It is indicated for the treatment of Wilsons disease in adults, adolescents and children five years of age or older who are intolerant to D-penicillamine therapy.The most common side effects include nausea, especially when starting treatment, skin rash, duodenitis (inflammation of the duodenum, the part of the gut leading out of the stomach), and severe colitis (inflammation in the large bowel causing pain and diarrhea). Society and culture
Controversies
In the United States, Valeant Pharmaceuticals International raised the price of its Syprine brand of TETA from $625 to $21,267 for 100 pills over five years. The New York Times said that this "egregious" price increase caused public outrage. Teva Pharmaceuticals developed a generic, which patients and doctors expected to be cheaper, but when it was introduced in February 2018, Tevas price was $18,375 for 100 pills. Aaron Kesselheim, who studies drug pricing at Harvard Medical School, said that drug companies price the product at what they think the market will bear. Production
TETA is prepared by heating ethylenediamine or ethanolamine/ammonia mixtures over an oxide catalyst. This process gives a variety of amines, especially ethylene amines which are separated by distillation and sublimation. Coordination chemistry
TETA is a tetradentate ligand in coordination chemistry, where it is referred to as trien. Octahedral complexes of the type M(trien)L2 can adopt several diastereomeric structures. References
External links
"Triethylenetetramine". Drug Information Portal. U.S. National Library of Medicine. "Trientine hydrochloride". Drug Information Portal. U.S. National Library of Medicine. "Trientine tetrahydrochloride". Drug Information Portal. U.S. National Library of Medicine.
Congenital hereditary corneal dystrophy (CHED) is a form of corneal endothelial dystrophy that presents at birth. CHED was previously subclassified into two subtypes: CHED1 and CHED2. However in 2015, the International Classification of Corneal Dystrophies (IC3D) renamed the condition "CHED1" to become posterior polymorphous corneal dystrophy, and renamed the condition "CHED2" to become, simply, CHED. Consequently, the scope of this article is restricted to the condition currently referred to as CHED

Signs and symptoms
CHED presents congenitally, but has a stationary course. The cornea exhibits a variable degree of clouding: from a diffuse haze, to a "ground glass" appearance, with occasional focal gray spots. The cornea thickens to between two and three times is normal thickness. Rarely, sub-epithelial band keratopathy and elevated intraocular pressure occur. Patients have blurred vision and nystagmus, however it is rare for the condition to be associated with either epiphora or photophobia with this. Genetics
CHED exhibits autosomal recessive inheritance, with 80% of cases linked to mutations in SLC4A11 gene. The SLC4A11 gene encodes solute carrier family 4, sodium borate transporter, member 11. Pathology
Histologically, the Descemets membrane in CHED becomes diffusely thickened and laminated. Multiple layers of basement membrane-like material appear to form on the posterior part of Descemets membrane. The endothelial cells are sparse - they become atrophic and degenerated, with many vacuoles. The corneal stroma becomes severely disorganised; the lamellar arrangement of the fibrils becomes disrupted. Diagnosis
Management
Management of CHED primarily involves corneal transplantation. The age that corneal transplantation is required is variable, however, it is usually necessary fairly early in life.