Methotrexate (or ‘MTX’ for short) keeps unhealthy cells from reproducing too quickly. Psoriasis and cancer are two examples of unhealthy cell proliferation, which MTX is designed to prevent.
The discovery of MTX led to what is now modern chemotherapy. As you might imagine, you don’t need as much of this drug to fight off psoriasis as you might need for cancer.
MTX keeps the enzyme dihydrofolate reductase from forming another compound called “tetrahydrofolate” which is needed for cell reproduction. It does this by posing as a folic acid molecule, thus binding to dihydrofolate reductase before real folic acid gets the chance. MTX is much more (1000 times more) prone to bind dihydrofolate reductase than folic acid, and thus is an effective antifolate (something that keeps folic acid from doing its job). When this process is allowed to proceed normally it is also called “metobolizing,” so methotrexate is also called an “antimetabolite.”
The risks of taking MTX to treat psoriasis are justified when a patient’s vital wellbeing is at stake. MTX doesn’t usually clear up psoriasis all the way, so sometimes it is administered long-term in smaller doses.
One of the main risk factors associated with methotrexate is the irreparable damage it can do to the liver. If a patient must take MTX for any length of time, periodic liver biopsies to check on the liver’s health are recommended.
MTX can also cause a severe drop in a person’s white blood cell count. Thus, doctors will often prescribe a testing period to make sure the patient’s blood-health is not adversely affected by the drug before prescribing it in doses that can actually start clearing up psoriasis.
Methotrexate is currently the only antimetabolite approved by the FDA as a treatment for psoriasis.
If methotrexate works by inhibiting the action of folic acid, would following a diet low in folic acid be beneficial? Would a diet filled with folic-acid-rich foods exacerbate symptoms?