Adverse effects
Very common (more than 10% of people) adverse effects include loss of appetite, weight loss, insomnia, drowsiness, ataxia, hypotonia, and dystonia.Common (between 1% and 10% of people) adverse effects include neutropenia (sometimes severe), aggressiveness, irritability, behavior disorders, opposing behavior, hyperexcitability, sleep disorders, hyperkinesias, nausea, vomiting, and elevated gamma-glutamyltransferase. Interactions
Stiripentol inhibits several cytochrome P450 isoenzymes and so interacts with many anticonvulsants and other medicines. Pharmacology
As with most anticonvulsants, the precise mechanism of action is unknown. Regardless, stiripentol has been shown to have anticonvulsant effects of its own. Stiripentol increases GABAergic activity. At clinically relevant concentrations, it enhances central GABA neurotransmission through a barbiturate-like effect, since it increases the duration of opening of GABA-A receptor channels in hippocampal slices. It has also been shown to increase GABA levels in brain tissues by interfering with its reuptake and metabolism. Specifically, it has been shown to inhibit lactate dehydrogenase, which is an important enzyme involved in the energy metabolism of neurons. Inhibition of this enzyme can make neurons less prone to fire action potentials, likely through activation of ATP-sensitive potassium channels.Stiripentol also improves the effectiveness of many other anticonvulsants, possibly due to its inhibition of certain enzymes, slowing the drugs metabolism and increasing blood plasma levels. Chemistry
Stiripentol is an α-ethylene alcohol; its chemical formula is 4,4-dimethyl-1-[3,4-(methylendioxy)-phenyl]-1penten-3-ol. It is chiral and used medically as the racemate. The R enantiomer appears to be around 2.5 times more active than the S enantiomer. History
Stiripentol was discovered in 1978 by scientists at Biocodex and clinical trials started over the next few years.
When such large amounts of water are being lost through perspiration, electrolytes, especially sodium, are also being lost.In most athletes exercising and sweating for 4–5 hours with a sweat sodium concentration of less than 50 mmol/L, the total sodium lost is less than 10% of total body stores (total stores are approximately 2,500 mmol, or 58 g for a 70-kg person). These losses appear to be well tolerated by most people. The inclusion of sodium in fluid replacement drinks has some theoretical benefits and poses little or no risk, so long as these fluids are hypotonic (since the mainstay of dehydration prevention is the replacement of free water losses). Treatment
The most effective treatment for minor dehydration is widely considered to be drinking water and reducing fluid loss. Plain water restores only the volume of the blood plasma, inhibiting the thirst mechanism before solute levels can be replenished. Solid foods can contribute to fluid loss from vomiting and diarrhea. Urine concentration and frequency will return to normal as dehydration resolves.In some cases, correction of a dehydrated state is accomplished by the replenishment of necessary water and electrolytes (through oral rehydration therapy, or fluid replacement by intravenous therapy). As oral rehydration is less painful, non-invasive, inexpensive, and easier to provide, it is the treatment of choice for mild dehydration. Solutions used for intravenous rehydration must be isotonic or hypertonic. Pure water injected into the veins will cause the breakdown (lysis) of red blood cells (erythrocytes).When fresh water is unavailable (e.g.