Mrs. S is a 28 year old female with no significant past medical history, who is at 27 weeks gestation. Her pregnancy to date has been normal, some nausea during the first trimester, but she has put on an appropriate amount of weight and is tolerating foods well. Her thyroid function tests done are as follows:
|8/17/04:||TSH: 0.046 (low ) T4: 9.9 T3 Uptake: 16.1( low) Free thyroxine index: 1.6|
|8/24/04:||TSH: 0.20 (0.34-5.60) FT4: 0.50 (0.58-1.64) FT3:2.6 (2.3-4.2)|
|8/26/04:||TSH; 0.246 (0.350-5.500) FT4: 0.88 (0.89-1.80) FT3: 2.4 (2.3-4.2)|
The patient has a normal thyroid on exam and no clinical features of hyper or hypothyroidism. Does she have secondary hypothyroidism? If so how do I work her up in pregnancy? Thank You,
Typically the elevated hCG levels in early pregnancy can suppress the TSH modestly. Also, free T4 or T3 assays may perform erratically in the presence of high TBG, which your patient should have. Please check the total T4, and the TSH again. Total T4 should be elevated. Probably she is well, and the tests are a bit off for these reasons. Kind regards,
L De Groot,MD
- I do not really know whether this patient has ‘central hypothyroidism’ since this diagnosis was solely based on the absence of a rise in serum total T4 during pregnancy, with real data not provided , no measurement of free T4 done, and in addition normal serum cortisol (whatever this really means !).
- In any case with hypothyroidism during a pregnancy (be it primary or supposedly secondary), I think that it is important to confirm the etiology of the condition before embarking on therapy : ultrasonography; thyroid antibodies; other pituitary hormone measurements; 24-hr urinary cortisol excretion; etc.
- The absence of a rise in total T4 might have other potential explanations : iodine deficiency (unlikely in Goa probably) or congenital absence of TBG (hemizygote in the case of females) for instance.
- If the patient has delivered now, it should be possible to re-evaluate the diagnosis of central hypothyroidism.
Prof Daniel GLINOER
- Thyroid hormone is essential for bone growth, and, therefore, bone age advancement. It appears that th CNS maturation that is necessary for puberty has the same determinants as those necessary for bone age maturation.; therefore, any disorder associated with delayed BA is associated with delayed puberty. In both sexes. The sex precocity seen in a tiny minority of hypothyroid children is poorly understood (see my chapter on female puberty in Sperling’s textbook of pediatric endocrinology).
- You can search PubMed as well as I for the latest. But this is a standard approach.
- I wouldn’t worry about DD unless he remains hypogonadotropic, which I presume he is (although polyclonal RIA’s for LH and FSH may give inaccurate results in hypothyroidism) after thyroid replacement.
Robert Rosenfield, MFD, Pediatrics, Univ of Chicago