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Frontiers in Endocrinology 2023Published data on the relationship between polycystic ovary syndrome (PCOS) and thyroid dysfunction are sparse and confusing. (Review)
Review
BACKGROUND
Published data on the relationship between polycystic ovary syndrome (PCOS) and thyroid dysfunction are sparse and confusing.
OBJECTIVE
To comprehensively review data available in the literature regarding the relationship between PCOS and the thyroid function, and its abnormalities.
METHODS
Nine main areas of interest were identified and analyzed according to the available evidence: 1) Evaluation of thyroid function for PCOS diagnosis; 2) Epidemiology data on thyroid function/disorders in patients with PCOS, and vice versa; 3) Experimental data supporting the relationship between thyroid function/disorders and PCOS; 4) Effects of thyroid function/disorders on PCOS features, and vice versa; 5) Effect of thyroid alterations on the cardiometabolic risk in women with PCOS; 6) Effect of thyroid abnormalities on reproductive outcomes in women with PCOS; 7) Relationship between thyroid function/abnormalities in patients with PCOS who are undergoing fertility treatment; 8) Effect of treatments for thyroid diseases on PCOS; and 9) Effect of treatments for PCOS on thyroid function. An extensive literature search for specific keywords was performed for articles published from 1970 to March 2023 using PubMed and Web of Science. Data were reported in a narrative fashion.
RESULTS
PCOS is a diagnosis of exclusion for which diagnosis is possible only after excluding disorders that mimic the PCOS phenotype, including thyroid dysfunctions. However, the tests and the cutoff values used for this are not specified. Many experimental and clinical data suggest a relationship between perturbations of the thyroid function and PCOS. Direct and unequivocal evidence on the effects of thyroid function/disorders on PCOS features are lacking. High thyroid-stimulating hormone levels and subclinical hypothyroidism may be associated with significant worsening of several intermediate endpoints of cardiometabolic risk in women with PCOS. Thyroid abnormalities may worsen reproductive outcomes, especially in patients undergoing fertility treatment. To date, there are no data demonstrating the efficacy of thyroid medications on fertility and cardiometabolic risk in women with PCOS. Lifestyle modification changes, metformin, and vitamin D seem to improve thyroid function in the general population.
CONCLUSION
PCOS and thyroid disorders are closely related, and their coexistence may identify patients with a higher reproductive and metabolic risk. Regular screening for thyroid function and thyroid-specific autoantibodies in women with PCOS, particularly before and during pregnancy, is highly recommended.
Topics: Female; Humans; Pregnancy; Polycystic Ovary Syndrome; Thyroid Diseases; Hypothyroidism; Thyroid Dysgenesis; Antibodies; Cardiovascular Diseases
PubMed: 37635968
DOI: 10.3389/fendo.2023.1251866 -
QJM : Monthly Journal of the... Jul 2023
Topics: Humans; Thyroid Dysgenesis; Ultrasonography
PubMed: 37021964
DOI: 10.1093/qjmed/hcad054 -
Borealin/CDCA8 deficiency alters thyroid development and results in papillary tumor-like structures.Frontiers in Endocrinology 2023/ mutations are associated with congenital hypothyroidism and thyroid dysgenesis. Borealin is involved in mitosis as part of the Chromosomal Passenger Complex. Although...
BACKGROUND
/ mutations are associated with congenital hypothyroidism and thyroid dysgenesis. Borealin is involved in mitosis as part of the Chromosomal Passenger Complex. Although mutations decrease thyrocyte adhesion and migration, little is known about the specific role of Borealin in the thyroid.
METHODS
We characterized thyroid development and function in Borealin-deficient ( ) mice using histology, transcriptomic analysis, and quantitative PCR.
RESULTS
Thyroid development was impaired with a hyperplastic anlage on embryonic day E9.5 followed by thyroid hypoplasia from E11.5 onward. Adult mice exhibited euthyroid goiter and defect in thyroid hormone synthesis. aged mice had disorganized follicles and papillary-like structures in thyroids due to ERK pathway activation and a strong increase of -like genes described by The Cancer Genome Atlas (TCGA) network of papillary thyroid carcinoma. Moreover, thyroids exhibited structural and transcriptomic similarities with papillary thyroid carcinoma tissue from a human patient harboring a mutation, suggesting a role in thyroid tumor susceptibility.
CONCLUSION
These findings demonstrate Borealin involvement in critical steps of thyroid structural development and function throughout life. They support a role for Borealin in thyroid dysgenesis with congenital hypothyroidism. Close monitoring for thyroid cancer seems warranted in patients carrying mutations.
Topics: Animals; Mice; Cell Cycle Proteins; Congenital Hypothyroidism; Thyroid Cancer, Papillary; Thyroid Dysgenesis; Thyroid Neoplasms
PubMed: 37964961
DOI: 10.3389/fendo.2023.1286747 -
Annals of Medicine and Surgery (2012) Jun 2023The pancreas develops from a small ventral bud and a larger dorsal bud. During the rotation of the foregut, the ventral pancreas rotates toward the dorsal pancreas and...
UNLABELLED
The pancreas develops from a small ventral bud and a larger dorsal bud. During the rotation of the foregut, the ventral pancreas rotates toward the dorsal pancreas and joins together to form a complete pancreas with ducts. Among the various developmental congenital anomalies, dorsal pancreatic agenesis is one of the rare entities, with less than a hundred cases reported so far. It involves the absence of the dorsal bud derivatives (head, body, and tail).
CASE PRESENTATION
Herein, we present a case of a 50-year-old woman who presented to general outpatient department with a complaint of abdominal pain. The patient was diagnosed with cholelithiasis with a contrast-enhanced computed tomography finding of dorsal pancreatic agenesis on a detailed workup. However, the patient did not have any other associated anomalies or symptoms associated with dorsal pancreatic agenesis. The patient was managed for cholelithiasis with laparoscopic cholecystectomy.
CLINICAL DISCUSSION
Failure in development due to aberrant embryogenesis may cause partial or complete agenesis of the dorsal pancreas. The minor papilla, the accessory pancreatic duct, the body, and the tail of the pancreas are not present in the case of complete dorsal agenesis. Most cases of dorsal pancreatic agenesis are asymptomatic and diagnosed incidentally, whereas some of the cases may present with other associated abnormalities. It is almost always diagnosed via imaging modalities.
CONCLUSION
Dorsal pancreatic agenesis is a very rare congenital anomaly of the pancreas. It can be diagnosed via various imaging modalities and almost always remains a radiological diagnosis with incidental findings.
PubMed: 37363558
DOI: 10.1097/MS9.0000000000000136 -
Medicina (Kaunas, Lithuania) Oct 2023Congenital hypothyroidism (CH) may have major detrimental effects on growth and neurological development, but early intervention leads to excellent outcomes. CH is...
Congenital hypothyroidism (CH) may have major detrimental effects on growth and neurological development, but early intervention leads to excellent outcomes. CH is classified as transient or permanent, primary or secondary, with primary CH being the most common neonatal endocrine disorder. Most patients with CH do not present any typical signs and symptoms of hypothyroidism shortly after birth, partly due to transplacental maternal thyroid hormone transfer and residual neonatal thyroid function. This paper reports on two CH cases. During the initial Neonatal Intensive Care Unit (NICU) admission phase, CH was not suspected due to nonspecific signs. The distinct characteristics of our cases are as follows: both infants were admitted to the NICU for respiratory distress syndrome, requiring invasive mechanical ventilation, and both were born to diabetic mothers. Following extubation, they both showed similar neurological issues, including reduced muscle tone and feeding difficulties. Initially, those symptoms were attributed to delayed clearance of analgesic and sedative medication. However, symptoms progressively worsened over time. Subsequent tests revealed both meeting CH diagnostic criteria: an unusual ultrasound indicating thyroid agenesis and abnormal hormone levels. Guided by the pediatric endocrinology team, prompt hormonal treatment was started with improvements in neurocognitive function and feeding. Usually, CH screening involves blood samples from healthy newborns at 2-3 days of life. Abnormal results require confirmation, prompting treatment within two weeks. Certain NICU-admitted infants face higher diagnosis delays, as seen in those two cases where CH screening was postponed. Thus, for all neonates with persistent pathologies unresponsive to standard etiological treatment, conducting a comprehensive anamnestic evaluation of the medical history, along with maternal preconceptional and prenatal nutrition, is recommended.
Topics: Infant; Pregnancy; Female; Humans; Infant, Newborn; Child; Congenital Hypothyroidism; Neonatal Screening; Thyroid Dysgenesis; Thyrotropin; Thyroxine
PubMed: 37893606
DOI: 10.3390/medicina59101887 -
Research Square Jul 2023Loss of GLI-Similar 3 (GLIS3) function in mice and humans causes congenital hypothyroidism (CH). In this study, we demonstrate that GLIS3 protein is first detectable at...
Loss of GLI-Similar 3 (GLIS3) function in mice and humans causes congenital hypothyroidism (CH). In this study, we demonstrate that GLIS3 protein is first detectable at E15.5 of murine thyroid development, a time when GLIS3 target genes, such as become also expressed. We further show that mice do not display any major changes in prenatal thyroid gland morphology indicating that CH in KO mice is due to dyshormonogenesis rather than thyroid dysgenesis. Analysis of thyroid-specific knockout (-Pax8Cre) mice fed either a normal or low-iodine diet (ND or LID) revealed that, in contrast to ubiquitous mice, thyroid follicular cell proliferation and the expression of cell cycle genes were not repressed suggesting that the inhibition of thyroid follicular cell proliferation in ubiquitous KO mice is related to loss of GLIS3 function in other cell types. However, the expression of several thyroid hormone biosynthesis-, extracellular matrix (ECM)-, and inflammation-related genes was still suppressed in -Pax8Cre mice particularly under conditions of high blood levels of thyroid stimulating hormone (TSH). We further demonstrate that treatment with TSH, protein kinase A (PKA) or adenylyl cyclase activators or expression of constitutively active PKA enhances GLIS3 protein and activity, suggesting that GLIS3 transcriptional activity is regulated in part by TSH/TSHR-mediated activation of the PKA pathway. This mechanism of regulation provides an explanation for the dramatic increase in GLIS3 protein expression and the subsequent induction of GLIS3 target genes, including several thyroid hormone biosynthetic genes, in thyroid follicular cells of mice fed a LID.
PubMed: 37461635
DOI: 10.21203/rs.3.rs-3044388/v1 -
Nature Communications Dec 2023The pathogenesis of thyroid dysgenesis (TD) is not well understood. Here, using a combination of single-cell RNA and spatial transcriptome sequencing, we identify a...
The pathogenesis of thyroid dysgenesis (TD) is not well understood. Here, using a combination of single-cell RNA and spatial transcriptome sequencing, we identify a subgroup of NF-κB-activated thyrocytes located at the center of thyroid tissues in postnatal mice, which maintained a partially mesenchymal phenotype. These cells actively protruded out of the thyroid primordium and generated new follicles in zebrafish embryos through continuous tracing. Suppressing NF-κB signaling affected thyrocyte migration and follicle formation, leading to a TD-like phenotype in both mice and zebrafish. Interestingly, during thyroid folliculogenesis, myeloid cells played a crucial role in promoting thyrocyte migration by maintaining close contact and secreting TNF-α. We found that cebpa mutant zebrafish, in which all myeloid cells were depleted, exhibited thyrocyte migration defects. Taken together, our results suggest that myeloid-derived TNF-α-induced NF-κB activation plays a critical role in promoting the migration of vertebrate thyrocytes for follicle generation.
Topics: Animals; Mice; Myeloid Cells; NF-kappa B; Thyroid Epithelial Cells; Tumor Necrosis Factor-alpha; Zebrafish
PubMed: 38057310
DOI: 10.1038/s41467-023-43895-8