Likewise, it is significantly more efficacious as an antiandrogen than other AR antagonists such as enzalutamide and spironolactone in scalp dermal papilla cells and sebocytes in vitro. Pharmacokinetics
Steady-state levels of clascoterone occur within 5 days of twice daily administration. At a dosage of 6 g clascoterone cream applied twice daily, maximal circulating levels of clascoterone were 4.5 ± 2.9 ng/mL, area-under-the-curve levels over the dosing interval were 37.1 ± 22.3 h*ng/mL, and average circulating levels of clascoterone were 3.1 ± 1.9 ng/mL. In rodents, clascoterone has been found to possess strong local antiandrogenic activity, but negligible systemic antiandrogenic activity when administered via subcutaneous injection. Along these lines, the medication is not progonadotropic in animals.The plasma protein binding of clascoterone is 84 to 89% regardless of concentration.Clascoterone is rapidly hydrolyzed into cortexolone (11-deoxycortisol) and this compound is a possible primary metabolite of clascoterone based on in-vitro studies in human liver cells. During treatment with clascoterone, cortexolone levels were detectable and generally below or near the low limit of quantification (0.5 ng/mL). Clascoterone may also produce other metabolites, including conjugates.The elimination of clascoterone has not been fully characterized in humans. Chemistry
Clascoterone, also known as cortexolone 17α-propionate or 11-deoxycortisol 17α-propionate, as well as 17α,21-dihydroxyprogesterone 17α-propionate or 17α,21-dihydroxypregn-4-en-3,20-dione 17α-propionate, is a synthetic pregnane steroid and a derivative of progesterone and 11-deoxycortisol (cortexolone). It is specifically the C17α propionate ester of 11-deoxycortisol.An analogue of clascoterone is 9,11-dehydrocortexolone 17α-butyrate (CB-03-04).Corticosteroids related to clascoterone, for instance cortisone acetate and prednisolone acetate, show antiandrogenic activity in animals similarly to clascoterone.
Liver function tests will typically be normal or unchanged from baseline as the infection does not involve the liver parenchyma. If a D-dimer is ordered, which it often is when there is pleuritic torso pain, it will usually be markedly elevated but other testing for pulmonary embolism will be normal. CT of the abdomen with IV contrast may show subtle enhancement of the liver capsule, but this may be missed by radiologists if they are not advised to look for it. Testing for gonorrhea and chlamydia should be performed to make the diagnosis. An endocervical or low vaginal swab should be taken to test for these organisms. Antibody testing is rarely required but may be considered if other tests are non-diagnostic and suspicion is high.Laparoscopy is also rarely required, but may be performed when the diagnosis is uncertain and may reveal "guitar string" adhesions of parietal peritoneum to liver. Treatment
Treatment involves a course of antibiotics to cover the appropriate organisms, typically ceftriaxone plus azithromycin. Laparoscopy for lysis of adhesions may be performed for refractory pain. References
Further reading
Pregerson, Brady (2010). Quick Essentials: Emergency Medicine (4th ed.). ISBN 978-0-9761552-3-2. Pregerson, D. Brady (2012). Tarascon Emergency Department Quick Reference Guide. Jones & Bartlett. ISBN 978-0-7637-8789-9. == External links ==