The parents of an individual with an autosomal recessive disorder both carry one copy of the defective gene, but usually do not experience any signs or symptoms of the disorder. Diagnosis
Other conditions such as Liddles Syndrome can mimic the clinical features of AME, so diagnosis can be made by calculating the ratio of free urinary cortisol to free urinary cortisone. Since AME patients create less cortisone, the ratio will much  be higher than non-affected patients. Alternatively, one could differentiate between the two syndromes by administering a potassium-sparing diuretic. Patients with Liddles syndrome will only respond to a diuretic that binds the ENaC channel, whereas those with AME will respond to a diuretic that binds to ENaC or the mineralcorticoid receptor. Treatment
The treatment for AME is based on the blood pressure control with Aldosterone antagonist like Spironolactone which also reverses the hypokalemic metabolic alkalosis and other anti-hypertensives. Renal transplant is found curative in almost all clinical cases.AME is exceedingly rare, with fewer than 100 cases recorded worldwide.Liquorice consumption may also cause a temporary form of AME due to its ability to block 11β-hydroxysteroid dehydrogenase type 2, in turn causing increased levels of cortisol. Cessation of licorice consumption will reverse this form of AME. See also
Inborn errors of steroid metabolism
11β-Hydroxylase I deficiency
Hyperaldosteronism
Pseudohyperaldosteronism
Glucocorticoid-remediable aldosteronism
Aldosterone and aldosterone synthase
Maria New

References
External links
Apparent mineralocorticoid excess at NIHs Office of Rare Diseases
Once CBV-TP is integrated into the viral DNA, transcription and HIV reverse transcriptase is inhibited. Pharmacokinetics
Abacavir is given orally and is rapidly absorbed with a high bioavailability of 83%. Solution and tablet have comparable concentrations and bioavailability. Abacavir can be taken with or without food.Abacavir can cross the blood-brain barrier. Abacavir is metabolized primarily through the enzymes alcohol dehydrogenase and glucuronyl transferase to an inactive carboxylate and glucuronide metabolites. It has a half-life of approximately 1.5-2.0 hours. If a person has liver failure, abacavirs half life is increased by 58%.Abacavir is eliminated via excretion in the urine (83%) and feces (16%). It is unclear whether abacavir can be removed by hemodialysis or peritoneal dialysis. History
Robert Vince and Susan Daluge along with Mei Hua, a visiting scientist from China, developed the medication in the 80s.Abacavir was approved by the U.S. Food and Drug Administration (FDA) on 18 December 1998, and is thus the fifteenth approved antiretroviral drug in the United States. Its patent expired in the United States on 26 December 2009. Synthesis
References
Further reading
External links

"Abacavir". Drug Information Portal. U.S. National Library of Medicine. "Abacavir sulfate". Drug Information Portal. U.S. National Library of Medicine. Abacavir pathway on PharmGKB