The Journal of laboratory and clinical medicine
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Proteins and allergens in natural rubber latex were characterized by a two-dimensional immunoblot method with serum samples from 17 patients with latex allergy of whom 10 had spina bifida and 7 were health care workers. We demonstrated in rubber tree sap approximately 240 polypeptides of which 57 bound immunoglobulin E (IgE) in patient serum samples. Forty-six of the 57 allergens were identified by patients with spina bifida, 19 of 57 allergens by health care workers, and 8 of 57 allergens by both patient groups. ⋯ This cluster of 11 allergens was identified by none of the 7 health care workers and by only 1 of 5 patients with spina bifida without demonstrable anaphylaxis. These preliminary findings indicate that patients with spina bifida in whom latex hypersensitivity has developed exhibit a strong anti-latex IgE immune response, which seems to differ markedly from the immune response of health care workers with latex allergy. The characteristic anti-latex IgE profile in patients with spina bifida and with a history of an anaphylactic reaction may be valuable in the evaluation of pathogenetic processes in latex allergy.
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Recombinant gamma interferon (rHuIFN-gamma) has been recognized to increase mRNA and protein levels of C1 inhibitor (C1 INH) in various human cells. Further, when administered to patients with colon cancer, it increased plasma C1 INH levels. A prospective trial was initiated to determine whether rHuIFN-gamma could elevate plasma C1 INH levels in six normal volunteers and two patients with type I angioedema. ⋯ It was found that immediately after rHuIFN-gamma treatment, tissue plasminogen activator activity and antigen levels were not significantly decreased in volunteers. Plasminogen activator inhibitor levels rose significantly, but this activity was not due to plasminogen activator inhibitor-1 antigen, whose value significantly fell. These data suggest that rHuIFN-gamma may stimulate the expression of another plasminogen activator inhibitor.(ABSTRACT TRUNCATED AT 250 WORDS)
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To explore the possible role of locally synthesized transforming growth factor beta-1 (TGF-beta 1) and procollagen gene expression in postburn hypertrophic scars, we have compared mRNA levels for type I and type III procollagen and TGF-beta 1 in human hypertrophic scar tissue with normal dermis obtained from the same patients as a control. Northern blot analysis of total RNA extracted from hypertrophic scar tissue and normal skin demonstrated two transcripts for the pro-alpha 1(I) chain (5.8 kb and 4.8 kb) and for the pro-alpha 1(III) chain (5.4 kb and 4.8 kb) and one transcript (4.9 kb) for TGF-beta 1. ⋯ Two transcripts (4.9 kb and 2.5 kb) for TGF-beta 1 were identified in cultured fibroblasts. In contrast to the results from tissue, the level of these transcripts in fibroblasts cultured from hypertrophic scar tissue and normal skin were not significantly different, suggesting that the synthesis of this growth factor is stimulated in tissue by a presently unknown mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)
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Clinical efficacy of plasma-derived products with factor VIII--bypassing activity in patients with factor VIII inhibitors is difficult to evaluate. It is also difficult to predict efficacy by coagulation assay. A test of thrombin generation in defibrinated plasma and in the presence of activated platelets was used to test the bypassing activity of the most currently used products (activated prothrombin complex concentrate from various origins, prothrombin complex concentrate, and factor VIIa). ⋯ In plasma with inhibitor, activated prothrombin complex concentrate elicited dose-dependent thrombin formation, whereas prothrombin complex concentrate and factor VIIa induced only minimal thrombin activity. Addition of tissue factor in the assay elicited thrombin generation in the presence of factor VIIa and prothrombin complex concentrate and allowed additional thrombin formation in the presence of activated prothrombin complex concentrate. Although it is hazardous to extend results of in vitro testing to clinical efficacy, our study sheds some light on the mechanism of action of the various substances used to treat bleeding episodes in patients with factor VIII inhibitors.
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To test the hypothesis that disseminated intravascular coagulation contributes to hemostatic failure in liver cirrhosis, fibrinopeptide A and fibrin(ogen) degradation fragment E were measured in 69 patients with stable liver cirrhosis and compared with fibrinopeptide A and fibrin(ogen) degradation fragment E in 32 healthy subjects, 33 patients with thromboembolism, and 10 patients with hypofibrinogenemic disseminated intravascular coagulation. Mean fibrinopeptide A in cirrhosis was slightly increased compared with healthy subjects (2.4 vs. 1.8 ng/ml, p < 0.005), but fourfold lower than in thromboembolism (mean fibrinopeptide A 9.7 ng/ml; p < 0.0001), and tenfold lower than in disseminated intravascular coagulation (mean FPA 24.3 ng/ml; p < 0.0001). Single fibrinopeptide A levels in cirrhosis were within the normal range in 75% of the patients, marginally increased in 9%, and definitely increased in 16%. ⋯ Among 17 patients with cirrhosis and hypofibrinogenemia, mean fibrinopeptide A (2.7 ng/ml) was tenfold lower compared with mean fibrinopeptide A in patients with hypofibrinogenemic disseminated intravascular coagulation (p < 0.0001), whereas the frequency of increased single fibrinopeptide A levels (29%) was not significantly different compared with the 52 cirrhotic patients without hypofibrinogenemia (single levels elevated in 23% of the cases). Moreover, the frequency of hypofibrinogenemia, thrombocytopenia, or abnormal clotting times was not significantly different in cirrhotic patients with normal fibrinopeptide A level when compared with cirrhotic patients with increased fibrinopeptide A. These findings do not support an important contribution of disseminated intravascular coagulation to coagulopathy of liver cirrhosis.