Doc: Does elevated TPO alone constitute hypothyroidism?
Dear Dr. Roach: I’m female, 68 years old with hypothyroidism, but no other medical problems. I exercise about 10 hours a week and try to eat healthy. During one of my physical checkups, my TSH was 0.002, so I saw an endocrinologist. After three months of blood tests, everything became normal even without medicine. My T4, T3, TSH and complete metabolic panel results all are in the normal range. The one that is not is the TPO level, which is greater than 600. She asked me to take 25 mcg of levothyroxine once a day. When I asked her if I need to continue the medication, she said yes, because of the presence of TPO. Is it true that once you have TPO, you have it for life and it won’t go away? Will I have to take the medicine for life? Please give me your opinion if I really have hypothyroidism.
Dear C.G.: There’s a lot of information here, but let’s start with the TPO (really, anti-TPO), which are antibodies to the enzyme thyroid peroxidase. This enzyme is critical in an important step in the production of thyroid hormone. High levels of anti-TPO are suggestive of Hashimoto’s thyroiditis. However, they can occur in other thyroid conditions, such as Graves’ disease, a common cause of hyperthyroidism. A low TSH, such as the 0.002 you initially had, is highly suggestive of hyperthyroidism. Transient hyperthyroidism happens in early stages of Hashimoto’s, which is what I think you most likely have. Right now, you are not hypothyroid.
However, most people with Hashimoto’s will progress to a prolonged period of hypothyroidism. This is particularly likely in people with high levels of anti-TPO antibodies.
Over time, the thyroid usually returns to normal, but this can take years. Most of the time, people with hypothyroidism from Hashimoto’s stay on replacement thyroid hormone, but it can be slowly tapered off under careful observation in most people.
I should note that 25 mcg of thyroxine is not a full replacement dose. Someone with no thyroid due to surgery needs full replacement, which is somewhere around 125 mcg, though it varies from person to person.
Dear Dr. Roach: I would like to know your opinion about taking vitamin K-2 for osteoporosis. I have not shown improvement with raloxifene, Fosamax or Actonel. I imagine that I am low in K-2 because I am on a low-cholesterol diet with no cheese or egg yolks. I am 72 and otherwise in good health. I do not take any other prescription medication. I would appreciate any information you can provide.
Dear J.F.C.: Vitamin K-2 has been used for years in Japan as a treatment for osteoporosis, a condition of weakened bone that predisposes to fracture. Most vitamin K-2 is synthesized in the gut by our bacteria, using K-1 as a source (K-1 is found in leafy green vegetables). You don’t need cheese or eggs (or any animal product) to get adequate K-2. However, studies outside of Japan have not shown significant benefit of K-2 supplements in preventing or treating osteoporosis, so it is seldom prescribed in North America.
When people don’t respond to medications for osteoporosis, it’s appropriate to look for a reason why. Vitamin D deficiency is a big possibility (the body also needs enough calcium), and vitamin D should be tested by blood level. Risendronate (Actonel) and alendronate (Fosamax) work the same way: by decreasing the activity of the osteoclasts, the cells that break down bone. Both require precise adherence in order to be absorbed properly, such as being taken while fasting (usually, just after waking). Raloxifene (Evista) works on the estrogen receptor and also seems to prevent bone resorption. For people who do not respond to those medications, I consider teriparatide, which works by stimulating new bone formation.
Email questions to ToYourGoodHealth@med.cornell.edu.