Torasemide, also known as torsemide, is a diuretic medication used to treat fluid overload due to heart failure, kidney disease, and liver disease and high blood pressure. It is a less preferred treatment for high blood pressure. It is taken by mouth or by injection into a vein.Common side effects include headache, increased urination, diarrhea, cough, and dizziness. Other side effects may include hearing loss and low blood potassium. Torasemide is a sulfonamide and loop diuretic. Use is not recommended in pregnancy or breastfeeding. It works by decreasing the reabsorption of sodium by the kidneys.Torasemide was patented in 1974 and came into medical use in 1993. It is on the World Health Organizations List of Essential Medicines. It is available as a generic medication. In 2019, it was the 227th most commonly prescribed medication in the United States, with more than 2 million prescriptions. Medical uses
It is used to treat fluid overload due to heart failure. It is sometimes used to treat high blood pressure. Compared with furosemide, torasemide is associated with a lower risk of rehospitalization for heart failure and an improvement in New York Heart Association class of heart failure. In heart failure it may be safer and more effective than furosemide. Long-term outcomes with torasemide may be better than with furosemide in patients with heart failure. Adverse effects
No evidence of torasemide-induced ototoxicity has been demonstrated in humans.Loop diuretics, including torsemide, may decrease total body thiamine, particularly in people with poor thiamine intake, and this depletion may worsen heart failure.
The nucleotide substitutions were discovered in the late 1990s by classical linkage analysis and are now known as p.R122H and p.N29I respectively, according to the amino acid substitution and position in the protein sequence. These mutations are rarely identified in general screens of patients with idiopathic disease and the phenotype of p.R122H and p.N29I is now well characterised with the p.A16V mutation recently characterised for the first time. There are many other rare mutations or polymorphisms of PRSS1 which remain less well understood and not all HP families have had the responsible genetic mutation identified. The mechanism by which these genetic mutations cause pancreatitis is not yet known; but is likely to be the result of increased autoactivation or reduced deactivation of trypsinogen. However, a novel mechanism has recently been identified in a p.R116C kindred. Diagnosis
Families are defined as having HP, if the phenotype is consistent with highly penetrant autosomal dominant inheritance. In simple terms, this would require two or more first degree relatives (or three or more second degree relatives) to have unexplained recurrent-acute or chronic pancreatitis in two or more generations. It is an autosomal dominant disease with penetrance that is generally accepted to be ≈80%. Management
Treatment of HP resemble that of chronic pancreatitis of other causes. Treatment focuses on enzyme and nutritional supplementation, pain management, pancreatic diabetes, and local organ complications, such as pseudocysts, bile duct or duodenal obstruction. (PMC1774562)

Prognosis
A 2009 study which followed 189 patients found no excess mortality despite the increased risk of pancreatic cancer. References


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