ABSTRACT
Management of B-thalassemia major with regular blood transfusion and iron chelation therapy with desferrioxamine [DFO] has markedly improved the prognosis of the disease but some patients continue to develop iron-related complications and to die despite the use of DFO. Deferiprone [DFP] is suggested to be the most promising oral iron chelator under development. The present study was conducted on 60 pediatric patients with Beta-thalassemia major to evaluate the effectiveness of combined therapy with DFO and DFP compared to DFO therapy alone. The patients were evaluated clinically with complete history taking, routine laboratory investigations, doppler echocardiography, serum ferritin and serum cardiac troponin T [cTnT] estimation. The results showed significant improvement in hemodynamic parameters and significant decrease in serum cTnT and decrease in serum ferritin post-treatment with DFO and combined DFO/DFP when compared with pre-treatment values of the patients. Combination therapy was more effective than DFO therapy alone in the improvement of hemodynamic parameters, reduction of the myocardial damage indicator [cTnT] and reduction of serum ferritin. The authors recommend the use of combined DFO/DFP therapy in the management of transfusional iron overload in beta-thalassemia major
ABSTRACT
This study was conducted on 360 adult albino rats of both sexes to evaluatesome of the chronic toxicity of two organotin compounds [TBTO and MBTCL]. Therats were grouped into two control groups orally received the vehicles and twoother groups orally received 1/10 of oral LD50 of TBTO and MBTCL. Monthly forthree months, biochemical and histopathological investigations were done. Tenrats were taken monthly from each group to make their chromosomal patterns. As regards nephrotoxicity, both compounds produced remarkable progressivehistopathological changes with no significant increase in blood urea andcreatinine. The hepatotoxin of both compounds were nearly the same throughthe study [biochemically and histopathologically]. Also, both compounds causeprogressive histopathological changes of almost the same degree in lungs,intestine, brain and heart. Regarding the cytogenetic study, TBTO was foundto be more toxic than MBTCL. This was deduced from the very highlysignificant increase in the number of cells with structural chromosomalanomalies and the total number of structural anomalies in the TBTO treatedgroup as compared with MBTCL treated group. It can be concluded that both TBTOand MBTCL were potentially toxic to the liver, kidneys and lungs. They hadalso mild to moderate toxic effects on intestine, brain and heart. Bothcompounds were highly genotoxic to albino rats. TBTO having more genotoxicpotential. Most of the toxic effects of both compounds were progressive