Thyroid autoimmunity and miscarriages: the corpus luteum hypothesis.

Area of Science:

• Reproductive Immunology
• Endocrinology
• Autoimmunity

Background:

• The link between first-trimester spontaneous miscarriages and thyroid autoimmunity is not fully understood.
• Glycoprotein hormone receptors share structural similarities, suggesting potential cross-reactivity.
• Thyrotropic action of human chorionic gonadotropin (hCG) and precocious puberty in juvenile hypothyroidism hint at receptor cross-reactivity.

Purpose of the Study:

• To propose a mechanism explaining how thyroid autoimmunity might lead to spontaneous miscarriages.
• To investigate the potential cross-reactivity between thyroid-stimulating hormone (TSH) and luteinizing hormone/chorionic gonadotropin receptors (LH/CG-R).
• To explore the role of TSH-receptor blocking autoantibodies in early pregnancy loss.

Main Methods:

• Hypothetical model based on structural similarities of glycoprotein hormone receptors.
• Analysis of cross-reactivity between TSH and LH/CG-R.
• Postulation of TSH-receptor blocking autoantibodies binding to LH/CG-R.

Main Results:

• Hypothesized that TSH-receptor blocking autoantibodies could bind and block LH/CG-R in the corpus luteum.
• This blockade may inhibit steroid hormone production essential for early pregnancy support.
• Proposed mechanism links thyroid autoimmunity to decreased progesterone levels and spontaneous miscarriage.

Conclusions:

• Thyroid autoimmunity may contribute to first-trimester spontaneous miscarriages via LH/CG-R blockade.
• This hypothesis offers a potential explanation for the observed association.
• Further research could lead to early detection of high-risk pregnancies and clarify progesterone's role in miscarriage prevention.