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)

The larval stages of Echinococcus granulosus and E. multilocularis are involved in parasitic diseases in humans: cystic echinococcosis (CE) ("hydatid disease") and alveolar echinococcosis (AE), respectively. Both diseases and parasites have tight links with allergy because of the immunological characteristics that contribute to maintain the larvae in their human host as well as their potential in inducing clinical anaphylactic reactions in some patients. Clinical observations in patients and data obtained from mass screenings in various countries have identified both forms of echinococcosis as "polar diseases," i.e., diseases where immunological background of the patients was related to the clinical presentation and course. In particular, abortive cases (i.e., spontaneous cures) have been found in many subjects in endemic areas. On the other hand, immune suppression was associated with severe disease. AE especially might be considered as an opportunistic infection. Experimental and clinical studies have shown that Th1-related immune response was associated with protection and Th2-related response was associated with parasite growth. Genetic characteristics of the host are related to both occurrence and severity of AE and are associated with the extent of IL-10 secretion, which is a major feature of chronic progressing echinococcosis. Anaphylactic reactions, including urticaria, edema, respiratory symptoms, and anaphylactic shock due to spontaneous or provoked rupture of the parasitic cyst, are well known in CE. Anaphylactic reactions in AE are far less frequent, and have been observed in rare cases at time of metastatic dissemination of the parasitic lesions. Echinococcus-specific IgE is present in most of the patients and associated with severity. Specific histamine release by circulating basophils stimulated with E. granulosus antigens is present in all patients with CE and AE. Echinococcus allergens include (1) AgB 12-kDa subunit, a protease inhibitor and a potent Th2 inducer; (2) Ag5, a serine protease; (3) EA 21, a specific cyclophilin, with a homology with other types of cyclophilins; (4) Eg EF-1 beta/delta an elongation factor, with a homology with Strongyloides stercoralis EF that shares the same IgE epitope. A clinical cross-reaction with Thiomucase, a mucopolysaccharidase used in arthritis treatment, has recently been published. However, despite the potential risk of allergic reactions, the dogma "never puncture a hydatid cyst" is no longer valid. International experience of therapeutic technique of "puncture, aspiration, injection, re-aspiration" of hydatid cysts developed at the beginning of the 1980s has proved to be successful in a variety of selected indications that have been reviewed by WHO recommendations. A better understanding of the immunological background of echinococcosis in humans has led to new therapeutic developments, such as immunomodulation using interferon alpha. Th2-driven immunological response and IL-10-related tolerance state are common characteristics of atopic allergy and echinococcosis. The example of echinococcosis stresses the ambiguous links that exist between parasitic and allergic diseases, and show the usefulness of comparing these diseases to better understand how immune deviation may lead to pathological events and to find new therapeutic and.or preventive agents.
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PMID:Echinococcosis and allergy. 1514 6

Chronic urticaria (CU), defined as recurrence of wheals with or without angioedema for more than 6 weeks, is a quite common disease that may severely worsen the quality of life. Studies carried out during the last 2 decades have demonstrated an autoimmune pathogenesis mediated by functionally active autoantibodies to the high affinity IgE receptor (FcepsilonRI) or to IgE which are able to induce histamine release from basophils and mast cells. However, such mechanism can be detected in less than 50% of patients only. The present article reviews recent findings showing an additional pathogenic mechanisms in CU patients: activation of the coagulation cascade resulting in thrombin production. Thrombin is a serine protease which may play a key role in urticaria, being able to induce edema through an increase in vascular permeability, mast cell activation and degranulation, and to induce the production of the anaphylotoxin C5a. Such mechanism seems to be active in the majority of CU patients, however their relationship with anti-FcepsilonRI or anti-IgE autoantibodies is still matter of research.
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PMID:Chronic urticaria: a disease at a crossroad between autoimmunity and coagulation. 1796 29

An 83-year-old woman was referred to our emergency department with acute urticaria and sudden shortness of breath approximately 30 min after taking rectal diclofenac potassium for lumbago. After treatment with adrenaline and corticosteroids, the patient became hemodynamically stable and left the hospital on the next day. She attended our hospital 1 week after the onset of anaphylaxis because of repeated postprandial epigastric pain. No abnormal lesions were found in endoscopy. Radiographic selective catheter angiography revealed chronic mesenteric ischemia caused by atherosclerosis and abundant collateral arteries between the celiac trunk, the superior mesenteric artery and the inferior mesenteric artery. Patients with chronic mesenteric ischemia usually present with a clinical syndrome characterized by painful abdominal cramps and colic occurring typically during the postprandial phase. Fear of eating resulted in malnutrition. She was prescribed proton pump inhibitor, digestants, anticholinergic agents, serine protease inhibitors, prokinetics, antiplatelet agents and transdermal nitroglycerin intermittently, but these had no beneficial effects. It was most probable that this patient with chronic atherosclerotic mesenteric ischemia was suffering from functional abdominal pain syndrome induced by anaphylaxis. Since psychiatric disorders were associated with alterations in the processing of visceral sensation, we facilitated the patient's understanding of functional abdominal pain syndrome with the psychologist. Postprandial abdominal pain gradually faded after administration of these drugs and the patient left the hospital. Developing a satisfactory patient-physician relationship was considered more effective for the management of persistent abdominal pain caused by complicated mechanisms.
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PMID:Chronic atherosclerotic mesenteric ischemia that started to develop symptoms just after anaphylaxis. 2275 90