Sarcosinemia (SAR), also called hypersarcosinemia and SARDH deficiency, is a rare autosomal recessive metabolic disorder characterized by an increased concentration of sarcosine in blood plasma and urine ("sarcosinuria"). It can result from an inborn error of sarcosine metabolism, or from severe folate deficiency related to the folate requirement for the conversion of sarcosine to glycine. It is thought to be a relatively benign condition. Cause
Sarcosinemia is thought to be caused by a mutation in the sarcosine dehydrogenase (SARDH) gene, which is located at human chromosome 9q34.The disease is inherited in an autosomal recessive manner, which means the defective gene responsible for the disorder is located on an autosome (chromosome 9 is an autosome), and two copies of the defective gene (one inherited from each parent) are required in order to be born with the disorder. The parents of an individual with an autosomal recessive disorder both carry one copy of the defective gene, but usually do not experience any signs or symptoms of the disorder. Diagnosis
Treatment
See also
Inborn errors of metabolism

References
External links
Sarcosinemia at NIHs Office of Rare Diseases
In a study with antimuscarinic drugs, more DDIs were investigated using a model of Rhesus monkeys. Dose combinations of vibegron and tolterodine showed increased bladder capacity, the effects of both drugs at low dosis strengthened each other, known as synergism. The addition of darifenacin to vibegron created greater bladder relaxation only when used at high doses. Additionally, co-administration with Imidafenacin shows an increase in bladder capacity and voided volume in comparison to monotherapy. Possibly, a widely adapted treatment will be the combination of beta-3-adrenergic agonist with a nonselective M2/M3 antagonist as the most prevalent option.Clinical studies show no significant drug–drug interaction (DDI), aside from a serum concentration increase of digoxin when taken with vibegron. Maximal concentrations and systemic exposure (Cmax and area under the curve (AUC)) of digoxin are both increased as a result of DDI. Apart from the no to little DDIs, Vibegron has an additional safety quality in that it does not cross the blood-brain barrier and therefore does not induce cognitive impairment. Furthermore, Vibegron can be taken with or without food, this does not have an effect on vibegron plasma concentrations. Toxicity
Effects on animals
Pregnant rats were given very high daily oral doses of Vibegron during the period of organogenesis and showed no embryo-fetal developmental toxicity up to 300 mg/kg/day. Similar data was found in rabbits. Maternal toxicity was observed when doses exceeded 100 mg/kg/day in lactating rats. Clinical studies show that Vibegron is not toxic, safe and well-tolerated in patients. References
External links
"Vibegron". Drug Information Portal. U.S. National Library of Medicine.