The Effect of Curcumin On Plasma Histamine Level, PEF Variation and Length of Stay of Patients With Acute Exacerbation Asthma

Introduction: Inflammation in asthma occured in airway especially in submucous layer, and involve eosinophil, neutrophil, lymphocytes T, epitheliat cel, basophil, mast cell, and lymphocytes B. Inflammatory cells produce inflammatory mediators (histamine, leucotrienes, and prostanoid), cytokines, and chemokines that can cause bronchocontriction. This study was conducted to determine and prove the effect of curcumin as adjunctive therapy in acute exacerbation asthma. Curcumin is expected to increase the quality therapy of acute exacerbation asthma. The effect of curcumin is known wiith evaluate plasma histamine level, PEF variation, and length of stay of patient with acute exacerbation asthma. Methods: This study is a quasi experimental study with pretest and posttest design. Sampel of study is 30 patients hospitalizes acute exacerbation asthma in Moewardi hospital and Sohadi Prijonegoro Sragen hospital in August 2016 until september 2016. The subject was taken with concecutive random sampling. Independent variable is curcumin 4x550 mg and dependent variables are plasma histamin level, PEF variation, and length of stay. Result: There is no significant difference (P=0.462) of decreasing plasma histamine level between treatment group 3,988±2,739 ng/ml and control group 3,376±1,606 ng/ml. There is no significant difference (P=0.501) of PEF variation between treatment group 28,126±7,886% and control group 30,400±10,217%. There is no significant difference (P=0.936) of length of stay between treatment group perlakuan 6,333±2,193 days and control group 6,400±2,292 days. Conclusion: Giving curcumin in acute exacerbation asthma while hospitalized didn’t reduce inflammatory marker plasma histamin, PEF variation, and length of stay. (J Respir Indo 2018; 38(2): 100-8)

Immunoglobulin E–dependent Active Fatal Anaphylaxis in Mast Cell–deficient Mice

Mast cells have long been believed to be the central effector cells in the development of immunoglobulin (Ig)E-dependent anaphylaxis. In this study, we investigated the role of mast cells in IgE-dependent hapten-induced active fatal anaphylaxis using mast cell–deficient WBB6F1- W/Wv (W/Wv) and congenic normal (+/+) mice. Although a 5-min delay in shock signs and death were observed in W/Wv mice, 100% fatal reactions to penicillin V (Pen V) occurred in both +/+ and W/Wv mice. Administration of monoclonal anti–IL-4 antibody completely prevented the fatal reactions, and the effect of anti–IL-4 was associated with its suppressive activity on Pen V–specific serum levels of IgE, but not IgG. The platelet-activating factor (PAF) antagonist, BN 50739, completely prevented the fatal reactions in both strains of mice. Our kinetic study revealed, in contrast to no elevation of plasma histamine level in W/Wv mice, high levels of PAF in the circulation after challenge in both +/+ and W/Wv mice, albeit to a lesser degree in the latter case. These data indicate that cells other than mast cells are sufficient to induce an IgE-dependent active fatal anaphylaxis by elaborating PAF, which is the critical mediator for fatal murine anaphylaxis.

Some effects of autologous and homologous blood or plasma overtransfusions in the dog

Plasma volume, protein concentration, mean arterial pressure, urticaria, and survival rates were observed in morphine-pentobarbitalized dogs overtransfused with either dextran, homologous blood, reconstituted homologous blood, autologous frozen stored, homologous frozen stored, or fresh plasma. The principal reaction and only difference between responses with autologous plasma and homologous blood and plasma was the development of urticaria with homologous blood (10%), homologous plasma (70–90%), and reconstituted homologous blood (100%). Significant amounts of fluid and protein were lost with all overtransfusions; this loss was not correlated with the urticaria. Of five dogs developing urticaria, three had an increased plasma histamine level. Diphenhydramine hydrochloride reduced the incidence of urticaria from 100 to 20%. Blood group incompatibility was not involved. There was a direct relationship between handling of blood and urticaria, and it is postulated that, during handling, a substance is activated which causes the release of endogenous histamine and production of urticaria.