Equine Hypothyroidism Study Guide

Overview and Clinical Importance

Hypothyroidism in horses is one of the most commonly diagnosed yet frequently misunderstood endocrine conditions in equine practice. True primary hypothyroidism is extremely rare in adult horses, with the most clinically significant presentations occurring in neonatal foals as congenital hypothyroidism and dysmaturity syndrome (CHD). This topic is critically important for the NAVLE because veterinarians must distinguish between true thyroid dysfunction and the far more common scenario of low thyroid hormone levels secondary to nonthyroidal illness syndrome (NTIS), also known as euthyroid sick syndrome.

Understanding the hypothalamic-pituitary-thyroid (HPT) axis and factors that influence thyroid hormone concentrations is essential for accurate diagnosis and appropriate clinical decision-making. The traditional clinical picture of an obese, laminitic horse being hypothyroid has been largely debunked, with these horses now recognized as suffering from equine metabolic syndrome (EMS) or pituitary pars intermedia dysfunction (PPID).

Thyroid Gland Anatomy and Physiology

Anatomical Location

The equine thyroid gland is a bilobed endocrine organ located dorsal to the trachea, just distal to the larynx. Each lobe measures approximately 2.5 cm × 2.5 cm × 5 cm and the total gland weighs approximately 0.04 g/kg body weight. The thyroid is not readily visible or palpable in normal horses, although it may become visible with aging or pathological enlargement (goiter).

Thyroid Hormone Synthesis

The thyroid gland is composed of follicles lined by cuboidal to columnar epithelial cells (thyrocytes) that produce thyroglobulin, a glycoprotein containing tyrosine residues. Thyroid hormone synthesis requires iodine, which is concentrated in the gland, oxidized, and bound to tyrosine to form monoiodotyrosine (MIT) and diiodotyrosine (DIT). Coupling of these molecules produces:

• Triiodothyronine (T3): One MIT + One DIT; the biologically active hormone
• Thyroxine (T4): Two DIT molecules; the primary secretory product, converted to T3 in peripheral tissues

Selenium is essential for the deiodinase enzymes that convert T4 to the active T3 in peripheral tissues. Selenium deficiency impairs this conversion and can contribute to low T3 states.

The Hypothalamic-Pituitary-Thyroid (HPT) Axis

Thyroid hormone production is regulated by a classic negative feedback loop. The hypothalamus releases thyrotropin-releasing hormone (TRH), which stimulates the anterior pituitary to secrete thyroid-stimulating hormone (TSH). TSH then stimulates the thyroid gland to produce and release T3 and T4. Elevated thyroid hormones exert negative feedback on both the hypothalamus and pituitary to suppress TRH and TSH release.

HPT Axis Components and Functions

Classification of Hypothyroidism

Hypothyroidism can be classified based on the level of the HPT axis affected:

Congenital Hypothyroidism and Dysmaturity Syndrome (CHD)

CHD is the most clinically significant form of hypothyroidism in horses, first described in western Canada in 1981. It remains an important cause of foal mortality and is now recognized in the United States, Australia, South America, and Europe.

Etiology and Risk Factors

CHD results from thyroid hormone deficiency during late gestation, leading to developmental abnormalities. Key risk factors include:

• Iodine deficiency or excess: Inadequate iodine intake or excessive kelp/seaweed supplementation in pregnant mares
• Dietary nitrates: High nitrate forage inhibits iodide uptake by the thyroid; mares fed greenfeed have 13.1× greater odds of affected foals
• Goitrogenic plants: Brassica species (mustard, cabbage) contain glucosinolates that interfere with thyroid function
• Selenium deficiency: Impairs T4 to T3 conversion and thyroid antioxidant protection
• Irrigated pastures: Associated with approximately 15× greater odds of affected foals
• No mineral supplementation: 5.6× greater odds of producing affected foal

Clinical Signs of CHD in Foals

Affected foals typically have prolonged gestation (average 357.6 days vs. 338.9 days in controls) yet appear dysmature:

Diagnosis of Equine Hypothyroidism

Diagnostic Approach Overview

Definitive diagnosis of primary hypothyroidism requires demonstration of inadequate thyroid gland response to stimulation. Low resting thyroid hormone concentrations alone are NOT diagnostic because numerous nonthyroidal factors affect these values.

Baseline Thyroid Hormone Testing

Important: Neonatal foals have thyroid hormone concentrations 5 to 10 times higher than adult horses. This high level is necessary for normal organ development and maturation.

TRH Stimulation Test

The TRH stimulation test is the gold standard for evaluating the entire HPT axis and confirming a diagnosis of hypothyroidism.

TRH Stimulation Test Protocol

• Collect baseline blood sample for T3 and T4
• Administer TRH intravenously: 1 mg for adult horses or 0.5 mg for ponies/miniature horses
• Collect blood at 2 hours post-injection for T3 measurement
• Collect blood at 4-6 hours post-injection for T4 measurement

Expected Response (Euthyroid): At least a doubling (greater than or equal to 2× baseline) of both T3 and T4 concentrations

Hypothyroid Response: Failure of T3 and T4 to increase adequately (fold change less than 2×)

Side Effects: Transient coughing, muscle fasciculations, and Flehmen response may occur but resolve within minutes without treatment

Diagnosis of CHD in Foals

Diagnosis of CHD is primarily based on clinical presentation and imaging findings:

• Clinical signs: Prolonged gestation, weakness, musculoskeletal abnormalities, possible goiter
• Radiography: Dorsopalmar and lateromedial views of carpus and tarsus to assess cuboidal bone ossification
• Skeletal Ossification Index (SOI): Grades 1-4 based on cuboidal bone development
• Thyroid biopsy: Demonstrates thyroid hyperplasia (definitive but rarely performed clinically)

Skeletal Ossification Index (SOI) Grading

Nonthyroidal Illness Syndrome (NTIS)

NTIS (also called euthyroid sick syndrome) is the most common cause of low thyroid hormone concentrations in adult horses. It represents a normal physiological response to illness, NOT true thyroid dysfunction.

Causes of Low Thyroid Hormones Without True Hypothyroidism

Pattern of Hormone Changes in NTIS: T3 decreases first, followed by T4 and fT4D with increasing illness severity. TSH fails to increase proportionally, indicating HPT axis dysregulation rather than primary thyroid failure.

Differentiating Hypothyroidism from EMS and PPID

The clinical signs historically attributed to hypothyroidism (obesity, regional adiposity, laminitis, poor fertility) have been clearly shown NOT to develop in experimentally thyroidectomized horses. These signs are now recognized as features of EMS and PPID.

Exam Focus: An overweight horse with a cresty neck and recurrent laminitis does NOT have hypothyroidism - think EMS! The traditional association of these signs with hypothyroidism has been disproven.

Treatment of Equine Hypothyroidism

Levothyroxine Sodium Supplementation

Treatment of confirmed hypothyroidism involves thyroid hormone replacement therapy with levothyroxine sodium (L-T4), a synthetic form of T4.

Contraindications and Precautions

• Use with caution in horses with cardiac disease, hypertension, or diabetes
• Not approved for use in pregnant mares but appears clinically safe
• Monitor for signs of hyperthyroidism: tachycardia, weight loss, nervousness, excessive sweating
• High doses associated with atrial fibrillation risk

Treatment of CHD in Foals

Treatment for CHD is primarily supportive as thyroid hormone supplementation does NOT reverse the musculoskeletal abnormalities:

• Exercise restriction: Essential to prevent collapse of poorly ossified cuboidal bones
• Splinting: Lightweight splints to prevent knuckling and support limbs; monitor closely for rub sores
• Pain management: As appropriate for comfort
• Nursing support: Assist weak foals to stand and nurse
• Prognosis: POOR for life and long-term soundness; many foals are euthanized within days of birth

Prevention of CHD

• Ensure adequate iodine: NRC recommends 0.35 mg/kg DM daily for pregnant mares; avoid excess from kelp
• Test forage for nitrates: Especially greenfeed and irrigated pastures
• Avoid goitrogenic plants: Remove Brassica species (mustard, cabbage) from pastures
• Ensure adequate selenium: Especially in selenium-deficient regions
• Provide mineral supplementation: To pregnant mares throughout gestation

Memory Aids for the NAVLE

CHD Foal Findings: "FOAL GROWS"

• Flexural deformities
• Ossification incomplete (cuboidal bones)
• Abnormal gestation (prolonged)
• Lethargy and weakness
• Goiter (may be present)
• Ruptured extensor tendons
• Overbite (mandibular prognathism)
• Weak suck reflex
• Sparse hair coat

NTIS Triggers: "PENS FASTING"

• Phenylbutazone
• Exercise (strenuous)
• NSAIDs
• Steroids (glucocorticoids)
• Fasting
• Any systemic illness
• Sulfonamides (TMS)
• Transport stress
• Infection
• Nutritional changes
• Gestation (pregnancy)