Abstract：
:Glucose-6-phospate dehydrogenase (G6PD) deficiency is estimated to affect more than 400 million people world-wide. This X-linked genetic deficiency puts stress on red blood cells (RBC), which may be further augmented under certain pathophysiological conditions and drug treatments. These conditions can cause hemolytic anemia and eventually lead to multi-organ failure and mortality. G6PD is involved in the rate-limiting step of the pentose phosphate pathway, which generates reduced nicotinamide adenine dinucleotide phosphate (NADPH). In RBCs, the NADPH/G6PD pathway is the only source for recycling reduced glutathione and provides protection from oxidative stress. Susceptibility of G6PD deficient populations to certain drug treatments and potential risks of hemolysis are important public health issues. A number of clinical trials are currently in progress investigating clinical factors associated with G6PD deficiency, validation of new diagnostic kits for G6PD deficiency, and evaluating drug safety, efficacy, and pathophysiology. More than 25 clinical studies in G6PD populations are currently in progress or have just been completed that have been examined for clinical pharmacology and potential therapeutic implications of G6PD deficiency. The information on clinical conditions, interventions, purpose, outcome, and status of these clinical trials has been studied. A critical review of ongoing clinical investigations on pharmacology and therapeutics of G6PD deficiency should be highly important for researchers, clinical pharmacologists, pharmaceutical companies, and global public health agencies. The information may be useful for developing strategies for treatment and control of hemolytic crisis and potential drug toxicities in G6PD deficient patients.
journal_name
Pharmacol Therjournal_title
Pharmacology & therapeuticsauthors
Ryan K,Tekwani BLdoi
10.1016/j.pharmthera.2020.107788subject
Has Abstractpub_date
2020-12-14 00:00:00pages
107788eissn
0163-7258issn
1879-016Xpii
S0163-7258(20)30319-3journal_volume
222pub_type
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