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

Neutrophil granulocyte function was determined in three patients with systemic staphylococcal infection, clinical manifestations of generalized allergic disease, and hyperimmunoglobulinemia E. Each of the patients had urticarial skin rashes before or at the time of development of staphylococcal suppurative lymphadenitis, pneumonia, or sepsis. Neutrophil chemotaxis, random migration, phagocytosis, and bactericidal capacity were assessed to determine if an abnormality in these functions might have contributed to the development of severe staphylococcal infections. Each of the three patients with generalized urticaria was found to have a marked defect in neutrophil chemotaxis. The mean chemotactic index of the patients was 12 +/- 4, whereas that of 20 controls was 72 +/- 11. Neutrophil random migration, phagocytosis, and bactericidal capacity were normal in each patient. The serum or plasma of the patients did not inhibit chemotaxis of control neutrophils and did not contain an increased concentration of the chemotactic-factor inactivator found in normal serum. Treatment of the neutrophils of these three patients with the competitive histamine H2 receptor blocking agent, burimamide, produced a significant increase in chemotactic responsiveness. These studies suggest the possibility of pharmacologic modification of neutrophil granulocyte function.
 ...
PMID:Severe staphylococcal disease associated with allergic manifestations, hyperimmunoglobulinemia E, and defective neutrophil chemotaxis. 97 42

Chronic urticaria is a common condition that can be very disabling when severe. A cause for chronic idiopathic urticaria (CIU) is only infrequently identified. Potential causes include reactions to food and drugs, infections (rarely) and, apart from an increased incidence of thyroid disease, uncomplicated urticaria is not usually associated with underlying systemic disease or malignancy. About one-third of patients with CIU have circulating functional autoantibodies against the high affinity IgE receptor or against IgE, although it is not known why such antibodies are produced, or how the presence of such antibodies alters the course of the disease or response to treatment. There are only a few publications relating to childhood urticaria, but it is probably similar to the adult form, except that adult urticaria is more common. The diagnosis is based on patient history and it is vital to spend time documenting this in detail. Extensive laboratory tests are not required in the vast majority of patients. Chronic urticaria resolves spontaneously in 30-55% of patients within 5 years, but it can persist for many years. Treatment is aimed firstly at avoiding underlying causative or exacerbating factors. Histamine H1 receptor antagonists remain the mainstay of oral treatment for all forms of urticaria. The newer low-sedating antihistamines desloratadine, fexofenadine, levocetirizine and mizolastine should be tried first. Sedating antihistamines have more adverse effects but are useful if symptoms are causing sleep disturbance. Low-dose dopexin is effective and especially suitable for patients with associated depression. There is controversy as to whether the addition of an histamine H2 receptor antagonist or a leukotriene antagonist is helpful. For CIU, second-line agents include ciclosporin (cyclosporine) [which is effective in approximately 75% of patients], short courses of oral corticosteroids, intravenous immunoglobulins and plasmapheresis, although the last two were found to be beneficial in small trials only. Treatments for CIU with only limited or anecdotal supportive evidence include sulphasalazine, methotrexate, stanazol, rofecoxib and cyclophosphamide. The efficacy of photo(chemo)therapy is controversial. Physical urticarias may respond to H1 receptor antagonists, although in delayed pressure urticaria, and cold, solar and aquagenic urticaria, the response may be disappointing. Second-line agents for physical urticarias vary depending on the urticaria and most have limited supportive evidence. The potential for spontaneous resolution, the variation in the disease activity and the unpredictable nature of the disease makes the efficacy of treatments difficult to assess.
 ...
PMID:Chronic urticaria: aetiology, management and current and future treatment options. 1551 52

The pathogenic mechanism of ASA-induced urticaria/angioedema (AIU) is still poorly understood, but it has been known that histamine releasing by cutaneous mast cell activation is considered to be an important role. Considering the importance of histamine in AIU, we speculated that a genetic abnormality of histamine-related genes such as a high-affinity IgE receptor, a metabolic enzyme of histamines and histamine receptors, may be involved in the development of AIU. Enrolled in the study were 110 patients with AIU, 53 patients without ASA hypersensitivity who had various drug allergies presenting as exanthematous skin symptoms, and 99 normal healthy controls (NC). Eleven single nucleotide polymorphisms (SNPs) of the beta chain of the high-affinity IgE receptor (FCER1B) and three histamine-related genes-histamine N-methyltransferase (HNMT), histamine H1 receptor (HRH1), histamine H2 receptor (HRH2)-were screened using the SNP-IT assay based on a single base extension method. No significant differences were observed in allele and genotype frequencies, and haplotype frequencies of all the SNPs of FCER1B, HNMT, HRH1, and HRH2 among the three groups (p>0.05, respectively). These results suggest that the polymorphisms of FCER1B and the three histamine-related genes may not contribute to the development of AIU phenotype in the Korean population.
 ...
PMID:Polymorphisms of high-affinity IgE receptor and histamine-related genes in patients with ASA-induced urticaria/angioedema. 1595 54