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Query: UMLS:C0042109 (
urticaria
)
6,569
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The authors report 5 cases whose main characteristics appeared very similar. Constantly, they found the same skin signs,
urticaria
without pruritus, recurring over a long period. The latter was accompanied by a very high E.S.R. and immuno-electrophoresis showed, in all cases, an increase in monoclonal IgB, permitting one to make the diagnosis of macroglobulinemia. In four cases out of five, this clinical picture was accompanied by bony pain associated with radiological signs of condensation. The symptoms were accompanied by prolonged fever and
lymphadenopathy
. After being well tolerated for a long period, the disease may become worse and lead to death. Thus this seems to be a true disease entity?
...
PMID:[Chronic urticarial lesions and macroglobulinemia. Apropos of 5 cases]. 18 33
Leo 1031, a chlorambucil ester of prednisolone, has been administered orally to 15 patients with chronic lymphocytic leukaemia (CLL) continuously for 1-29 months (mean 12.5). Seven patients were previously untreated and eight had been treated with prednisolone, radiotherapy and/or alkylating agents. The initial daily dose was generally 8-16 mg and the maintenance dose was 6-8 mg. Allopurinol was given concurrently. In 14 of 15 patients a reduction of the leucocyte count was observed and a reduction, in most instances, of
lymphadenopathy
or splenomegaly, or both. In seven patients the Hb concentration was improved. Significant toxic effects on bone marrow function have been observed in one patient. Two patients developed
urticaria
. Our study suggests that the drug is effective in the treatment of CLL.
...
PMID:Therapeutic effect of Leo 1031, an alkylating corticosteroid ester, in lymphoproliferative disorders. I. chronic lymphocytic leukaemia. 113 62
Twenty patients with the acquired immunodeficiency syndrome (AIDS), AIDS-related complex (ARC) or asymptomatic HIV infection (HIV+) were given 20 mcg kg-3 trichosanthin (TCS; 'Compound Q'), a ribosome-inactivating protein with in vitro antiviral activity against human immunodeficiency virus (HIV) once every four weeks for up to 12 weeks. With the concurrent administration of prostaglandin inhibitors, the drug was moderately well tolerated, with most subjects experiencing mild arthralgia,
hives
and malaise. Additionally, four patients experienced neurological complications which resolved spontaneously without intervention. Four of 20 subjects in this open label pilot study showed progressive although transient reductions in viral activity as measured by p-24 antigen level decreases. Subjects also experienced decreases in levels of beta 2-microglobulin. Ten HIV+ and healthy ARC subjects demonstrated improved immunological status as measured by significant increases in percentage of CD4+ cells and augmentations in delayed hypersensitivity reactions. Eight of 20 subjects reported improved appetites and increased energy levels. The group as a whole had a weight gain of 3.2 kg. Eight of 20 subjects who presented with persistent generalized
lymphadenopathy
exhibited a marked diminution in the size of their lymph nodes after the first treatment. No subject who presented with oral candidiasis experienced an improvement in that condition. We conclude that, in the short term, TCS seems to have the ability to reduce viral activity and improve certain symptoms in healthy ARC patients and HIV + asymptomatics although it may not be able to restore immune competence in persons with advanced AIDS or poor prognosis ARC. Additionally, the drug may pose a special risk for patients with HIV-related dementia.
...
PMID:Trichosanthin treatment of HIV-induced immune dysregulation. 157 89
Schnitzler's syndrome is characterized by chronic urticaria, recurrent fever, bone pain, and
lymphadenopathy
in conjunction with a serum IgM M component in a concentration that is usually less than 10,000 mg/L. Complement activation and cryoprecipitation do not appear to be involved. We report two additional patients who share many of the characteristics of this entity. These patients differ from patients previously reported because of the markedly elevated IgM M-component concentration in one patient and the severity of anemia in the second patient. An increased frequency of IgG autoantibodies to interleukin-1-alpha has been reported by other investigators; it has been suggested that an antibody-mediated prolongation of the half-life of interleukin-1-alpha might account for some of the symptoms and signs of this disorder. However, neither the mediators involved in the induction of nonpruritic
urticaria
nor the role of the IgM M component has been established.
...
PMID:Schnitzler's syndrome: a broader clinical spectrum. 182 7
We report the skin manifestations and abnormalities of subacute necrotizing lymphadenitis. As far as we are aware, this is the first report of this disease in the dermatology literature. The main features of subacute necrotizing lymphadenitis are fever, a cervical
lymphadenopathy
, and, occasionally, a skin eruption resembling
urticaria
, rubella, or a drug-induced erythema. A skin biopsy specimen showed a mild lymphohistiocytic perivascular infiltrate of cells in the papillary and mid dermis and deposition of fibrinogen around the capillary vessels. Subacute necrotizing lymphadenitis responds to oral corticosteroid therapy but not to antibiotics.
...
PMID:Subacute necrotizing lymphadenitis. 233 83
A 19 year-old youth was taking oral minocycline and after 8 days he presented all four cardinal symptoms of serum sickness (
urticaria
, fever,
lymphadenopathy
and joint symptoms). C3, C4 and CH50 evolution imitate experimental serum sickness complement evolution. We exclude other causes of this syndrome. Although other hypersensitivity reactions have occurred with minocycline usage, to our knowledge serum sickness-like syndrome has not been previously reported with this drug.
...
PMID:Serum sickness-like syndrome associated with minocycline therapy. 238 98
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.
...
PMID:Human serum sickness: a prospective analysis of 35 patients treated with equine anti-thymocyte globulin for bone marrow failure. 325 88
A previously well young woman presented with an acute hepatitis resembling viral hepatitis and a liver biopsy after 5 weeks showed features of acute hepatitis. Infection with identifiable viruses or other organisms known to cause hepatitis was excluded. Evidence for autoimmune chronic active hepatitis ab initio included prolonged fever,
lymphadenopathy
,
urticaria
, arthralgia, Coombs' positive hemolytic anemia, lymphopenia, a markedly raised level of immunoglobulin G and a positive antinuclear antibody test. Liver biopsies after 4 and 28 months showed typical histologic features of autoimmune chronic active hepatitis and the subsequent clinical course was typical, being marked by relapses and remissions responsive to prednisolone. Thus, described here is a woman in whom an acute onset of autoimmune chronic active hepatitis was clinically and histologically identified.
...
PMID:'Acute' autoimmune hepatitis. 375 17
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.
...
PMID:Cutaneous manifestations of serum sickness in patients receiving antithymocyte globulin. 387 81
Angioimmunoblastic lymphadenopathy often begins with constitutional symptoms, such as fever, malaise, and weight loss. Most patients have generalized
lymphadenopathy
, and about 40 per cent have skin lesions with maculopapular erythema, purpura,
urticaria
, or exfoliative erythroderma. Lymph-node biopsy specimens demonstrate the most characteristic histopathologic features: extensive effacement of lymph nodal architecture; a pleomorphic population of immunoblasts, plasma cells, lymphocytes, and eosinophils; interstitial deposits of eosinophilic material; and prominent vascular proliferation, with "arborization" of small vessels. The pathogenesis of angioimmunoblastic
lymphadenopathy
is still unknown, but its histopathologic features and laboratory findings strongly suggest that it is an immunologically mediated disorder. Some clinical and laboratory evidence supports the possibility that angioimmunoblastic
lymphadenopathy
is a benign reactive or proliferative process, whereas other studies suggest that it might be a malignant disease. In some patients, it can develop into immunoblastic sarcoma or other types of malignant lymphoma or leukemia. It is probably reasonable to consider angioimmunoblastic
lymphadenopathy
a prelymphomatous state of immunoblastic sarcoma.
...
PMID:Angioimmunoblastic lymphadenopathy. 391 79
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