This is produced in the trophoblast cells of the placental tissue. Hyperglycosylated hCG is the main form of hCG during the implantation phase of pregnancy, with invasive molar pregnancies, and with choriocarcinoma.Gonadotropin preparations of hCG can be produced for pharmaceutical use from animal or synthetic sources. Some of these are medically justified, whereas others are of a quack nature. Testing
Blood or urine tests measure hCG. These can be pregnancy tests. hCG-positive can indicate an implanted blastocyst and mammalian embryogenesis or can be detected for a short time following  childbirth or pregnancy loss. Tests can be done to diagnose and monitor germ cell tumors and gestational trophoblastic diseases. Concentrations are commonly reported in thousandth international units per milliliter (mIU/mL). The international unit of hCG was originally established in 1938 and has been redefined in 1964 and in 1980. At the present time, 1 international unit is equal to approximately 2.35×10−12 moles, or about 6×10−8 grams.It is also possible to test for hCG to have an approximation of the gestational age. Methodology
Most tests employ a monoclonal antibody, which is specific to the β-subunit of hCG (β-hCG). This procedure is employed to ensure that tests do not make false positives by confusing hCG with LH and FSH. (The latter two are always present at varying levels in the body, whereas the presence of hCG almost always indicates pregnancy.) Many hCG immunoassays are based on the sandwich principle, which uses antibodies to hCG labeled with an enzyme or a conventional or luminescent dye.
Contraindications
Atrioventricular (AV) block, complete, without implanted pacemaker or at high risk of complete AV block
Concomitant use with drugs containing quinidine, quinine, or mefloquine
Concomitant use with drugs that both prolong the QT interval and are metabolized by CYP2D6 (e.g., thioridazine, pimozide); effects on QT interval may be increased
Concomitant use with MAOIs or use of MAOIs within 14 days; risk of serious, potentially fatal, drug interactions including serotonin syndrome
Heart failure
Hypersensitivity to dextromethorphan
Hypersensitivity to quinine, mefloquine, quinidine, or dextromethorphan/quinidine with a history of thrombocytopenia, hepatitis, bone marrow depression or lupus-like syndrome induced by these drugs
QT interval, prolonged or congenital long QT syndrome or a history suggesting torsades de pointes

Adverse effects
Common risks and side effects include:
Abdominal pain
Asthenia
Cough
Diarrhea (reported in 13% of patients)
Dizziness
Elevated gamma glutamyltransferase
Flu-like symptoms
Flatulence
Prolonged QT interval
Muscle spasm
Peripheral edema
Urinary tract infection
Vomiting

Interactions
Desipramine (CYP2D6 substrate) levels increase 8-fold with co-administration
Paroxetine (CYP2D6 inhibitor and substrate)
Memantine

Pharmacology
Pharmacodynamics
Dextromethorphan acts as a σ1 receptor agonist, serotonin–norepinephrine reuptake inhibitor, and NMDA receptor antagonist, while quinidine is an antiarrhythmic agent acting as a CYP2D6 inhibitor. Quinidine prevents the metabolism of dextromethorphan into its active metabolite dextrorphan, which is a much more potent NMDA receptor antagonist but much less potent serotonin reuptake inhibitor than dextromethorphan. The mechanism of action of dextromethorphan/quinidine in the treatment of PBA is unknown. Research
Dextromethorphan/quinidine was investigated for the treatment of agitation associated with dementia, diabetic neuropathy, drug-induced dyskinesia, migraine, and neuropathic pain, but development for these indications was discontinued. Another formulation, deudextromethorphan/quinidine, is still under investigation for various indications. These include agitation, schizophrenia, and major depressive disorder, among others.