Management
Eradication therapy
Once the diagnosis of H. pylori is confirmed, the first-line treatment would be a triple regimen in which pantoprazole and clarithromycin are combined with either amoxicillin or metronidazole. This treatment regimen can be given for 7–14 days. However, its effectiveness in eradicating H. pylori has been reducing from 90% to 70%. However, the rate of eradication can be increased by doubling the dosage of pantoprazole or increasing the duration of treatment to 14 days. Quadruple therapy (pantoprazole, clarithromycin, amoxicillin, and metronidazole) can also be used. The quadruple therapy can achieve an eradication rate of 90%. If the clarithromycin resistance rate is higher than 15% in an area, the usage of clarithromycin should be abandoned. Instead, bismuth-containing quadruple therapy can be used (pantoprazole, bismuth citrate, tetracycline, and metronidazole) for 14 days. The bismuth therapy can also achieve an eradication rate of 90% and can be used as second-line therapy when the first-line triple-regimen therapy has failed

NSAIDs induced ulcers
NSAID-associated ulcers heal in 6 to 8 weeks provided the NSAIDs are withdrawn with the introduction of proton pump inhibitors (PPI). Bleeding
For those with bleeding peptic ulcers, fluid replacement with crystalloids is sometimes given to maintain volume in the blood vessels. Maintaining haemoglobin at greater than 7 g/dL (70 g/L) through restrictive blood transfusion has been associated with reduced rate of death. Glasgow-Blatchford score is used to determine whether a person should be treated inside a hospital or as an outpatient. Intravenous PPIs can suppress stomach bleeding more quickly than oral ones.
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