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A Malbrán

Publications and source records attributed to A Malbrán.

8 recordsLinked to original sources

Diclofenac induces basophil degranulation without increasing CD63 expression in sensitive patients.

Diclofenac (Dc) induces an IgE-independent basophil (Ba) degranulation in susceptible individuals. CD63 Ba expression is utilized as an in vitro test for diagnosis of drug hypersensitivity. We tested the ability of Dc to induce CD63 Ba expression by flow cytometry (BAT) and Ba degranulation using light microscopy (HBDT) in patients sensitive to Dc. We studied 14 patients with diclofenac hypersensitivity, also two patients sensitive to Dermatophagoides pteronyssinus (Dp), and 12 normal controls. HBDT was performed by mononuclear cells toluidine blue staining. BAT determined CD63 expression in antiCD63/anti-IgE/anti-CD45-labelled whole blood. In each case, the percentage of activated Ba post-stimulation with 1 and 10 microg/ml Dc was determined. Positive controls included N-formyl-methionyl-leucyl-phenylalanine (fMLP) peptide-induced activation. IgE-mediated Ba activation was induced with a Dp allergenic extract. With Dc 1 microg/ml, mean HBDT in Dc-susceptible individuals was 33.62 +/- 18.35% and 8.49 +/- 4.79% in controls (P = 0.0001). Mean BAT was 2.04 +/- 1.68% and 1.93 +/- 1.40% in controls (P = 0.8). Ba preincubation with Dc did not affect fMLP-induced CD63 expression, neither in Dc-sensitive individuals (P = 0.8) (n = 4) nor in subjects without Dc hypersensitivity (P = 0.25) (n = 4). Ba from the two patients sensitive both to Dc and Dp responded to Dp but not to Dc by BAT: Dc, 1.99 +/- 0.78%; Dp: 60.87 +/- 9.28%; but showed degranulation by HBDT: Dc, 30.53 +/- 1.02%, Dp: 48.78 +/- 22.17%. Dc induces Ba degranulation in sensitive patients in a way that does not induce CD63 expression and is different from IgE-mediated and fMLP-mediated degranulation. Our results suggest that CD63 expression is not a reliable diagnostic method for diclofenac allergy.

Allergens↗

[Kikuchi-Fujimoto necrotizing lymphadenitis. Report of 2 cases].

Kikuchi-Fujimoto disease (KFD) is a form of necrotizing lymphadenitis. The disease is a usually benign, self limited cause of lymph node enlargement affecting predominantly young women. Several other clinical manifestations have been described, though the only consistent findings are a macular eruption and a fever. Occasionally, the disease has presented as a fever of unknown origin. Lymph node specimens show areas of necrosis without neutrophilic infiltration. Lymphocyte mediated apoptotic mechanisms are responsible for the necrosis observed. Clinically, it should be differentiated from many different conditions, including infections such as cat scratch disease and rheumatological diseases like Still's disease and Systemic Lupus Erythematosus. Pathologically, it should be differentiated from lymphomas. KFD is widely known in the Far East, but very rare in Latin America. As a matter of fact, we have only detected four reported cases from Argentina, Brazil and Chile. We here describe two additional cases from Argentina. Both occurred in young women. One had a mediastinal compromise and a recurrent course, only observed in 4% of cases. The second one had a classical cervical presentation. The diagnosis in both was made by lymph node biopsy, although, in areas of great prevalence, an aspiration may be sufficient to establish the disease. We anticipate that the real prevalence of this unusual disease is highly underrepresented.

Adult↗

[Effect of complement type 1 receptor pre-binding on the phagocytosis mediated by Fc receptor].

As a result of IgG-Fc interaction, sheep erythrocytes sensitized with IgG (E-IgG) are constitutively phagocytosed by resting PMN, although in low numbers. The low efficiency of the system can be improved by opsonization with C3b, since the combination of C3b and IgG makes a powerful opsonic signal. It is accepted that the mechanism of C3b enhancement of IgG mediated phagocytosis is achieved by increasing the adherence of the targets to the phagocyte. Recently, a non-opsonic role for C3b enhancement of IgG mediated phagocytosis has been proposed, in cultured human monocytes. These cells, when adhered on glass surfaces precoated with C3b, showed a marked increase in E-IgG internalization. The effect was dose dependent and it was reproduced utilizing a monoclonal antibody against CR1 (C3b receptor). In the present work we studied the existence of this phenomenon in resting neutrophils and in neutrophils stimulated with two kinds of agents: a phorbol ester (PDBu), which activates the CR1 and fMLP, which increases the expression of this receptor. In previous experiments we determined that the adherence of resting neutrophils on different concentrations of iC3 (which binds CR1 and exerts the same effect that C3b), did not increase the phagocytosis of the E-IgG, using as a control neutrophils adhered on the same concentrations of human serum albumin (HSA) (data not shown).(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗

Partial neutralization of a lupus anticoagulant by human immunoglobulin.

In a patient with a Lupus Anticoagulant (LA) and recurrent fetal loss, we observed a significant shortening of the APTT after high-dose intravenous immunoglobulin infusion (IVIg). The LA activity present in patient's serum and purified IgG was partially neutralized by IVIg in a dose-dependent way. In addition, IgG purified from IVIg and its F(ab')2 fragment neutralized LA activity of the patient's IgG. In both cases, the neutralization was dose-dependent and it was obtained with similar molar ratios. The "in vitro" neutralization of LA activity and the immediate shortening of the APTT after IVIg infusion, might be mediated through idiotype/antiidiotype interactions. On the other hand, the long-lasting effect of IVIg in this patient indicates that it may induce specific inhibition of autoantibody synthesis. We believe that IVIg should be considered as a therapeutic alternative for LA-related clinical disorders.

Abortion, Spontaneous↗