can somone explain the different antibodies tests??
hi everyone i do have hypothryoidism and until today i was told that i do not have antibodies there fore no hashi's.
but one of the antibodies tests came back positive. my thyroid peroxidase ab came back negative but my thyroglobulin ab came back at 4.2 with a range of 0- 2.0
i posted on a thyroid website about this and was told that unless both tests come back positive that it doenst necessarily mean hashi's.
but my new doc who did these new tests say i do have hashi's.
does anyone know much about this?? arghs still confused!!! xoxo jenn
__________________ jennifer, 33years old
long island, new york
dxd 2001
searching for new therapies/meds for pcos
met/gluc not working as well..but on 1000mgxr
married on 9/28/06 to keith
The thyroid perioxidase ab (TPO antibodies test) is usually more sensitive than the thyroglobulin ab test (95% of Hashi's patients will test positive for TPO antibodies; 80% will test positive for the latter), so some docs only use the TPO test to diagnose Hashi's. If you have thyroid enlargement (goiter) and hypothyroidism, then it seems reasonable for the doc to diagnose you with Hashi's if you also have presence of antibodies (no matter which one, though many people have both that's not necessarily the case). The thing is, you might gave Grave's instead, because a person can be hypo with Grave's too (thought most people think of Grave's as a form of hyperthyroidism).
Selenium supplements (200 mcg daily) can help lower antibody levels. Hopefully the doc has tested your free T3 levels, since many Hashi's patients don't convert T4 to T3 well and need to either take Armour or add Cytomel to their usual T4 med.
The only way to know 100% that a person has Hashi's is to examine the thyroid gland (biopsy), but that is rarely done to diagnose. Instead, diagnosis is usually based on differential diagnosis (ruling out other causes), symptoms, and presence of antibodies. You might want to try talking to your doc again and asking him why he is diagnosing you with Hashi's and not Grave's (there may be something particular about your situation and confirmed the diagnosis for him).
Here's some info you may find helpful about thyroid antibodies:
Patients with autoimmune thyroid diseases (AITD’s), such as Graves’ disease (GD), usually have a combination of thyroid autoantibodies present in their blood. One type, thyroglobulin antibodies, is known to destroy thyroid cells. Another type, TSH (thyrotropin) receptor antibodies (TRAb) bind with the TSH receptor in thyroid cells. Here they can act in different ways, depending on their specific type, described later in this article.
Antibodies are proteins produced by the immune system in response to a foreign stimulus or antigen. Antibodies are composed of proteins known as immunoglobulins (Ig’s). Immunoglobulins have several subtypes, including A, M, G, E, and D, which have different functions. Most autoantibodies, including thyroid antibodies, are made of immunoglobulins of the G subclass (IgG). IgG antibodies last for about 120 days, although they are continuously being produced in active GD. In pregnant patients with GD, TRAb can cross the placental barrier and cause transient disease symptoms in the newborn. For this reason, pregnant patients, especially those who have been previously treated with radioiodine, are tested for these antibodies.
Immunoglobulins have antibody properties, that is, they can attach and bind, and ultimately destroy, the antigen that caused their production. For instance, when we have an immune reaction to a virus, our immune system produces antibodies that react with and destroy this virus on a subsequent exposure. When we’re vaccinated, we’re exposed to treated complexes of specific live viral antigens.
Our immune systems react and produce antibodies to the specific virus present in the vaccine. Upon subsequent exposure to this virus, these vaccine-induced antibodies destroy the virus keeping us free from disease. If we were unable to produce antibodies, if, for instance, we have inadequate immunoglobulin levels, we'd have symptoms of immune deficiency. That is, we wouldn't be able to fight off colds and viruses and if we received vaccines, they wouldn’t result in antibody production or “wouldn't take.”
In autoimmune disorders, our immune systems become tricked (by triggers such as viral particles which mimic our cells) into producing antibodies against our body’s cells, which are immunologically referred to as self-components. Autoantibodies don’t target specific organs, rather they target cell parts such as the cell nucleus or cell receptor of tissue in certain organs.
Autoantibodies are present in 20% of the population, but only 3% of the population develop autoimmune diseases. Individuals with autoantibodies are said to have autoimmunity. When these individuals go on to develop symptoms of the particular disease these antibodies are associated with, they are said to have an autoimmune disease. For instance, individuals who have thyroid autoantibodies and symptoms of thyroid disease (demonstrated by abnormal laboratory tests) have autoimmune thyroid disease. GD is caused by a defect in T lymphocytes, which causes genetically susceptible individuals to develop thyroid autoantibodies. Patients with GD generally have a combination of thyroid autoantibodies. Thyroid autoantibody tests are used to differentiate GD from non-autoimmune hyperthyroid disorders, such as those which are due to nodules, infections, tumors, and other conditions. Patients with any AITD, including GD, may experience symptoms of hyperthyroidism, hypothyroidism and thyroid failure or primary myxedema at different times during their lifetime. Most patients exhibit symptoms of hypothyroidism prior to their GD diagnosis. Also, patients with GD go into spontaneous remission at the rate of 10% to 25% each year.
Antithyroid drug (ATD) therapy in GD slows down the immune system and reduces autoantibody production. Many patients are tested before and during ATD therapy. A lowered TSI antibody titer indicates that the patient is responding treatment, and is a good candidate for remission.
Besides GD, autoimmune thyroid diseases include 1) autoimmune thyroiditis, which is also known as Hashimoto's thyroiditis (HT); 2) Ha****oxicosis, a condition characterized by symptoms of hyperthyroidism occurring in patients with HT; 3) atrophic thyroiditis which is also known as primary myxedema or autoimmune thyroid failure, 4) autoimmune thyroid lymphoma.
The first thyroid antibodies discovered, thyroglobulin antibodies are the thyroid antibody test most frequently ordered. When found in patients with hyperthyroidism, thyroglobulin antibodies indicate that the patient has an AITD, but they are not diagnostic for GD. Tests for stimulating TRAb (TSI) are diagnostic for GD. Although they're present in 50% of patients with GD, thyroglobin antibodies are more often seen in HT, and in HT their titers are generally higher. Thyroglobulin antibodies (also called antithyroglobulin antibodies or ATG) cause thyroid cell destruction. Reference Range= < 2 IU/ml. GD patients with high titers of ATG are likely to eventually become hypothyroid. Thyroid Peroxidase (TPO) autoantibodies refer to antibodies directed against thyroid peroxidase, an enzyme required for thyroid hormone synthesis. The TPO antibody test has replaced the test for antimicrosomal antibodies since TPO is a more sensitive indicator of the microsomal component of thyroid cells. Like ATG, TPO autoantibodies may be seen in 30% of normal elderly patients, although their titers are generally not as high as those seen in AITD. TPO antibodies are increased in patients with HT, GD and postpartum thyroiditis. Reference Range= < 2 IU/ml. TRAb may be 1) stimulatory, mimicking the pituitary hormone TSH and causing hyperthyroidism, 2) blocking, preventing TSH from binding to the cell receptor and thereby causing hypothyroidism, and 3) binding, interfering with normal activity of TSH at the cell receptor. Stimulating TRAb are classified as binding antibodies in some laboratories since they bind to the receptor. Most patients with AITD’s have a combination of TRAb The predominating antibody type determines which specific disorder is present. Stimulating TRAb predominate in GD, and blocking TRAb predominate in autoimmune hypothyroidism. Binding antibodies may also reflect the presence of stimulating antibodies, or they may interfere with other activity at the TSH receptor.
Reference Ranges: Stimulating TRAb (TSI)= < 130% basal activity; Binding TRAb (TBII)= < 10% inhibition; TRAb blocking antibodies= < 10% inhibition TSH, T4 and T3 autoantibodies are also rarely present and may interfere with test results. These tests are generally ordered when one of the laboratory thyroid function tests doesn’t fit the clinical picture.
HTH,
Linda
__________________ dx pcos 1984, type II diabetes 2001, also hypertension
Met 2000mg since 2001, started Glucophage XR 4/22/04, then switched to Met ER 6/04; also: multi, Vit. C, Vit. E, B12/folic acid combo, fish oil & borage oil combo, garlic capsules, cinnamon, Vitex, calcium with magnesium/zinc, biotin, CoQ10, selenium,iron
Other meds: Verapamil and Altace(for blood pressure)
Started laser hair removal 7/29/03, completed 3/04 (it works!)
UAE for fibroid 3/24/03 and 3/16/04
well when i asked the doc what having antibodies meant and if it meant hashi's he said yes.
i am assuming bc my tsh has been high and my t3 and t4 levels have been low..thats why we would go towards hashi's right???
i am now on armour and my t3 t4 and tsh is okay. much better than before.
why would i or anyone that matter be dx'd with graves if the labs go hypo and their is weight gain??
also , i read online sooo manypeople dxd with hashi's hypo who have not had a biopsy, just blood work.
should i not consider i have autoimmune thyroid prob since i wont have a biopsy ( no goiter) and just consider it hypo?? does it matter??
just curious as to your thoughts..thank you...
btw my tsh is now 2.58 range .4- 5.5
free t4 is 1.0 range .8 -1.8
free t3 range 230-420
my tsh used to be 3.7 ish with my free t4 and t3 being below range ...with the t3 and t4 flipflopping as to which one would go below range.
currently on 1 grain armour
thanks linda!! xo jenn
__________________ jennifer, 33years old
long island, new york
dxd 2001
searching for new therapies/meds for pcos
met/gluc not working as well..but on 1000mgxr
married on 9/28/06 to keith
Looks like you are making progress, but your TSH and T4 could be optimized even more. If you do have Hashi's, it is best to suppress the TSH as much as possible (less than 1.0). Your T4 should be at least 1.3 (that would be midrange). You accidentally left out your FT3 result (you listed the range but not your test result). If that is at least midrange, then you may want to talk to your doc about adding some T4 (i.e. synthroid) along with your Armour. If the T3 is below mid range, then increasing the Armour may be the way to get your numbers into optimal range.
I guess at this point the most important thing is that you are getting treatment, and the treatment whether you have Hashi's or some other form of hypothyroidism wouldn't be any different. But if you do have Hashi's you are at an increased risk of other autoimmune diseases (fibromylagia, lupus, psoriasis, to name a few), so it's good to know whether or not you do (and stay on the lookout for other symptoms). Most normal people won't test positive for antibodies, so the fact that you have them along with your symptoms and other test results (along with PCOS) is pretty much a slam dunk that you do have Hashi's (docs don't do biopsies to diagnose Hashi's; I said that was the only wasy to be 100% sure). Since you don't have a goiter or other symptoms of Graves, that can probably be ruled out (although it's the thyroglobulin ab's that usually go along with Graves, and as said earlier, you can have Graves and go through hypo periods).
Linda
__________________ dx pcos 1984, type II diabetes 2001, also hypertension
Met 2000mg since 2001, started Glucophage XR 4/22/04, then switched to Met ER 6/04; also: multi, Vit. C, Vit. E, B12/folic acid combo, fish oil & borage oil combo, garlic capsules, cinnamon, Vitex, calcium with magnesium/zinc, biotin, CoQ10, selenium,iron
Other meds: Verapamil and Altace(for blood pressure)
Started laser hair removal 7/29/03, completed 3/04 (it works!)
UAE for fibroid 3/24/03 and 3/16/04
sorry bout the free t3... it was 281 with a range of 230- 420
as far as thyroglobulin ab goes.. you said its more common with graves right? can someone with graves be very overwieght though??
just a side note linda since you are a wealth of info do you know much about hemochromatosis by any chance?? xo jenn
__________________ jennifer, 33years old
long island, new york
dxd 2001
searching for new therapies/meds for pcos
met/gluc not working as well..but on 1000mgxr
married on 9/28/06 to keith
sorry bout the free t3... it was 281 with a range of 230- 420
as far as thyroglobulin ab goes.. you said its more common with graves right? can someone with graves be very overwieght though??
just a side note linda since you are a wealth of info do you know much about hemochromatosis by any chance?? xo jenn
Jenn, your Free T3 is still low; 325 would be the midpoint of the lab range. The target is to get up in the upper quadrant if possible (in your case, 367-420), or at least to the midpoint of 325. I think asking your doc about upping your Armour dose is warranted.
Presence of thyroglobulin ab's can occur with either Hashi's or Graves, but with Hashi's the TPO ab's are usually present as well (but everyone is different and that isn't always the case). Although your bloodwork is a little unusual, along with your symptoms and other thyroid blood tests I think it is reasonable for your doc to diagnose you with Hashi's.
I know hemochromatosis is a genetic disorder that involves iron overload (which can be very serious). Here is a link to a website for the American Hemochromatosis Society that has a wealth of information for you:
__________________ dx pcos 1984, type II diabetes 2001, also hypertension
Met 2000mg since 2001, started Glucophage XR 4/22/04, then switched to Met ER 6/04; also: multi, Vit. C, Vit. E, B12/folic acid combo, fish oil & borage oil combo, garlic capsules, cinnamon, Vitex, calcium with magnesium/zinc, biotin, CoQ10, selenium,iron
Other meds: Verapamil and Altace(for blood pressure)
Started laser hair removal 7/29/03, completed 3/04 (it works!)
UAE for fibroid 3/24/03 and 3/16/04
do you know if a person WITHOUT either hash's or graves could have either tpo or thyro ab antibodies??
being that i guess i am not the norm sincei i only have thyro antibodies..i was just curious about that.
for instance there are alot of antibodies healthy regular people have for example to viruses but that doesnt mean they are sick.
or is the evidence that i have at least they thryro ab evidence enought that i have an autoimmune thryoid problem ie hash's or graves??
veryyy confusing.
thanks for the link about hemochromatosis. one of my levels came back funny so its something i need to look further into.
how are you btw?
i do agree i think i need more thryoid meds. funny thing is my labs a couple months ago were dead on excellent!! grrrr lol
oxoxo jenn
__________________ jennifer, 33years old
long island, new york
dxd 2001
searching for new therapies/meds for pcos
met/gluc not working as well..but on 1000mgxr
married on 9/28/06 to keith
Yes, a person can have thyroid antibodies and not have Hashi's or Graves. This is especially true for the elderly. I think the percentage is something like 5% of those with antibodies being normal (without autoimmune thyroid disease). Presence of antibodies can also be a temporary thing when one has transient hypothroidism from a virus or from pregnancy.
I have only a couple of possible hypothyroid symptoms (slow weight loss, low body temps, but that's it). Last year, when I had my first TPO antibodies test, my result was 58 and the range was ">60" (meaning over 60 would indicate a problem). This was very confusing to me because although I was below the range, I still seemed to have antibodies. Also the lab range was strange and didn't fit with others I had seen. I started taking selenium just in case and eventually went to a "top thyroid doc". He told me if I had presence of antibodies, even if not in range, and I had symptoms, then I had Hashi's. He felt my thyroid gland and told me it was enlarged. He prescribed Cytomel, and said that was the only med he prescribed. I insisted on tests (this was several months after my last tests, and all were normal), and he said when a person has Hashi's the test results are meaningless and he goes by symptoms and body temps only to monitor treatment. I didn't like his style, and I had a hunch he was prescribing Cytomel for weight loss more than anything else (he had signs up in his office with info to his "weight loss patients"). I decided not to take the Cytomel but got him to send me to a lab for tests. This time, my TPO test showed no presence of antibodies at all. In the months since I have visited my PCP and my gyn, and both said my thyroid gland isn't enlarged at all. I also had another TPO test and it was negative, too. Meanwhile, my TSH which was once 3 something is now down to 1.12, and my free T's are just fine, too. My temps are a little higher, but still somewhat low (96's during first half of my cycle). So I'm keeping an eye on things but at the present time don't consider myself hypothyroid (I sure have learned a lot though!). I do wonder if the selenium I have taken now for sometime somehow lowered any antibodies I might have had (research says that it can).
Take care,
Linda
__________________ dx pcos 1984, type II diabetes 2001, also hypertension
Met 2000mg since 2001, started Glucophage XR 4/22/04, then switched to Met ER 6/04; also: multi, Vit. C, Vit. E, B12/folic acid combo, fish oil & borage oil combo, garlic capsules, cinnamon, Vitex, calcium with magnesium/zinc, biotin, CoQ10, selenium,iron
Other meds: Verapamil and Altace(for blood pressure)
Started laser hair removal 7/29/03, completed 3/04 (it works!)
UAE for fibroid 3/24/03 and 3/16/04
wow your antibody history is a trip...there and then not there!! hmm maybe the selenium is helping????
dang it linda,,, now i dont know if what the dr said about me having hashis i true or not!!! or do i just have plain hypo??? i know it shouldnt matter cause the treatment is the same, but i like to know what deck i am holding if you get my drift lol
xo jenn
__________________ jennifer, 33years old
long island, new york
dxd 2001
searching for new therapies/meds for pcos
met/gluc not working as well..but on 1000mgxr
married on 9/28/06 to keith
Jenn, the odds are very high that you do have Hashi's, because you have symptoms, low thyroid output, AND presence of antibodies. You can always have the antibodies tests repeated (and if your doc won't do it, you can get those run yourself at healthcheckusa.com for $60). A good doc would want to repeat those tests (both of them) anyway sometime in the future to monitor your progress anyway.
Here's the link to the healthcheckusa thyroid antibodies tests if you're interested:
__________________ dx pcos 1984, type II diabetes 2001, also hypertension
Met 2000mg since 2001, started Glucophage XR 4/22/04, then switched to Met ER 6/04; also: multi, Vit. C, Vit. E, B12/folic acid combo, fish oil & borage oil combo, garlic capsules, cinnamon, Vitex, calcium with magnesium/zinc, biotin, CoQ10, selenium,iron
Other meds: Verapamil and Altace(for blood pressure)
Started laser hair removal 7/29/03, completed 3/04 (it works!)
UAE for fibroid 3/24/03 and 3/16/04
linda, thanks for responding. i just make myself nuts lol
ps thanks for the armour recall info xoxo jenn
__________________ jennifer, 33years old
long island, new york
dxd 2001
searching for new therapies/meds for pcos
met/gluc not working as well..but on 1000mgxr
married on 9/28/06 to keith