Hypothyroxinemia In Pregnancy Research Articles

A Systematic Review and Meta-Analysis Examining the Risk of Adverse Pregnancy and Neonatal Outcomes in Women with Isolated Hypothyroxinemia in Pregnancy.

Background: The relationship between isolated hypothyroxinemia (IH) in pregnancy and adverse pregnancy outcomes is controversial, with no consensus on the need for treatment. Summary: We conducted a systematic review and meta-analysis examining adverse pregnancy and neonatal outcomes in women with IH in pregnancy. We searched PubMed, Embase, Web of Science, and the Cochrane Central Register of Controlled Trials for publications from inception to December 2022. Randomized clinical trials and cohort studies were included. Random-effects meta-analyses were used to estimate pooled relative risks (RRs) for each outcome. We included 21 articles, of which 19 investigated the relationship between IH and maternal and neonatal outcomes and 4 investigated the efficacy of levothyroxine (LT4) treatment. Compared with euthyroid pregnancies, IH pregnancies were associated with an increased risk of preterm birth (RR 1.35 [confidence interval, CI, 1.16-1.56]; I2 = 9%), premature rupture of membranes (RR 1.41 [CI 1.08-1.84]; I2 = 0%), gestational diabetes (RR 1.34 [CI 1.07-1.67]; I2 = 76%), macrosomia (RR 1.62 [CI 1.31-2.02]; I2 = 42%), and fetal distress (RR 1.72 [CI 1.15-2.56]; I2 = 0%). However, no statistically significant differences were noted in adverse outcomes according to LT4 treatment status. Conclusions: There is evidence suggesting that IH in pregnancy may be associated with an increased risk of adverse pregnancy and neonatal outcomes. However, it is unclear whether LT4 may mitigate the risk of these adverse outcomes.

Early Levothyroxine Treatment for Subclinical Hypothyroidism or Hypothyroxinemia in Pregnancy: The St Carlos Gestational and Thyroid Protocol.

The optimal maternal levels of thyroid hormones (TH) during the first trimester of gestation have not been established, nor has the ideal moment to initiate levothyroxine treatment (LT) to improve the evolution of gestation and fetal development. Cut-off points for Thyroid-stimulating hormone (TSH) <2.5 µIU/mL and free thyroxine (FT4)>7.5 pg/mL have been recommended. There are no data on whether initiation of LT <9th Gestational Week (GW) can have a favourable impact.ObjectiveTo define the TSH/FT4 percentiles corresponding with 2.5 µIU/mL and 7.5 pg/mL levels, respectively, at GW8 (Study 1), and evaluate the effects of protocol-based LT before GW9 on gestation evolution, in women with TSH ≥2.5 µIU/mL and/or FT4≤ 7.5 pg/mL (study 2).Subjects2768 consecutive pregnant women attending the first gestational visit from 2013-2014 and 3026 from 2015-2016 were eligible for Study I and 2 respectively. A final 2043 (study 1) and 2069 (study 2) women were assessed in these studies.ResultsStudy 1: The FT4 level of 7.5 pg/mL corresponds with the 17.9th percentile, a TSH level of 2.5 µIU/mL with the 75.8th. Women with TSH ≥2.5 µIU/mL had a history of fetal losses more frequently than those <2.5 (OR 2.33 (95%CI): 1.58-3.12), as did those with FT4 ≤7.5 pg/ml compared to those >7.5 (OR 4.81; 3.25-8.89). Study 2: A total of 1259 women had optimal TSH/FT4 levels (Group 1), 672 (32.4%, Group 2) had suboptimal TSH or T4l, and 138 (6.7%, Group 3) had suboptimal values of both. 393 (58.5%) in Group 2 and 88 (63.8%) in Group 3 started LT before GW9. Mean (SD) GW24 levels were TSH: 1.96 ± 1.22 µIU/mL and FT4: 7.07 ± 1.25 pg/mL. The highest FT4 value was 12.84 pg/mL. The adjusted risk for an adverse event if LT was started early was 0.71 (0.43-0.91) for Group 2 and 0.80 (0.66-0.94) for Group 3.ConclusionsEarly LT in women with suboptimum levels of TSH/FT4 (≥2.5µIU/mL/≤7.5 pg/ml) at or before GW9 is safe and improves gestation progression. These data support the recommendation to adopt these cut-off points for LT initiation, which should be started as early as possible.

Hypothyroidism and Hypothyroxinemia in Pregnancy: An Overview in the Time of Coronavirus Disease 2019

In normal pregnancy, the maternal thyroid gland undergoes alterations to maintain the necessary levels of thyroid hormones (THs) in each gestational period. However, various factors may reduce TH levels, potentially impacting the onset and development of pregnancy. Such cases of thyroid dysfunction are divided into overt (clinical) hypothyroidism, subclinical hypothyroidism, or isolated hypothyroxinemia, depending on the severity of deficiency. The reported incidence of overt hypothyroidism in p

How low can you go? Isolated hypothyroxinaemia in pregnancy

How low can you go? Isolated hypothyroxinaemia in pregnancy

Treatment of Subclinical Hypothyroidism or Hypothyroxinemia in Pregnancy

(Abstracted from N Engl J Med 2017;376:815–825) Subclinical hypothyroidism (SCH) during pregnancy has been associated with impaired fetal neuropsychological development. Several organizations recommend treatment of subclinical thyroid dysfunction, although the Controlled Antenatal Thyroid Screening study found mothers who were treated with levothyroxine for hypothyroidism or hypothyroxinemia did not have children with improved cognitive function compared with controls.

The Treatment of Hypothyroidism in Pregnancy

Abstract Hypothyroidism is a pathologic condition generated by the thyroid hormone deficiency. The American Thyroid Association advises for the screening of hypothyroidism beginning at 35 years and thereafter every 5 years in people at high risk for this condition: females older than 60 years, pregnant women, patients with other autoimmune disease or patients with a history of neck irradiation. In pregnant women, hypothyroidism can been associated with adverse effect for both mother and child. The „Guidelines of the American Thyroid Association for the Diagnosis and Management of Thyroid Disease During Pregnancy and Postpartum“ recommends the treatment of maternal overt hypothyroidism: females with a thyrotropin (TSH) level higher than the trimester-specific reference interval and decreased free thyroxine (FT4), and females for which TSH level is higher than 10.0 mIU/L, irrespective of the FT4 value, with administration of oral levothyroxine. The goal of treatment of maternal overt hypothyroidism is to bring back the serum TSH values to the reference range specific for the pregnancy trimester. The Guidelines of the „European Thyroid Association for the Management of Subclinical Hypothyroidism in Pregnancy and in Children“ recommends treatment of pregnancy associated subclinical hypothyroidism with the following levothyroxine doses: „1.20 μg/kg/day for TSH≤4.2 mU/l, 1.42 μg/kg/day for TSH &gt;4.2-10 and 2.33 μg/kg/day for overt hypothyroidism“. The „Guidelines of the American Thyroid Association for the Diagnosis and Management of Thyroid Disease During Pregnancy and Postpartum“ and the „European Thyroid Association for the Management of Subclinical Hypothyroidism in Pregnancy and in Children“ do not recommend the treatment of isolated hypothyroxinemia in pregnancy.

Levothyroxine Therapy of Subclinical Hypothyroidism or Hypothyroxinemia in Pregnancy Does Not Improve Cognitive Function in the Offspring

Clinical ThyroidologyVol. 29, No. 4 SummariesLevothyroxine Therapy of Subclinical Hypothyroidism or Hypothyroxinemia in Pregnancy Does Not Improve Cognitive Function in the OffspringJerome M. HershmanJerome M. Hershman*The author is grateful to Tim Korevaar and Jorge Mestman for their helpful suggestions.Search for more papers by this authorPublished Online:1 Apr 2017https://doi.org/10.1089/ct.2017;29.132-135AboutSectionsView articleView Full TextPDF/EPUB Permissions & CitationsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail View articleFiguresReferencesRelatedDetailsCited bySubclinical Hypothyroidism with Negative for Thyroid Peroxidase Antibodies in Pregnancy: Intellectual Development of Offspring Jiajia Chen, Jing Zhu, Xianping Huang, Shenzhi Zhao, Huiqiu Xiang, Panpan Zhou, Tong Zhou, and Zhangye Xu11 April 2022 | Thyroid, Vol. 32, No. 4 Volume 29Issue 4Apr 2017 InformationCopyright 2017 American Thyroid Association, Inc.To cite this article:Jerome M. Hershman.Levothyroxine Therapy of Subclinical Hypothyroidism or Hypothyroxinemia in Pregnancy Does Not Improve Cognitive Function in the Offspring.Clinical Thyroidology.Apr 2017.132-135.http://doi.org/10.1089/ct.2017;29.132-135Published in Volume: 29 Issue 4: April 1, 2017PDF download

Treatment of Subclinical Hypothyroidism or Hypothyroxinemia in Pregnancy

BackgroundSubclinical thyroid disease during pregnancy may be associated with adverse outcomes, including a lower-than-normal IQ in offspring. It is unknown whether levothyroxine treatment of women who are identified as having subclinical hypothyroidism or hypothyroxinemia during pregnancy improves cognitive function in their children.MethodsWe screened women with a singleton pregnancy before 20 weeks of gestation for subclinical hypothyroidism, defined as a thyrotropin level of 4.00 mU or more per liter and a normal free thyroxine (T4) level (0.86 to 1.90 ng per deciliter [11 to 24 pmol per liter]), and for hypothyroxinemia, defined as a normal thyrotropin level (0.08 to 3.99 mU per liter) and a low free T4 level (<0.86 ng per deciliter). In separate trials for the two conditions, women were randomly assigned to receive levothyroxine or placebo. Thyroid function was assessed monthly, and the levothyroxine dose was adjusted to attain a normal thyrotropin or free T4 level (depending on the trial), with sham adjustments for placebo. Children underwent annual developmental and behavioral testing for 5 years. The primary outcome was the IQ score at 5 years of age (or at 3 years of age if the 5-year examination was missing) or death at an age of less than 3 years.ResultsA total of 677 women with subclinical hypothyroidism underwent randomization at a mean of 16.7 weeks of gestation, and 526 with hypothyroxinemia at a mean of 17.8 weeks of gestation. In the subclinical hypothyroidism trial, the median IQ score of the children was 97 (95% confidence interval [CI], 94 to 99) in the levothyroxine group and 94 (95% CI, 92 to 96) in the placebo group (P=0.71). In the hypothyroxinemia trial, the median IQ score was 94 (95% CI, 91 to 95) in the levothyroxine group and 91 (95% CI, 89 to 93) in the placebo group (P=0.30). In each trial, IQ scores were missing for 4% of the children. There were no significant between-group differences in either trial in any other neurocognitive or pregnancy outcomes or in the incidence of adverse events, which was low in both groups.ConclusionsTreatment for subclinical hypothyroidism or hypothyroxinemia beginning between 8 and 20 weeks of gestation did not result in significantly better cognitive outcomes in children through 5 years of age than no treatment for those conditions. (Funded by the Eunice Kennedy Shriver National Institute of Child Health and Human Development and the National Institute of Neurological Disorders and Stroke; ClinicalTrials.gov number, NCT00388297.)

Treatment of Subclinical Hypothyroidism or Hypothyroxinemia in Pregnancy

Treatment of Subclinical Hypothyroidism or Hypothyroxinemia in Pregnancy

Maternal hypothyroxinaemia in pregnancy is associated with obesity and adverse maternal metabolic parameters.

ObjectiveSubclinical hypothyroidism and isolated hypothyroxinaemia in pregnancy have been associated with an increased risk of gestational diabetes. We aimed to ascertain if these women have a worse metabolic phenotype than euthyroid pregnant women.Design, subjects and methodsWe recruited 956 healthy Caucasian women with singleton, non-diabetic pregnancies from routine antenatal clinics. Detailed anthropometric measurements (including BMI and skinfold thickness) and fasting blood samples (for TSH, free thyroxine (FT4), free triiodothyronine (FT3), HbA1c, lipid profile, plasma glucose and insulin resistance (HOMA-IR) analysis) were obtained at 28 weeks gestation.ResultsIn comparison to euthyroid women (n=741), women with isolated hypothyroxinaemia (n=82) had significantly increased BMI (29.5 vs 27.5 kg/m2, P<0.001), sum of skinfolds (57.5 vs 51.3 mm, P=0.002), fasting plasma glucose (4.5 vs 4.3 mmol/l, P=0.01), triglycerides (2.3 vs 2.0 mmol/l, P<0.001) and HOMA-IR (2.0 vs 1.3, P=0.001). Metabolic parameters in women with subclinical hypothyroidism (n=133) were similar to those in euthyroid women. Maternal FT4 was negatively associated with BMI (r=−0.22), HbA1c (r=−0.14), triglycerides (r=−0.17), HOMA-IR (r=−0.15) but not total/HDL cholesterol ratio (r=−0.03). Maternal FT3:FT4 ratio was positively associated with BMI (r=0.4), HbA1c (r=0.21), triglycerides (r=0.2), HOMA–IR (r=0.33) and total/HDL cholesterol ratio (r=0.07). TSH was not associated with the metabolic parameters assessed.ConclusionsIsolated hypothyroxinaemia, but not subclinical hypothyroidism, is associated with adverse metabolic phenotype in pregnancy, as is decreasing maternal FT4 and increasing FT3:FT4 ratio. These associations may be a reflection of changes in the thyroid hormone levels secondary to increase in BMI rather than changes in thyroid hormone levels affecting body weight and related metabolic parameters.

Maternal Hypothyroxinemia in Pregnancy Is Associated with Increased Risk for ADHD Symptoms in Children

Clinical ThyroidologyVol. 27, No. 8 SummariesMaternal Hypothyroxinemia in Pregnancy Is Associated with Increased Risk for ADHD Symptoms in ChildrenElizabeth N. PearceElizabeth N. PearceSearch for more papers by this authorPublished Online:10 Aug 2015https://doi.org/10.1089/ct.2015;27.212-214AboutSectionsView articleView Full TextPDF/EPUB Permissions & CitationsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail View articleFiguresReferencesRelatedDetailsCited byThyroid-disrupting chemicals and brain development: an updateEndocrine Connections, Vol. 7, No. 4 Volume 27Issue 8Aug 2015 InformationCopyright 2015 American Thyroid Association, Inc.To cite this article:Elizabeth N. Pearce.Maternal Hypothyroxinemia in Pregnancy Is Associated with Increased Risk for ADHD Symptoms in Children.Clinical Thyroidology.Aug 2015.212-214.http://doi.org/10.1089/ct.2015;27.212-214Published in Volume: 27 Issue 8: August 10, 2015PDF download

Could Isolated Hypothyroxinemia in Pregnancy Be Caused by Iron Deficiency?

Clinical ThyroidologyVol. 27, No. 4 SummariesCould Isolated Hypothyroxinemia in Pregnancy Be Caused by Iron Deficiency?Jorge H. MestmanJorge H. MestmanSearch for more papers by this authorPublished Online:8 Apr 2015https://doi.org/10.1089/ct.2015;27.83-85AboutSectionsView articleView Full TextPDF/EPUB ToolsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail View articleFiguresReferencesRelatedDetails Volume 27Issue 4Apr 2015 InformationCopyright 2015 American Thyroid Association, Inc.To cite this article:Jorge H. Mestman.Could Isolated Hypothyroxinemia in Pregnancy Be Caused by Iron Deficiency?.Clinical Thyroidology.Apr 2015.83-85.http://doi.org/10.1089/ct.2015;27.83-85Published in Volume: 27 Issue 4: April 8, 2015PDF download

Iron Deficiency, An Independent Risk Factor for Isolated Hypothyroxinemia in Pregnant and Nonpregnant Women of Childbearing Age in China

Isolated hypothyroxinemia during early pregnancy may irreversibly damage the neurodevelopment of offspring. However, the causes are not well clarified. To explore the association of iron deficiency (ID) with hypothyroid function of women in early pregnancy and nonpregnant women. A total of 7953 pregnant women of ≤ 12 weeks gestation and 2000 childbearing-aged women were recruited. A subpopulation including 3340 pregnant women and 1052 nonpregnant women with sufficient iodine intake and negative thyroid peroxidase antibody were studied. Mild and severe cases of hypothyroxinemia were defined as free T4 levels below the 10th percentile and the 5th percentile, respectively, with normal TSH. Total body iron, serum ferritin, and serum transferrin receptor were used as indicators for iron nutrition. Serum free T4 levels were significantly lower in both pregnant and nonpregnant women with ID compared with the corresponding groups without ID (both P < .05). The prevalence of mild and severe hypothyroxinemia was markedly higher in women with ID than those without, in both pregnant and nonpregnant women (all P < .01). Logistic regression indicated that ID was an independent risk factor for both mild and severe hypothyroxinemia in pregnancy (odds ratio [OR] = 2.440, 95% confidence interval [CI]: 1.324-4.496, P = .004; and OR = 3.278, 95% CI: 1.443-7.446, P = .005, respectively) and nonpregnancy (OR = 2.662, 95% CI: 1.330-5.329, P = .006; and OR = 3.254, 95% CI: 1.375-7.700, P = .007, respectively). An association between ID and isolated hypothyroxinemia was found in both pregnant and nonpregnant childbearing-aged women, independent of the effects of iodine and thyroid autoimmunity. We speculate that ID may be a pathogenic factor for hypothyroxinemia, even in pregnant women during the first trimester.

Fetal-Maternal Outcomes of Isolated Hypothyroxinemia in Pregnancy

Fetal-Maternal Outcomes of Isolated Hypothyroxinemia in Pregnancy

Optimal management of hypothyroidism, hypothyroxinaemia and euthyroid TPO antibody positivity preconception and in pregnancy.

Normal physiological changes of pregnancy warrant the need to employ gestation specific reference ranges for the interpretation of thyroid function tests. Thyroid hormones play crucial roles in foetal growth and neurodevelopment which are dependent on adequate supply of maternal thyroid hormones from early gestation onwards. The prevention of significant adverse obstetric and neurodevelopmental outcomes from hypothyroidism requires a strategy of empirical levothyroxine dose increases and predictive dose adjustments in pregnancy combined with regular thyroid function testing, starting before pregnancy and until the postpartum period. Subclinical hypothyroidism has been associated with an increased risk of pregnancy loss and neurocognitive deficits in children, especially when diagnosed before or during early pregnancy. Whilst trials of levothyroxine replacement for mild hypothyroidism in pregnancy have not indicated definite evidence of improvements in these outcomes, professional guidelines recommend treatment, especially if evidence of underlying thyroid autoimmunity is present. Studies of isolated hypothyroxinaemia in pregnancy have shown conflicting evidence with regards to adverse obstetric and neurodevelopmental outcomes and no causative relationships have been determined. Treatment of this condition in pregnancy may be considered in those with underlying thyroid autoimmunity. Whilst the evidence for a link between the presence of anti-TPO antibodies and increased risks of pregnancy loss and infertility is compelling, the results of ongoing randomized trials of levothyroxine in euthyroid women with underlying autoimmunity are currently awaited. Further studies to define the selection of women who require levothyroxine replacement and to determine the benefits of a predictive dose adjustment strategy are required.

PMM.59 Maternal hypothyroxinaemia in pregnancy is associated with altered maternal metabolic parameters

BackgroundIn euthyroid healthy adults thyroid function is known to be associated with obesity, insulin resistance, glycaemia, and dyslipidaemia. Little is known of similar associations in pregnancy, where maternal subclinical hypothyroidism...

Five-Year Follow-Up for Women With Subclinical Hypothyroidism in Pregnancy

Context:Increasing numbers of women are being treated with l-thyroxine in pregnancy for mild thyroid dysfunction because of its association with impaired neuropsychological development in their offspring and other adverse obstetric outcomes. However, there are limited data to indicate whether treatment should be continued outside of pregnancy.Objectives:We aimed to determine whether subclinical hypothyroidism and maternal hypothyroxinemia resolve postdelivery.Design, Setting, and Participants:A total of 523 pregnant healthy women with no known thyroid disorders were recruited during routine antenatal care and provided blood samples at 28 weeks of pregnancy and at a mean of 4.9 years postpregnancy.Main Outcome Measures:TSH, free T4, free T3, and thyroid peroxidase antibody levels were measured in serum taken in pregnancy and at follow-up.Results:Subclinical hypothyroidism in pregnancy (TSH >3 mIU/L) was present in 65 of 523 (12.4%) women. Of these, 49 (75.4%) women had normal thyroid function postpregnancy; 16 of 65 (24.6%) had persistent high TSH (TSH >4.5 mIU/L postpregnancy) with 3 women receiving l-thyroxine treatment. A total of 44 of 523 (8.4%) women had isolated maternal hypothyroxinemia in pregnancy (free T4 <10th centile and TSH ≤3 mIU/L). Only 2 of 44 (4.5%) had TSH >4.5 mIU/L outside pregnancy. Of the women with subclinical hypothyroidism in pregnancy with antibody measurements available, those with thyroid peroxidase antibodies in pregnancy were more likely to have persistently elevated TSH or be receiving l-thyroxine replacement after pregnancy (6 of 7 [86%] vs 10 of 57 [18%], P < .001).Conclusions:The majority of cases of subclinical hypothyroidism in pregnancy are transient, so treatment with l-thyroxine in these patients should be reviewed because it may not be warranted after pregnancy.

Overweight increases risk of first trimester hypothyroxinaemia in iodine‐deficient pregnant women

Hypothyroxinaemia early in pregnancy may impair fetal brain development. Increased body weight has been associated with low thyroxine concentrations in non-pregnant women. In pregnant women, morbid maternal obesity is a risk factor for thyroid dysfunction. But whether lesser degrees of overweight that are much more common could be a risk factor for hypothyroxinaemia in pregnancy is unclear. The objective of this study was to investigate if overweight increases risk for thyroid dysfunction, and specifically hypothyroxinaemia, in iodine-deficient pregnant women. We performed a cross-sectional study at first hospital visit among healthy Thai pregnant women. We measured weight and height, urinary iodine concentration (UIC), serum thyroid hormones and thyroglobulin. Pre-pregnancy weight and relevant dietary factors were determined by questionnaire, and body mass index (BMI) was used to classify weight status. Among 514 women (mean gestational age, 11 weeks) with a median UIC of 111 μg dL(-1) , indicating mild iodine deficiency, 12% had low free thyroxine (fT4) concentrations: 3% had overt hypothyroidism; 7% had subclinical hypothyroidism; and 8% had isolated hypothyroxinaemia. Based on pre-pregnancy BMI, 26% of women were overweight or obese. In a multiple regression model, BMI was a negative predictor of fT4 (β = -0.20, P < 0.001). Compared to normal weight women, the prevalence ratio (95% CI) of a low fT4 in overweight women was 3.64 (2.08-6.37) (P < 0.01). Iodine-deficient pregnant Thai women who are overweight have a 3.6-fold higher risk of hypothyroxinaemia in the first trimester compared to normal weight women. Targeted screening should consider overweight a potential risk factor for thyroid dysfunction in pregnant women in iodine-deficient areas.

Thyroid and pregnancy.

Thyroid and pregnancy.

Are Detection and Treatment of Thyroid Insufficiency in Pregnancy Feasible?

A workshop entitled, "The Impact of Maternal Thyroid Diseases on the Developing Fetus: Implications for Diagnosis, Treatment, and Screening," was held in Atlanta, Georgia, January 12-13, 2004. The workshop was sponsored jointly by The National Center on Birth Defects and Developmental Disabilities of The Centers for Disease Control and Prevention (CDC) and The American Thyroid Association. This paper reports on the individual session that examined the ability to detect and treat thyroid dysfunction during pregnancy. For this session, presented papers included: "Laboratory Reference Values in Pregnancy" and "Criteria for Diagnosis and Treatment of Hypothyroidism in Pregnancy." These presentations were formally discussed by invited respondents and by others in attendance. Salient points from this session about which there was agreement include the following: thyrotropin (TSH) can be used as marker for hypothyroidism in pregnancy, except when there is iodine deficiency usually evidenced by elevated serum thyroglobulin (Tg). We need more longitudinal studies of TSH during pregnancy in iodine-sufficient populations without evidence of autoimmune thyroid disease to develop trimester-specific TSH reference ranges. Current free thyroxine (FT4) estimate methods are sensitive to abnormal binding-protein states such as pregnancy. There is no absolute FT4 value that will define hypothyroxinemia across methods. Total thyroxine (TT4) changes in pregnancy are predictable and not method-specific. TT4 below 100 nmol/L (7.8 microg/dL) is a reasonable indicator of hypothyroxinemia in pregnancy. Women with known hypothyroidism and receiving levothyroxine (LT4) before pregnancy should plan to increase their dosage by 30% to 60% early in pregnancy. Women with autoimmune thyroid disease prior to pregnancy are at increased risk for thyroid insufficiency during pregnancy and postpartum thyroiditis and should be monitored with TSH during pregnancy.