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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this review I have described the pathophysiology of allergic disorders of the gastrointestinal tract. Situations where the intestine cannot be a complete barrier to foreign allergens and antigens were discussed and etiological factors of gastrointestinal allergy were detailed. Clinical features of gastrointestinal allergy include diarrhea, vomiting, abdominal pain and colic, intestinal hemorrhage and malabsorption as well as symptoms and signs outside the gastrointestinal tract such as chronic rhinitis and asthma in the respiratory system, urticaria, angioedema and eczema as dermatological signs, headache, insomnia, hyperkinesis as central nervous system manifestations, failure to thrive and anaphylaxis as constitutional reactions. Milk allergy was discussed as an example of food allergy. Immunology of the gastrointestinal tract was presented, with examples of four types of hypersensitivity reactions, and gastrointestinal disturbances of immunodeficiency disorders and syndromes were named. Lastly, the autoimmune mechanism and the gut were described, with particular discussion of ulcerative colitis as an example of an autoimmune disease.
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PMID:The intestine in allergic diseases. 78 84

Chronic urticaria remains one of the major unsolved clinical problems in dermatology. My group has employed an integrated experimental approach in order to shed light on the pathophysiology and treatment of this group of disorders. Using delayed pressure urticaria as a model, evidence has emerged of the role of eosinophil major basic protein (MBP) and of interleukin-6 (IL-6) as important molecular mediators, possibly explaining the poor response to H1 antihistamines. Our recent work in chronic idiopathic urticaria has led to identification of a circulating greater than 100 kD factor which causes wealing following intradermal injection and which releases histamine from normal leukocytes in vitro. Further characterisation confirmed that this skin and histamine releasing reactivity is due mainly to an IgG anti-IgE autoantibody. That this autoantibody is functionally significant is supported not only by its ability to release histamine and cause local wealing, but also by the results of removal by plasmapheresis which we have shown to cause clinical improvement in seven out of eight patients with severe unremitting chronic urticaria. It is concluded that chronic 'idiopathic' urticaria is an autoimmune disease due, in most patients, to a functionally significant IgG anti-IgE autoantibody. Immunotherapy offers the best long-term prospects of relief in severe unremitting cases.
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PMID:Urticaria: new molecular insights and treatments. The Parkes Weber Lecture 1991. 137 92

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

Twelve cases of chronic urticaria with histopathologic features of lecocitoclastic allergic angitis are studied. The type of cutaneous lesion, personal and familiar atopic history and the presence of autoimmune disease are described. Light microscopy, direct immunofluorescence, anti DNA, antinuclear, antithyroid, Ro, La, Rnp and Sm antibodies, total complement levels, C3 and C4, rheumatoid factor, latex, ASTO, cryoglobulines and complete workup were investigated, taking into account natural progression and response to therapy. Two different groups are defined: 1) normocomplementemic (5 patients) and 2) hypocomplementemic (7 patients). They were all women except one. The cutaneous lesions were indistinguishable in the two groups. Only in the second group there was an associated disease (systemic lupus erythematosus, Sjogren syndrome disease, lupus-Sjogren overlap, autoimmune thyroid disease). Urticaria had been present from the onset of the disease in 4 patients, and occurred later during its course in 8 others. Five patients had thyroid disease (Hashimoto thyroiditis or Graves disease), two of them being mother and daughter. Another patient had a family history of Grave's disease and urticaria. Anti DNA antibodies were found in 7 cases, and anti Ro + La + in 3 cases. Response to treatment was variable with spontaneous cycles of worsening and remissions. One of the patients found a relationship with certain foods. Histopathologic results are related in both clinical normocomplementemic and hypocomplementemic groups. No significant differences were found between the two groups, but Ro+ and La+ patients exhibit more intense cariorexis and neutrophilic infiltrates.
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PMID:[Vasculitic urticaria: study of 12 cases]. 226 94

Cytokines such as Interleukin-1 (IL-1) are important modulators of the cell-mediated immune response and play a paramount role in inflammatory autoimmune disease. We report on preliminary clinical experiences with a new, tricyclic substance [( 10-Methoxy-4H-benzo[4,5]cyclo-hepta-[1,2-b]thiophene-4- ylidene]acetic acid, MW 284), which inhibits the release of interleukin-1 alpha and -beta from cultured murine macrophages or human mononuclear cells. The study included 12 patients (rheumatoid arthritis, n = 9; hemochromatotic arthropathy, n = 1; psoriatic arthropathy, n = 1; seronegative spondylarthropathy, n = 1). Eight patients were treated for a total of 8 weeks, receiving a median dose of 800 mg/d of the substance. Due to significant clinical benefits, two patients continued for a total of six months. Administration of the drug was discontinued in two patients because of severe urticaria and lack of compliance, respectively. Four out of 10 patients showed clinical improvement according to Ritchie-Index, pain score, ESR and CRP. Side effects were diffuse gastrointestinal symptoms (4/12), temporary impairment of liver function (4/12) and allergic skin reactions (3/12).
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PMID:[Initial clinical experiences in the treatment of chronic polyarthritis with a new monokine release inhibitor]. 267 92

From a pool of 624 patients with idiopathic chronic urticaria and angioedema, 90 patients had evidence of associated thyroid autoimmunity (TA). Since the number expected by chance alone is 37, given that less than 6% of normal subjects have TA, the association is significant (p less than 0.01; chi-square test). Age and sex distribution was typical of patients with TA. Clinically, most patients suffered relentless and severe urticaria and/or angioedema. With the exception of thyroid function and thyroid antibody tests, other laboratory tests were not rewarding. In most cases, treatment with 1 thyroxine did not improve urticaria or angioedema, but a few patients demonstrated a dramatic response. Awareness of the association resulted in the identification of previously undiagnosed thyroid disease. The authors hypothesize that a subset of idiopathic chronic urticaria and angioedema may be an autoimmune disease.
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PMID:Syndrome of idiopathic chronic urticaria and angioedema with thyroid autoimmunity: a study of 90 patients. 275 46

Complement may play a primary or exacerbating factor in the production of urticaria and/or angioedema. As we have seen, the absence of inhibitor proteins, such as ClINH, C3bINA, or Carboxypeptidase N Anaphylatoxin Inactivator) can permit small amounts of active complement fragments, liberated "normally" through the action of nonspecific effector pathways, to produce generalized urticaria or angioedema. Abnormal degrees of complement activation, produced by circulating immune complexes, cryoglobulins, paraproteins, may also cause angioedema and/or urticaria. Autoimmune diseases, lymphoreticular malignancy, infections, drug reactions, and syndromes currently termed idioipathic may be associated with urticaria and angioedema due to pathologic complement activation. Direct effects of complement on blood vessels, either by anaphylatoxins or by the deposition of complement fixing immune complexes, may produce the vascular permeability requisite to these syndromes. Secondary effects, produced by the recruitment of inflammatory cells and/or the liberation of other vasoactive mediators from these cells may also occur. Finally, complement may act in a potent synergistic fashion with mediators such as prostaglandins to produce vascular permeability. Current studies, using antigenic, hemolytic, and immunofluorescent techniques for detecting complement involvement have identified a relatively limited number of syndromes in which complement is involved. It is anticipated that the use of more sensitive assays for anaphylatoxins, such as radioimmunoassay, neutrophil aggregation, and others, coupled with an understanding of the potential synergism between these and other mediators, will lead to the recognition of a wider role for complement in urticaria and angioedema.
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PMID:The role of complement in urticaria and angioedema. 676 76

We retrospectively studied 94 children with urticaria longer than six weeks in duration. The disease was equally distributed among the sexes and the following age subgroups (0-3.9 years, 4.0-7.9 years, 8.0-11.9 years and 12.0-15.9 years). A cause of the urticaria was identified or suspected in 15 of the patients. These included eight patients with cold urticaria, two with infection (hepatitis, sinusitis), two with food allergy, one patient with juvenile rheumatoid arthritis, one with arthralgia associated with a positive ANA and one with a low level of total hemolytic complement (CH50). Follow-up of a year of more on 52 patients revealed a median duration of urticarial symptoms of 16.0 months, with 58% of children becoming symptom free for six months or more, whereas the remaining 42% continued to have recurrent symptoms but without the development of an underlying serious illness. Results of the present study indicate that the etiology of chronic urticaria in childhood remains mostly undetermined but that the prognosis is generally favorable. However, one must consider an underlying infection or autoimmune disease as a potential etiology.
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PMID:Chronic urticaria in childhood: natural course and etiology. 688 5

In the literature there are a few occasional case reports of rheumatic manifestations following vaccination. The link between vaccination and musculoskeletal complaints was established on the grounds of the chronological succession between the two events. The occurrence of an individual genetic predisposition has been stressed many times. With regard to immunopathological mechanisms, it has been proposed the vaccination as a trigger of a very autoimmune disease or an immune complex-induced disease. In this paper we describe two females who underwent vaccination against hepatitis B virus. One complained of polyarticular pain that, even if self-limiting, was accompanied by the positivity of RA-test and Waaler-Rose reaction; the other showed migratory arthritis, urticaria and oedema of the glottis and the upper lip, all successfully treated with a short course of corticosteroids. We think these reports are of interest at the time when vaccination against hepatitis B virus is becoming a mass practice.
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PMID:[Rheumatological manifestations following hepatitis B vaccination. A report of 2 clinical cases]. 793 76

The authors undertook a case-control study to explore the many factors that have been postulated to be related to the etiology of systemic lupus erythematosus. A total of 195 cases of systemic lupus diagnosed in the Philadelphia, Pennsylvania, metropolitan area between 1985 and 1987 were compared with 143 controls, friends of the cases matched to them according to age (+/- 5 years) and sex. Through personal interviews and chart reviews, data were collected on demographic factors, personal and familial medical history, reproductive history, medication history, and environmental exposures. Associations were found between systemic lupus erythematosus and having a family history of autoimmune disease (age-, sex-, and race-adjusted odds ratio (OR) = 2.3, 95% confidence interval (CI) 1.2-4.6), a history of shingles (adjusted OR = 6.4, 95% CI 1.4-28.0), a history of hives (adjusted OR = 1.8, 95% CI 1.1-3.0), and a history of medication allergies (adjusted OR = 2.6, 95% CI 1.5-4.5). No association was present between systemic lupus erythematosus and either any use or recent use of oral contraceptives (e.g., OR = 0.6 (95% CI 0.2-1.4) for use in the 3 years prior to diagnosis), family history of multiple other diseases, or a history of numerous other infections or various other types of allergies. Thus, these data indicate that systemic lupus erythematosus is associated with a family history of autoimmune diseases, a history of shingles, and a history of allergies. In contrast, if the development of systemic lupus is affected by use of oral contraceptives, this effect must be extremely modest. These findings may help clarify the possible pathogenesis of systemic lupus erythematosus, and they provide clues as to when the presence of systemic lupus should be suspected.
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PMID:Shingles, allergies, family medical history, oral contraceptives, and other potential risk factors for systemic lupus erythematosus. 794 63


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