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High antibodies
Hello, this is my first question here. I'm really stressed and confused it's like 4.00 and am awake. My question is that my obgyn is not going to give me therapy for high antibodies (around 400) because he said my thyroid works normal. Am wondering is this right ?? I read a lot of articles online that women with high antibodies have a lot of risk of miscarriage etc plus those women need to start therapy before pregnancy. especially when my doctor knows that me and my husband are trying to have a baby.. I don't know if I should trust him he change his mind a lot about the fact I'm not pregnant yet. I'm confused. Please help me.
COMMUNITY LEADER
Can you get the results of the FT3 and FT4 tests, along with reference ranges? Without those, there's not really a whole lot we can comment on. You should always try to get a copy of all blood work or other test results and keep them for your records.
Thanks both for the reply. I have hashimotos unused to take pill when I was younger but then all my levels were natural so I stopped. The antibodies from thyroid i don't really know exactly but all the other levels were normal I tested for ft3 ft4 tsh and those were ok. I don't really have the results the doctors do
Excerpt from Medscape: Thyroid Autoimmunity, Infertility and Miscarriage...
"Pathophysiological Mechanisms That May Explain the Association Between TAI Diseases & Miscarriage...
"The exact mechanism underlying the association between TAI disease and miscarriage remains largely unknown. Three possible explanations have been proposed:
The first hypothesis postulates that the presence of thyroid Abs reflects a generalized activation of the immune system and a generally heightened autoimmune state against the fetal–placental unit;[17] thus, women with thyroid Abs may have a generalized autoimmune predisposition, including autoimmune responses against the fetus. Using the paradigm of antiphospholipid Abs, pregnancy tends to occur later (mean: 22 weeks),[51] compared with the timing of mis-carriages in women with TPO Abs,[24] which is usually in the first trimester of gestation, a phase during gestation when the fetus is critically dependent on maternal thyroid hormones.[52] It is of interest that, in mice, a direct action of Tg Abs on the placenta has been described, although no similar data are available in humans.[3]
Thyroid Abs may impair fertility, so that affected women conceive at an older age and, therefore, have a higher risk of miscarriage.[53,54] However, the study performed by Poppe et al. showed that the mean age of the thyroid autoAb-positive women was not significantly different from that of thyroid autoAb-negative women.[24] Kontiainen et al. found an increase in the prevalence of TPO Abs with age, but this correlation was not statistically significant.[55] In a study conducted by Kutteh et al., patients with recurrent pregnancy loss demonstrated an elevated autoAb titer as their age increased, up until the age range of 31–35 years, after which a decreased frequency was observed.[20]
Finally, the presence of thyroid Abs in euthyroid women could be associated with a subtle deficiency in thyroid hormone concentrations or a lesser ability of the thyroid to adapt adequately to the changes associated with the pregnancy. Indeed, mean serum TSH values (although within the normal range) have been found to be significantly higher in thyroid autoAb-positive women compared with controls. Pregnancy may, therefore, unmask a reduced thyroidal reserve when the demands for thyroid hormones is increased.[5] In thyroid autoAb-positive women, serum TSH levels increased progressively as gestation progressed, with 19% of them experiencing an increased serum TSH at delivery. Serum TSH levels also increased in the control group but to a much lesser extent.[48,56]
The different explanations provided above are not in contradiction with one another. It is possible that the increased risk of miscarriage in thyroid Ab-positive women has multiple etiologies and is a result of a combination of several factors.
Animal data, although scarce, also links TAI and miscarriage. Imaizumi et al., who attempted to investigate the influence of autoimmune thyroiditis on pregnancy, studied the impact of murine experimental autoimmune thyroiditis on pregnancy outcome by using Tg-immunized CBA/J (H2[k]) female mice.[57] They concluded that pregnancy loss was increased in experimental autoimmune thyroiditis in a manner that was dependent on paternal antigens. In 2003, Matalon et al. examined whether active immunization with Tg could elicit anti-Tg autoAbs and reproductive failure without interfering with thyroid function in mice.[58] They concluded that immunization with Tg results in the production of Tg Abs and fetal resorption. These effects occurred in the absence of thyroid dysfunction."
"Pathophysiological Mechanisms That May Explain the Association Between TAI Diseases & Miscarriage...
"The exact mechanism underlying the association between TAI disease and miscarriage remains largely unknown. Three possible explanations have been proposed:
The first hypothesis postulates that the presence of thyroid Abs reflects a generalized activation of the immune system and a generally heightened autoimmune state against the fetal–placental unit;[17] thus, women with thyroid Abs may have a generalized autoimmune predisposition, including autoimmune responses against the fetus. Using the paradigm of antiphospholipid Abs, pregnancy tends to occur later (mean: 22 weeks),[51] compared with the timing of mis-carriages in women with TPO Abs,[24] which is usually in the first trimester of gestation, a phase during gestation when the fetus is critically dependent on maternal thyroid hormones.[52] It is of interest that, in mice, a direct action of Tg Abs on the placenta has been described, although no similar data are available in humans.[3]
Thyroid Abs may impair fertility, so that affected women conceive at an older age and, therefore, have a higher risk of miscarriage.[53,54] However, the study performed by Poppe et al. showed that the mean age of the thyroid autoAb-positive women was not significantly different from that of thyroid autoAb-negative women.[24] Kontiainen et al. found an increase in the prevalence of TPO Abs with age, but this correlation was not statistically significant.[55] In a study conducted by Kutteh et al., patients with recurrent pregnancy loss demonstrated an elevated autoAb titer as their age increased, up until the age range of 31–35 years, after which a decreased frequency was observed.[20]
Finally, the presence of thyroid Abs in euthyroid women could be associated with a subtle deficiency in thyroid hormone concentrations or a lesser ability of the thyroid to adapt adequately to the changes associated with the pregnancy. Indeed, mean serum TSH values (although within the normal range) have been found to be significantly higher in thyroid autoAb-positive women compared with controls. Pregnancy may, therefore, unmask a reduced thyroidal reserve when the demands for thyroid hormones is increased.[5] In thyroid autoAb-positive women, serum TSH levels increased progressively as gestation progressed, with 19% of them experiencing an increased serum TSH at delivery. Serum TSH levels also increased in the control group but to a much lesser extent.[48,56]
The different explanations provided above are not in contradiction with one another. It is possible that the increased risk of miscarriage in thyroid Ab-positive women has multiple etiologies and is a result of a combination of several factors.
Animal data, although scarce, also links TAI and miscarriage. Imaizumi et al., who attempted to investigate the influence of autoimmune thyroiditis on pregnancy, studied the impact of murine experimental autoimmune thyroiditis on pregnancy outcome by using Tg-immunized CBA/J (H2[k]) female mice.[57] They concluded that pregnancy loss was increased in experimental autoimmune thyroiditis in a manner that was dependent on paternal antigens. In 2003, Matalon et al. examined whether active immunization with Tg could elicit anti-Tg autoAbs and reproductive failure without interfering with thyroid function in mice.[58] They concluded that immunization with Tg results in the production of Tg Abs and fetal resorption. These effects occurred in the absence of thyroid dysfunction."
COMMUNITY LEADER
What antibodies were tested? What are your actual thyroid hormone levels? You should also have been tested for Free T3, Free T4 and TSH. Those are what would determine whether or not you need treatment.
It sounds like you have an autoimmune thyroid disease, either Hashimoto's or Graves Disease. You can have thyroid antibodies and still have a fully functional thyroid, because the antibodies may not have done enough damage to your thyroid yet.
It's not the antibodies that get treated. It's resulting hypothyroidism or hyperthyroidism.
There are 3 different thyroid antibodies (2 to diagnose Hashimoto's and 1 to diagnose Graves), so without knowing which test was done, we can't determine what might be wrong.
What prompted the antibody test? Do you have symptoms of a thyroid condition? Overactive (hyper) or under active (hypo)?
It sounds like you have an autoimmune thyroid disease, either Hashimoto's or Graves Disease. You can have thyroid antibodies and still have a fully functional thyroid, because the antibodies may not have done enough damage to your thyroid yet.
It's not the antibodies that get treated. It's resulting hypothyroidism or hyperthyroidism.
There are 3 different thyroid antibodies (2 to diagnose Hashimoto's and 1 to diagnose Graves), so without knowing which test was done, we can't determine what might be wrong.
What prompted the antibody test? Do you have symptoms of a thyroid condition? Overactive (hyper) or under active (hypo)?
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