TSH (0.3–4.7 mIU/mL)
FT4 (0.8–1.8 ng/dL)
TT3 (60–180 ng/dL)
FT3 (2.3–4.2 pg/mL)
TgAb (<60 U/mL)
TPOAb (<60 U/mL)
At diagnosis
8.2
0.9
3 months follow-up
10.1
0.9
6 months follow-up
On N-T 16.25 mcg BID
8.1
1 year follow-up
On N-T 32.5 mcg BID
0.8
0.8
164
18 month follow-up
7 weeks 5 days pregnant
On N-T 32. mcg BID
2.18
8 weeks pregnant
On N-T 32.5 mcg BID
3.32
0.6
216
4.1
143
38
12 weeks pregnant
On levothyroxine 137 mcg/day
1.5
1
At the 3 months follow-up, she complained of cold intolerance, constipation, dry skin, and feeling fatigued to the point of requiring a nap in the afternoon. The laboratory tests confirmed overt hypothyroidism (Table 12.1). Again, the recommendation was made to start levothyroxine. She opted not to be treated conventionally with levothyroxine. Rather, after consulting with an alternative medicine physician, she started Nature-Throid (N-T) 16.25 mg BID. Nature-Throid® (Thyroid USP) tablets of desiccated thyroid for oral use is a preparation derived from porcine thyroid glands. The preparation provides 38 mcg levothyroxine (T4) and 9 mcg liothyronine (T3) for each 65 mg (1 Grain) tablet. T3 is approximately four times as potent as T4 on a microgram for microgram basis.
Subsequently, TSH was monitored approximately every 3–6 months. N-T was adjusted accordingly once after 3 months of treatment when it was increased to 32.5 mg BID, as at that point TSH was still elevated (Table 12.1).
At the 1 year follow up, after 6 months on desiccated thyroid 32.5 mg BID: TSH, FT4, TT3 were obtained and were normal (Table 12.1).
At the 18th month mark, 6 months after the last TSH was obtained, the patient became pregnant. She established care with a nurse midwife at the local natural birth center. At the initial pregnancy visit, 7 weeks, 5 days of gestation, the TSH was normal for the first trimester of pregnancy at 2.18 mIU/mL. The patient was referred for endocrinology consultation for treatment of hypothyroidism in pregnancy, as the nurse midwife was unfamiliar with adjusting desiccated thyroid.
Two days later, the patient was seen in endocrinology consultation. She was 8 weeks pregnant. She complained of feeling stressed and fatigued; she continued to complain of cold intolerance, palpitations, and insomnia, all of which were present long before the diagnosis of hypothyroidism. She reported a new complaint of nausea without vomiting in the morning, which she attributes to her pregnancy.
She was taking Nature-Throid 32.5 mg BID and prenatal vitamins at bedtime containing iodine derived from kelp.
Her family history and social history were unremarkable.
On exam, she was well appearing with a nontender palpable thyroid without nodules. No neck lymphadenopathy. She had a fine tremor of the outstretched fingers. The remainder of the physical exam was unremarkable.
Laboratory tests done when the patient was 8 weeks pregnant are reported in Table 12.1.
After reviewing the laboratory tests, the patient was informed that her hypothyroidism was due to Hashimoto’s thyroiditis and that one of her thyroid hormone, T4 was low. She was advised that her current treatment with desiccated thyroid did not provide sufficient thyroid hormone to the fetus. I explained that the total T3 was still within normal range for pregnancy (upper range for pregnancy 1.5× upper normal range).
Desiccated thyroid was discontinued and brand name levothyroxine was recommended instead.
Her N-T 65 mg daily was converted to levothyroxine 100 mcg/day using a conversion chart. In addition, a 30–40 % increase in her pre-pregnancy thyroid hormone replacement dose was calculated. As a result, she was prescribed brand name levothyroxine, 137 mcg/day.
In addition, after noticing that her prenatal vitamin contained iodine derived from kelp, recommendation was made to switch to a multivitamin containing iodine in the form of potassium iodide 150 mcg/day.
One week later, at the ninth week of pregnancy, she called to discuss her worries. After viewing her laboratory tests on the patient portal, she searched online the effects of low maternal thyroid hormone in pregnancy. She was seeking advice on termination of her pregnancy. I explained to her that it is still debated whether hypothyroxinemia alone causes adverse effects on the developing fetus. I advise her against termination of pregnancy.
At her 12th weeks of pregnancy laboratory tests were obtained and both TSH and free T4 were in normal range for pregnancy (Table 12.1).
Recommendation was made to continue brand name levothyroxine 137 mcg/day.
Review on How the Diagnosis Was Made
The fetal thyroid begins concentrating iodine at 10–12 weeks of gestation and is controlled by pituitary TSH by approximately 20 weeks of gestation. Fetal serum levels of TSH, TBG, FT4, and FT3 increase throughout gestation, reaching mean adult levels at approximately 36 weeks of gestation.
Maternal thyroid stimulating hormone does not cross the placenta, and only small amounts of maternal thyroxine (T4) and minimal amount of triiodothyronine (T3) cross the placenta. T4 crosses the placenta much more than T3 does [1]. Maternal T4 is therefore the only significant source of thyroid hormone before the development of the fetal thyroid at 13–15 weeks gestation.
When assessing a pregnant woman with hypothyroidism, appropriate maternal TSH levels in patients treated with T3 or T4/T3 combinations may be accompanied by insufficient fetal thyroid hormone levels. In the case presented, the diagnosis was made by obtaining not only the TSH but also FT4 by immunoassay. In spite of a normal TSH, FT4 was low. The results were confirmed by equilibrium dialysis. The normal TSH measured at week 8 of pregnancy was misleading. The maternal TSH was disproportionately affected by the orally administered T3 which exerts a negative feedback on the maternal TSH while only minimally reaching the fetus. In other words, a normal TSH was achieved in this woman with lower than usual daily T4 dose. Indeed her FT4 was low reflecting the abnormal T4/T3 ratio contained in desiccated porcine thyroid.
Women with hypothyroidism are at increased risk for both complications of pregnancy and adverse neonatal outcomes. If the hypothyroidism is not treated, there is increased risk of a miscarriage, gestational hypertension, placental abruption, and postpartum hemorrhage. Overt untreated maternal hypothyroidism is associated with premature birth, low birth weight, and neonatal respiratory distress. Just as importantly, a study showed that children born from untreated women with hypothyroidism had an IQ a few points below the IQ of children born from healthy women and the IQ of children born from adequately treated women with hypothyroidism [1]. Other studies observed an IQ reduction in the offspring of mothers with hypothyroidism and with isolated hypothyroxinemia in the first trimester [2–4].
Regarding our patient’s iodine status, one may be tempted to assume that since she has always lived in the USA, her iodine intake is probably sufficient. A study done in the Boston area, however, surprisingly found that approximately 40 % of the women sampled may have mild iodine deficiency [5].
Lessons Learned
Thyroid Hormone Preparations for Treatment of Hypothyroidism in Pregnancy
The appropriate treatment and follow up of hypothyroidism in pregnancy is extremely important in order to avoid the consequences of lack of thyroid hormone on the mother, on the pregnancy, on the neonate, and on the fetal brain development. One should not assume that normal TSH in pregnant women treated with T3 or T4/T3 combination reflects fetal exposure to normal maternal thyroid hormone. In this case the developing fetus was likely exposed to insufficient levels of maternal T4.
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