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 cause of angioedema with eosinophilia (AE) is unknown. Patients with AE sometimes develop pruritic eruptions or urticaria before the onset of edema. We report a case of a 37-year-old woman with nonepisodic AE who presented with erythema and livedo reticularis before the onset of edema. The patient noticed erythema on both heels as well as livedo reticularis on her right great toe 1 month prior to presentation. A biopsy specimen from the heel revealed numerous eosinophils with degranulation infiltrating the subcutaneous tissue. One month later, she developed edema on the legs. Histopathologic findings of biopsy specimens obtained from the legs revealed edema and eosinophils in the subcutaneous tissue. Some patients with AE present with pruritic eruptions prior to the onset of edema. The diagnosis of AE in our patient with leg edema of unknown cause was considered prior to the appearance of any pruritic eruptions.
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PMID:A case of nonepisodic angioedema with eosinophilia associated with livedo reticularis and erythema before onset of edema of the legs. 2450 82

Cutaneous adverse drug reactions (CADR) represent a heterogeneous field including various clinical patterns without specific features suggesting drug causality. Exanthematous eruptions, urticaria and vasculitis are the most common forms of CADR. Fixed eruption is uncommon in western countries. Serious reactions (fatal outcome, sequelae) represent 2% of CADR: bullous reactions (Stevens-Johnson syndrome, toxic epidermal necrolysis), DRESS (drug reaction with eosinophilia and systemic symptoms or drug-induced hypersensitivity syndrome) and acute generalized exanthematous pustulosis (AGEP). These forms must be quickly diagnosed to guide their management. The main risk factors are immunosuppression, autoimmunity and some HLA alleles in bullous reactions and DRESS. Most systemic drugs may induce cutaneous adverse reactions, especially antibiotics, anticonvulsivants, antineoplastic drugs, non-steroidal anti-inflammatory drugs, allopurinol and contrast media. Pathogenesis includes immediate or delayed immunologic mechanism, usually not related to dose, and pharmacologic/toxic mechanism, commonly dose-dependent or time-dependent. In case of immunologic mechanism, allergologic exploration is possible to clarify drug causality, with a variable sensitivity according to the drug and to the CADR type. It includes epicutaneous patch testing, prick test and intradermal test. However, no in vivo or in vitro test can confirm the drug causality. To determine the cause of the eruption, a logical approach based on clinical characteristics, chronologic factors and elimination of differential diagnosis is required, completed with a literature search. A reporting to pharmacovigilance network is essential in case of a serious CADR whatever the suspected drug and in any case if the involved drug is a newly marketed one or unusually related to cutaneous reactions.
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PMID:[Cutaneous adverse drug reactions]. 2545 66

Eosinophilic skin diseases, commonly termed as eosinophilic dermatoses, refer to a broad spectrum of skin diseases characterized by eosinophil infiltration and/or degranulation in skin lesions, with or without blood eosinophilia. The majority of eosinophilic dermatoses lie in the allergy-related group, including allergic drug eruption, urticaria, allergic contact dermatitis, atopic dermatitis, and eczema. Parasitic infestations, arthropod bites, and autoimmune blistering skin diseases such as bullous pemphigoid, are also common. Besides these, there are several rare types of eosinophilic dermatoses with unknown origin, in which eosinophil infiltration is a central component and affects specific tissue layers or adnexal structures of the skin, such as the dermis, subcutaneous fat, fascia, follicles, and cutaneous vessels. Some typical examples are eosinophilic cellulitis, granuloma faciale, eosinophilic pustular folliculitis, recurrent cutaneous eosinophilic vasculitis, and eosinophilic fasciitis. Although tissue eosinophilia is a common feature shared by these disorders, their clinical and pathological properties differ dramatically. Among these rare entities, eosinophilic pustular folliculitis may be associated with human immunodeficiency virus (HIV) infection or malignancies, and some other diseases, like eosinophilic fasciitis and eosinophilic cellulitis, may be associated with an underlying hematological disorder, while others are considered idiopathic. However, for most of these rare eosinophilic dermatoses, the causes and the pathogenic mechanisms remain largely unknown, and systemic, high-quality clinical investigations are needed for advances in better strategies for clinical diagnosis and treatment. Here, we present a comprehensive review on the etiology, pathogenesis, clinical features, and management of these rare entities, with an emphasis on recent advances and current consensus.
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PMID:Eosinophilic Skin Diseases: A Comprehensive Review. 2587 39

Acute infection with viral pathogens in the herpesviridae family can trigger acute urticaria, and reactivation of herpesviridae is associated with cutaneous urticarial-like syndromes such as drug-induced hypersensitivity syndrome/drug reaction with eosinophilia and systemic symptoms (DRESS). Reactivation of latent herpesviridae has not been studied systematically in chronic idiopathic/spontaneous urticaria (CIU). This review proposes that CIU is an inflammatory disorder with autoimmune features (termed 'CVU' for chronic viral urticaria), based on serology consistent with the hypothesis that reactivation of a latent herpesvirus or -viruses may play a role in CIU. Serology obtained from a cohort of omalizumab (Xolair)-dependent patients with severe CIU was consistent with previous HHV-6 infection, persistent viral gene expression and replication. CIU patients also exhibited serological evidence of increased immune response to HHV-4 (Epstein-Barr virus, or EBV) but not all CIU patients were infected with EBV. These observations, combined with case reports of CIU response to anti-viral therapy, suggest that HHV-6, possibly interacting with HHV-4 in cutaneous tissues, is a candidate for further prospective study as a co-factor in CIU.
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PMID:Serological evidence that activation of ubiquitous human herpesvirus-6 (HHV-6) plays a role in chronic idiopathic/spontaneous urticaria (CIU). 2636 16

Eosinophilic ascites is a rare feature of eosinophilic gastroenteritis. We would like to highlight this increasingly recognised diagnosis in a case of unexplained ascites. We present a challenging case of a woman aged 25 years who presented with nausea, vomiting, diarrhoea, generalised abdominal pain and swelling 8-week following delivery of her first baby. Her symptoms were primarily aggravated by eating, and she had also noticed postprandial itching and self-limiting generalised rash. She had a strong history of atopy. Physical examination revealed abdominal tenderness and distension with shifting dullness. Urticarial skin rash was noted on the face, neck, chest and abdomen. Routine biochemistry was normal apart from peripheral eosinophilia. Imaging confirmed moderate ascites. Diagnostic paracentesis showed exudative ascites with numerous eosinophils. Histology of the upper and lower gastrointestinal tract showed infiltration of the oesophageogastroduodenal and rectosigmoid mucosa with eosinophils. The patient significantly improved following a course of steroids and six-food elimination diet.
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PMID:Eosinophilic ascites: a diagnostic challenge. 2760 59

The tapeworm Taenia (T.) solium can be responsible for two different conditions: taeniasis and cysticercosis. Helminth infections in human host cause an immune response associated with elevated levels of IgE, tissue eosinophilia and mastocytosis, and with the presence of CD4+ T cells that preferentially produce IL-4, IL-5, and IL-13. Individuals exposed to helminth infections may have allergic inflammatory responses to parasites and parasite antigens. PubMed search of human cases of allergic reactions occurring during T. solium infestation was performed combining the terms (allergy, urticaria, angioedema, asthma, anaphylaxis) with T. solium. A study was considered eligible for inclusion in the review if it reported data on patients with T. solium infestation who had signs or symptoms of allergy. In literature we found six articles reporting the association between an allergic reaction and T. solium infestation: two cases of urticaria, two cases of relapsing angioedema, one case of asthma and two cases of anaphylaxis. Despite the large diffusion of T. solium infestation, we found only a few cases of concomitant allergic reaction and the presence of Taenia in the host. The association between T. solium infestation and allergic manifestations has never been clearly demonstrated, and in absence of a well-documented causality the hypotheses are merely speculative. Therefore, the association between Taenia infection and allergy needs to be thoroughly studied to better clarify if this association may really exist and which is the pathogenetic mechanism supported.
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PMID:Different clinical allergological features of Taenia solium infestation. 2798 Apr 57

Important changes in the understanding and management of drug hypersensitivity reactions during the last years result from the increasing importance of biologics in medical practice, which differ in their spectrum of adverse drug reactions (ADRs) from the classical covalent drugs. With regard to covalent drugs, ampicillin and amoxicillin as well as clavulanic acid play an increasing role among ADRs to betalactam antibiotics. Fluoroquinolones are mainly the cause of anaphylactic and photosensitivity reactions. Especially in allergic reactions to NSAIDs, pseudoallergic reactions should be considered in the differential diagnosis. In opposite to the main cutaneous allergic drug reactions such as urticaria or maculopapular skin rash, in which antibiotics are the main culprits, in severe drug allergic reactions such as SJS (Stevens-Johnson Syndrome), TEN (Toxic Epidermal Necrolysis), or DRESS (Drug Reaction with Eosinophilia and Systemic Symptoms) Syndrome, compounds like allopurinol and anticonvulsants are the main causes. Similar mutations in the IL36R gene, which were found in both patients with an AGEP (Acute Generalized Exanthematous Pustulosis) and pustular psoriasis, make the differential diagnosis more difficult and raise the question whether there is a difference between these diseases or whether AGEP is not just a drug induced pustular psoriasis. Finally, some special aspects of side effects of biologics and targeted therapies respectively are discussed.
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PMID:Cutaneous allergic drug reactions: update on pathophysiology, diagnostic procedures and differential diagnosic. 2841 64

Episodic angio-oedema with eosinophilia (EAE) or Gleich's syndrome is a rare condition characterised by recurrent episodes of oedema and eosinophilia, accompanied by urticaria, fever and weight gain. The presence of ascites has not been reported so far. We report a 21-year-old Caucasian woman who presented with marked ocular oedema and ascites. Laboratory evaluation revealed marked eosinophilia. During the last 3 months, three episodes of facial and neck oedema were reported, which resolved spontaneously over a period of 3-5 days. The diagnosis of EAE was established after exclusion of secondary causes (infections, allergic reactions, collagen diseases, neoplasms) and clonal disorders associated with marked eosinophilia. Low-dose steroids resulted in eosinophil decrease and complete resolution of symptoms, including ascites. This case highlights that ascites can be a very rare manifestation of EAE particularly if other more frequent causes of ascites have been excluded and the clinical and laboratory findings are supportive of EAE.
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PMID:Ascites in a patient with episodic angio-oedema and eosinophilia: thinking outside the box. 2843 71

Paragonimiasis is a zoonosis caused by many species of Paragonimus commonly P. westermani. Human get infected by eating raw, salted, pickled, smoked, partially cooked crustaceans (crayfish or crabs). Clinical manifestations ranges from non-specific symptoms like pain abdomen, diarrhea, urticarial rashes, fever to pleuropulmonary symptoms like cough, hemoptysis, chest pain and dyspnea. A 48 years, female presented at TUTH emergency with fever on and off for nine months, cough and shortness of breath for three months, lethargy, malaise and urticaria with history of raw crab intake one month prior to the onset of symptoms. Blood and pleural fluid analysis revealed raised total counts with eosinophilia and x-ray showed bilateral infiltration of lower lobes with pleural effusion. Diagnosis was confirmed by microscopic examination of sputum for Paragonimus. She responded well to Praziquantel. Pulmonary paragonimiasis must be considered in the differential diagnosis of unresolving pneumonia and unexplained hypereosinophilia.
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PMID:Unresolving Pneumonia with Pleural effusion: Pulmonary Paragonimiasis. 2874 28

Drug hypersensitivity may manifest ranging from milder skin reactions (e.g., maculopapular exanthema and urticaria) to severe systemic reactions, such as anaphylaxis, drug reactions with eosinophilia and systemic symptoms (DRESS)/drug-induced hypersensitivity syndrome (DIHS), or Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN). Current pharmacogenomic studies have made important strides in the prevention of some drug hypersensitivity through the identification of relevant genetic variants, particularly for genes encoding drug-metabolizing enzymes and human leukocyte antigens (HLAs). The associations identified by these studies are usually drug, phenotype, and ethnic specific. The drug presentation models that explain how small drug antigens might interact with HLA and T cell receptor (TCR) molecules in drug hypersensitivity include the hapten theory, the p-i concept, the altered peptide repertoire model, and the altered TCR repertoire model. The broad spectrum of clinical manifestations of drug hypersensitivity involving different drugs, as well as the various pathomechanisms involved, makes the diagnosis and management of it more challenging. This review highlights recent advances in our understanding of the predisposing factors, immune mechanisms, pathogenesis, diagnostic tools, and therapeutic approaches for drug hypersensitivity.
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PMID:An Updated Review of the Molecular Mechanisms in Drug Hypersensitivity. 3136 35


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