Abnormal Thyroid Function Tests Research Articles

Misleading free t4 due to auto-t4 antibodies resulting in abnormal thyroid function tests: a case report

Introduction: The presence of elevated TSH with high free T4 is considered as an abnormal thyroid function test. This may be due to false elevation of serum T4 associated with autoantibodies to T4. We report a case that presented with high serum freeT4 and TSH associated with autoantibodies to T4. Case presentation: A 40 year old female patient presented with tiredness and sweating. She was diagnosed with primary hypothyroidism two years ago based on elevated TSH. She was treated with thyroxine 50mcg per day for 6 months and then she was defaulted. Examination revealed a thin lady with BMI of 18.5 Kgm-2 with a mild goiter. She was otherwise clinically euthyroid. Investigations revealed abnormal thyroid function test (TFT) with TSH of 43.6mIU/l and freeT4 of 3.06ng/dl. Her TFT was repeated on three laboratories which showed elevated TSH and upper normal to elevated freeT4. She had high titres of anti thyroid peroxidase (TPO antibodies) > 1300mIU. Her thyroid scan revealed small multinodular goiter and fine needle aspiration cytology confirmed Hushimoto’s thyroiditis. In view of the clinical findings the following possibilities were considered; assay interference, TSHoma and thyroid hormone resistance. TSHoma seemed less likely due to normal pituitary gland on MRI and normal SHBG. Further analysis of the sample was done with comparison between one step and two step methods using Cantaur and Delfia assays respectively. There was no evidence of assay interference in respect of TSH (38.73 vs 44.1mIU/l) and free T3 (3.9 vs 5.3pmol/l), however the freeT4 measurements were not consistent across the two platforms (25.6 vs 11.8 pmol/l). In addition, the total T4 measurement was elevated (219nmol/l; normal range 69-141) with 32% recovery after PEG treatment. Taken together, the results were suggestive of autoimmune hypothyroidism with evidence of freeT4 (and total T4) assay interference due to anti-T4 autoantibodies. The patient was treated with thyroxine and thereafter monitored using a TSH assay alone to guide treatment adequacy. Conclusions: Clinicians must be aware of possible assay interference including the measurement of freeT4 in the differential diagnosis of abnormal TFT that do not fit the patient’s clinical presentation.

Unstable Thyroid Function in Older Adults Is Caused by Alterations in Both Thyroid and Pituitary Physiology and Is Associated with Increased Mortality

Average thyrotropin (TSH) levels are known to be higher in older adults when measured in cross-sectional populations. Possible etiologies include differential survival, neutral aging changes, or increased disease prevalence at older ages. This study aimed to elucidate the mechanisms underlying changing thyroid function during aging, and to determine the association of changes with survival, by analyzing the individual thyroid axis over time. Individual patterns of changing TSH and free thyroxine (fT4) were determined in 640 participants in the Baltimore Longitudinal Study of Aging who had at least three measures of serum TSH and fT4, not on medications, over an average of seven years of follow-up. Participants with changing phenotypes were identified based on quintiles for both slopes. Those with alterations in primary thyroid gland function demonstrated intact negative feedback (rising TSH with declining fT4 or declining TSH with rising fT4). Other participants had a parallel rise or fall of TSH and fT4 levels, consistent with pituitary dysfunction. Predictors of phenotype were analyzed by logistic regression. Differential survival between thyroid aging phenotypes was analyzed using multivariate Cox regression. While the majority of participants at all ages had stable thyroid function, changes were more common among older adults, with 32.3% of those aged >80 years but only 9.5% of those aged <60 years demonstrating thyroid function changes in the highest and lowest quintiles. Regression to the mean accounts for some of the changes, for example increased baseline TSH was associated with a falling TSH pattern (odds ratio = 1.4 [confidence interval 1.1-1.7] per 1 mIU/L). Importantly, changing thyroid function in either the upper or lower quintiles of slope for TSH and fT4 was associated with increased risk of death compared to stable thyroid status (hazard ratio = 5.4 [confidence interval 3.1-9.5]). Changing thyroid hormone function is increasingly common at older ages and is associated with decreased survival. Nonetheless, the tendency for abnormal thyroid function tests to resolve, along with altered pituitary responsiveness underlying some TSH elevations, suggests that an elevated TSH level should be not assumed to represent subclinical hypothyroidism in older adults. Thus, caution is appropriate when determining the need for thyroid hormone supplements in older adults.

Rapid Evolution of Thyroid Dysfunction in Patients Treated with Nivolumab

To describe the evolution of thyroid dysfunction in a series of patients with cancer treated with the immune checkpoint inhibitor anti-programmed cell death protein-1 (PD-1) monoclonal antibody, nivolumab. Cases of thyroid dysfunction after initiation of checkpoint inhibitor treatment were identified from the Division of Endocrinology clinical practice at Mount Sinai Hospital, New York from April 2016 to February 2017. Charts were reviewed to identify patients treated with nivolumab with new onset of thyroid dysfunction. Nine cases of thyroid function in patients who were treated with nivolumab were identified. There were 4 male and 5 female patients, with a mean age of 66 years (range 50-76 years). Seven patients ultimately developed hypothyroidism. Five of the 7 patients developed abnormal thyroid function tests within the first 90 days of starting therapy (range 21-84 days), 3 of whom had transient hyperthyroidism. Transient hyperthyroidism evolved rapidly to hypothyroidism; elevated thyroid-stimulating hormone (TSH) levels were detected within 16 to 32 days of the last documented low TSH. In the 2 patients without a hyperthyroid phase, TSH levels >50 were found 18 to 28 days after the last normal TSH value. As the use of immune checkpoint inhibitor therapy increases, the need for prompt diagnosis and treatment of drug-induced thyroid disease will become more important. As illustrated in this case series, in contrast to other causes of auto-immune thyroiditis, hypothyroidism can develop rapidly within 3 months of treatment. Close monitoring is necessary to detect the development of thyroid dysfunction and avoid preventable morbidity. Anti-TPO Abs = anti-thyroglobulin antibodies; CT = computed tomography; CTLA-4 = cytotoxic T-lymphocyte-associated protein 4; FDA = U.S. Food & Drug Administration; FDG-PET = fluorodeoxyglucose-positron emission tomography; PD-1 = programmed cell death protein-1; PD-L1 = programmed death-ligand 1; T3 = triiodothyronine; T4 = thyroxine; TG = thyroglobulin; TPO = thyroperoxidase; TSH = thyroid-stimulating hormone.

Identification of Genetic Disorders Causing Disruption of Selenoprotein Biosynthesis.

Disorders of selenoprotein biosynthesis in humans, due to mutations in three genes (SECISBP2, TRU-TCA1-1, and SEPSECS) involved in the selenocysteine insertion pathway, have been described. Patients with SECISBP2 and TRU-TCA1-1 defects manifest a multisystem disorder with a biochemical signature of abnormal thyroid function tests due to the impaired activity of deiodinase selenoenzymes, myopathic features linked to SEPN1 deficiency and phenotypes resulting from increased levels of reactive oxygen species attributable to lack of antioxidant selenoenzymes. In patients harboring SEPSECS mutations, severe, progressive, cerebello-cerebral atrophy (pontocerebellar hypoplasia type 2D) dominates the phenotype and it is not known whether the disorder is associated with thyroid dysfunction.

Relationship of thyroid peroxidase antibody test with abnormal thyroid function tests

Background: Autoimmune thyroid disease results from a complex interaction between genetic and enviromental factors. The aim of this study was to find association of anti-thyroid peroxidase antibody with abnormal thyroid function tests. Materials and Methods: This is a retrospective study, conducted in 160 patients who showed abnormal thyroid function tests in grande city clinic and hospital services and Kantipur dental college for duration of 18 months since Baisakh 2072.Results: Among 160 individuals , 126(78.8%) were female and 34(21.2%) were male. Subclinical hypothyroidism (56.3%) were most common than overthyperthyroidism (18.0%), overthypothyroidism (16.9%) and subclinical hyperthyroidism (8.8%). Anti thyroid peroxidase antibodies test was shown positive in 102/160 (63.8% ) cases.Conclusion: According to the present study, anti- thyroid peroxidase antibody has been significantly associated with thyroid dysfunction, it can be used as diagnostic marker for thyroid autoimmune diathesis.

Association between thyroid dysfunction and dysglycaemia: a prospective cohort study.

To compare the incidence of hyperglycaemia among participants with low, elevated and normal serum thyroid-stimulating hormone concentration, as well as the incidence of abnormal thyroid function test results among participants with normal blood glucose and those with hyperglycaemia. In a prospective study, a cohort of 72 003 participants with normal, low and elevated serum thyroid-stimulating hormone concentration were followed from the study beginning to the first report of diabetes and prediabetes. A proportional hazards regression model was used to calculate the hazard ratios and 95% CIs for each outcome, adjusting for age, sex, education level, smoking, alcohol consumption and obesity. Analyses for the association between dysglycaemia and incident abnormal thyroid function test were also conducted. During a median 2.6 year follow-up, the incident rates for dysglycaemia, particularly prediabetes, were substantially higher in participants with elevated thyroid-stimulating hormone concentrations at baseline, while the rates for participants with normal and low thyroid-stimulating hormone were similar. After controlling for risk factors, participants with elevated thyroid-stimulating hormone retained a 15% increase in risk of prediabetes (adjusted hazard ratio 1.15, 95% CI 1.04-1.26), but were not at greater risk of diabetes (adjusted hazard ratio 0.96, 95% CI 0.64-1.44). By contrast, participants with normal and low thyroid-stimulating hormone concentrations had similar dysglycaemia risks. Participants with diabetes and prediabetes were not at greater risks of developing abnormal thyroid function test results when compared with participants with euglycaemia. People with elevated serum thyroid-stimulating hormone concentration are at greater risk of developing prediabetes. Whether this includes a greater risk of developing frank diabetes may require an extended period of follow-up to clarify.

Anemia in Patients With Resistance to Thyroid Hormone α: A Role for Thyroid Hormone Receptor α in Human Erythropoiesis

Context:Patients with resistance to thyroid hormone (TH) α (RTHα) are characterized by growth retardation, macrocephaly, constipation, and abnormal thyroid function tests. In addition, almost all RTHα patients have mild anemia, the pathogenesis of which is unknown. Animal studies suggest an important role for TH and TH receptor (TR)α in erythropoiesis.Objective:To investigate whether a defect in TRα affects the maturation of red blood cells in RTHα patients.Design, Setting, and Patients:Cultures of primary human erythroid progenitor cells (HEPs), from peripheral blood of RTHα patients (n = 11) harboring different inactivating mutations in TRα (P398R, F397fs406X, C392X, R384H, A382fs388X, A263V, A263S), were compared with healthy controls (n = 11). During differentiation, erythroid cells become smaller, accumulate hemoglobin, and express different cell surface markers. We assessed cell number and cell size, and used cell staining and fluorescence-activated cell sorter analysis to monitor maturation at different time points.Results:After ∼14 days of ex vivo expansion, both control and patient-derived progenitors differentiated spontaneously. However, RTHα-derived cells differentiated more slowly. During spontaneous differentiation, RTHα-derived HEPs were larger, more positive for c-Kit (a proliferation marker), and less positive for glycophorin A (a differentiation marker). The degree of abnormal spontaneous maturation of RTHα-derived progenitors did not correlate with severity of underlying TRα defect. Both control and RTHα-derived progenitors responded similarly when differentiation was induced. T3 exposure accelerated differentiation of both control- and RTHα patient–derived HEPs.Conclusions:Inactivating mutations in human TRα affect the balance between proliferation and differentiation of progenitor cells during erythropoiesis, which may contribute to the mild anemia seen in most RTHα patients.

Euthyroid athyroxinemia - a novel endocrine syndrome.

A 55-year-old female was referred with abnormal thyroid function tests (TFTs); the free thyroxine level (FT4) was undetectable <3.3 pmol/L (normal: 7.9–14.4), while her FT3, TSH and urinary iodine levels were normal. She was clinically euthyroid with a large soft lobulated goitre that had been present for more than thirty years. She received an injection of recombinant human TSH (rhTSH) following which there was a progressive rise of the FT3 and TSH levels to 23 pmol/L and >100 mIU/L respectively at 24 h, The FT4 however remained undetectable throughout. Being on thyroxine 100 µg/day for one month, her FT4 level increased to 15 pmol/L and TSH fell to 0.08 mIU/L. Four years earlier at another hospital, her FT4 level had been low (6.8 pmol/L) with a normal TSH and a raised Tc-99 uptake of 20% (normal<4%). We checked the TFTs and Tc-99 scans in 3 of her children; one was completely normal and 2 had euthyroid with soft lobulated goitres. Their Tc-99 scan uptakes were raised at 17% and 15%, with normal TFTs apart from a low FT4 7.2 pmol/L in the son with the largest thyroid nodule. This is a previously unreported form of dyshormonogenesis in which, with time, patients gradually lose their ability to synthesize thyroxine (T4) but not triiodothyroxine (T3).Learning points:This is a previously unreported form of dyshormonogenetic goitre.This goitre progressively loses its ability to synthesize T4 but not T3.The inability to synthesize T4 was demonstrated by giving rhTSH.

Incidence of thyroid function test abnormalities in patients receiving immune checkpoint inhibitor therapy for cancer: A single institution retrospective review.

e14569 Background: With the advent of immune-checkpoint inhibitor (ICI) therapy, thyroid function test abnormalities (TFTA) are common with reported incidence range of 2-15%. Our aim was to describe the incidence of TFTAs retrospectively in patients (pts) on ICI therapy. Methods: 285 pts reviewed (178 male, 107 female; ages 16-94) of which 218 had no baseline TFTA, 61 had baseline TFTAs, and 6 had thyroidectomy (excluded). Pts received at least one dose of ipilimumab (I) and/or nivolumab (N) or pembrolizumab (P). Post-treatment TFTA was classified according to definitions of thyroid abnormalities when possible. Results: A total of 35% (76/218) pts had new onset TFTAs on ICI. Of note, 70.5% (43/61) had baseline TFTA that were exacerbated by ICI. Median time to new onset or exacerbated baseline TFTA were 46 &amp; 33 days respectively. Of note, 65% (20/31) of pts on both I+N had new onset TFTA, compared to 31.3% (15/48) with I, 31.5% (28/89) N, 26% (13/50) P. Conclusions: Incidence of TFTAs with ICI was higher than expected in our pts. Pts with baseline TFTA and/or I+N combination therapy had higher incidence of TFTA than one agent ICI therapy. In conclusion, we recommend more frequent evaluation of TFT in the first two months, especially in those with baseline TFTA. [Table: see text]

Three-year follow-up of children with abnormal newborn screening results for congenital hypothyroidism

To analyze predictive factors suggesting transient congenital hypothyroidism (TCH) compared to permanent congenital hypothyroidism (PCH) or transient thyroid function test (TFT) abnormalities among children who had positive screening results at our centers over the past decade. A retrospective chart review of 105 subjects who presented elevated TSH levels on a newborn screening test (NST) was done. TCH was defined when a trial-off therapy was successful, and PCH was defined when a trial failed or when the subject was kept on medication beyond 3years of age. A transient TFT abnormality was defined when follow-up TFTs were normalized without levothyroxine (LT4) therapy. Congenital hypothyroidism (CH) was diagnosed in 75.2% (TCH 35.2% and PCH 40.0%) of all subjects; the others (24.8%) showed transient TFT abnormalities. Initial NST-TSH levels (optimal cutoff point, 31.0 μIU/mL), the LT4 dose at 2years of age (4.1μg/kg/day), and the maximal LT4 dose (50μg/day) merged as significant predictive factors discriminating between TCH and PCH. The initial serum level of free T4 (1.06ng/dL) and not TSH (27.2μIU/mL) was the only discriminating factor between transient TFT abnormalities and TCH. Earlier re-evaluation might be possible when a patient's initial NST-TSH levels and maximal or 2-year LT4 doses are low, as both are important predictors of successful trial-off therapy in CH patients. When the initial serum level of free T4 is above the average value in neonates with mildly elevated TSH levels, TFTs may be more likely to normalize on theirown.

Association between chronic spontaneous urticaria and thyroid autoimmunity: a case control study from a tertiary care centre

&lt;p class="abstract"&gt;&lt;strong&gt;Background:&lt;/strong&gt; The exact etiology of chronic spontaneous urticaria is unknown in the majority of patients. A subset of chronic spontaneous urticaria can be autoimmune and may be associated with thyroid autoimmunity&lt;span lang="EN-IN"&gt;.&lt;/span&gt;&lt;/p&gt;&lt;p class="abstract"&gt;&lt;strong&gt;Methods:&lt;/strong&gt; Serum anti thyroid peroxidase (anti-TPO) antibody level and thyroid function tests (TFT) including triiodothyronine (T3), thyroxine (T4) and thyroid stimulating hormone (TSH) levels were estimated in 100patients with chronic spontaneous urticaria and 50 controls. Autologous serum skin test (ASST) was done in 84 chronic urticaria patients and 21 patients with high anti-TPO antibody.&lt;strong&gt;&lt;/strong&gt;&lt;/p&gt;&lt;p class="abstract"&gt;&lt;strong&gt;Results:&lt;/strong&gt; High anti-TPO antibodies and abnormal thyroid function were seen in 24 (24%) patients each. High anti-TPO antibody levels were seen in nine (18%) and abnormal TFT in 11 (22%) controls. Abnormal TSH was seen in 22 patients (22%) and 6 (12%) controls. Autologous serum skin test was positive in 53 patients with chronic spontaneous urticaria. It was positive in 16 and negative in five out of 21 patients with high anti-TPO antibody levels&lt;span lang="EN-IN"&gt;. &lt;/span&gt;&lt;/p&gt;&lt;p class="abstract"&gt;&lt;strong&gt;Conclusions:&lt;/strong&gt; Though there was a slight increase in abnormal anti-TPO antibody level and thyroid dysfunction in patients with chronic spontaneous urticaria compared to controls, it was not statistically significant&lt;span lang="EN-IN"&gt;.&lt;/span&gt;&lt;/p&gt;

Thyroid stimulating hormone (TSH) ≥2.5 mU/l in early pregnancy: Prevalence and subsequent outcomes

ObjectiveThere remains controversy over how women with abnormal thyroid function tests in pregnancy should be classified. In this study we assessed the proportion of women with thyroid stimulating hormone (TSH)≥2.5mU/l in a large obstetric cohort, and examined how many have gone on to develop thyroid disease in the years since their pregnancy. Study design4643 women were recruited and samples taken in early pregnancy between 2007 and 2010. Thyroid function tests were analysed in 2014; in women with raised TSH computerised health records and prescription databases were used to identify thyroid disease detected since pregnancy. Results58 women (1.5%) had a TSH over 5mU/l and 396 women (10.3%) had TSH between 2.5 and 5mU/l. Women with TSH>5mU/l delivered infants of lower birthweight than those with TSH<2.5mU/l; there were no other differences in obstetric outcomes between the groups. Of those who have had thyroid tests since their pregnancy, 78% of those with TSH>5mU/l and 19% of those with TSH between 2.5 and 5mU/l have gone on to be diagnosed with thyroid disease. ConclusionsUsing a TSH cut-off of 2.5mU/l in keeping with European and US guidelines means that over 12% of women in this cohort would be classified as having subclinical hypothyroidism. Treatment and monitoring of these women would have major implications for planning of obstetric services.

Sub-Clinical Thyroid Disorders in Patients With Hepatitis C Before and After Conventional Treatment

Objective: Thyroid dysfunction represents one of the commonest endocrine manifestations of chronic hepatitis C infection, exaggerated by interferon based treatment. The purpose of this study was to assess the frequency of hepatitis C virus and sub-clinical thyroid disorder in patients with hepatitis C before and after treatment. Methods: This is an observational, cross sectional analysis conducted in Lyari general hospital and Abbasi Shaheed hospital from January 2009 to December 2015. Patients with a positive rt-PCR and genotype 3 were included in the study. After a positive rt-PCR, patients were screened by thyroid stimulating hormone before starting the treatment. All patients were given therapy of conventional interferons (3 million units thrice weekly) and ribavirin (800 mg per day in two divided doses) for a period of 6 months. Patient with normal TSH level was included and patients with a co-existing hepatitis B or D were excluded from the study. After 6 months of therapy all patients had a repeat rt-PCR to see the end treatment response to therapy and a thyroid stimulating hormone to screen for thyroid disorders. Results: A total of 129,430 patients have visited the medical outpatient department of which, 4069 were HCV RNA PCR positive. The prevalence of unrecognized hepatitis C Virus was 13.4% in the study population. The prevalence of sub-clinical thyroid disorders was 9%. Of which 6.5% had sub-clinical hypothyroidism and 2.5% had overt or subclinical hyperthyroidism. A total of 2196 patients were included in the analysis. Mean age was 36.22 ±10.01 years range from 16 to 63 years. Among all 36.9% were male and 5.1% were known diabetics. On the whole 14.8% were non-responders, 80.9% achieved an end treatment response and 4.3% lost to follow up. We observed an association between the post treatment TSH level and the ETR of HCV (p=0.015). A statistically significant difference (p<0.001; 95% CI -3.008-1.577) was observed in the thyroid stimulating hormone at the baseline and following the conventional interferon and ribavirin therapy for a period of 6 months. 388 (17.6%) patients had abnormal thyroid function tests after conventional interferon treatment. These 388 patients were further followed up for 6 months. Conclusion: In conclusion, this study results shows 13.4% prevalence of HCV in Karachi and the prevalence of sub-clinical thyroid disorders was 9%, of which 6.5% and 2.5% had overt hypothyroidism and hyperthyroidism respectively.

Diagnostic Dilemma In Discordant Thyroid Function Tests Due To Thyroid Hormone Autoantibodies

Assay interference could be the cause of abnormal thyroid function tests. Early recognition prevents inappropriate patient management. The objective of this report is to present a case with discordant thyroid function tests in different thyroid assay platforms due to thyroid autoantibodies. We present a case her family, laboratory data and methods that investigate immunoassay interference. A 21-year-old woman with autoimmune thyroid disease was treated for hypothyroidism with levothyroxine and noted to have elevated total and free thyroxine, free triiodothyronine but normal thyroid-stimulating hormone. Repeat thyroid function tests using different platforms revealed discrepant results. Further investigation showed that the patient had positive thyroid hormone autoantibodies (THAAbs). We demonstrates abnormal thyroid function tests caused by THAAbs. The latter were the cause of interference with assays resulting in discrepant test results inconsistent with the clinical presentation. Early recognition would prevent inappropriate patient management.

A Novel Mutation Causing Complete Thyroid Binding Globulin Deficiency (Tbg-Cd Mia) In A Male With Coexisting Graves Disease

An asymptomatic male was found on screening to have a low serum TSH and total T4. The diagnosis of Graves' disease was made with positive thyroid stimulating immunoglobulin (TSI) and elevated free T4 in the presence of complete TBG deficiency (TBG-CD). Genetic testing of the patient and family members revealed a novel frameshift mutation in the TBG (SERPINA7) gene resulting in a complete deficiency of the protein. The laboratory testing included total T4, free T4 by analog method and direct dialysis and TBG measurements. Sequencing of genomic DNA was performed from peripheral blood. A 35-year-old East Indian male was referred to endocrinology because of abnormal thyroid function tests (TFTs): TSH 0.01 mIU/L (0.4-3.6), total T4 3.0 µg/dl (5.5-10.5) done as part of a "routine office visit". Upon further testing, the serum free T4 2.0 ng/dl (0.8-1.8) and TSI 355% (<140% baseline) were elevated and the diagnosis of Graves' disease was made. TBG deficiency was suspected because the total T4 concentration was inconsistent with hyperthyroidism and further testing confirmed TBG was undetectable. Sequencing of the TBG gene revealed a novel hemizygous frameshift mutation: p.Ala64ProfsTer106, TBG-CD Mia (numbering excludes 20 a.a. signal peptide) associated with the complete deficiency of TBG in a patient with Graves' disease. Patients with Graves' disease harboring a TBG mutation have conflicting TFTs. If a clinically hyperthyroid patient presents with normal or low total T4, serum TBG should be measured to identify an abnormality and prevent unnecessary testing.

Early Pregnancy Thyroid Function Test Abnormalities in Biobank Sera from Women Clinically Diagnosed with Thyroid Dysfunction Before or After Pregnancy.

Maternal thyroid disease may complicate pregnancy. A high frequency of abnormal thyroid function test results in pregnant women with known thyroid disease has been reported, but the frequency of unidentified thyroid dysfunction in women first clinically diagnosed with thyroid disease after a pregnancy is not known. This was a population-based study of pregnant women in the Danish National Birth Cohort (DNBC) who had a blood sample drawn in early pregnancy and terminated the pregnancy with a singleton live-birth in the period between 1997 and 2003. Participants were all women in the DNBC who had a registration of thyroid disease before and/or up to five years after the pregnancy in nationwide health registers (n = 2445) and a 12% random sample of all women in the cohort (n = 7624). Thyrotropin and free thyroxine were measured with an immunoassay in sera stored in the Danish National Biobank. Method- and pregnancy week-specific references ranges were used for classification of thyroid function test abnormalities. The frequency of abnormal thyroid function in early pregnancy was 12.5% in the random sample and 35.7% among women clinically diagnosed with thyroid disease before or after blood sampling (55.7% among women on current treatment). One third of women clinically diagnosed with thyroid disease after blood sampling had unidentified thyroid dysfunction in the early pregnancy blood sample (most frequently [52.0%] unidentified hypothyroidism in women with a later diagnosis of hypothyroidism). More than 50% of Danish pregnant women on current treatment for thyroid disease had thyrotropin and/or free thyroxine outside the week-specific reference ranges, and the frequency of unidentified early pregnancy thyroid dysfunction in women clinically diagnosed after the pregnancy was also high.

Headache Disorders May Be a Risk Factor for the Development of New Onset Hypothyroidism.

To determine whether headache disorders are a risk factor for the development of new onset hypothyroidism. Past studies have reported associations between headache disorders and hypothyroidism, but the directionality of the association is unknown. This was a longitudinal retrospective cohort study using data from the Fernald Medical Monitoring Program (FMMP). Residents received physical examinations and thyroid function testing every 3 years during the 20 year program. Residents were excluded from the cohort if there was evidence of past thyroid disease or abnormal thyroid function tests at the first office visit. A diagnosis of a headache disorder was established by self-report of "frequent headaches," use of any headache-specific medication, or a physician diagnosis of a headache disorder. The primary outcome measure was new onset hypothyroidism defined as the initiation of thyroid replacement therapy or TSH ≥ 10 without thyroid medication. A Cox survival analysis with time dependent variables were used for the model. Headache disorders, age, sex, body mass index, income, smoking, narcotic use, and hypothyroidism-producing medications were independent variables in the model. Data from 8412 residents enrolled in the FMMP were used in the current study. Headache disorders were present in about 26% of the residents and new onset hypothyroidism developed in ∼7%. The hazard ratio for the development of new onset hypothyroidism was 1.21 (95% CI = 1.001, 1.462) for those with headache disorders. Headache disorders may be associated with an increased risk for the development of new onset hypothyroidism.

Incidence and Predicting Factors for Abnormal Thyroid Function Test in Adult Patients Post Hematopoietic Stem Cell Transplantation at King Hussein Cancer Center

Incidence and Predicting Factors for Abnormal Thyroid Function Test in Adult Patients Post Hematopoietic Stem Cell Transplantation at King Hussein Cancer Center

Evaluation of thyroid function tests of acne vulgaris patients treated with systemic isotretinoin

Background: Isotretinoin is a systemic retinoid used to treat acne and it binds receptors which are the member of steroid–thyroid hormone superfamily. Certain types of retinoids may cause abnormalities in serum thyroid function tests (sTFTs) by suppressing thyroid stimulating hormone (TSH). However, it is uncertain whether systemic isotretinoin has any effect on sTFTs.Objective: The aim of the study was to find out if there is any alteration in sTFTs of patients with acne vulgaris treated with systemic isotretinoin.Methods: A total of 51 patients (male/female: 22/29) with severe acne vulgaris treated with a total dose of 120 mg/kg isotretinoin were included into the study prospectively. Serum free T3 (fT3), free T4 (fT4) and TSH levels were measured at baseline, 3rd and 6th months of treatment.Results: Mean serum TSH levels at baseline, 3rd and 6th months of treatment were 1.57 ± 0.67, 2.07 ± 0.88 and 2.25 ± 0.86 uIU/mL, respectively. Mean serum TSH levels increased significantly following isotretinoin therapy (p < 0.01, p = 0.007 and p < 0.01, respectively). Mean serum fT3 levels at baseline, 3rd and 6th months of treatment were 3.59 ± 0.57, 3.19 ± 0.45 and 3.09 ± 0.61 pmol/L, respectively. Mean serum fT4 levels at baseline, 3rd and 6th months of treatment were 1.21 ± 0.19, 1.09 ± 0.16 and 1.11 ± 0.19 pmol/L, respectively. Mean serum fT3 and fT4 levels decreased significantly at 3rd and 6th months compared to baseline levels (p < 0.01 and p < 0.01, p < 0.01 and p = 0.001, respectively).Conclusion: Systemic isotretinoin therapy causes significant alterations in sTFTs. Dose dependent or long-term effects of systemic isotretinoin on sTFTs needs further evaluation.

Is there an association between subclinical hypothyroidism and preterm uterine contractions? A prospective observational study*

Objective: To investigate the association between subclinical hypothyroidism and preterm contractions. Methods: Prospective observational study among women at 23 + 0/7 and 34 + 6/7 weeks of gestation, with no known thyroid function abnormality, and preterm uterine contractions (PTC). All patients underwent laboratory evaluation of Thyroid Stimulating Hormone (TSH) and Free Thyroxin (FT4). Patients with and without PTC were compared. Results: No association was found between PTC and subclinical hypothyroidism. Rate of spontaneous preterm delivery (PTD) was comparable between women with abnormal and normal thyroid function tests. Excluding indicated PTD, patients in the study group had a higher rate of spontaneous PTD (24.7% versus 9.6%, p = 0.03). Patients with past PTD and preterm contractions had higher rates of hypothyroxinemia compared with patients without past PTD (54.6% versus 19.0% and 31.2%, p = 0.001), and patients with past PTD (regardless of the presence or absence of PTC) had higher rate of subclinical hypothyroidism compared with patients with PTC and without PTD (59.1% and 66.7% versus 31.6%, p = 0.017). Conclusions: No association was found between PTC and subclinical hypothyroidism in the entire cohort, except for patients with preterm contractions and a history of past PTD. This specific group of patients might benefit from thyroid function evaluation.