It says:
MTHFR deficiency can cause problems with “neurological symptoms, premature arteriosclerosis, and venous and arterial thrombosis.”
MTHFR mutations come in heterozygous or homozygous. Heterozygous means there are two different genes at the allele (or locus, or the location of the gene). Homozygous means the two genes are the same.
(You get one gene from each parent. They could be the same gene (the same one from each parent) or different genes (again, one from each parent, but different ones this time), or a mutation of one or the other or both.)
If there are two different genes, the dominant gene is usually the ‘boss.’ The other one is recessive. If the genes are they same, then they do the same thing as each other.
The mutation C677T causes the most problems. This mutation causes an increase in homocysteine in the patient’s blood. Homocysteine may be associated with increased risk for cardiovascular and peripheral vascular disease. Someone with this mutation may experience an increase in homocysteine levels when exposed to nitrous oxide.
Now, I have access to the article. It is a case report of one patient. Consider single case reports carefully. Single cases are interesting but do not speak to the larger idea well.
The woman, 44, had a homozygous MTHFR mutation and a predisposition to vascular clots (from the mutation?).
She was prescribed coumadin, a blood thinner.
Six months later, she was admitted to the hospital with a GI bleed. She received blood and plasma, but then developed a clot in an artery in one of her kidneys. She recovered and went home.
She returned again with cellulitis of the foot. (She had stepped on a screw.) She was admitted to the hospital where she got antibiotics and blood thinners, but the toe also had gangrene and needed to be amputated. I believe her labs say she was already ill. I think it says her clotting factors were off and that her blood was too thin.
In preparation for the surgery, which would be done under general anesthetic, she got two units of plasma. Thirty minutes later, she had an episode of bronchospasm.
She had the surgery and nitrous oxide was not used.
She then developed pneumonia. She was already ill. She got worse. She was intubated and sent to the ICU. They tried different anticoagulents including heparin, coumadin and lovenox to manage her bleeding times which were abnormal. She also had many other abnormal labs.
Her blood pressure dropped, requiring treatment. Her heart labs were abnormal indicating damage, and that was also treated. Then on day 7,her kidneys failed, due to a clot in her kidney, requiring dialysis. On day 7 she also got a tracheotomy (yay- off the vent).
She did not get better until day 10 of her hospital stay and finally got out of the ICU on day 17. Her kidneys (and other things) slowly began to recover and she went home on day 39, but she still needed kidney dialysis as an outpatient. She continued to take coumadin and folate on an outpatient basis.
This article goes on to cite another study using 20 patients with the C677T defect where 10 got nitrous oxide and 10 did not. The ones who got the nitrous oxide had large increases in homocysteine levels after the nitrous oxide. The article points out that a study of 20 is too small to make generalizations.
The article concludes with the idea that “It is recommended that N2O be avoided in patients with MTHFR deficiency undergoing general anesthesia,” that the patients always be properly anticoagulated, and also well hydrated, monitored for clots, and that liver and kidney function be closely monitored since they clear medications from the system (and it is important they function as well as possible, especially when one is very ill). Even healthy patients should do things to avoid clots.
Anyone else read “MTHFR” as something entirely different? 