The volume of gas produced is partially dependent upon the composition of the intestinal microbiota, which is normally very resistant to change, but is also very different in different individuals. Some patients are predisposed to increased endogenous gas production by virtue of their gut microbiota composition. The greatest concentration of gut bacteria is in the colon, while the small intestine is normally nearly sterile. Fermentation occurs when unabsorbed food residues arrive in the colon. Therefore, even more than the composition of the microbiota, diet is the primary factor that dictates the volume of flatus produced. Diets that aim to reduce the amount of undigested fermentable food residues arriving in the colon have been shown to significantly reduce the volume of flatus produced. Again, increased volume of intestinal gas will not cause bloating and pain in normal subjects. Abnormal intestinal gas dynamics will create pain, distension, and bloating, regardless of whether there is high or low total flatus volume. Odor
Although flatus possesses an odor, this may be abnormally increased in some patients and cause social distress to the patient. Increased odor of flatus presents a distinct clinical issue from other complaints related to intestinal gas. Some patients may exhibit over-sensitivity to bad flatus odor, and in extreme forms, olfactory reference syndrome may be diagnosed. Recent informal research found a correlation between flatus odor and both loudness and humidity content. Incontinence of flatus
"Gas incontinence" could be defined as loss of voluntary control over the passage of flatus.
Glu275 and Lys268 have also been shown to contribute to the active site, indicating there are four active sites, each of which is formed from regions of three subunits. ADSL deficiency in different people is often caused by different mutations to the enzyme, more than 50 different mutations in the ADSL gene have been discovered

Diagnosis
In terms of the diagnosis of adenylosuccinate lyase deficiency one should look for (or exam/method):
MRI
Demonstration of succinylpurines in extracellular fluids like plasma, cerebrospinal fluid and/or urine using high-pressure liquid chromatography, with or without mass spectroscopy
Genetic testing - genomic cDNA sequencing of the ADSL gene and characterization of mutant proteins. Treatment
Treatment of adenylosuccinate lyase deficiency can be done via epilepsy management with anticonvulsive drugs. Additionally the following options include:

D-ribose and uridine administration
Ketogenic diet
S-adenosyl-l-methionine

Prognosis
The prognosis of this condition in childhood usually has a stable outcome, whereas in neonatal is almost always fatal, according to Jurecka, et al. See also
Adenylosuccinate
Adenylosuccinate lyase
List of genetic disorders

References
Further reading
Saudubray, Jean-Marie; Berghe, Georges van den; Walter, John H. (2011-11-16). Inborn Metabolic Diseases: Diagnosis and Treatment. Springer Science & Business Media. ISBN 9783642157202. Blau, Nenad; Hoffmann, Georg F.; Leonard, J. V.; Clarke, Joe T. R. (2006-01-16). Physicians Guide to the Treatment and Follow-Up of Metabolic Diseases. Springer Science & Business Media. ISBN 9783540289623. == External links ==