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This sidebar originally appeared in the June 4th, 1997 issue of Smart Drug News [Volume 5, Number 9]. All rights reserved.

Piracetam and Sickle Cell Anemia

Piracetam’s fundamental lack of toxicity has prompted numerous pediatric uses over more than two decades of clinical use. One of the latest appears to be sickle cell anemia and beta-thalassemia. Piracetam shows a strong anti-sickling influence in vitro and in vivo, and a Saudi Arabian double-blinded clinical study found a significant reduction in “the clinical severity of the disease, the number of crises, the extent of hospitalization and the blood transfusion requirements” in children in the 3-12-year age range [El-Hazmi et al., 1996]. Although these clinical improvements were highly statistically significant (P<0.001) and continued for several months after discontinuation of the piracetam, there were no corresponding changes in haematological or biochemical parameters associated with sickle cell disease.

El-Hazmi MAF, Warsy AS, Al-Fawaz I et al. Piracetam is useful in the treatment of children with sickle cell disease. Acta Haematologica (Basel) 96(4): 221-26, 1996.

Piracetam in Angelman Syndrome

Angelman syndrome is a genetic condition characterized by a deletion of part of maternal chromosome 15 (15q11-13), which is associated with severe mental retardation, ataxic (uncoordinated) gait, tremulousness, and jerky movements. Although not yet fully studied, the critical region of the 15th chromosome contains several genes that code for GABA-A receptor subunits. The GABA-A receptor is the most common GABA receptor in the brain. GABA-A receptors regulate the flow of chloride ions (Cl-) across neuron membranes, which decreases neuron excitability. In Angelman syndrome, the lack of adequate GABA-A influence increases neuronal (CNS) excitability and results in myoclonic (muscle twitching) activity, which was reported to be significantly reduced in 5 patients by treatment with piracetam [Guerrini et al., 1966].

Guerrini R, De Lorey TM, Bonanni P et al. Cortical myoclonus in Angelman syndrome. Annals of Neurology 40(1): 39-48, 1996.