The most popular method for reducing ephedrine to methamphetamine is similar to the Birch reduction, in that it uses anhydrous ammonia and lithium metal in the reaction. The second-most popular method uses red phosphorus and iodine in the reaction with ephedrine. Moreover, ephedrine can be synthesized into methcathinone via simple oxidation. As such, ephedrine is listed as a table-I precursor under the United Nations Convention Against Illicit Traffic in Narcotic Drugs and Psychotropic Substances. Detection of use
Ephedrine may be quantified in blood, plasma, or urine to monitor possible abuse by athletes, confirm a diagnosis of poisoning, or assist in a medicolegal death investigation. Many commercial immunoassay screening tests directed at the amphetamines cross-react appreciably with ephedrine, but chromatographic techniques can easily distinguish ephedrine from other phenethylamine derivatives. Blood or plasma ephedrine concentrations are typically in the 20–200 µg/L range in persons taking the drug therapeutically, 300–3000 µg/L in abusers or poisoned patients and 3–20 mg/L in cases of acute fatal overdosage. The current World Anti-Doping Agency (WADA) limit for ephedrine in an athletes urine is 10 µg/mL. Contraindications
Ephedrine should not be used in conjunction with certain antidepressants, namely norepinephrine-dopamine reuptake inhibitors (NDRIs), as this increases the risk of symptoms due to excessive serum levels of norepinephrine. Bupropion is an example of an antidepressant with an amphetamine-like structure similar to ephedrine, and it is an NDRI.
Hydrolases secreted into the blood stream cause little problem as they are inactivate at the near neutral pH of blood (7.4). It can be associated with N-acetylglucosamine-1-phosphate transferase (GNPTA). In a case report, I-cell disease was complicated by severe dilative cardiomyopathy (DCM).Though rare, a deficiency of phosphodiesterase which would cleave GlcNAc from the mannose-6-phosphate tag will also cause I-cell disease. The presence of lipids, glycosaminoglycans (GAGs) and carbohydrates in the blood provide for the distinguishing characteristic to separate I-cell from Hurler Syndrome. In Hurlers, only glycosaminoglycans would be present. Diagnosis
Diagnostic measures can include the following. Before birth:

Abnormally low concentrations of UDP-N-acetylglucosamine-1-phosphotransferase enzyme activity in amniotic fluid cells or chorionic villiIn infants:

Elevated plasma lysosomal enzyme concentrations 
Decreased concentration of lysosomal enzymes in cultured fibroblasts and increased in the surrounding medium 
Presence of inclusion bodies in peripheral blood lymphocytes
Low concentrations of UDP-N-acetylglucosamine-1-phosphotransferase enzyme activity as measured in white blood cells

Treatment
There is no cure  for I-Cell disease/Mucolipidosis II disease; treatment is limited to controlling or reducing symptoms. Nutritional supplements, particularly iron and vitamin B12, are often recommended. Physical therapy to improve motor delays and speech therapy to improve language acquisition are treatment options. Surgery can remove the thin layer of corneal clouding to temporarily improve the complication. It is possible that bone marrow transplant may be helpful in delaying or correcting the neurological deterioration that occurs with I-Cell disease.