Interpretation of laboratory investigations relies on reference intervals. Physiological changes in pregnancy may result in significant changes in normal values for many biochemical assays, and as such results may be misinterpreted as abnormal or mask a pathological state. The aims of this review are as follows: 1. To review the major physiological changes in biochemical tests in normal pregnancy. 2. To outline where these physiological changes are important in interpreting laboratory investigations in pregnancy. 3. To document the most common causes of abnormalities in biochemical tests in pregnancy, as well as important pregnancy-specific causes.

Changes in biochemical tests in pregnancy and their clinical significance.

Recurrent Pregnancy Loss (RPL) affects between 1% to 5% of women of reproductive age. It is widely believed that RPL is a complex disorder that is influenced by chromosomal abnormalities, genetic mutations, uterine anatomic deformity, endocrine dysfunction, immunologic factors, infections, and the environment. Thrombotic disorders are a frequent cause of RPL, accounting for almost half of all cases; however, in the rest of the cases, the cause of RPL remains unclear. Therefore, in this study, it was planned to determine the genetic mutations involved in RPL during the first and second trimester of pregnancy. An observational retrospective cohort study was conducted in 2021, collecting data from 157 first trimester miscarriages and 54 s trimester pregnancies. All patients with a panel of laboratory and genetic analysis for thrombophilia were included for data analysis. It was observed that four factors were significantly more prevalent in one of the groups. Factor V Leiden (FVL) homozygosity and antiphospholipid syndrome (APS) antibodies were statistically significantly more common in pregnant women who suffered first trimester pregnancy losses. On the other hand, Protein C deficiency and Glycoprotein Ia polymorphism were statistically significantly more frequent in the second trimester group. The strongest independent risk factors for first trimester pregnancy loss were FVL and prothrombin (PT) compound mutations (OR = 3.11), followed by FVL homozygous mutation (OR = 3.66), and APS antibodies (OR = 4.47). Regarding second trimester pregnancy loss risk factors, the strongest were FVL and PT compound (OR = 3.24), followed by Glycoprotein Ia polymorphism (OR = 3.61), and respectively, APS antibodies (OR = 3.85). Numerous thrombophilic risk factors for early and late pregnancy loss have been found, including several mutations that seem to occur more often either during the first or the second trimester. Even though we are aware of risk-free and efficient diagnostics for thrombophilia abnormalities, no intervention has been proved to be clearly successful after the detection of these variables.

/pdf/a-retrospective-assessment-of-thrombophilia-in-pregnant-1hh35xve.pdf

A Retrospective Assessment of Thrombophilia in Pregnant Women with First and Second Trimester Pregnancy Loss

After encountering two women with serum thyrotropin (TSH) levels greater in periovulatory phase than in other days of the menstrual cycle, we hypothesized that TSH levels could be sensitive to changes in circulating estrogens in women. The objective of this study was to evaluate whether serum TSH increases after an induced acute increase of serum estradiol, and compare serum TSH increase with that of prolactin (PRL) which is a classic estradiol-upregulated pituitary hormone. In this retrospective study, we resorted to stored frozen sera from 55 women who had undergone the GnRH agonist (buserelin)-acute stimulation test of ovarian steroidogenesis. This test, that is preceded by dexamethasone administration to suppress adrenal steroidogenesis, had been performed to show an increased buserelin-stimulated response of 17-hydroxyprogesterone, a response that is frequent in polycystic ovary syndrome. Fifty-five women had enough serum volume at pertinent times (first observation early in the follicular phase and all times of the test) to permit assay of serum estradiol, TSH and PRL. Before dexamethasone administration, estradiol averaged 26.4 ± 15.5 pg/ml (reference range 23–139, follicular phase), TSH 1.78 ± 0.86 mU/L (reference range 0.3–4.2) and PRL 409.4 ± 356 mU/L (reference range 70.8–556) (mean ± SD). Serum estradiol, TSH and PRL averaged 47.2 ± 27 pg/ml, 0.77 ± 0.48 mU/L and 246.4 ± 206.8 mU/L just prior to the buserelin injection, but they peaked at 253.4 ± 113.5 pg/ml (nv 83–495, midcycle), 3.30 ± 1.65 mU/L and 540.3 ± 695.2 mU/L after injection. The responses to buserelin of estradiol, TSH and PRL were of wide magnitude. There was a significant correlation between TSH peak and serum estradiol peak, betweeen AUC0-24 h-TSH and AUC0-24 h-estradiol, or between PRL peak and estradiol peak and AUC0-24 h -PRL and AUC0-24 h-estradiol in only a subgroup of women. Therefore, women with estradiol-dependent increase in serum TSH do exist. Reference bands of serum TSH dependent on the phases of the menstrual cycle should be available.

https://arpi.unipi.it/bitstream/11568/923210/1/J%20Clin%20Transl%20Endocrinol%202018.pdf

Circulating thyrotropin is upregulated by estradiol.

Thyroid dysfunction is frequent in pregnant women and is often associated with an increased risk of adverse maternal and fetal outcome. In the present work, thyroid function of pregnant women from Benin republic was studied. Two hundred forty (240) pregnant women, without thyroid disease history, have been included in the study. A blood sample was drawn for measurement of TSH, free T3 and free T4 serum levels. From the first to the third trimester, plasma levels of free T3 and free T4 decreased when plasma levels of TSH increased. Using recommendations of the 2011 American Thyroid Association (ATA) guidelines, thyroid dysfunction was observed in 24.17% of subjects. Hypothyroidism was present in 22.50% of subjects with 19.17% of subclinical hypothyroidism, 0.83% of overt hypothyroidism and 2.50% of hypothyroxinemia and hyperthyroidism was observed in 1.67% of subjects. An increase from 15.52% to 28.07% was observed in the frequency of hypothyroidism from the first to the third trimester of pregnancy. When an upper cut-off value of 4 mU/L was used for TSH, as recommended in the 2017 ATA guidelines, prevalence of thyroid disorders was 14.58% with 12.91% of hypothyroidism but no hypothyroidism was observed in women in the first trimester of pregnancy. A rise in hypothyroidism frequency was observed when pregnant women age increased. Hypothyroidism was very common in pregnant women in Benin. To allow accurate assessment of thyroid status in pregnant women in Benin, pregnancy specific range for plasma level of TSH and thyroid hormones should be established.

/pdf/thyroid-function-in-pregnant-women-from-a-west-african-wysnvzf03v.pdf

Thyroid Function in Pregnant Women from a West-African Population

Guidelines for TrimesTer‐specific Thyroid‐sTimulaTinG hormone Current guidelines on the management of thyroid disorders during pregnancy strongly recommend the establishment of population-based trimester-specific reference ranges for thyroid-stimulating hormone (TSH).[1] This is an important aspect of clinical endocrinology, as the reference range directly impacts clinical decision-making and institution of therapy. Population-based reference ranges are expected to be calculated based on data of healthy pregnant women, with no personal or family history of thyroid dysfunction, no visible or palpable goiter; history of thyroid disease, with optimal iodine intake; and negative thyroid peroxidase antibody status. In accordance with the International Federation of Clinical Chemistry,[2] reference intervals should extend from the 2.5th to 97.5th percentile.[3,4] While standard investigations require a minimum of 120 measurements for the establishment of normal ranges, thyroid function tests need a minimum of 400 individual measurements for validation of healthy reference ranges.[5] This is due to the high interindividual variability and skewness of data.

Trimester-specific Thyroid-stimulating Hormone: An Indian Perspective.

Background: Reference intervals for thyroid hormone during pregnancy need to be gestational age, method , and population specific and there is need to establish trimester-specific thyroid levels for the different population across the world. The aim of this study was to establish trimester-specific reference range for thyroid hormone during pregnancy in a tertiary care center in Haryana. Materials and Methods: A total of 1430 pregnant women were recruited for the study. Participants having any history of chronic illness, goiter on physical examination, thyroid illness in the past or present, consuming thyroid medications, family history of thyroid illness, presence of anti-thyroid peroxidase antibody, poor obstetrics history were excluded from the study and reference population was identified to calculate serum free triiodothyronine (FT3), free thyroxine (FT4) and thyrotropin (TSH) for each trimester of pregnancy. Results: The 2.5–97.5th percentiles for FT3, FT4, and TSH obtained in this study were 2.53–4.54 pg/ml, 0.88–1.78 ng/ml and 0.37–3.69 μIU/ml in the first trimester, 2.0–4.73 pg/ml, 0.91–1.78 ng/ml and 0.54–4.47 μIU/ml in the second trimester, 2.01–4.01 pg/ml, 0.83–1.73 ng/ml, and 0.70–4.64 μIU/ml in the third trimester of pregnancy. Mean TSH increased and mean FT3 decreased significantly with the progression of gestational period. FT4 decreased from trimester 1–3rd, but the decrease was nonsignificant from 2nd to 3rd trimester. Conclusions: Existing results for trimester-specific reference intervals for thyroid hormones are inconsistent and cannot be extrapolated due to differences in ethnicity, maternal iodine status, laboratory assay method, and rigor for selection of reference population. Thus, establishment of reference intervals in each region is of great importance.

Trimester-specific reference interval for thyroid hormones during pregnancy at a Tertiary Care Hospital in Haryana, India.

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Trimester-specific reference interval for thyroid hormones during pregnancy at a Tertiary Care Hospital in Haryana, India.