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 study of one hundred and fifty cases of chronic urticaria observed, gave the following results: higher female frequency, usual beginning at adult age, relative absence of digestive problems. For the last of these results we nevertheless noted numerous insignificant functional features, a few examples of colitis, a number of cases of non-functioning gall-bladder. Frequency of sensitivity to foods, preservatives, colouring agents, medical substances, principally shown by provocation tests (the latter present a considerable interest, and merit frequent use); importance of bacterian, mycotic, parasitic origins; little importance of atopy; frequency of minor psychogenic disorders. A contributing role might be played by spasmophily. The therapy includes the following basic treatment; antihistaminic drugs (mainly hydroxyzine hydrochloride and cyproheptadine hydrochloride) and a diet which eliminates recognized urticaria causing foods. In addition, a supplementary treatment destined to eliminate the factors shown to be responsible for the outbreak, must be prescribed.
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PMID:[Chronic urticaria. Etiologic and therapeutic evaluation of 150 cases. (author's transl)]. 3 29

Histamine release from peripheral blood leukocytes challenged with anti-human IgE was studied in patients with chronic urticaria and nonatopic controls. 19 of 23 controls, but only 6 of 20 patients, released over 20% of the total available leukocyte histamine. The response to anti-IgE concentrations of 1.66, 0.33, 0.066, and 0.013 mug antibody N/ml was significantly lower in patients than in controls. Serum IgE levels were significantly higher in the patients but total histamine content of about 10(7) leukocytes was not. Deuterium oxide (D2O) greatly increased histamine release (in both groups), indicating that the anti-IgE interacted with the basophils of urticaria patients. Passive sensitization of leukocytes with biologically active IgE was achieved in both patients and control subjects whose cells responded to anti-IgE, but was not achieved in either patients or control subjects whose cells were nonresponsive to anti-IgE challenge. 125I-anti-IgE autoradiographic studies revealed no obvious quantitative abnormality in the amount of basophil-bound IgE in chronic urticaria patients. Ionophore stimulation of aliquots of the same leukocytes used for anti-IgE challenge demonstrated that the urticaria patients' basophils were capable of releasing normal amounts of histamine. Leukocyte cyclic AMP levels in the two groups were not significantly different either in base-line levels or in responsiveness to stimulation with isoproterenol. These data indicate that chronic urticaria patients have a (acquired?) defect in leukocyte histamine release that occurs after the anti-IgE-IgE interaction, but before the actual (second-stage) release process, and that is comparable to the phenomenon of desensitization.
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PMID:Defective histamine release in chronic urticaria. 5 21

The erythema and wealing resulting from the application of thurfyl nicotinate ointment (Trafuril) and from the inoculation of kallikrein has been studied in patients with chronic urticaria and normal controls. Polyphloretin phosphate (PPP) suppressed the reaction in controls but in patients with urticaria it increased the reactions to Trafuril and had little effect on the kallikrein reaction. PPP also suppressed the PGE2-induced erythma in normal controls but not in urticaria patients. In a separate study using fibrinolysis autography, prostaglandin (PG) E2 and PGF2alpha depressed fibrinolysis in the skin of two pigs and both kallikrein and Trafuril suppressed fibrinolysis in human skin. It is suggested that the inflammatory reaction induced by thurfyl nicotinate and kallikrein is mediated in part by a prostaglandin-like action. Several anomalies in the action of Trafuril in skin diseases can be explained if such prostaglandin-like activity is mediated in part through inhibition of fibrinolysis.
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PMID:The cutaneous reactions to kallikrein, prostaglandin and thurfyl nicotinate in chronic urticaria and the effect of polyphloretin phosphate. 5 6

The hypothesis that deficiencies of plasma protease inhibitors might play a role in the pathogenesis of chronic urticaria was evaluated. Plasma levels were measured in patients with urticaria and a matched control group for alpha1-antitrypsin, alpha2-macroglobulin, total trypsin-inhibiting capacity, kallikrein-inhibiting capacity, and the complement factors C1 esterase inhibitor, C3, and C4. A total of 92 patients with chronic urticaria or more than three months' duration was studied. Patients with acquired cold urticaria had significantly decreased levels of alpha1-antitrypsin and total antitrypsin activity. In patients with acquired angioneurotic edema, alpha1-antitrypsin levels and antichymotrypsin activities were lowered, with less significant decreases in anti-trypsin and antikallikrein activities. Levels of C1 esterase inhibitor , C3, and C4 were normal in all groups. There was no correlation between the increased sensitivity to intracutaneously administered kallikrein injection and deficiencies of of protease inhibitors.
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PMID:Protease inhibitors in plasma of patients with chronic urticaria. 6 Sep 15

Five patients with delayed cold urticaria are described. The urticarial skin response was present between 24 and 72 hours after ice challenge. In two of the patients the cold sensitivity was of clinical relevance. Some of the patients displayed low alpha1-antitrypsin and increased C4 levels in their serum. Our findings may justify the introduction of cold provocation as a routine procedure in the investigation of a patient with chronic urticaria.
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PMID:Delayed cold urticaria. 8 39

Some etiologic possibilities which must be considered are foods, drugs, infection, inhalant sensitivity, psychic factors, physical agents, underlying connective tissue disease or neoplasm, insect bite or stings and genetic abnormalities. A painstaking history and a complete physical examination are, of course, mandatory. These are followed by appropriate studies for whatever etiologic factors are suggested by the history and physical examination. Certain routine or more sophisticated studies might be indicated including a complete blood count, urinalysis, stools for ova and parasites, antinuclear antibody titer, complete complement, sedimentation rate, sinus, chest and dental X rays and any other specified test depending on where the clues lead. O'Loughlin described a practical approach in the use of laboratory studies for the diagnosis of chronic urticaria. Skin tests can be helpful especially for inhalants, but food tests are usually not reliable in the diagnosis of chronic urticaria. The acute urticaria reaction to a food is clinically obvious and this type of patient does not usually seek medical attention or need extensive investigation. Treatment includes a few basic medications. Hydroxyzine (Atarax, Vistaril), which combines tranquilizer and antihistamine action, is frequently effective. Cyproheptadine HCL (Periactin) both a serotonin and histamine antagonist with anticholinergic effect, is also helpful--especially in combination with hydroxyzine. Antihistamines, ephedrine, epinephrine, aminophyllin and occasionally corticosteroids are helpful. Immunotherapy with inhalants is occasionally indicated. Eliminating possible offending foods, dyes or drugs has been previously discussed. Anti-candidal therapy and low yeast diet is effective when indicated. The final aspect of the investigation and treatment process might best be described as "patient support"--patience on the part of the physician. It should be realized that in 75% of the cases of chronic urticaria, no convincing etiology is found. It should also be realized that urticaria all too frequently "settles down" due as much to the natural course as to the careful ministrations of the physician.
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PMID:An allergist looks at urticaria. 13 66

The C1q precipitin test was performed in serum samples from five groups of patients: (1) 20 patients with acomplementemic systemic lupus erythematosus glomerulonephritis (SLE), (2) 2 patients with serum sickness due to the administration of horse serum, (3) 2 patients with serum sickness preceding hepatitis B, (4) 50 patients with chronic urticaria, and (5) 30 normal controls. Positive C1q precipitin tests were found in all patients with SLE and the four cases of serum sickness. Positive tests correlated with depressed serum complement (C3 and C4) levels and were found only in the early phase of serum sickness. Urticaria patients uniformly had negative C1q precipitin tests and normal serum complement levels.
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PMID:Studies of urticaria and acute serum sickness with the C1q precipitin test. 13 55

Serum immunoglobulins, complement and alpha 1-antitrypsin were assayed in forty-eight patients with chronic urticaria. Thirteen cases had chronic cold urticaria and thirty-two had chronic idiopathic urticaria. Elevated mean serum IgM was found in chronic cold urticaria. Seven patients had partial immunoglobulin deficiencies. IgE was elevated in sixteen cases of chronic idiopathic and in two with chronic cold urticaria. Eight patients had depressed serum total haemolytic complement activity. Low C3 and normal C4 serum protein concentrations in four cases suggested alternative complement pathway activation. Twenty of forty-six patients were atopic, although specific allergies responsible for the urticaria were not identified in any of them. alpha 1-antitrypsin levels were normal in all patients. The data suggest that the aetiology and pathogenesis of chronic urticarias in this study are heterogeneous. No evidence of abnormality of the protease inhibitor system in either chronic idiopathic or chronic cold urticaria was found.
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PMID:Immunological parameters and alpha 1-antitrypsinin chronic urticaria. 31 14

Twelve of 54 patients with systemic lupus erythematosus (SLE) had nonpuric, chronic urticaria-like lessions. Skin biopsy of the lesions was performed in 11 cases, and nine showed necrotizing vasculitis. The 54 patients, in general, had severe disease, and laboratory and clinical data suggested a postivite relationship between the urticaria-like lesions and disease severity. There was no consistent relationship between the course of the urticaria-like lesions and the serologic findings and clinical activity of the SLE. The frequency and importance of urticaria-like lesions in SLE deserve further study.
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PMID:Chronic urticaria-like lesions in systemic lupus erythematosus. A review of 12 cases. 35 70

The cause of urticaria and angioedema often is difficult to ascertain. In most cases the conditions are transient, but a chronic idiopathic form does occur and may be intractable. Acute urticaria and angioedema usually result from an IgE-mediated mechanism; success in treatment depends on recognition of the underlying factor. Chronic urticaria may ultimately necessitate use of corticosteroids. Hereditary angioedema is easily differentiated from idiopathic angioedema by the family history and absence of pruritus.
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PMID:Urticaria and angioedema. Common clinical problems. 42 57


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