Medications
Somatostatin analogues
The primary current medical treatment of acromegaly is to use somatostatin analogues – octreotide (Sandostatin) or lanreotide (Somatuline). These somatostatin analogues are synthetic forms of a brain hormone, somatostatin, which stops GH production. The long-acting forms of these drugs must be injected every 2 to 4 weeks for effective treatment. Most people with acromegaly respond to this medication. In many people with acromegaly, GH levels fall within one hour and headaches improve within minutes after the injection. Octreotide and lanreotide are effective for long-term treatment. Octreotide and lanreotide have also been used successfully to treat people with acromegaly caused by non-pituitary tumors.Somatostatin analogues are also sometimes used to shrink large tumors before surgery.Because octreotide inhibits gastrointestinal and pancreatic function, long-term use causes digestive problems such as loose stools, nausea, and gas in one third of people. In addition, approximately 25 percent of people with acromegaly develop gallstones, which are usually asymptomatic. In some cases, octreotide treatment can cause diabetes due to the fact that somatostatin and its analogues can inhibit the release of insulin. With an aggressive adenoma that is not able to be operated on, there may be a resistance to octreotide and in which case a second generation SSA, pasireotide, may be used for tumor control. However, insulin and glucose levels should be carefully monitored as pasireotide has been associated with hyperglycemia by reducing insulin secretion.
X-linked endothelial corneal dystrophy (XECD) is a rare form of corneal dystrophy described first in 2006, based on a 4-generation family of 60 members with 9 affected males and 35 trait carriers, which led to mapping the XECD locus to Xq25. It manifests as severe corneal opacification or clouding, sometimes congenital, in the form of a ground glass, milky corneal tissue, and moon crater-like changes of corneal endothelium. Trait carriers manifest only endothelial alterations resembling moon craters.As of December 2014, the molecular basis for this disease remained unknown, although 181 genes were known to be within the XECD locus, of which 68 were known to be protein-coding. References


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