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 case of a 10 month-old girl with a history of recurrent urticaria and diarrhoea is presented. Immunological study was carried out and secretory component in sputum, duodenal juice and stool was not found, while IgA was detected. Peroral biopsy of intestinum was also carried out and histology revealed partial villous atrophy. Immunofluorescent staining showed only a few IgA and IgG producing cells scattered within the villous stroma, while the IgM producing cells were increased in number. Serum concentration of IgA, IgM and particularly IgG was increased. Both parents had measurable IgA in the serum, however, the secretory component was not detectable neither in mother nor in father. The deficiency of secretory component and deficiency of IgA producing cells in the jejunal villous stroma led to local immunodeficiency of the intestinal mucosa and that caused recurrent urticaria and diarrhoea in the girl presented.
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PMID:Local immunodeficiency of the intestinal mucosa--a contribution to etiopathogenesis of recurrent urticaria and diarrhoea. 293 37

The authors evaluated the clinical efficacy of an adjunctive treatment with spores of Bacillus subtilis in 20 adult patients with urticaria-angioedema syndrome from food allergy. The patients treated with B. subtilis showed a significant reduction in frequency and severity of clinical features in respect to the patients who received no treatment. Bacillus subtilis spores may increase S-IgA synthesis or protect gastroenteric mucosa.
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PMID:Effects of an adjunctive treatment with Bacillus subtilis for food allergy. 310 71

We have prospectively evaluated the clinical and immunological features of serum sickness in 35 patients treated for bone marrow failure with anti-thymocyte globulin (ATG 15 mg/kg/day) and methylprednisolone (1 to 1.5 mg/kg/day). Twenty-one patients were treated for 10 days and 14 were treated for 28 days. Clinical evidence of serum sickness developed in 30 patients (86%) and included fever and malaise (100%), cutaneous eruptions (93%), arthralgias (67%), gastrointestinal complaints (67%), cephalgia (57%), blurring of vision (37%), arthritis, (30%) and lymphadenopathy (13%). Clinical serum sickness began on day 7 +/- 1 (X +/- S.E.M.) and lasted for 10 +/- 2 days in the 18 affected patients receiving the shorter course of ATG. In the 12 affected patients receiving the longer course of ATG, serum sickness began on day 9 +/- 1. The earliest manifestations of serum sickness were fever, malaise, and cutaneous eruptions. Cutaneous findings consisted of morbilliform eruptions (n = 19) and urticaria (n = 1) or a combination (n = 8) that lasted 10 to 14 days. Twenty-one patients (75%) developed a highly characteristic serpiginous band of erythema and purpura along the sides of the fingers, toes, palms and soles 12 to 48 hours before other symptoms of serum sickness. Biopsies of lesional skin during the course of serum sickness revealed immune deposits (IgM, IgE, IgA and C3) in dermal vasculature in 7 of 9 patients. Immunological changes that occurred during the course of serum sickness included increased serum levels of IgG, IgM, IgA, and IgE. Circulating immune complexes, as measured by the C1q-binding assay, increased from a mean value of 12% to 45% on day 13 +/- 1. Complement levels (C3, C4, and CH50) decreased 50 to 80% from their baseline levels on day 10 +/- 2. Acute phase reactants increased: erythrocyte sedimentation rate, C-reactive protein and beta-2 microglobulin. Abnormal urinalysis developed in 17 patients (57%) over the course of serum sickness and included proteinuria, hematuria and hemoglobinuria on day 10 +/- 3. Hematopoietic response occurred in 43%. All 5 patients who did not develop serum sickness recovered from bone marrow failure. Our data document the clinical and immunopathological findings in human serum sickness and suggest that the principles of antigen-antibody interaction, complement activation, and resultant inflammatory response as seen in the previous animal studies are directly applicable to studies of patients with serum sickness.
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PMID:Human serum sickness: a prospective analysis of 35 patients treated with equine anti-thymocyte globulin for bone marrow failure. 325 88

104 patients with erythema migrans disease (EMD), 7 patients with borrelia lymphocytoma (BL), and 21 patients with acrodermatitis chronica atrophicans (ACA) were prospectively followed for a median of 20, 14, and 12 months, respectively. 99 patients with EMD and 6 with BL were treated with antibiotics early for their illness. 72 patients with EMD had 1 to 10 constitutional symptoms besides the erythema migrans, 32 had erythema migrans alone, and a child with BL had urticaria. Out of 39 patients with EMD, 23 acquired arthralgia, 18 signs and symptoms consistent with neurologic manifestations and 8 with cardiac involvement before or after therapy. 4 patients with EMD and 1 with BL had up to 10 multiple erythema migrans lesions. 3 patients with EMD experienced a reinfection and 1 with ACA a relapse. Several patients with ACA developed signs and symptoms consistent with neurologic, cardiac and joint involvement, and 2 had a history of EMD. Elevated antibody titers against Borrelia burgdorferi were present in 48% of 69 patients with EMD, 5 with BL and 11 with ACA, and in 93% of another group with EMD, 2 with BL and 10 with ACA, when tested against other borreliae. Increased values of the ESR, IgG, IgA and IgM were found in more patients with ACA than with EMD. The median of IgA and IgM was significantly higher in ACA than in EMD. Borreliae were found in brain and liver of a newborn. Early EMD appears to be quite similar to early Lyme disease.
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PMID:Clinical features of early erythema migrans disease and related disorders. 357 81

The acquired form of cold induced urticarial syndrome can be found associated with serum cryoproteins, in idiopathic form (generally IgE mediated) and transitory forms associated with other factors. The viral infections, specially infectious mononucleosis and hepatitis B can cause urticaria, mostly chronic, although infrequently produces cold urticaria. We present a case of a 13 year old patient with history suggestive of cold urticaria wherein we have found the existence of a mixed polyclonal cryoglobulinemia, IgG-IgA (exceptionally associated) and serologic markers of hepatitis B, HBsAb and HBsAb (the last being suggestive of a recent infection) 3 months from the urticaria, without recent or past history of hepatitis B infection. We also observed an elevated total serum IgE and peripheral blood eosinophilia. The provocation test presented an evolution similar to the cryoglobulinemia and markers of hepatitis B (after 18 months were negative) but serum IgE and eosinophilia remain elevated until the present time. All of this make us think that the patient could have suffered a subclinical form of hepatitis B which triggered off a cryoglobulinemia, presenting as cold urticaria.
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PMID:[Cold urticaria associated with serologic markers of hepatitis B and cryoglobulinemia]. 366 57

Urticaria and angioedema are common disorders that affect approximately 1/5 of the population at some stage in their lives. Although the clinical diagnosis of this disorder is made without difficulty, its etiology and pathogenesis remain obscure. Extensive clinical studies and the application of different laboratory techniques seldom manage to detect the etiology of chronic urticaria or determine its supposed pathogenic mechanism. Thus, a large number of causal agents have been held responsible for the symptoms of chronic urticaria and/or chronic urticaria and angioedema and for the variety of immunologic and nonimmunologic factors involved in its pathogenesis. The controversial laboratory findings in this type of patients prompted us to undertake this study on 48 subjects with chronic urticaria and/or angioedema. We studied the levels of serum immunoglobulins (IgG, IgA, IgM and IgE), the haemolytic activity of the complement (CH50), the levels of the complement components (C1 inhibitor, C3 and C4), the possible presence of circulating immune complexes and the percentages of the T lymphoid subpopulations (using OKT3, OKT4 and OKT8 markers) and the B population. The results obtained showed an alteration of the complement (CH50) and of some of its components (C3 and C4) as well as of the cytotoxic/suppressor lymphocyte subpopulation (OKT8).
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PMID:[Immunologic parameters in chronic urticaria]. 379 6

We have prospectively evaluated the cutaneous manifestations of serum sickness in thirty-five patients treated with horse antithymocyte globulin for bone marrow failure. Twenty-one patients (21/35) were treated with antithymocyte globulin (15 mg/kg/day) for 10 days, and fourteen of thirty-five patients were treated with antithymocyte globulin (15 mg/kg/day) for 14 days and then every other day for an additional 14 days. Clinical evidence of serum sickness developed in thirty patients and included fever and malaise (100%), cutaneous eruptions (93%), arthralgias and myalgias (67%), gastrointestinal complaints (67%), and lymphadenopathy (13%). Cutaneous findings consisted of morbilliform eruptions (n = 19), urticaria (n = 1), or a combination of these two reaction patterns (n = 8). Cutaneous manifestations of serum sickness began on day 7 +/- 1 and lasted for 12 +/- 2 days for the group as a whole. Biopsies of lesional skin revealed mild perivascular lymphohistiocytic infiltrates by light microscopy in these leukopenic patients. Direct immunofluorescence microscopy of lesional skin from patients with serum sickness demonstrated immunoreactants in seven of nine subjects (78%). Immunoreactants were confined to the walls of dermal blood vessels and consisted of IgM (7/9), C3 (6/9), IgE (5/9), and IgA (4/9). IgG (horse or human) was not identified in any of these specimens. Twenty-one patients (21/28) also developed an erythematous eruption on the sides of the fingers, toes, palms, and soles 12 to 48 hours prior to their morbilliform eruption. This study describes the cutaneous manifestations of human serum sickness occurring during therapy with horse antithymocyte globulin, documents a cutaneous sign of serum sickness, and suggests that the cutaneous eruptions associated with human serum sickness are immunologically mediated.
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PMID:Cutaneous manifestations of serum sickness in patients receiving antithymocyte globulin. 387 81

The serum concentrations of "pregnancy-associated" alpha 2-glycoprotein (alpha 2-PAG) were measured in 129 healthy women and 141 healthy men to establish a normal range, using a sensitive enzyme linked immunosorbent assay. In the normal population 2.8% of men and 5.4% of women had low serum alpha 2-PAG concentrations. Low concentrations occur, however, much more commonly in patients, particularly male patients, with certain diseases, including dermatitis herpetiformis (three of 12 or 25%) and urticaria (two of five or 40%). One female patient with absolute deficiency was also identified. In view of the recently confirmed association of alpha 2-PAG with IgA and the fact that alpha 2-PAG seems to have immunosuppressive properties, it seems likely that deficiency of alpha 2-PAG could result in the subject becoming sensitised to various dietary antigens. Interestingly, none of the 24 patients with IgA deficiency showed concomitant deficiency of alpha 2-PAG.
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PMID:Deficiency of serum "pregnancy-associated" alpha 2-glycoprotein alpha 2-PAG): association with disease. 395 41

A total of 158 patients with pollinosis, bronchial asthma, urticaria and Quincke's edema were examined. The immunoglobulin and C3 levels in sera and the immunoglobulin and albumin levels in saliva were determined by the method of single radial immunodiffusion with the corresponding monospecific antisera. In all the groups of patients subjected to examination the presence of polyclonal hypergammaglobulinemia was detected, which was manifested by a rise in the levels of IgG, IgA and especially IgM; the level of IgD was low. A decrease in the level of C3 was detected in pollinosis patients in the absence of the exacerbation of the disease. No circulating immune complexes were detected. An essential increase in the level of IgG in saliva was revealed, which was due to the local synthesis of this immunoglobulin. In winter the level of salivary IgA in pollinosis patients was found to be essentially below normal, but at the period of exacerbation it increased twofold, probably in response to local stimulation with antigen-allergen. Patients with bronchial asthma and pollinosis were found to have a high level of free secretory component (SC); in pollinosis the level of free SC sharply increased during the stage of exacerbation, which was due to the increase of its synthesis and secretion by the epithelial cells of the mucous membranes. The importance of these data for the pathogenesis of allergic diseases are discussed.
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PMID:[Serum and secretory immunoglobulins in allergic diseases]. 405 Feb 21

An antiserum was raised against a monoclonal IgMk macroglobulin isolated from serum of a patient with recurrent urticaria. The antiserum was made idiotype-specific through adequate absorptions. The anti-idiotype antiserum reacted only with the immunizing protein and its Fab fragments and not with other monoclonal proteins of IgM and IgA class or pooled IgG as assayed in an enzyme-linked immunosorbent assay. IgM antibodies with the same idiotype as the monoclonal IgM protein were detected in the dermal/epidermal junction area of diseased skin. The similar idiotypic determinants could also be demonstrated on membrane-bound molecules of peripheral blood B and T lymphocytes using the immunofluorescence methods.
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PMID:Unique antigenic determinants (idiotypes) used as markers in a patient with macroglobulinemia and urticaria. Similar idiotypes demonstrated in the skin and on peripheral blood lymphocytes. 615 59


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