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.