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1.
Hemoglobin ; 38(5): 351-4, 2014.
Article in English | MEDLINE | ID: mdl-25271993

ABSTRACT

The increase in survival rate of ß-thalassemia (ß-thal) patients allowed for the appearance and manifestation of several complications in almost every organ system. Priapism in ß-thal patients is rarely reported in the literature. We herein report and investigate the occurrence of two cases of priapism in two young patients with ß-thal intermedia (ß-TI). The potential mechanisms are due to either a cellular mechanism involving a thrombus obstructing the efferent venules of the corpora cavernosa leading to priapism, or a recently elucidated functional mechanism that causes alteration of nitric oxide (NO) response of the penis, ultimately causing priapism. This should incite clinicians for a close follow-up and monitoring of high risk patients who are susceptible to developing priapism.


Subject(s)
Priapism/etiology , beta-Thalassemia/physiopathology , Adrenergic beta-Antagonists/therapeutic use , Adult , Combined Modality Therapy , Drug Combinations , Histamine H1 Antagonists/therapeutic use , Humans , Male , Priapism/prevention & control , Propranolol/therapeutic use , Pseudoephedrine/therapeutic use , Severity of Illness Index , Treatment Outcome , Triprolidine/therapeutic use , beta-Thalassemia/drug therapy , beta-Thalassemia/therapy
2.
Biomed Res Int ; 2014: 350432, 2014.
Article in English | MEDLINE | ID: mdl-25121095

ABSTRACT

The term Nontransfusion dependent thalassaemia (NTDT) was suggested to describe patients who had clinical manifestations that are too severe to be termed minor yet too mild to be termed major. Those patients are not entirely dependent on transfusions for survival. If left untreated, three main factors are responsible for the clinical sequelae of NTDT: ineffective erythropoiesis, chronic hemolytic anemia, and iron overload. Reactive oxygen species (ROS) generation in NTDT patients is caused by 2 major mechanisms. The first one is chronic hypoxia resulting from chronic anemia and ineffective erythropoiesis leading to mitochondrial damage and the second is iron overload also due to chronic anemia and tissue hypoxia leading to increase intestinal iron absorption in thalassemic patients. Oxidative damage by reactive oxygen species (generated by free globin chains and labile plasma iron) is believed to be one of the main contributors to cell injury, tissue damage, and hypercoagulability in patients with thalassemia. Independently increased ROS has been linked to a myriad of pathological outcomes such as leg ulcers, decreased wound healing, pulmonary hypertension, silent brain infarcts, and increased thrombosis to count a few. Interestingly many of those complications overlap with those found in NTDT patients.


Subject(s)
Blood Transfusion , Reactive Oxygen Species/metabolism , Thalassemia/metabolism , Thalassemia/therapy , Humans , Hypoxia/pathology , Iron Overload/metabolism , Iron Overload/therapy , NADPH Oxidases/metabolism
4.
Crit Rev Oncol Hematol ; 87(2): 122-31, 2013 Aug.
Article in English | MEDLINE | ID: mdl-23375349

ABSTRACT

Inhibition of angiogenic pathways has proven an effective strategy for the treatment of several common solid tumors however its role in the management of prostate cancer is yet to be defined. Advances in clinical research have resulted in five new treatments for metastatic prostate cancer in the last two years. The immunotherapy sipuleucel-T, the cytotoxic cabazitaxel, the androgen biosynthesis inhibitor abiraterone acetate, the radioisotope radium-223 and the antiandrogen enzalutamide have all been shown to improve overall survival in randomized phase III studies treatment paradigms are changing rapidly. Angiogenesis is known to play a central role in the progression of advanced prostate cancer however established antiangiogenic therapies including bevacizumab and sunitinib have failed to improve survival in randomized trials to date. Novel treatment combinations and novel agents such as cabozantinib are showing promising early results and it is hoped that further well-designed studies will validate the strong biological hypothesis for the benefit of antiangiogenic therapy to improve outcomes for patients with prostate cancer.


Subject(s)
Angiogenesis Inhibitors/therapeutic use , Antineoplastic Agents/therapeutic use , Neovascularization, Pathologic/drug therapy , Prostatic Neoplasms/drug therapy , Prostatic Neoplasms/pathology , Humans , Male , Neoplasm Staging , Treatment Outcome
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