Search results
Results from the WOW.Com Content Network
Treatments for Glycerol Kinase Deficiency are targeted to treat the symptoms because there are no permanent treatments for this disease. The main way to treat these symptoms is by using corticosteroids, glucose infusion, or mineralocorticoids. Corticosteroids are steroid hormones that are naturally produced in the adrenal glands.
Hyperglycerolemia, also known as glycerol kinase deficiency (GKD), is a genetic disorder where the enzyme glycerol kinase is deficient resulting in a build-up of glycerol in the body. Glycerol kinase is responsible for synthesizing triglycerides and glycerophospholipids in the body. Excess amounts of glycerol can be found in the blood and/ or ...
ERT has also been used to treat patients with severe combined immunodeficiency (SCID) resulting from an adenosine deaminase deficiency . [2] Other treatment options for patients with enzyme or protein deficiencies include substrate reduction therapy, gene therapy, and bone-marrow derived stem cell transplantation. [1] [3] [4]
take (often effectively a noun meaning "prescription"—medical prescription or prescription drug) rep. repetatur: let it be repeated s. signa: write (write on the label) s.a. secundum artem: according to the art (accepted practice or best practice) SC subcutaneous "SC" can be mistaken for "SL," meaning sublingual. See also SQ: sem. semen seed
Alipogene tiparvovec (Glybera): AAV-based treatment for lipoprotein lipase deficiency (no longer commercially available) Axicabtagene ciloleucel (Yescarta): treatment for large B-cell lymphoma [1] Beremagene geperpavec (Vyjuvek): treatment of wounds. [2] Betibeglogene autotemcel (Zynteglo): treatment for beta thalassemia [3]
Since drug-induced nonautoimmune hemolytic anemia often occurs due to oxidative mechanisms, it is commonly seen in those with antioxidant enzyme deficiencies such as in Glucose-6-phosphate dehydrogenase deficiency or Hemoglobin H disease, often in response to drugs such as primaquine or dapsone. [2]
Thiazolidinedione ligand dependent transactivation is responsible for the majority of anti-diabetic effects. The activated PPAR/RXR heterodimer binds to peroxisome proliferator hormone response elements upstream of target genes in complex with a number of coactivators such as nuclear receptor coactivator 1 and CREB binding protein, this causes upregulation of genes (for a full list see PPARγ):
Treatment for glycogen storage disease type III may involve a high-protein diet, to facilitate gluconeogenesis. Additionally the individual may need: [2] [1] [10] IV glucose (if oral route is inadvisable) Nutritional specialist; Vitamin D (for osteoporosis/secondary complication) Hepatic transplant (if a complication occurs)