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)

A case of localized urticaria in an otherwise healthy young woman, produced only by direct contact of the skin with heat, is described. The minimal temperature of urtication was 44 degrees C (immersion of the forearm in hot water for 5 min). Redness and painful oedema immediately developed without reflex flare. Total serum IgG, IgA, IgM, IgE, complement factors C3 and C4, and alpha1-antitrypsin were in the normal range, whereas the C1-inhibitor level was slightly decreased. There was no evidence of circulating immune complexes in the serum. A skin test and a RAST with house dust were positive, but there were no signs of respiratory atopy. An attempt for passive transfer of heat urticaria into the abdominal skin of a rhesus monkey failed, but was successful for house dust. A treatment trial with ketotifen, a new, perorally acting anti-allergic drug, was poorly effective, but dexchlorpheniramine maleate, a classical antihistaminic, in a dose of 12 mg daily completely suppressed the swelling evoked by heat, but not the erythema, suggesting that other tissue or plasma factors than histamine may be involved in the mechanism of heat urticaria in this patient.
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PMID:[Clinical and immunological studies on acquired heat contact urticaria (author's transl)]. 3 3

A survey was made on workers handling powdered drugs in a pharmaceutical factory. In this factory, two kinds of anti-inflammatory enzyme (bromelain and trypsin), one anti-inflammatory agent (flufenamic acid), one antispasmodic (flopropion) and two kinds of antibiotics (ampicillin and cephalexin) are mainly produced. Twenty four workers were examined by interviews and checked by Cornell Medical Index, and 18 of them complained of respiratory symptoms. These 18 workers were physically examined by skin scratch tests, pulmonary function tests and serum immunological tests. Among 24 workers, 9 handled powdered drugs (A group), 5 handled the same in the past and had already been transferred to other sections for their symptoms (B group), 3 engaged in the process of capsul-filling (C group) and 7 handled several times occasionally during one year (D group). Their average months spent in handling powdered drugs were, in the case of anti-inflammatory enzyme, A group 53.2, B group 66.2, and in the case of antibiotics, 5 workers in A group 24.0, 2 workers in B group 7.0, 3 workers in C group 25.7. Twenty workers complained of symptoms which were mainly irritation of mucosa including the respiratory system and itching of the skin while they were working, and accelerated nasal discharge, urticaria and asthma after working. Group A and group B were higher than group D in the rate of respiratory complaints in C.M.I. (p less than 0.001). Fourteen workers pointed out anti-inflammatory enzyme as a cause of main symptoms, 7 workers flufenamic acid, 3 workers flopropion, 4 workers antibiotics. Three workers who had past history of asthma or articular rheumatism had been transferred to other sections. Of 18 workers who were physically examined, 11 workers showed positive reactions to skin scratch tests with handling drugs. On 8 workers of them, some kinds of drugs which were pointed out as drugs causing main symptoms reacted positively. Numbers of workers with increased immunoglobin values were, IgE 3, IgM 2, IgA 4, IgM 2. Two workers showed decreased FVC and FEV (1.0 sec.) values in pulmonary function tests. The causes of the occupational allergic reaction in this factory are guessed as follows: 1) control of powdered materials was incomplete in the process of production, 2) various kinds of sensitizing drugs were handled by the same workers.
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PMID:[Some experiments on the allergic reaction among workers in a pharmaceutical factory (author's transl)]. 16 Apr 71

Six patients suffering from anaphylactoid reactions after infusion of pasteurized plasma (PP) or human serum albumin (HSA) were investigated. Clinical symptoms ranged from urticaria and hypotension to cardiac arrest. Immunoglobulin levels, especially of IgA, were normal, as were concentrations of complement factors C3, C4 and factor B. In skin and lymphocyte transformation tests patients, with the exception of one severely allergic to protein, did not react to the monomeric pure HSA. Five out of six patients reacted against HSA aggregates and three patients to the HSA modified by caprylate added as stabilizer during commercial HSA production. It is concluded that the anaphylactoid reactions developing after PP or HSA infusion result from a non-specific reaction to protein aggregates and in some cases possibly from a specific immune response to the caprylate-modified HSA.
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PMID:Anaphylactoid reactions to infusions of plasma protein and human serum albumin. Role of aggregated proteins and of stabilizers added during production. 42 39

Results of a study in 62 patients with urticaria and 30 controls, all under 12 years of age, are reported. The study involved history taking and assays of immunoglobulins A, G, M, D, E, of complement fractions C3c and C4 and estimation of C1 estease inactivator activity in the plasma. Acute urticaria is more frequent than chronic urticaria in children, expecially in subjects with atopic diathesis; papular urticaria (or strophulus infantum) is particularly frequent in children under 6 years of age and in the male. Assays of plasma immunoglobulins demonstrated selective deficiency of IgA in two and significant reduction of this immunoglobulin in a further three cases. The mean levels of IgE proved normal in chronic urticaria, raised in acute urticaria, and very high in papular urticaria. Complement assays demonstrated, in one case, a reduction of C3c below 60 mg/100 ml, persisting after the disappearance of urticaria.
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PMID:Pathogenetic factors in utricaria in children. A clinico-experimental study. 85 23

Schnitzler's syndrome, first described in 1974, is defined by chronic non-pruritic urticaria, osteocondentation, and a monoclonal IgM dysproteinemia, but without criteria of lymphoproliferative disease. We report a patient with chronic urticaria and macroglobulinemia. In addition, he had double monoconal dysproteinemia IgM kappa (31.3 g/l) and IgA lambda, osteocondensation, and some cutaneous lesions of pseudoxanthoma elasticum. Only 20 cases of Schnitzler's syndrome have been reported hitherto. This is the first case associated with pseudoxanthoma elasticum, which was localized and discovered at the same time as Schnitzler's syndrome. We discuss the possible role of monoclonal immunoglobulin in the occurrence of localized elastorrexhis.
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PMID:Schnitzler's syndrome (urticaria and macroglobulinemia) associated with pseudoxanthoma elasticum. 135 Jan 35

To study immune responses that may play a role in immediate-type allergic reactions (ITAR) and serum-sickness-like reactions that have been reported with administration of monoclonal antibodies (MAb), we measured by enzyme-linked immunosorbent assay serum levels of IgE, IgG, and IgA human antimurine antibody (HAMA) to T101, a murine IgG2a antibody that has been used in the treatment of cutaneous T cell lymphoma (CTCL) and chronic lymphocytic leukemia (CLL). None of 8 patients (4 with CLL, 4 CTCL) pretreated with T101 had elevated titers of any HAMA class tested as compared to normal control sera. All CTCL patients who had elevated total serum IgE levels, but normal total serum levels of other antibody classes, had significant rises in IgE, IgG, and IgA HAMA to T101 after intravenous MAb infusion. However, the CLL patients who were hypogammaglobulinemic failed to develop significant rises in HAMA. Three patients (2 CLL, 1 CTCL) had ITAR (e.g., urticaria, angioedema, bronchospasm) associated with infusion of T101; prophylactic medication regimens based upon the control of radiographic contrast media reactions were used with apparent benefit in subsequent infusions in these patients. All 8 patients had negative immediate intradermal skin tests (1 microgram/ml) to T101 prior to its infusion. Our data confirm that (1) non-IgE-mediated mechanisms cause ITAR from this MAb, possibly by a mechanism inherent in the action of this MAb against lymphocytes, and (2) that isotypic antibody responses to MAb vary with the type of malignancy being treated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Human IgE, IgG and IgA antibody responses to T101, a murine monoclonal antibody against human lymphocytes: implications for pathogenesis, risk and avoidance of adverse immunologic reactions. 224 27

Thirty seven patients with chronic urticaria were prospectively studied from August 1984 to July 1986. These patients were submitted to regular and immunological laboratory tests. Biopsies were taken from recent urticarial lesions for histologic analysis and also to direct immunofluorescence and immunohistochemistry studies. Vasculitis was found in 27% of the patients. Most of them showed only urticarial lesions except two (20%), that presented residual macula; angioedema occurred in 20% of the urticarial vasculitis (UV) patients; most cases had no systemic manifestations. Serum immunoglobulins and circulant immunocomplexes were increased in both groups. Complement reduction was considered an evidence of vascular aggression, being found in 55% of the UV patients. Direct immunofluorescence studies showed only 10% of positive IgM fluorescence in the vessel walls in the UV group. Immunohistochemical evaluation in the same group revealed mainly slight deposition of immunoglobulins IgG, IgM and IgA in the plasma cells of 80% of the samples and in only 10% there was immunoglobulin deposition in the vessel walls. The authors concluded that conventional histopathology is the best diagnosis method for urticarial vasculitis, direct immunofluorescence and immunoperoxidase being ancillary tools. Therefore, a special group of patients was detected, clinically and therapeutically resembling common urticaria patients, but presenting vasculitis in the histologic exam. This fact leads to the hypothesis that there is a range between common urticaria and urticarial vasculitis with systemic involvement.
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PMID:Urticarial vasculitis. 226 52

Study was made of immune responses in cow's milk allergy by a new immunoassay that measures total Ig-secreting cells and specific antibody-secreting cells during their maturation cycle in peripheral blood. These primed gut-associated lymphoid tissue-derived lymphocytes are assumed to reflect the intestinal immune responses. During diagnostic milk provocation, 15 patients had acute urticarial skin eruptions, eight patients had slow onset of eczema, and 15 showed symptoms from the gastrointestinal tract. A significant increase in IgM-secreting cells (means with 95% confidence intervals) from 382.2 (265, 552) to 621.4 (381, 1013)/10(6) cells, p less than 0.01, but not IgA- and IgG-secreting cells was associated with acute urticaria. In patients with eczematous skin eruptions and gastrointestinal symptoms, the response involved all these Ig isotypes. The magnitude of the postchallenge Ig-secreting cell responses in patients with gastrointestinal symptoms in the IgM class [from 657.9 (428, 1012) to 3544.0 (1696, 7406)/10(6) cells, p less than 0.001] and the IgA class [from 974.6 (590, 1610) to 2482.4 (1528, 4028)/10(6) cells, p = 0.001] significantly exceeded that of the patients with cutaneous symptoms. Notwithstanding the distinct increase in the total number of Ig-secreting cells, the specific antibody-secreting cell response specifically directed against beta-lactoglobulin and alpha-casein was small and inconsistent. These findings indicate that immune exclusion of milk antigens is defective in cow's milk allergy. The quality and extent of the response varied in the three reaction types, suggesting that different immunopathogenic mechanisms are operative in cow's milk allergy.
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PMID:Local immune response measured in blood lymphocytes reflects the clinical reactivity of children with cow's milk allergy. 228 53

We assessed the relationships of clinical symptoms and serum antibody levels during follow-up of 47 patients, aged 3 to 66 months, who were shown by formal milk challenge to have cow milk allergy. Three groups of patients were identified. Group 1 patients (n = 15) were sensitized to IgE and responded rapidly to small volumes of milk with urticaria, an exacerbation of eczema, wheeze, or vomiting. In the second group (n = 24), symptoms of milk enteropathy (vomiting and diarrhea) developed between 1 and 20 hours after milk ingestion. In the group 3 patients (n = 8), coughing, diarrhea, eczematoid rashes, or a combination of these developed more than 20 hours after normal volumes of milk were given. Serum levels of IgG, IgA, IgM, and IgE and of milk-specific anti-cow milk antibodies of these isotypes were measured initially and then at a median follow-up time of 16 months (range 6 to 39 months). In this investigation, changes in these immunologic measures during the study period were related to whether or not clinical tolerance to cow milk was achieved. At follow-up, six patients from group 1, ten from group 2, and two from group 3 were milk tolerant. No consistent change in any of the immunologic measurements was associated with remission of the disease. These findings raise the question of whether acquisition of clinical tolerance to cow milk in cow milk allergy can be attributed solely to immunologic events.
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PMID:Recovery from milk allergy in early childhood: antibody studies. 271 89

Spontaneous plaque-forming cells (S-PFC) were followed in 67 bone marrow transplantation (BMT) recipients and 41 controls. Patients with no acute graft-versus-host disease (GVHD) had decreased IgA and IgM S-PFC up to 7 weeks after BMT compared with controls. Patients with acute GVHD had increased IgG, IgA, and IgM PFC compared with controls and patients without GVHD during the first 4 weeks after BMT. The maximum number of S-PFC increased with increasing severity of acute GVHD. However, at diagnosis of GVHD there was no difference in S-PFC in patients who resolved their GVHD or in those who developed more severe GVHD. After 6 weeks, patients with acute GVHD had significantly decreased IgA and IgM S-PFC compared with normal. No major changes in S-PFC were induced during various infections. However, a patient who developed urticaria had a dramatic increase in S-PFC. Patients studied more than a year after BMT had reduced IgM S-PFC compared with controls. It is concluded that S-PFC are reduced after BMT, but markedly enhanced during acute GVHD.
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PMID:Polyclonal antibody secretion during acute graft-versus-host disease. 282 43


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