Levonorgestrel is metabolized in the liver, via reduction, hydroxylation, and conjugation (specifically glucuronidation and sulfation). Oxidation occurs primarily at the C2α and C16β positions, while reduction occurs in the A ring. 5α-Dihydrolevonorgestrel is produced as an active metabolite of levonorgestrel by 5α-reductase. The elimination half-life of levonorgestrel is 24 to 32 hours, although values as short as 8 hours and as great as 45 hours have been reported. About 20 to 67% of a single oral dose of levonorgestrel is eliminated in urine and 21 to 34% in feces. Chemistry
Levonorgestrel, also known as 17α-ethynyl-18-methyl-19-nortestosterone or as 17α-ethynyl-18-methylestr-4-en-17β-ol-3-one, is a synthetic estrane steroid and a derivative of testosterone. It is the C13β or levorotatory stereoisomer and enantiopure form of norgestrel, the C13α or dextrorotatory isomer being inactive. Levonorgestrel is more specifically a derivative of norethisterone (17α-ethynyl-19-nortestosterone) and is the parent compound of the gonane (18-methylestrane or 13β-ethylgonane) subgroup of the 19-nortestosterone family of progestins. Besides levonorgestrel itself, this group includes desogestrel, dienogest, etonogestrel, gestodene, norelgestromin, norgestimate, and norgestrel. Levonorgestrel acetate and levonorgestrel butanoate are C17β esters of levonorgestrel. Levonorgestrel has a molecular weight of 312.45 g/mol and a partition coefficient (log P) of 3.8. History
Norgestrel (rac-13-ethyl-17α-ethynyl-19-nortestosterone), the racemic mixture containing levonorgestrel and dextronorgestrel, was discovered by Hughes and colleagues at Wyeth in 1963 via structural modification of norethisterone (17α-ethynyl-19-nortestosterone). It was the first progestogen to be manufactured via total chemical synthesis.
Chondrocalcinosis or cartilage calcification is calcification (accumulation of calcium salts) in hyaline cartilage and/or fibrocartilage. It can be seen on radiography. Causes
Buildup of calcium phosphate in the ankle joints has been found in about 50% of the general population, and may be associated with osteoarthritis.Another common cause of chondrocalcinosis is calcium pyrophosphate dihydrate crystal deposition disease (CPPD). CPPD is estimated to affect 4% to 7% of the adult populations of Europe and the United States. Previous studies have overestimated the prevalence by simply estimating the prevalence of chondrocalcinosis regardless of cause.A magnesium deficiency may cause chondrocalcinosis, and magnesium supplementation may reduce or alleviate symptoms. In some cases, arthritis from injury can cause chondrocalcinosis. Other causes of chondrocalcinosis include:
Hypercalcaemia, especially when caused by hyperparathyroidism
Arthritis
Pseudogout
Wilson disease
Hemochromatosis
Ochronosis
Hypophosphatasia
Hypothyroidism
Hyperoxalemia
Acromegaly
Gitelman syndrome

Diagnosis
Chondrocalcinosis can be visualized on projectional radiography, CT scan, MRI, US, and nuclear medicine. CT scans and MRIs show calcific masses (usually within the ligamentum flavum or joint capsule), however radiography is more successful. At ultrasound, chondrocalcinosis may be depicted as echogenic foci with no acoustic shadow within the hyaline cartilage. As with most conditions, chondrocalcinosis can present with similarity to other diseases such as ankylosing spondylitis and gout. == References ==