Cutaneous larva migrans (abbreviated CLM) is a skin disease in humans, caused by the larvae of various nematode parasites of the hookworm family (Ancylostomatidae). These parasites live in the intestines of dogs, cats, and wild animals and should not be confused with other members of the hookworm family for which humans are definitive hosts, namely Ancylostoma duodenale and Necator americanus. Colloquially called creeping eruption due to its presentation, the disease is also somewhat ambiguously known as "ground itch" or (in some parts of the southern United States) "sandworms", as the larvae like to live in sandy soil. Another vernacular name is plumbers itch. The medical term CLM literally means "wandering larvae in the skin". Symptoms and signs
The infection causes a red, intensely pruritic (itchy) eruption, and may look like twirling lesions. The itching can become very painful and if scratched may allow a secondary bacterial infection to develop. Cutaneous larva migrans usually heals spontaneously over weeks to months and has been known to last as long as one year. However, the severity of the symptoms usually causes those infected to seek medical treatment before spontaneous resolution occurs. Following proper treatment, migration of the larvae within the skin is halted and relief of the associated itching can occur in less than 48 hours (reported for thiabendazole).This is separate from the similar cutaneous larva currens which is caused by Strongyloides.
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