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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cell-mediated immunity is generally considered as the principal immunological response to dermatophyte infection. However, certain clinical manifestations associated with a humoral antibody response occasionally occur as complications to dermatophytosis (e.g. vasculitis, urticaria). Immediate wheal reaction to intradermal application of "trichophytin" is frequent in patients with chronic T. rubrum infection and can be passively transferred with serum, which demonstrates the presence of specific IgE antibodies in these patients. Crossed immunoelectrophoresis and modifications thereof were applied for studies of (i) the antigenic structure of dermatophytes in sera from patients with dermatophytosis. The antigenic composition was found to differ between species but was characteristic and constant for different strains of the same species. Partial cross reactivity between different species, especially T. rubrum and T. mentagrophytes was noted. The presence of specific IgG antibodies towards corresponding dermatophytes was associated with tinea capitis (100%), tinea pedis with dermatophytid eruption (62%) and chronic T. rubrum infection (25%). Sera from 50 healthy persons were all negative. Specific IgE antibodies toward T. rubrum were demonstrated in serum from eight patients with chronic T. rubrum infection while specific IgE antibodies were not present in sera from ten patients with tinea capitis and four controls. The possible role of IgG and IgE antibodies in inflammatory and non-inflammatory dermatophyte infections is discussed.
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PMID:Humoral antibody responses in the immunopathogenesis of dermatophytosis. 242 54

The prevalence of autoantibodies of immunoglobulin G (IgG) and immunoglobulin M (IgM) classes directed against myeloma immunoglobulin E (IgE) were determined in distinct subsets of urticaria, using an enzyme immunoassay. IgG anti-IgE antibodies were found in five of nine patients (55%) with cold urticaria, four of eight patients (50%) with urticarial vasculitis, and three of six patients (50%) with chronic urticaria. IgM anti-IgE antibodies were found exclusively in cold urticaria (two of nine patients, 22%). Heating of these sera increased the binding to IgE, suggesting immune complex formation. Several positive sera were capable of inducing histamine release from normal peripheral basophils and caused a wheal-flare response upon intradermal injection. Sera containing such autoantibodies from three cold urticaria patients were studied for passive transfer of cold sensitivity. One serum containing IgG anti-IgE gave a strongly positive transfer test at 5 h but not 48 h, suggesting a pathogenic role for the IgG.
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PMID:Prevalence and functional role of anti-IgE autoantibodies in urticarial syndromes. 244 92

The histopathology, immunofluorescence and ultrastructure of skin in idiopathic cold-contact urticaria have been studied over the 24 h following the application of a cold stimulus sufficient to provoke a confluent weal on the anterior thigh. Biopsies were taken 10 min, 2 h and 24 h after ice removal. Considerable epidermal and dermal oedema was present. Type I and Type II mast-cell degranulation was noted but was not universal. Lymphatics and capillaries were dilated and endothelial cells showed an increase in micropinocytotic activity, without evident vasculitis. In two cases packed platelets were seen within vessel lumina. There was no change in the infiltrating dermal cell population and direct immunofluorescence was negative. The evidence suggests that idiopathic cold-contact urticaria is an exudative rather than an infiltrative process.
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PMID:A timed study of the histopathology, direct immunofluorescence and ultrastructural findings in idiopathic cold-contact urticaria over a 24-h period. 269 Nov 33

In two patients with leukocytoclastic vasculitis allergic reactions to foods were shown to be of clinical relevance. Intracutaneous tests with food allergens produced not only immediate wheal and flare reactions but also distinct inflammatory reactions after 8-24 h, which showed the histological and immunopathological characteristics of leukocytoclastic vasculitis. After controlled oral provocation with specific foods exacerbation of petechial lesions was observed. A striking improvement in the patients' condition was achieved by avoidance of the relevant foods and oral administration of cromoglycate.
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PMID:[Allergic vasculitis caused by food allergy]. 340 68

Two cases of urticarial vasculitis (UV) accompanying systemic lupus erythematosus (SLE) are reported. Both patients developed characteristic wheal and purpuric lesions of UV followed by pigmentation, and histological examination revealed leucocytoclastic vasculitis. Although oral prednisolone was beneficial for the systemic symptoms and various serological abnormalities, one patient needed dapsone and the other needed dapsone and cyclophosphamide to control the UV. In both patients, hypocomplementemia with no evidence of congenital complement deficiency or complement consumption persisted even after all other laboratory data and symptoms improved.
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PMID:Urticarial vasculitis in systemic lupus erythematosus: fair response to prednisolone/dapsone and persistent hypocomplementemia. 992 Sep 91

There are many types of urticaria and the principal form of assessment is by clinical history and examination. Urticarial weal formation involves acute, reversible vasodilatation and increased vascular permeability. If the process is deeper the more diffuse swelling is termed angio-oedema. The major types of urticaria include allergic, physical and idiopathic forms. In allergic urticaria, IgE-mediated degranulation of mast cells results in weals of short duration which typically respond well to antihistamines. Physical urticarias are induced by physical insults including pressure, scratch, cold, etc. The distribution and duration of individual weals may suggest the causal factor. Chronic idiopathic urticaria can be very variable, with individual weals lasting between 90 min and 24 hours. Longer-lasting weals are less responsive to anti-histamines and clearly involve other mediators. When long-lasting weals fade leaving a bruised appearance urticarial vasculitis is present which may only respond to systemic corticosteroids. In a proportion of individuals with chronic idiopathic urticaria, auto-antibodies are present with specificity for the high affinity receptor for IgE or sometimes, for IgE itself. In general laboratory tests for allergic factors or other assessments of general health are completely unhelpful.
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PMID:Assessment of urticaria and angio-oedema. 1044 23

H1-antihistamines are the cornerstone of symptomatic treatment in acute and chronic urticaria, in which they not only relieve itching, but also reduce the number, size, and duration of urticarial lesions. Relief of whealing, flaring, and erythema may be incomplete as the vascular effects of histamine are mediated to its action at H2-receptors as well as at H1-receptors, and other vasoactive substances may also be involved. In randomized, prospective, placebo-controlled, double-blind studies, the new low-sedating H1-antihistamines have been found to be effective and safe in urticaria. Sedating antihistamines, although effective, place patients at risk for adverse effects, including decreased psychomotor performance. The response to H1-antihistamines in some types of urticaria, for example, in urticarial vasculitis, is unsatisfactory. An H2-antihistamine administered concurrently with an H1-antihistamine may modestly enhance relief of itching and wheal formation in some patients with urticaria refractory to treatment with an H1-antihistamine alone. The available evidence does not justify the routine addition of H2-antihistamine treatment to H1-antihistamine treatment.
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PMID:Antihistamines in urticaria and angioedema. 1211 19

Wasp stings generally cause local reactions like pain, wheal, flare, edema and swelling, which are generally self-limiting. Multiple stings can lead to vomiting, diarrhea, generalized edema, dyspnea, hypotension, collapse, renal failure or death. Unusually, they may cause serum sickness, vasculitis, neuritis or encephalitis. We report a case of a 40 year old male who developed focal neurological deficit 10 hours following a wasp sting, which was confirmed to be ponto-cerebellar infarction on MRI scan, and recovered within five days.
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PMID:Wasp sting induced neurological manifestations. 1239 66

Urticaria is a common complaint characterized by the eruption of cutaneous wheals, accompanied by redness and itching and in which mast cells are thought to play a central role. Wheals range from a few millimeters to several centimeters in diameter and are usually short lasting, except in case of urticarial vasculitis in which they last longer than 24 hours. Urticaria may occur alone or be associated with angioedema, that can be defined as a deep dermal and subcutaneous edema typically affecting the lips, face, hands, feet, penis or scrotum. Angioedema may also involve the submucosal tissue, and when the swellings occur in the oropharynx they can be alarming and occasionally life-threatening. In many cases the cause of acute urticaria or angioedema may be determined, whilst the pathogenetic and diagnostic aspects of the chronic forms are more complex and variable. The clinical features of, as well as the diagnostic and therapeutic approaches to the different forms of urticaria and angioedema are here reviewed, focusing on chronic idiopathic urticaria.
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PMID:[Urticaria and angioedema]. 1273 24

Chronic urticaria is an umbrella term, which encompasses physical urticarias, chronic "idiopathic" urticaria and urticarial vasculitis. It is important to recognize patients with physical urticarias as the investigation and treatment differs in important ways from patients with idiopathic chronic urticaria or urticarial vasculitis. Although relatively uncommon, urticarial vasculitis is an important diagnosis to make and requires histological confirmation by biopsy. Underlying systemic disease and systemic involvement, especially of the kidneys, should be sought. It is now recognized that chronic "idiopathic" urticaria includes a subset with an autoimmune basis caused by circulating autoantibodies against the high affinity IgE receptor (FceR1) and less commonly against IgE. Although the autologous serum skin test has been proven useful in prompting search for and characterization of circulating wheal-producing factors in chronic urticaria, its specificity as a screening test for presence of functional anti-FceR1 is low, and confirmation by demonstration of histamine-releasing activity in the patient's serum must be the benchmark test in establishing this diagnosis. Improved screening tests are being sought; for example, ability of the chronic urticaria patient's serum to evoke expression of CD 203c on donor human basophils is showing some promise. The strong association between autoimmune thyroid disease and autoimmune urticaria is also an area of ongoing research. Drug treatment continues to be centered on the H1 antihistamines, and the newer second-generation compounds appear to be safe and effective even in off-label dosage. Use of systemic steroids should be confined to special circumstances such as tapering regimens for acute flare-ups. Use of leukotriene antagonists is becoming popular, but the evidence for efficacy is conflicting. Cyclosporin is also effective and can be used in selected cases of autoimmune urticaria, and it is also effective in non-autoimmune cases, although less so.
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PMID:Chronic urticaria: recent advances. 1809 52


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