Similarly, the degree to which transthyretin amyloidosis-associated polyneuropathy and carpal tunnel syndrome is under investigation. Prior carpal tunnel release is often noted in individuals who later present with transthyretin amyloid-associated cardiomyopathy. There is consideration that bilateral carpal tunnel syndrome could be a reason to consider amyloidosis, timely diagnosis of which could improve heart health. Amyloidosis is rare, even among people with carpal tunnel syndrome (0.55% incidence within 10 years of carpal tunnel release). In the absence of other factors associated with a notable probability of amyloidosis, its not clear that biopsy at the time of carpal tunnel release has a suitable balance between potential harms and potential benefits.Other specific pathophysiologies that can cause median neuropathy via pressure include:

Rheumatoid arthritis and other diseases that cause inflammation of the flexor tendons. With severe untreated hypothyroidism, generalized myxedema causes deposition of mucopolysaccharides within both the perineurium of the median nerve, as well as the tendons passing through the carpal tunnel. Association of CTS and IMNCT with lesser degrees of hypothyroidism is questioned. Pregnancy may bring out symptoms in genetically predisposed individuals. Perhaps the changes in hormones and fluid increase pressure temporarily in the carpal tunnel. High progesterone levels and water retention may increase the size of  the synovium. Bleeding and swelling from a fracture or dislocation. This is referred to as acute carpal tunnel syndrome. Acromegaly causes excessive secretion of growth hormones.
Xanthinuria, also known as xanthine oxidase deficiency, is a rare genetic disorder causing the accumulation of xanthine. It is caused by a deficiency of the enzyme xanthine oxidase. It was first formally characterized in 1954. Presentation
Sufferers have unusually high concentrations of xanthine in their blood and urine, which can lead to health problems such as renal failure and xanthine kidney stones, one of the rarest types of kidney stones. Causes
Type I xanthinuria can be caused by a deficiency of xanthine oxidase, which is an enzyme necessary for converting xanthine to uric acid. Type II xanthinuria and molybdenum cofactor deficiency lack one or two other enzyme activities in addition to xanthine oxidase. Treatment
There is no specific treatment beyond maintaining a high fluid intake and avoiding foods that are high in purine. References
External links

Xanthinuria at NIHs Office of Rare Diseases