and 14.9% of mmFA (p < .0005). Aspirin, NSAIDs, betablockers and ACEI were associated with respectively 15.8%, 6.6%, 10.5% and 5.3% of SA, and with 1.7%, 0.9%, 1.7% and 0.4% of mmFA (p < .003). The respective odds ratios were 10.8, 8.2, 6.8 and 13.0. No other drugs were associated with FA. Exercise and alcohol intake were associated to drugs with respectively 10.5% and 27.6% of SA and 0.4% and 8.1% of mmFA (p < .0005). Exercise drastically increased the risk of drugs. We conclude that aspirin, NSAIDs, betablockers and ACEI are significant risk factors for severe IgE-dependent food allergy. The underlying mechanisms are discussed. Adults with food allergy or sensitization should avoid taking aspirin and NSAIDs before meals and should receive drug families other than ACEI and betablockers for hypertension. In case of pre-existing heart disease, the benefit-risk ratio of ACEI and beta-blockers has to be carefully considered.
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PMID:[Drugs as risk factors of food anaphylaxis in adults: a case-control study]. 1971 92

Anaphylaxis is the most severe type of food allergy. Factors of risk are advanced age, cardiopathy, asthma, mastocytosis. Age may be linked to an increased consumption of drugs: aspirin, nonsteroidal anti-inflammatory drugs, beta-blockers, inhibitors of angiotensin converting enzyme (ACE). A case-control study comparing anaphylaxis and mild food allergies has shown a sharp increase of consumption of these drugs in patients with anaphylaxis, with odds ratio respectively of 10.8 [CI 95%: 3.10-41.3], 8.2 [CI 95%: 1.37-62.51], 6.8 [CI 95%: 1.78-27.78] and 13 [CI 95%: 1.34-310.38]. Besides, exercise potentiates the relative risk of drug consumption. Predominant mechanisms could be an increase of gut permeability enhancing the passage of food allergens in the mucosa and in blood, and the inhibition of ACE, so that the angiotensin homeostatic mechanism deteriorates. Main sites of interference may be endothelium and gut epithelium. Preventive measures excluding the intake of aspirin and nonsteroidal anti-inflammatory drugs before the meals can be recommended for food allergic and food sensitized adults. Treatment of hypertension can address to other families of drugs than ACE inhibitors (ACEI) and beta blockers. The benefit-risk ratio of beta blockers and ACEI has to be carefully considered in the case of cardiopathy. double dagger.
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PMID:[Drugs as risk factors of food anaphylaxis in adults]. 2081 8

Pompe disease is an inherited lysosomal disease in which there is a decrease or absence of acid alpha-glucosidase activity. This enzyme defect induces glycogen storage in different tissues, especially muscle and heart, resulting in muscle weakness, respiratory failure and heart disease. Substitutive enzyme replacement therapy (ERT) dispensed every two weeks is the only treatment that has shown benefits. However, this treatment induces hypersensitivity for half of the treated patients. Reactions range from mild to severe, sometimes requiring ERT suspension and anti-anaphylaxis drug administration. Understandably, high amount of acid alpha-glucosidase infusion seems to be identified by the immune system as a danger associated molecular pattern, and induce an immune reaction, involving sometimes, but not always, immunoglobulin E (IgE) production and activating mast and basophil polynuclear cells. Considering the lack of therapeutic alternatives and the proved benefit of ERT, desensitization finds its place here. We hereby report the case of a patient for whom a simplified desensitization protocol ("SWORD": Start With One Regular Drop) was successfully achieved, allowing ERT to be pursued, resulting eventually in clinical improvement.
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PMID:SWORD: A simplified desensitization protocol for enzyme replacement therapy in adult Pompe disease. 2763 92

Anaphylactic reaction to gelatin-containing hemostatic agents has been reported in the orthopedic literature, most commonly during scoliosis repair in adolescents. However, the risk, differential diagnosis, and management of anaphylaxis in patients with complex congenital heart disease undergoing noncardiac procedures have not been previously reported. We describe the case of an adolescent with a history of repaired truncus arteriosus undergoing posterior spinal fusion who developed sudden and profound hypotension that was ultimately confirmed to be an anaphylactic reaction to Surgiflo. Echocardiography was used to aid in diagnosis and management of the cardiovascular effects of anaphylaxis in this patient with residual cardiac pathophysiology.
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PMID:Anaphylaxis to Surgiflo During Posterior Spinal Fusion in an Adolescent Status Post Truncus Arteriosus Repair: A Case Report. 2906 3

We experienced rocuronium-induced anaphylaxis in a 62-year-old man who was scheduled for laparoscopic ileocecal excision for cecal cancer under general anes- thesia. The patient did not have a preoperative history and examinations suggestive of heart disease, or pre- disposing factors for myocardial infarction. Just after induction of anesthesia, we noticed abnormally low blood pressure and ST segment elevation on his elec- trocardiogram. The surgery was postponed and percu- taneous coronary intervention was performed to treat coronary artery stenosis. Re-operation was planned 73-days after the first operation. The patient suffered cardiac arrest just after induction of general anesthesia At the same time, we noticed systemic erythema all over his body, which led to the diagnosis of anaphy- laxis. Cardiopulmonary resuscitation was performed and the surgery was postponed once again. Cardiovas- cular agents, including adrenaline, noradrenaline, atro- pine and amiodarone, improved his hemodynamics. In addition, steroids and anti-histamines were also admin- istered to treat anaphylaxis. We advised him to undergo skin tests to determine the causative agent of anaphylaxis, but he declined. Instead, a basophil activa- tion test was performed, which showed a positive reac- tion to rocuronium. Therefore, we planned general anesthesia without using muscle relaxants such as rocuronium for the third attempt at surgery. The sur- gery was performed safely with this protocol. It is likely that his symptoms in the first general anesthesia were caused by Kounis syndrome. We conclude that the basophil activation test seems to be valuable in determining the causative agent of anaphylaxis, partic- ularly when a patient does not agree to undergo skin tests.
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PMID:[A Case of Rocuronium-induced Anaphylaxis in a Man with Kounis Syndrome in which Basophil Activation Test was Valuable in Determining the Causative Agent]. 3038 47