The de novo pathway is stimulated due to an excess of PRPP (5-phospho-D-ribosyl-1-pyrophosphate or simply phosphoribosyl-pyrophosphate).It was previously unclear whether the neurological abnormalities in LNS were due to uric acid neurotoxicity or to a relative shortage in "new" purine nucleotides during essential synthesis steps. Genetic mutations affecting the enzymes of the de novo synthesis pathway may possibly contribute to the disease, although these are rare or unknown. Uric acid has been suggested as a possible cause of neurotoxicity but this is unproven.Importantly, evidence suggests that one or more lesions in striatal dopaminergic pathways may be central to the neurological deficits, especially the choreoathetoid dyskinesia and self-mutilation. 6-hydroxydopamine toxicity in rodents may be a useful animal model for the syndrome, although this is not proven. However, the link between dopamine and purine synthesis is a nucleotide called guanosine triphosphate or GTP. The first step of dopamine synthesis is GTP cyclohydrolase, and significantly a deficiency of this step produces a syndrome that has a neuropathology similar to LNS. Thus a lack of HGPRT may produce a nucleotide deficiency (specifically: GTP deficiency) disorder, resulting in dopamine deficiency.Another animal model for LNS has been proposed to arise from oxidative damage, caused by the hyperuricemia accompanying LNS. This is based on the theory that uric acid is a powerful reducing agent and likely an important human antioxidant, in high concentration in blood.
Nizatidine is a histamine H2 receptor antagonist that inhibits stomach acid production, and is commonly used in the treatment of peptic ulcer disease and gastroesophageal reflux disease.It was patented in 1980 and approved for medical use in 1988. It was developed by Eli Lilly. Brand names include Tazac and Axid. Medical use
Nizatidine is used to treat duodenal ulcers, gastric ulcers, and gastroesophageal reflux disease (GERD/GORD), and to prevent stress ulcers. Adverse effects
Side effects are uncommon, usually minor, and include diarrhea, constipation, fatigue, drowsiness, headache, and muscle aches. History and development
Nizatidine was developed by Eli Lilly, and was first marketed in 1988. It is considered to be equipotent with ranitidine and differs by the substitution of a thiazole ring in place of the furan ring in ranitidine. In September 2000, Eli Lilly announced they would sell the sales and marketing rights for Axid to Reliant Pharmaceuticals. Subsequently, Reliant developed the oral solution of Axid, marketing this in 2004, after gaining approval from the U.S. Food and Drug Administration (FDA). However, a year later, they sold rights of the Axid Oral Solution (including the issued patent protecting the product) to Braintree Laboratories.Nizatidine proved to be the last new histamine H2 receptor antagonist introduced prior to the advent of proton pump inhibitors.Axid (nizatidine) drug recalled due to presence of NDMA. See also
Famotidine (Pepcid) — another popular H2 receptor antagonist

References
External links
"Nizatidine". Drug Information Portal. U.S. National Library of Medicine.