Equis ISSN 2398-2977

Endocrine: hypothyroidism

Contributor(s): Graham Munroe, Ramiro Toribio, Han van der Kolk

Introduction

  • Hypothyroidism is defined as a deficiency of thyroid hormones, a deficient thyroid gland activity, or as a disruption in the hypothalamus-pituitary-thyroid axis.
  • Hypothyroidism occurs from diseases that affect thyroid function, from compounds that interfere with TH synthesis, and less frequently by disorders of the hypothalamus or pituitary gland.
  • The clinical presentation is the result of the actions of TH on cell differentiation and metabolic rate regulation.
  • This endocrine abnormality is uncommon in horses.
  • Cause: there are 3 types of hypothyroidism:
    • Primary - thyroid gland hypothyroidism
    • Secondary - hypothalamus-pituitary dysfunction.
    • Tertiary - target organ refractoriness to thyroid hormones.
  • Signs:
    • Foals: either weak/dysmature or musculoskeletal abnormalities.
    • Adults: skin lesions, exercise intolerance, laminitis, infertility and lethargy/poor performance, obesity.
  • Diagnosis: ancillary tests including measurement of T3   Endocrine: T3 assay  and T4   Endocrine: T4 assay  levels and response to TSH   Endocrine: TSH stimulation test - thyroid function  /TRH   Endocrine: TRH stimulation test - thyroid function  stimulation tests; diet analysis and radiographic evaluation in foals with musculoskeletal abnormalities. Clinical history is important in foals.
  • Treatment: involves dietary supplementation with iodide.
  • Prognosis:
    • Foals: poor.
    • Adults: guarded to good depending on the cause.
  • Important note:
    • Low thyroid hormone concentrationsper sedoes not mean hypothyroidism.
    • Functional tests are required to assess thyroid gland function.
    • Several drugs of veterinary use decrease thyroid hormone concentrations to cause a pseudohypothyroidism (phenylbutazone, dexamethasone).
    • Many non-thyroidal diseases decrease thyroid hormones but this does not mean hypothyroidism.
    • Low thyroid hormones during disease = Euthyroid Sick Syndrome.

Pathogenesis

Etiology

  • A specific cause is often not identified.

Primary

  • Inadequate production from thyroid gland of thyroxine (T4) or tri-iodothyronine (T3).
  • Iodine deficiency or excess intake in the diet of the individual or dam.
  • Ingestion of goitrogenic compounds, eg nitrates, that block thyroid hormone synthesis.
  • Neoplasia   Thyroid gland: adenoma  .
  • Thyroiditis.
  • Biochemical defects in thyroid hormone synthesis.
  • Thyroid agenesis.

Secondary

  • Hypothalamic or pituitary dysfunction that   →   inadequate thyrotropin release hormone (TRH)   →    inadequate thyroid-stimulating hormone (TSH   Endocrine: TSH stimulation test - thyroid function  ) release   →    thyroid gland dysfunction follicular cell atrophy.

Tertiary

  • Defect in thyroid hormone utilization at the peripheral tissues (not described in horses).
  • It has been proposed that phenylbutazone   Phenylbutazone  administration, high-energy   Nutrition: energy  or high-protein   Nutrition: protein  diets, diets high in zinc or copper   Nutrition: minerals  , glucocorticoid administration, food deprivation, ingestion of endophyte-infected fescue grass   Toxicity: fescue grass  , interfere with thyroid hormone conversion and actions at the target sites.

Pathophysiology

  • Loss of thyroid tissue or suppression of function.
  • Two separate entities because of differing actions of thyroid hormone on cell differentiation, growth and metabolic rate regulation.
  • Primary, secondary or tertiary hypothyroidism.

Foal

  • Decreased thyroid function in the developing fetus and foal due to inadequate or excessive iodine intake (iodine-containing drugs/solutions or ingestion of goitrogenic plants/iodide preparations) by the mare.
  • There is also evidence that forages rich in nitrates can impair thyroid gland function. Fescue plants are also commonly infected by an endophytic fungus (Neotyphodium coenophialum) that can alter thyroid function, particularly in pregnant mares and their foals.
  • T4 is transported transplacentally and via the milk. The placenta is permeable to many plant goitrogens and to iodide.
  • Congenital goiter may occur.
  • The dam may or may not be affected.
  • Differentiation of the nervous system and growth of the musculoskeletal system may be affected by ameliogenesis and epiphyseal dysgenesis.
  • Thyroid hormones are required for the biochemical maturation, hypertrophy and capillary penetration of growing cartilage. Indirect effects on chondrogenesis may occur via T3 stimulating growth hormone secretion/production.
  • Thyroxine may also play a role in the maturation of the lungs and in surfactant production.
  • Chances of recovery are unlikely once critical developmental stages are passed.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Koikkalainen K et al (2014) Congenital hypothyroidism and dysmaturity syndrome in foals: First reported cases in Europe. Equine Vet Educ 26 (4), 181-189.
  • Allen A L (2014) Congenital hypothyroidism in horses: Looking back and looking ahead. Equine Vet Educ 26 (4), 190-193.
  • Breuhaus B A (2003) Thyroid function in mature horses ingesting endophyte-infected fescue seed. JAVMA 223, 340-345 PubMed.
  • Breuhaus B A (2002) Thyroid-stimulating hormone in adult euthyroid and hypothyroid horses. J Vet Intern Med 16, 109-115 PubMed.
  • Allen A L, Townsend H G, Doige C E & Fretz P B (1996) A case-control study of the congenital hypothyroidism and dysmaturity syndrome of foals. Can Vet J 37, 354-358 PubMed.
  • Harris P, Marlin D & Gray J (1992) Equine thyroid function tests - a preliminary investigation. Br Vet J 148, 71-80 PubMed.
  • Irvine C H G (1984) Hypothyroidism in the foal. Equine Vet J 16, 302-306 PubMed.

Other sources of information

  • Toribio R E & Duckett W M (2004) Thyroid Gland. In: Equine Internal Medicine. Eds: Reed S M, Bayly W M, & Sellon D C. 2nd edn. Saunders, USA. pp 1340-1356.


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