OB-GYN-L Messages for May, 2006: Re: T3 level in pregnancy

Re: T3 level in pregnancy
From: Terrence.Jones@kp.org
Tue May 23 21:21:53 2006

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Hank, this might be a good patent to refer to a Medical Endocrinologist. The new sensitive TSH assays should not be influenced by HCG to an extent that would be measurably suppressed. Besides, You have a T3 which is measurably elevated. Now there's an explanation for the TSH suppression. That T4 is normal argues against Grave's (diffuse hyperfunction due to TSIg), and more toward toxic nodule or adenoma (local clone with mutation in TSH receptor). That there is still some TSH measurable suggests a compensated adenoma (autonomous hormone production not yet fully suppressive). Tho 4-5% of these will lead to thyrotoxicosis per year, this tends to be in older Patients, and less likely in pregnancy due to increased TBG, and volume of distribution (plasma volume). Follow FT3/TSH during pregnancy, then radionuclide scan postpartum (99mTc) with excision based on uptake, age, and size. (Wortsman, Arch Int Med 1988; Corvilain, Ann Endocrinol, 2003.)
Tho nml FT4 (and therefore not likely to be Grave's), the hx of Bell's (autoimmunity) might suggest measuring TSIg anyway, as this is the mechanism in which Grave's can affect the fetus (IgG - crosses placenta); when levels are > 600% nml. The recent fatigue may be due to a relative decrease in FT3, as this is more susceptible (0.3% bound, compared to 0.02% with T4) to the estrogen mediated increase in hepatic TBG production by pregnancy. So She may be more tired, 'cause She's less hyperthyroid. (She's not a health care worker who is excessively weight conscious?) However, fatigue may also be secondary to viral illness and its sequelae (recent episode of bronchitis?); particularly EBV which causes all sorts of changes in thyroid function and testing parameters. Lastly, although unusual at this age, neoplasia is always a consideration. So a Medical Endocrinologist could help sort this out.
Dan, the T3RU (resin uptake) refers to the amount of radiolabelled T3 that binds to a resin, following incubation with the Patient's blood. Since T3 has greater affinity for TBG than T4, it was chosen as the marker. It will be bound to the remaining open TBG-binding sites. The more TBG (say from pregnancy, HRT, or OCP's) the less of the marker to bind to the resin. Using this inverse relationship to TBG the product of Total T4 and T3RU could confirm a normal FTI (free thyroxine index) in Patients with elevated total T4, not due to hyperthyroidism.
Neither T3 nor T4 cross very well, so these are not the cause of any ill fetal effects. Rather, diffuse hyperfunction due to increased TSIg is the culprit. The antibody crosses the placenta, and can induce hyperactivity in the fetus when the gland becomes active (end of first trimester). The only way a pregnant Patient is going to produce sufficient antibody to affect the fetus (>600% nml activity) and NOT be symptomatic, is either prior Surgical excision, or (more likely) prior radio-ablation. The latter Patients are frequently rendered hypothyroid by the ablative therapy, and so, may even require LT4 supps. The fetus can be protected from the antibody by maternal Thioamide (PTU), which does cross. /tj
The TSH only drops if the FREE T3 & FREE T4 rise. In normal pregnancy the total T3 & Total T4 go up but the FREE T3 & FREE T4 stay the same. As the T3 goes up the T3 Resin Uptake goes down. We don't measure the T3 Resin Uptake anymore. With the LOW TSH, she is chemically hyperthyroid. Even without symptoms in pregnancy, the fetus can be affected. If there is any question, I would repeat the TSH about 1 week after the first just to make sure the lab didn't make an error.
Dan
------------------------------------------------------------------------------- ---------------------------------------------------------------------------=20 ---------------------------------------------------------------------------On 5/23/06, Atkinson, Samuel M <ATKINSONS@ecu.edu> wrote: T3 is elevated in pregnancy and usually comes down after 20 weeks. It is inversely proportional to HCG. As her TSH is low she is appropriately dropping it as T3 goes up. As you said, clinically she isn't hyperthyroid. As with any test that doesn't compute, repeat it in one month. sAm
Subject: T3 level in pregnancy The views of listers would be appreciated. A 35yo G1P1A2 (VIP 1, sab 1) presented at 8+wks EGA by dates, exam and sono. 1st preg'y was VIP. 2nd delivered at term, approx 5 yrs ago with PIH as well as antenatal Bell's Palsy. 3rd preg'y was SAB at 6wks, in '05. Patient's only meds in last three months were Imitrex and antibiotic of unknown type for bronchitis. She quick smoking upon recognition of pregnancy. She had complaints of fatigue which seemed beyond that usually attibutable to pregnancy or family/occupational activities, so a TSH was drawn with her prenatal lab panel. TSH was dec'd to .021. FT4 was nl at 1.64 ( .89 - 1.80 ). FT3 was increased at 4.9 ( 2.3- 4.2 ). She is without clinical or ROS findings suggestive of hyperthyroidism and has a negative PH of thyroid ds. At first I thought perhaps HCG was contributing ... even tho' I understand it to be rather weak as a thryotropin, the levels are possibly high enough...however the T4 was normal. Is this a T3 toxicosis that should be considered pathologic and treated? Should a range of thyroid antibody studies be checked....?? Opinions appreciated. Hank
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         Hank, this might be a good patent to refer to a Medical Endocrinologist. The new sensitive TSH assays should not be influenced by HCG to an extent that would be measurably suppressed. Besides, You have a T3 which is measurably elevated. Now there's an explanation for the TSH suppression. That T4 is normal argues against Grave's (diffuse hyperfunction due to TSIg), and more toward toxic nodule or adenoma (local clone with mutation in TSH receptor). That there is still some TSH measurable suggests  a compensated adenoma (autonomous hormone production not yet fully suppressive). Tho 4-5% of these will lead to thyrotoxicosis per year, this tends to be in older Patients, and less likely in pregnancy due to increased TBG, and volume of distribution (plasma volume). Follow FT3/TSH during pregnancy, then radionuclide scan postpartum (99mTc) with excision based on uptake, age, and size. (Wortsman, Arch Int Med 1988; Corvilain, Ann Endocrinol, 2003.)         Tho nml FT4 (and therefore not likely to be Grave's), the hx of Bell's (autoimmunity) might suggest measuring TSIg anyway, as this is the mechanism in which Grave's can affect the fetus (IgG - crosses placenta); when levels are > 600% nml. The recent fatigue may be due to a relative decrease in FT3, as this is more susceptible (0.3% bound, compared to 0.02% with T4) to the estrogen mediated increase in hepatic TBG production by pregnancy. So She may be more tired, 'cause She's less hyperthyroid. (She's not a health care worker who is excessively weight conscious?) However, fatigue may also be secondary to viral illness and its sequelae (recent episode of bronchitis?); particularly EBV which causes all sorts of changes in thyroid function and testing parameters. Lastly, although unusual at this age, neoplasia is always a consideration. So a Medical Endocrinologist could help sort this out.         Dan, the T3RU (resin uptake) refers to the amount of radiolabelled T3 that binds to a resin, following incubation with the Patient's blood. Since T3 has greater affinity for TBG than T4,  it was chosen as the marker. It will be bound to the remaining open TBG-binding sites. The more TBG (say from pregnancy, HRT, or OCP's) the less of the marker to bind to the resin. Using this inverse relationship to TBG the product of Total T4 and T3RU could confirm a normal FTI (free thyroxine index) in Patients with elevated total T4, not due to hyperthyroidism.         Neither T3 nor T4 cross very well, so these are not the cause of any ill fetal effects. Rather, diffuse hyperfunction due to increased TSIg is the culprit. The antibody crosses the placenta, and can induce hyperactivity in the fetus when the gland becomes active (end of first trimester). The only way a pregnant Patient is going to produce sufficient antibody to affect the fetus (>600% nml activity) and NOT be symptomatic, is either prior Surgical excision, or (more likely) prior radio-ablation. The latter Patients are frequently rendered hypothyroid by the ablative therapy, and so, may even require LT4 supps. The fetus can be protected from the antibody by maternal Thioamide (PTU), which does cross. /tj                 The TSH only drops if the FREE T3 & FREE T4 rise. In normal pregnancy the total T3 & Total T4 go up but the FREE T3 & FREE T4 stay the same. As the T3 goes up the T3 Resin Uptake goes down. We don't measure the T3 Resin Uptake anymore. With the LOW TSH, she is chemically hyperthyroid. Even without symptoms in pregnancy, the fetus can be affected. If there is any question, I would repeat the TSH about 1 week after the first just to make sure the lab didn't make an error.   Dan ------------------------------- ------------------------------- On 5/23/06, Atkinson, Samuel= ------------------------------- M <<a href=mailto:ATKINSONS@ecu.edu>ATKINSONS@ecu.edu</a>> wrote: T3 is elevated in pregnancy and usually comes down after 20 weeks.  It is inversely proportional to HCG.  As her TSH is low she is appropriately dropping it as T3 goes up. As you said, clinically she isn't hyperthyroid.  As with any test that doesn't compute, repeat it in one month. sAm   <div alignÎnter> <hr></div> Subject: T3 level in pregnancy  The views of listers would be appreciated. A 35yo G1P1A2 (VIP 1, sab 1) presented at 8+wks EGA by dates, exam and sono. 1st preg'y was VIP. 2nd delivered at term, approx 5 yrs ago with PIH as well as antenatal Bell's Palsy. 3rd preg'y was SAB at 6wks, in '05.  Patient's only meds in last three months were Imitrex and antibiotic of unknown type for bronchitis. She quick smoking upon recognition of pregnancy. She had complaints of fatigue which seemed beyond that usually attibutable to pregnancy or family/occupational activities, so a TSH was drawn with her prenatal lab panel.  TSH was dec'd to .021. FT4 was nl at 1.64 ( .89 - 1.80 ). FT3 was increased at 4.9 ( 2.3- 4.2 ).  She is without clinical or ROS findings suggestive of hyperthyroidism and has a negative PH of thyroid ds.  At first I thought perhaps HCG was contributing ... even tho' I understand it to be rather weak as a thryotropin, the levels are possibly high enough...however the T4 was normal. Is this a T3 toxicosis that should be considered pathologic and treated? Should a range of thyroid antibody studies be checked....??  Opinions appreciated.  Hank   <div alignÎnter> <hr></div> Ring'em or ping'em. Make <a href="http://us.rd.yahoo.com/mail_us/taglines/postman11/*http:/us.rd.yahoo.com/evt9666/*http:/voice.yahoo.com" target=_blank>PC-to-phone calls as low as 1¢/min</a> with Yahoo! Messenger with Voice. -- R. Daniel Braun       "The way to health is an aromatic bath and scented massage everyday".                                Hippocrates 

Next message: Joanne Bulley, MD: "Breat Cancer and Celiac Disease"
Previous message: Joe: "Re: Operating time"
Maybe in reply to: Henry Gregor: "T3 level in pregnancy"
Next in thread: Henry Gregor: "Re: T3 level in pregnancy"
Reply: Henry Gregor: "Re: T3 level in pregnancy"

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