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 immune status of the individual is an additional variable which has to be taken into account in any consideration of factors which influence the metabolism and toxicity of metals. The commonly occurring phenomena are described resulting from increased cellular reactivity to platinum, mercury, gold, nickel, chromium, and beryllium, and an attempt has attempt has been made to classify these into the four types of immune response. The clinical effects can be very varied, giving rise to conjunctivitis, rhinitis, asthma, urticaria, contact dermatitis, proteinuria, nephrotic syndrome or blood dyscrasia. Of these effects, cutaneous hypersensitivity is the most common, affecting both industrial and general population groups. Metal compounds used in therapeutics and metals used in prostheses have also been responsible for hypersensitive reactions.
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PMID:The role of hypersensitivity and the immune response in influencing susceptibility to metal toxicity. 72 Feb 96

The paper comprises 63 patients with diagnosed vasculitis of the skin who had abnormal findings in the urine. Thirteen of these patients had positive skin findings and abnormal findings in the urine, with concomitant attacks of dyspnea as seen in bronchial asthma. These patients account for 20% of the entire group, while there was an incidence of 37% of systemic manifestations. Skin findings: 45% had a maculopapular rash, 36% had urticarial findings, 13% had urticaria and angioedema and 6% had angioedema alone. Nonspecific biologic syndrome of evolution was statistically significant while no significant changes were found in the number of white blood cells and eosinophils. The degree of proteinuria ranged from 0.1 g/L to 1.16 g/L. Most patients with proteinuria above 0.25 g/L had microhematuria. Slightly over 50% of the patients had signs of complement activation by the alternative pathway, along with the presence of cryoglobulins. Increased histamine in the serum was found in over 50% of the patients although the values of histamine did not correlate with the degree of proteinuria. Proteinuria was not detected in patients with very high values of histamine (and without signs of vasculitis), which indicates that histamine itself responsible for changes in the glomeruli. There is a possibility that local tissue hyperhistaminemia is responsible for the increased permeability of the basal membrane of the glomeruli. According to the obtained results, the etiology of proteinuria and microhematuria should be pursued in the pathogenesis of vasculitis as signs of complement activation indicate. Other possible causes for proteinuria were excluded. The proteinuria was selective, benign according to its course and degree, occurred concomitantly with skin findings and was absent during remission of the disease.
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PMID:[Proteinuria in dermal vasculitis (incidence, degree and possible mechanisms of onset)]. 191 47

Sixteen children with severe juvenile chronic arthritis received high dose intravenous immunoglobulin (IVGG). Extra-articular symptoms improved to some degree in 6 of ten patients. A decrease in the number of active joints occurred in 7 patients of the 11 who received more than ten months of IVGG. Hemoglobin levels increased, the ESR and platelet counts decreased and the IgG levels diminished in most of the patients who received long term treatment. The treatment was totally ineffective in three children who had very severe disease. Two children had respectively a vasculitic rash and urticaria thought to be side effects of the treatment. One had proteinuria. This last might have been due to other therapeutic agents given. Although clinical and biological benefits occurred in some, the state of the patients who had short term (m = 2-3 months) or long term (m = 2-7 years) therapy was not different at the last visit.
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PMID:High dose immunoglobulin therapy in severe juvenile chronic arthritis: long-term follow-up in 16 patients. 228 32

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

An 8-year-old boy developed anaphylaxis after receiving his maintenance dose of immunotherapy and proceeded to display the signs and symptoms of serum sickness. These consisted of fever, arthralgia, arthritis, urticaria followed by a hemorrhagic palpable rash, edema, lymphadenopathy, splenomegaly, abdominal pain, proteinuria, and neurologic manifestations consistent with vascular compromise of the posterior cerebral circulation. A skin biopsy specimen revealed perivascular infiltrates of lymphocytes and few polymorphonuclear neutrophils. The timing of events in this patient suggests that immunotherapy initiated a chain of events beginning with anaphylaxis and leading to serum sickness. It is hypothesized that the enhanced vascular permeability that accompanied the anaphylaxis allowed immune complexes that may have preexisted in the circulation to deposit in the blood vessels of the patient. These complexes may or may not have been related to the immunotherapy itself. Because antihistamines are known to prevent the induction of serum sickness, early and aggressive treatment of anaphylaxis during immunotherapy may prevent the occurrence of immune complex disease.
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PMID:Serum sickness triggered by anaphylaxis: a complication of immunotherapy. 405 55

Eleven patients with severe, treatment-resistant essential or renovascular hypertension were treated with captopril after withdrawal of various multiple drug regimes. If supine diastolic blood pressure remained greater than 90 mm Hg on a maximum daily dose of 450 mg captopril, a diuretic and then a beta-adrenoceptor blocker were added. Patient-volunteered complaints were carefully noted. Mean (+/- SE) systolic and diastolic blood pressures fell from 225 +/- 6.8/131 +/- 4.4 mm Hg on various multiple drug regimes to 182 +/- 9.0/105 +/- 5.0 mm Hg on a regime including captopril. The reported and observed incidence of adverse effects were as follows: maculopapular rash (one patient); urticaria and pruritus (three patients); loss of taste (one patient); tachycardia (four patients); increased frequency of trivial infections (three patients); severe myalgia (one patient); and deterioration in renal function (one patient). However, these patients were able to continue captopril after either temporary withdrawal or dose reduction. Captopril was discontinued permanently in five patients, in two because of poor blood pressure control, in one who developed persistent severe urticaria, and in one because of marked proteinuria. In the fifth patient intractable diarrhoea occurred. Captopril lowers blood pressure very effectively in patients with severe hypertension refractory to other agents. Adverse effects are common but acceptable in this situation where prognosis is poor if blood pressure is not adequately controlled.
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PMID:Efficacy and adverse effects of captopril in severe refractory hypertension. 617 29

Urticarial skin lesions may occur in patients as a manifestation of necrotizing vasculitis. We describe a series of forty patients with idiopathic chronic urticaria and histologic features of necrotizing vasculitis. On the basis of clinical evaluation, we have classified urticarial vasculitis into two major groups: (1) hypocomplementemic (sixteen patients, ten of whom had evidence of renal disease) and (2) normocomplementemic (twelve patients with systemic disease and twelve with only cutaneous involvement). Most patients with hypocomplementemia presented with arthritis, and some had abdominal pain or airway compromise. Although patients with normocomplementemia and systemic disease had a less severe clinical course, four exhibited renal disease that was characterized by microhematuria and proteinuria. Direct immunofluorescence microscopy of the skin aids in assessing renal involvement in some cases of hypocomplementemic urticarial vasculitis, particularly when IgG and IgM are deposited at the basement membrane. There seems to be a spectrum of disease in urticarial vasculitis, ranging from benign cutaneous lesions to systemic disease.
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PMID:The clinical and histopathologic spectrums of urticarial vasculitis: study of forty cases. 675 76

We report a case of hypocomplementemic urticarial vasculitis syndrome (HUVS) with membranous glomerulopathy in a 62-year-old man who had a 2-month history of secondary iritis. He was transferred to our hospital because of uncontrollable edema and respiratory dysfunction. Physical examination revealed anasarca, pulmonary edema, hypertension and urticaria-like eruption on his arms. Urinalysis, blood chemistry and serological studies showed massive proteinuria (10.5g/day) with numerous granular casts, hypoalbuminemia (1.5g/dl), renal dysfunction (creatinine; 1.6mg/dl, BUN; 86mg/dl), hypercholesterolemia (total cholesterol; 455mg/dl), positive results for antinuclear factor, microsome test, thyroid test, lupus anticoaglant, antithyroglobulin test and rheumatoid factor, but LE cell or double-strand anti DNA antibody was negative. Serum complement levels were persistently low as CH50 of 13 U/ml and Clq of 6.0 micrograms/dl. The patient serum precipitated with normal human Clq by immunodiffusion analysis, indicating the presence of anti-Clq antibody. Renal biopsy revealed membranous glomerulopathy with prominent fine granular deposition of Clq along the glomerular basement membrane by immunofluorescent study and subepithelial dense deposit by electron microscopy. Corticosteroid treatment was ineffective for hypocomplementemia and nephrotic syndrome. Acute subendocardial infarction occurred on the 25th hospital day and he died of acute respiratory distress syndrome on the 45th hospital day. Autopsy revealed leucocytoclastic vasculitis in the alveolar wall. HUVS was confirmed by clinical symptoms, such as iritis and urticaria-like eruption, serum anti-Clq antibody, the absence of any specific autoantibody for systemic lupus erythematosus (SLE) and leucocytoclastic vasculitis in the alveolar wall.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Nephrotic syndrome due to membranous glomerulopathy in hypocomplementemic urticarial vasculitis syndrome;--a case report]. 807 26

In diabetic nephropathy, heparan sulfate glycosaminoglycan side chains are reduced in glomerular basement membranes proportionally to the degree of proteinuria. Recently, it was demonstrated that additional therapy with danaparoid sodium, a mixture of sulfated glycosaminoglycans with mainly heparan sulfate, lowered proteinuria in type 1 diabetes patients with diabetic nephropathy. A randomized placebo-controlled parallel study was performed with 750 anti-Xa units of danaparoid sodium once daily in type 2 diabetes patients with severe proteinuria. The aim of the study was to evaluate the possible effects of danaparoid sodium on proteinuria, endothelial dysfunction, and hard exudates in the retina and to determine the safety/tolerability of this drug. Twenty-two patients completed the study, and one patient had to stop prematurely after 6 wk of danaparoid sodium treatment because of urticaria at the injection sites. Apart from a small decrease of hemoglobin and minor skin hematomas at the injection site in five patients in the danaparoid sodium group, no other safety parameters showed any clinically or statistically significant difference between and within groups. The relative change in time of both the urinary albumin and protein excretion rate corrected for creatinine did not differ between both treatment arms (P = 0.2 and 0.49, respectively). No retinal complications or changes of hard exudates occurred. von Willebrand factor was elevated in both groups, but was not influenced by either treatment modality. Contrary to the beneficial effects that occurred in type 1 diabetes patients with diabetic nephropathy, treatment for 8 wk with 750 anti-Xa units of danaparoid sodium gave no reduction of proteinuria, hard exudates, and von Willebrand factor.
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PMID:Effect of danaparoid sodium on proteinuria, von Willebrand factor, and hard exudates in patients with diabetes mellitus type 2. 1036 73

We report a case of hypocomplementemic urticarial vasculitis (HUV). The clinical course was characterized by urticaria, angio-edema, pericarditis, joint pain and conjunctivitis. The laboratory findings revealed moderate proteinuria, erythrocyturia, normal renal function, normotension, reduction of C3, C4 and C1q complement with elevated C1q antibodies. Antinuclear antibodies were inconstantly positive. Renal biopsy showed a mild form of membranous glomerulonephritis. Despite intensive therapeutic measures (dapsone, immunosuppressives and immunoglobulins), relapses of urticaria occurred frequently. HUV is probably a minor form of systemic lupus erythematosus.
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PMID:[Kidney involvement in hypocomplementemic urticaria-vasculitis syndrome--a simulated systemic lupus erythematosis]. 1137 Jun 7


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