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 six-year-old girl with recurrent urticaria and angioedema, vasculitis, and probable renal disease exhibited marked blood eosinophilia, increased levels of serum IgE, circulating Clq precipitins, and hypocomplementemia with evidence of activation of complement by the classic pathway. Biopsies of skin and muscle revealed heavy infiltrations of the vessel walls with eosinophils. Immunofluorescence studies revealed deposition of IgM, IgE, and C3 in the vessel walls. Exacerbations of the disease were associated with an increase in the eosinophil count and a decrease in the serum levels of C4 and C3. Remission was achieved with corticosteroid therapy. This patient has many features in common with the syndrome of skin lesions, angioedema, and hypocomplementemia recently described in adults.
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PMID:Skin lesions, angioedema, eosinophilia, and hypocomplementemia. 78 39

To determine the cost-effectiveness of selective use of nonionic low-osmolality contrast material, the authors randomly assigned 955 patients to receive high-osmolality and 1,158 to receive low-osmolality intravenous contrast material. All patients had one or more of the following perceived risk factors for adverse reactions: prior reaction to contrast material, allergies, asthma, diabetes, cardiac or renal disease, anxiety, severe illness, and age greater than 50 years. The occurrence of any adverse event, need for therapy, or subjective symptoms was assessed in a double-blind fashion. An adverse reaction necessitating the attention of a physician occurred in 3.9% (n = 37) of patients in the high-osmolality and 0.9% (n = 10) of patients in the low-osmolality groups (P less than .000005). Therapy was administered to 1.4% (n = 13) and 0.5% (n = 6), respectively (P = .035). The difference was due to a reduction in urticaria and other mild anaphylactoid reactions. In a multivariate analysis, only prior reactions and allergy were independent risk factors. Selective use of intravenous nonionic contrast material is best justified in those with prior reactions, allergy, or asthma; at least 67% of reactions would be prevented.
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PMID:Nonionic low-osmolality versus ionic high-osmolality contrast material for intravenous use in patients perceived to be at high risk: randomized trial. 154 74

We encountered 4 patients (3 women, 1 man) with cutaneous vasculitis: three have a delayed pressure urticaria, two a vascular purpura with which a mixt cryoglobulinemia. Histology show a leukocytoclastic vasculitis. Initially all studies for lupus erythematosus were negative. However, after 3 to 10 years of follow-up, the 4 patients developed clinical, serological and histological features of systemic lupus erythematosus meeting four or more criteria of the American Rheumatism Association for the diagnosis of SLE. In one case there is a moderate renal disease. In three others cases there are a severe visceral injury: one with aseptic valvula's injury treated by surgery, another who died from a septicemic incident. The last who died from a neurological complication of systemic lupus. During the isolated cutaneous vasculitis phasis antinuclear antibodies and antibodies to double stranded DNA were all negative. At the time of SLE's diagnosis anti-DNA antibodies were present with or without ANA. In all four cases hypocomplementaemia was not initially seen which distinguish these cases from others previously reported in the literature. The syndrome recognized in these patients may constitute an "ante" serological and clinical phasis of SLE.
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PMID:[Seronegative leukocytoclastic vasculitis preceding the onset of disseminated systemic lupus erythematosus]. 229 Oct 68

We report a patient who developed recurrent urticaria and angioedema at age 2 years, severe hypocomplementemic glomerulonephritis at 11 years, and end-stage renal disease at 14 years. His disease resembled the hypocomplementemic vasculitis syndrome but was atypical in its early age of presentation, severe hypocomplementemia, and progression to end-stage renal disease. Serum C1q levels were extremely low, and C4, C2, C3, and C5 levels were significantly reduced. Serum C1 inhibitor (C1INH) levels were slightly low, presumably from consumption. Circulating C1INH-C1r-C1s complexes were evidenced by reduced ratios of functional to antigenic C1INH and antigenic C1r to C1s. Family members had normal functional and antigenic levels of all complement components studied. The patient's serum, erythrocytes, platelets, and mononuclear cells did not activate complement when mixed with normal target serum. Absence of a circulating complement activator and the low serum C3 and C5 levels suggested the presence of a solid-phase complement activator, possibly related to renal or systemic vascular endothelium. As in patients with homozygous deficiencies of classical pathway components, a severe, prolonged, acquired C1q deficiency may have predisposed this patient to the development of glomerulonephritis.
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PMID:Atypical hypocomplementemic vasculitis syndrome in a child. 298 70

Aspirin (ASA) and nonsteroidal anti-inflammatory drugs (NSAIDs) share common pharmacologic effects in the prevention of inflammation, at least in part through inhibition of prostaglandin formation. ASA and NSAIDs have predictable side effects such as gastric pain, ecchymosis, and tinnitus. They also cause anaphylactoid shock, urticaria/angioedema, nephropathy, and hepatitis in individuals who appear to be normal and in whom prediction of such reactions cannot be made. Two selected populations of patients are likely to experience hypersensitivity reactions to both ASA and NSAIDs. Patients with asthma have an 8% to 20% chance of experiencing asthmatic attacks after ingesting ASA and NSAID. If such patients have associated rhinosinusitis (polyps), prevalence increases to 30% to 40%. Patients with chronic urticaria/angioedema have a 21% to 30% chance of experiencing an urticarial flare after ingesting ASA and NSAIDs.
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PMID:Diagnosis, prevention, and treatment of adverse reactions to aspirin and nonsteroidal anti-inflammatory drugs. 643 54

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

Ten of 143 systemic lupus erythematosus patients demonstrated urticaria-like lesions. Lesional biopsies in 7 of 9 patients tested revealed a leukocytoclastic angiitis and in 2, a mononuclear perivascular infiltrate. Direct immunofluorescent studies in 2 of 6 patients tested revealed IgM and C3 deposition in and about dermal blood vessels. Nine of the 10 systemic lupus erythematosus, patients displayed active clinical disease (e.g., arthritis, renal disease, etc.), a positive lupus band test, antibodies against deoxyribonucleic acid or Sm macromolecules, serum hypocomplementemia and markedly elevated quantities of serum immune complexes as determined by an immunoradiometric assay employing Raji cells. Similar lesions were not detected in 35 discoid lupus erythematosus patients. These studies strongly suggest: (1) urticaria-like lesions are uncommon cutaneous manifestations of systemic lupus erythematosus. (2) These urticaria-like lesions do not represent a classic IgE mediated urticaria. (3) These urticaria-like lesions generally occur in lupus erythematosus patients demonstrating clinical and/or serological evidence of systemic disease activity. (4) These lesions are probably secondary to immune complex deposition. We, therefore, conclude that all urticarial lesions in lupus erythematosus patients should be biopsied and the patient evaluated for active systemic disease.
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PMID:Unusual cutaneous manifestations of systemic lupus erythematosus: I. Urticaria-like lesions. Correlation with clinical and serological abnormalities. 700 29

Bumetanide was compared with furosemide in a total of 43 outpatients with edema due to renal disease, selected from three clinics following a uniform protocol. By random selection, 31 patients received 1 to 10 mg/day bumetanide, and 12 received 40 to 400 mg/day furosemide for at least six months. The patients were evaluated clinically, by standard laboratory tests, as well as by ECG, audiometry, eye examination, and mammary examination. Pooled statistical analysis of the results was done. Edema, body weight, and abdominal girth were reduced during both treatments. There was no significant difference in the mean response to the two diuretic agents by the two sided probability test in the other parameters studied, e.g., supine and standing blood pressure and pulse, serum electrolytes (sodium, potassium, chloride), and uric acid. There were no differences in liver function tests, hematology, or chest x-ray, and no remarkable effects on hearing. Gynecomastia improved in some patients while being treated with bumetanide after spironolactone was discontinued. Adverse reactions in patients on bumetanide which were considered possibly or probably related to the drug were muscle cramps (two patients); and vertigo, headache, muscle pain, urticaria, chest pain, arthritis, dehydration, postural hypotension, and leg cramps (one each). Laboratory abnormalities in both groups were generally those that could be attributed to the pharmacologic action of the diuretics or due to the patients' underlying disease states. No drug-related adverse effects were noted in ECG, ophthalmologic examinations, or chest x-rays. Two patients in the furosemide group had a probably or possibly drug-related loss of hearing sensitivity. In summary, bumetanide appeared to be as safe and as efficacious as furosemide in controlling edema and hypertension in patients with renal disease.
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PMID:Long-term bumetanide treatment of patients with edema due to renal disease. Cooperative studies. 704 Apr 92

Muckle-Wells syndrome (MWS) is a rare condition characterized by urticaria, arthralgias, deafness and amyloid nephropathy. The arthropathy is poorly documented. We describe the arthropathy occurring in four cases of MWS and discuss the management. Each patient developed recurrent bouts of transient synovitis. One patient developed a persistent sterile pyoarthrosis.
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PMID:The arthropathy of the Muckle-Wells syndrome. 800 Jul 53

The term Muckle-Wells syndrome (MWS) describes an autosomal dominant disorder characterised by various combinations of urticaria, sensorineural deafness, amyloidosis, arthralgia and skeletal abnormalities. We describe a family with nephropathy and several symptoms of MWS, but no evidence of deafness or amyloidosis. Since nephropathy without amyloidosis has never been reported in MWS, but deafness is a feature of all reported pedigrees, we conclude that members of this family have a previously unreported inherited predisposition to urticaria, arthralgia and nephropathy which is distinct from the MWS phenotype.
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PMID:Urticaria, arthralgia, and nephropathy without amyloidosis: another variant of the Muckle-Wells syndrome? 873 77


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