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)

Histamine release from dispersed skin mast cells may be used for functional studies on the mast cell. However, technical difficulties have hampered such studies. In the present study a new fiberglass-based histamine assay was applied to previously described dispersion techniques, using excision biopsies from 7 patients with urticaria pigmentosa, 3 with psoriasis as well as 4 with urticaria. However, sufficient mast cell numbers for performing histamine release could only be obtained from patients with urticaria pigmentosa. The average mast cell yield was 935 +/- 470 cells (mean +/- SD) per mg wet weight of tissue. The skin mast cells from these patients responded with dose-dependent histamine release to anti-IgE, calcium ionophore A23187, and N-formyl-methionyl-leucyl-phenylalanine challenge without previous passive sensitization. The pattern of histamine release of mast cells and corresponding blood basophils did not indicate substantial differences between the two cell types.
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PMID:Histamine release from skin mast cells and basophils in patients with urticaria pigmentosa. 169 Apr 93

Circulating histamine-releasing factors have been identified in the serum and plasma of chronic-urticaria patients by in vivo skin testing and in vitro histamine release from heterologous mixed leukocytes. Quantitative mast cell studies of serum skin test biopsies and electron microscopy indicate that the serum factors release histamine by mast cell degranulation. Peripheral blood basophils and total cellular blood histamine are reduced in chronic-urticaria patients suggesting that the circulating serum factors cause sustained degranulation. Histamine-releasing activity has been identified by skin testing in ultrafiltered serum fractions less than 30 kDa and greater than 100 kDa. In vitro histamine-releasing activity was confined to ultrafiltered serum fractions greater than 100 kDa and was present in IgG purified from some chronic-urticaria sera by protein G affinity chromatography. The dose-response relationship and kinetics of histamine release in vitro were similar to those of anti-human IgE. 'Desensitisation' of basophils by prior incubation with anti-IgE in the absence of calcium and competitive inhibition studies with myeloma IgE serum indicated that histamine-releasing autoantibodies in chronic-urticaria sera and purified IgG have the properties of anti-IgE. Plasma exchange in 4 patients with active chronic urticaria refractory to antihistamine therapy showing in vivo and in vitro histamine-releasing activity was followed by temporary remission of disease activity in 2 of them. It is possible that chronic urticaria is an autoimmune disease.
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PMID:Histamine-releasing autoantibodies in chronic urticaria. 172 16

Basophil and mastocyte degranulation is calcium-dependent. Calcium-antagonists can inhibit synthesis of and release in vitro some mediators in various types of cells. Both immunologically stimulated and non-immunologically stimulated release of material from basophils isolated from normal and allergic subjects can be antagonized by calcium blockers. The present study was aimed at testing the therapeutic effects and side effects of nimodipine therapy, a new dihydropyridine anti-calcium derivative for physical stimulus-induced urticaria, in comparison with a standard H1-antihistamine therapy. The study was done in 32 outpatients who had physical stimulus-induced urticaria: 20 patients received nimodipine three times a day in a daily dose of 180 mg, 12 patients were treated with terfenadine in a dose of 120 mg. In the majority of patients treated with both nimodipine and terfenadine, satisfactory clinical results were obtained after 3 weeks of therapy. There were, however significant (P less than 0.05) differences in responses. Complete clearance after 3 weeks was noted in 50% patients treated with nimodipine, whereas only 16% of patients on terfenadine were completely clear, and some showed only slight improvement. The treatment was easily manageable, and with few side effects.
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PMID:Nimodipine versus terfenadine in the treatment of physical stimulus-induced urticaria. 196 27

Histamine release from peripheral blood basophils challenged with C5a, f-met-peptides and calcium ionophore was studied in patients with cold urticaria before and after exposure to low environmental temperatures. Compared to healthy controls, stimulated mediator release before cold exposure was increased in 7 of 11 patients. When challenged by cold exposure mediator release from in vitro-stimulated basophils was decreased. This decrease was more pronounced after stimulation with receptor-mediated stimuli (e.g. C5a) as compared to receptor-unrelated stimuli, e.g. calcium ionophore. In 4 of 11 patients stimulated mediator release before cold exposure was moderately increased. Also after cold exposure only a weak decrease of stimulated histamine release was seen. Levels of activated complement components (C3a) before and after cold exposure failed to provide evidence for complement activation in vivo. Also the number of circulating basophils as well as their cellular histamine content remained normal after cold exposure. The results show that in these patients release of histamine is altered before and after cold exposure. These changes in basophil responsiveness are not due to complement activation in vivo.
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PMID:Decreased releasability of basophils from patients with cold urticaria after cold exposure. 247 11

Twenty seven cases of actionomycotic mycetoma caused either by Actinomadura madurae or Actinomadura pelletierii have been described. Infection by A. madurae has been more common than A. pelletierii. Left foot in A. madurae and right foot in A. pelletierii infections were involved more commonly in adult males, whereas right foot of the females was frequently affected in A. madurae infection. Large, soft, white grains in A. madurae and small, firm, red grains in A. pelletierii were consistently seen. Deep hematoxylin stained grains with scalloped margin and prominent eosinophilic club in A. madurae and such deep stained grains with smooth margin and horizontal cracks appearing as portions of a spherical mass in A. pelletierri were diagnostic. Large numbers of plasma cells and Russel bodies were also characteristic of A. madurae infection. Both the grains were stainable with Von Kossa method for calcium. Bone changes were similar in both the infections. Oral tetracycline produced soft tissue and bone resolution to almost normalcy in those who regularly consumed the drug any time from 2 to 6 years. Mild glucose intolerance, facial hyperpigmentation and urticaria were the side effects observed in a few. Two patients developed cataract following tetracycline therapy. The value of medical therapy with oral tetracycline in Actionomadura mycetomas is emphasized.
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PMID:A clinico-pathological study of actinomycotic mycetomas caused by Actinomadura madurae and Actinomadura pelletierii. 357 38

The antimalarials, chloroquine, hydroxychloroquine, and quinacrine, are used primarily for malaria; but they can be beneficial for cutaneous lupus erythematosus (LE), polymorphous light eruption, solar urticaria, and porphyria cutanea tarda. Antimalarials bind to deoxyribonucleic acid (DNA) which prevents DNA and ribonucleic acid (RNA) polymerase reactions and DNA heat inactivation; and they inhibit the LE cell phenomenon, antinuclear antibody reactions, and suppress lymphocyte transformation. By competing with calcium ion, they stabilize membranes and have an anesthetic effect. Their anti-inflammatory potential is due to their inhibition of hydrolytic enzymes, stabilization of lysosomes, interference with prostaglandin synthesis, blocking of chemotaxis, and antagonism of histamine responses. The antimalarials have no sunscreening properties. The most common toxic effects are cutaneous pigmentation, nausea, vomiting, diarrhea, mild ileus, and cycloplegia. There has been a reluctance to use chloroquine and hydroxychloroquine because of the possibility of retinopathy. However, if the "safe" daily dose limit of chloroquine, 2 mg per pound of body weight, and of hydroxychloroquine, 3.5 mg per pound of body weight, is followed, the chance of retinopathy is slight. Quinacrine does not cause retinopathy, but it has more cutaneous side effects than the other two agents.
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PMID:Antimalarials. 616 44

Histamine release from human peripheral leukocytes was studied in patients with urticaria, pollinosis, and psoriasis and compared with the release in normal healthy donors using anti-IgE or the calcium-ionophore A 23187 as stimuli in the presence of three calcium mineral solutions (Frubiase Calcium). It was observed that among 35 donors 29 revealed a calcium dependent inhibition of histamine release. The inhibition was also evident when calcium mineral solution was added to an ongoing histamine release. The membrane biochemical effects of calcium mediated inhibition are currently under investigation.
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PMID:Effect of calcium mineral solutions on the histamine release from human peripheral leukocytes. 620 Jan 23

Mast cells with their stores of vasoactive and chemotactic mediators are central to the pathogenesis of allergic diseases. The cross-linking of receptorbound IgE molecules on the surface of mast cells initiates a complex chain of events, including calcium ion influx, phospholipid methylation and turnover and cyclic nucleotide metabolism, ultimately resulting in the release of mediators of immediate hypersensitivity. These mast cell mediators are important in smooth muscle reactivity, in the recruitment of eosinophilic and neutrophilic leukocytes and in the generation of secondary chemical mediators. Histologic evidence of mast cell degranulation, biochemical evidence of mast cell mediators in blood and tissues and clinical evidence of signs and symptoms reproducible by these mediators have strongly supported the crucial role of mast cells in asthma, urticaria, anaphylaxis, rhinitis and mastocytosis. Because of their unique location at host environment interfaces, mast cells may both participate in allergic diseases and promote homeostasis.
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PMID:Mast cells in allergic diseases and mastocytosis. 629 4

Hormones of the thyroid gland (thyroxine, tri-iodothyronine) control the metabolism of cells and tissue of the body, while parathormone and calcitonine are balancing the intra- and extracellular levels of calcium and phosphorus by governing some metabolic functions of bones, kidney and small intestine. Growth, maturation and metabolic homeostasis of the organism depend, among other intrinsic factors, on a normal production and secretory rate of both thyroidal and parathyroidal hormones. Clinical conditions of hyperthyroidism induce 1. increased metabolic turnover of the body with transcutaneous heat loss, 2. disordered growth of hairs and nails, 3. hyperpigmentation of skin, 4. pruritus with or without urticaria. Pretibial (usually symmetrical) myxedema may be associated with conditions of either hyper- or hypothyroidism (e.g., Hashimoto's thyroiditis); if combined with bilateral exophthalmus and acropachyderma of fingers and toes, it is called Diamond syndrome, or E.M.O. syndrome. In hypothyroidism, the skin feels chilly and dry, looks pale, and may present follicular keratoses with or without secondary eczema. The hair appears dull and sparse due to disordered anagen phase. Skin wounds heal with delay. Diffuse myxedema originates in the papillary and periadnexal connective tissue and eventually extends to the dermis as a whole. Clinical conditions of hyperparathyroidism rarely cause secondary calcification of the skin; they may induce severe pruritus, particularly in secondary hyperparathyroidism due to renal failure. Impetigo herpetiformis or generalized pustular psoriasis, resp., may be set off by excessive surgical removal of the goiter. Congenital maldevelopment of both thymus and parathyroid gland leads to cellular immune deficiency with secondary chronic muco-cutaneous candidosis.
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PMID:[The thyroid gland, the parathyroid gland and the skin]. 648 58

The urticarias are a complex group of disorders characterised by transient whealing or swelling of the skin. Understanding the many possible causes is the first step in assessing urticaria. Allergic and drug-induced urticaria respond to removal of the cause. The physical urticarias, particularly delayed pressure urticaria and also urticarial vasculitis, require separate consideration. For the majority of patients with chronic idiopathic urticaria, nonsedating antihistamines are the mainstay of treatment. There are several to choose from, including cetirizine, astemizole, loratadine, terfenadine and acrivastine, each with its own pharmacokinetics and antiallergic properties. When these fail, histamine H2-antagonists may help either alone or in combination with H1-antagonists. Older sedative antihistamines are still useful. Ketotifen, oxatomide and azelastine have mast cell stabilising effects that are considered an advantage in treating these disorders. Second-line therapies include a wide range of drugs such as doxepin, dapsone, attenuated androgens, calcium antagonists, antimalarials, gold and methotrexate. The most effective and regularly used second-line agents are corticosteroids. These are best limited to short term crisis management, except in severe recalcitrant cases, and in patients with pressure urticaria or urticarial vasculitis. Recent work on circulating histamine releasing autoantibodies suggests that there is scope for more aggressive immunosuppression in selected patients. However, effective treatment with immunosuppression often requires plasma exchange and more toxic agents such as cyclosporin. Such treatments are only likely to be entertained in exceptional cases.
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PMID:Urticaria. Recognition, causes and treatment. 753 Jun 29


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