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)

Many diseases caused by occupational exposures may have an allergic or immunopathogenetic basis. These include asthma, hypersensitivity pneumonitis, the pulmonary disease-anemia syndrome, allergic contact dermatitis, and contact urticaria. This article discusses concepts important to the understanding of occupational forms of these diseases and provides approaches to their diagnosis, treatment, and prevention.
Prim Care 1987 Sep
PMID:Occupational respiratory and dermatologic disease. 295 77

At a major fish factory in northern Norway, workers employed in fish-stick and fillet production participated in a survey on skin diseases. 122 (80.1%) of the workers in the fish-stick section responded, but only 60.7% of the fillet workers. Clinical examination and patch testing revealed 16 cases of occupational dermatitis among workers in fish stick production, 3 of whom had contact urticaria from mustard and 8 from fish. There were only found 6 cases of occupational dermatitis among fillet workers; 3 reacted to fish and 3 had irritant contact dermatitis. Working conditions are described for both locations. A greater exposure to irritants may in part explain the 10.7% occupational dermatitis in the fish-stick section compared to only 3.5% in the fillet section.
Contact Dermatitis 1987 Sep
PMID:Contact urticaria from mustard in fish-stick production. 296 Apr 85

The anaphylactic shock is a life-threatening reaction produced by the release of pharmacologically active substances (histamine, leukotriene...) by most cells and basophils. The release of these mediators may be immunologically mediated (anaphylactic reaction a typical immediate hypersensitivity reaction mediated by IgE) or not (anaphylactic reaction when not mediated by an antigen-antibody process). These mediators in turn specific end-organ responses in the cardio-vascular system, (vasodilatation, change in inotropy, increased capillary permeability), the respiratory system (bronchospasm upper airway oedema) and the skin (urticaria). Because of its etiology (mainly drugs, contrast media and colloids) the treatment of anaphylactic or anaphylactic reactions must be prophylactic. When it occurs, its cure is based upon adrenaline and fluid loading and eventually bronchodilators.
Allerg Immunol (Paris) 1988 Sep
PMID:[Anaphylactic shock]. 305 90

Benoxaprofen (BPF) induces a clinical photosensitivity which resembles idiopathic solar urticaria. This response is mediated by degranulation of mast cells. Since mast-cell degranulation is known to be modulated by phospholipid alteration, we examined the effect of BPF and ultraviolet radiation (UV) on phospholipid metabolism of C3H 10 T1/2 cells in culture. BPF + UVB (280-320 nm) induced release of [3H]arachidonic acid (AA) but did not alter the release of [3H]choline from prelabelled cells. This suggests that BPF photosensitizes phospholipase A2 activation. Such activation probably represents an integral step in the mechanism of BPF photosensitization of mast-cell degranulation.
Toxicol Lett 1986 Sep
PMID:Benoxaprofen photosensitization of phospholipase activation in mammalian cells in culture. 309 56

The differential regulation of immunoactive FSH and LH secretion by endogenous GnRH was studied using a GnRH antagonist, [Ac-D2Nal1,D4FPhe2,DTrp3,DArg6]GnRH (the NAL-ARG antagonist), in normal women in the early follicular phase of the menstrual cycle, and their responses were compared to those in two groups of control women. Pulsatile LH secretion was examined as an index of the completeness of blockade of endogenous GnRH secretion. There was a dose-dependent decrease in both the frequency and amplitude of LH pulses. At the highest dose, LH pulses were completely abolished within 20 min after sc administration of the GnRH antagonist and for a minimum of 8 h in all women. The mean plasma LH levels were reduced within the first 4 h after antagonist administration at all doses (P less than 0.001). The duration of LH suppression was influenced by antagonist dose, with a continued effect 24 h after administration of the 500 micrograms/kg dose only. The maximum degree of LH suppression was 40% after 50 micrograms/kg (n = 6), 60% after 150 micrograms/kg (n = 6), and 59% after 500 micrograms/kg (n = 5). In contrast, plasma immunoreactive FSH levels did not change after these doses of the NAL-ARG GnRH antagonist. The maximum degree of FSH suppression was 16%, and the changes in plasma FSH concentrations were not dose dependent. Serum antagonist concentrations rose within 30 min after its administration to mean peak levels of 7.5 +/- 2.1 (+/- SE), 20.4 +/- 6.1, and 151 +/- 21 ng/mL after the 50, 150, and 500 micrograms/kg doses, respectively. The half-time of the disappearance of the NAL-ARG GnRH antagonist from plasma was 8.8 +/- 1.5 h. While there were no effects of antagonist administration on hematological, hepatic, or renal function, three women developed urticaria distant from the site of injection when administered the highest dose. We conclude that blockade of GnRH receptors by a GnRH antagonist 1) effectively antagonizes the action of GnRH, as assessed by its ability to block pulsatile LH secretion and reduce mean plasma LH levels; and 2) inhibits LH release to a considerably greater degree than FSH release, providing further evidence of possible GnRH-independent FSH secretion.
J Clin Endocrinol Metab 1988 Sep
PMID:Evidence of differential control of FSH and LH secretion by gonadotropin-releasing hormone (GnRH) from the use of a GnRH antagonist. 313 43

In a study of cows' milk allergy (CMA) in infancy, 135 consecutive challenges were performed on children with a good clinical history of the disorder. Of these, only half of the patients were shown to have the disease. Highly atopic patients responded rapidly to small volumes of milk with acute urticaria, wheezing, stridor and eczema, whereas patients who were relatively non-atopic developed symptoms of eczema, bronchitis and wheezing over several hours or days. In a statistical evaluation of the diagnostic value of skin tests and RAST it was shown for the extracts used in this investigation, and for the population studied, all patients with SPT greater than or equal to 4 had CMA. The results highlight the potential diagnostic value of SPT in the identification of children with some forms of CMA if standardized cows' milk allergen extracts can be prepared.
Clin Allergy 1988 Sep
PMID:Clinical manifestations of cows' milk allergy in childhood. II. The diagnostic value of skin tests and RAST. 323 25

Urticaria and angioedema are common medical problems. This article presents a classification and review of the diverse etiologic factors that can trigger these problems. A practical approach to differential diagnosis and various therapeutic modalities are also explained.
Prim Care 1987 Sep
PMID:Urticaria and angioedema. 331 60

During the last few years, the structure and function of human C1-inhibitor have been elucidated. Chromogenic substrate assays for determination of C1-inhibitor activity in plasma are available, and have proved to be of value not only for the diagnosis of hereditary angioedema but also in acquired diseases involving C1-inhibitor, such as cold urticaria and autoimmune disorders as well as acute-phase types of disease states.
Clin Rheumatol 1987 Sep
PMID:Aspects of C1-inhibitor biochemistry and pathophysiology. 332 41

Eight patients with cutaneous T cell lymphomas (CTCL) and five with various other T cell malignancies were treated with mouse monoclonal antibody (MoAb) T101. Doses of 1 to 500 mg were administered weekly over a two-hour period and resulted in one complete remission (convoluted T cell lymphoma) and one partial remission (CTCL). Remission duration was 6 weeks and 3 months, respectively. Frequent toxicities were pruritus, hives, flushing, and shortness of breath. Supraventricular arrhythmias and blood pressure instability were also observed. Complete targeting of peripheral blood T cells was achieved with 1 mg of MoAb in the nonleukemic patients (WBC less than 10,000/microL), and free, bioavailable antibody was present at the next (10-mg) dose level. Even higher doses resulted in substantial antibody excess that persisted for as long as 6 weeks. Serum concentrations of MoAb decreased with increasing number of peripheral blood T cells, and 25 to 35 mg of T101 were required for induction of antibody excess in leukemic patients. Excess antibody induced antigenic modulation, which was of consequence only if MoAb excess persisted to the next treatment. In the original treatment, the rapidly administered MoAb was able to target and remove peripheral blood T cells before the development of antigenic modulation. Antimouse antibodies developed in three patients. Their presence rendered further therapy ineffective and was associated with an anaphylactic reaction in one patient. Development of these antibodies could not be predicted by lymphoproliferative assays. In these assays, however, the T101 protein strongly stimulated the mononuclear cells of the patient who reached the only complete remission of this trial. Immunologic stimulation by the MoAb thus might have played a role in this patient's antitumor response. In summary, therapy with MoAb T101 was specific but only modestly efficacious. Rapid infusion of nonmodulating doses of antibody provided excellent targeting and removal of peripheral blood T cells and might be a valid approach in future trials with immunoconjugated T101.
Blood 1986 Sep
PMID:Monoclonal antibody T101 in T cell malignancies: a clinical, pharmacokinetic, and immunologic correlation. 348 78

The murine IgG3 monoclonal antibody (MoAb) 3F8, specific for the ganglioside GD2, activates human complement, is active in antibody-dependent cell-mediated cytotoxicity (ADCC), and can target specifically to human neuroblastoma in patients with metastatic disease. In a phase I study, 3F8 was administered intravenously (IV) to 17 patients with metastatic GD2 positive neuroblastoma or malignant melanoma at doses of 5, 20, 50, and 100 mg/m2. Serum 3F8 levels achieved were proportional to the dose of 3F8 infused. However, serum antimouse antibody levels did not increase with the amount of 3F8 administered. Toxicities included pain, hypertension, urticaria, and complement depletion. All acute side effects were controllable with symptomatic therapy. No long-term side effects were detected in patients observed for more than 14 months. None of the 17 patients received any antitumor therapy postantibody treatment. Antitumor responses occurred in seven of 17 patients. These ranged from complete clinical remissions to mixed responses. The murine monoclonal antibody (MoAb) 3F8 has clinical utility for the diagnosis and therapy of neuroblastoma and melanoma.
J Clin Oncol 1987 Sep
PMID:Ganglioside GD2 specific monoclonal antibody 3F8: a phase I study in patients with neuroblastoma and malignant melanoma. 154 29


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