HASHIMOTO THYROIDITIS

✓ Medically ReviewedDISEASEID: MDBT0288🚨 TRIAGE: URGENTICD-10: E06.3

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Definition

CLINICAL DEFINITION

Hashimoto thyroiditis is a chronic autoimmune inflammation of the thyroid gland characterised by lymphocytic infiltration and the presence of circulating autoantibodies directed against thyroid peroxidase (TPO) and, less commonly, thyroglobulin (Tg). The disease produces a spectrum of functional outcomes, ranging from euthyroidism to subclinical or overt hypothyroidism, and may be associated with either a diffuse goitre or glandular atrophy. Diagnosis is established by the combination of a diffusely enlarged, firm thyroid, elevated titres of TPO antibodies, and biochemical evidence of thyroid dysfunction when present.

IN PLAIN ENGLISH

Hashimoto thyroiditis is a condition where the body's immune system mistakenly attacks the thyroid gland, a butterfly-shaped organ in the neck that controls metabolism. Over time, this attack can damage the gland and reduce its ability to produce thyroid hormones, leading to symptoms such as fatigue, weight gain, and feeling cold.

COMMON MISCONCEPTION / WHAT IT DOES NOT MEAN

Hashimoto thyroiditis is NOT simply 'hypothyroidism'; it is a specific autoimmune disease that is the most common cause of hypothyroidism in iodine-sufficient regions, but many individuals with Hashimoto thyroiditis remain euthyroid or have only subclinical dysfunction for years. It is also NOT Graves disease, although both are autoimmune thyroid disorders and rare transitions between the two can occur.

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Word Breakdown

Hashimoto

=Named after the Japanese physician Haruto Hashimoto (also rendered Hakaru Hashimoto), who first described the condition in 1912 as 'struma lymphomatosa'

-itis

=inflammation (from Greek '-itis')

Literal Meaning: Inflammation of the thyroid gland as described by Hashimoto

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Abbreviations

HT=Hashimoto Thyroiditis — the standard clinical abbreviation

TPOAb=Thyroid Peroxidase Antibody — the most sensitive diagnostic marker for HT

TgAb=Thyroglobulin Antibody — a second thyroid autoantibody commonly tested in HT

LT4=Levothyroxine — the first-line hormone replacement therapy for HT-related hypothyroidism

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Synonyms & Variants

Chronic Autoimmune Thyroiditis›Chronic Lymphocytic Thyroiditis›Autoimmune Thyroiditis›

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Category-Specific Context

Hashimoto thyroiditis is a Disease in the Medobo classification because it is a defined pathological condition with recognised diagnostic criteria (thyroid autoantibodies, lymphocytic infiltration, and functional thyroid status) and a well-characterised clinical spectrum from euthyroidism through subclinical to overt hypothyroidism. It is the most common cause of hypothyroidism in iodine-sufficient regions and is frequently associated with other autoimmune disorders, underscoring its systemic context.

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Clinical Context & Usage

CLINICAL SETTINGS

Endocrinology Outpatient ClinicGeneral Medicine WardPrimary Care ClinicObstetrics and Antenatal ClinicPaediatric Endocrinology ClinicEmergency Department (for myxedema coma)

USAGE & DOCUMENTATION NOTES

In clinical documentation, Hashimoto thyroiditis is often abbreviated as HT. Notes typically record the thyroid function status (euthyroid, subclinical hypothyroid, or overt hypothyroid), the titre of TPO antibodies, and the presence or absence of goitre. A common phrase is 'TPO antibody–positive Hashimoto thyroiditis with subclinical hypothyroidism.' When treatment is initiated, the note documents the levothyroxine dose and the TSH target. Referral letters often emphasise the need for monitoring of thyroid function, especially during pregnancy or when symptoms persist despite normal TSH.

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Primary Causes & Pathophysiology

PATHOPHYSIOLOGY

Hashimoto thyroiditis arises from a loss of immune self-tolerance to thyroid antigens, driven by a combination of genetic susceptibility and environmental triggers. Defective regulatory T-cell (Treg) function and increased Th17 proinflammatory activity permit autoreactive CD4+ T cells to activate B cells, leading to the production of polyclonal antibodies against thyroid peroxidase (TPO) and thyroglobulin (Tg). Cytotoxic CD8+ T cells and antibody-dependent cell-mediated cytotoxicity then mediate progressive destruction of thyroid follicular cells, producing lymphocytic infiltration and fibrosis. As follicular cells are lost, thyroid hormone synthesis declines, and TSH rises in compensation; this may maintain euthyroidism for a period before subclinical and then overt hypothyroidism develop. Some individuals experience a transient thyrotoxic phase (hashitoxicosis) due to release of preformed hormone from destroyed follicles.

PRIMARY CAUSES

Genetic susceptibility (HLA and immune-regulatory gene polymorphisms)

Inherited variants in HLA, CTLA-4, PTPN22, CD40, FoxP3, and thyroid-specific genes (TSH receptor, thyroglobulin) lower the threshold for loss of self-tolerance to thyroid antigens; twin studies indicate that genetic factors account for approximately 70–80% of liability.

Environmental triggers (excess iodine intake, selenium or vitamin D deficiency, infections)

Chronic excess iodine increases the immunogenicity of thyroglobulin; low selenium and vitamin D may impair antioxidant and immunomodulatory defences; infections may provoke autoimmunity in genetically susceptible individuals.

Female sex and reproductive hormonal factors

The markedly higher prevalence in women (female-to-male ratio approximately 7–10:1) implicates oestrogen-related immune modulation and X-chromosome–linked immune regulation, although the precise mechanisms are incompletely defined.

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Epidemiology

Prevalence:The global prevalence of Hashimoto thyroiditis is estimated at approximately 7.5%, with higher estimates (10–12%) in some general-population cohorts; it is the most common autoimmune disease and the most common cause of hypothyroidism in iodine-sufficient regions. Thyroid antibody positivity is present in roughly 5–20% of the general population, and TPO antibodies are found in 5–14% of pregnant individuals.

Age Group:Hashimoto thyroiditis can occur at any age but most commonly presents in middle-aged adults, with peak incidence between 45 and 55 years in many series; it may also present in children and adolescents, and the prevalence increases with advancing age.

Sex Predilection:Female

Geographic Distribution:Hashimoto thyroiditis is more prevalent in populations with adequate or excessive iodine intake and is less common in areas of severe iodine deficiency; prevalence is highest in White populations and lowest in Black populations, and the incidence is higher in countries with lower iodine-deficiency prevalence.

Red Flags & Triage ★

TRIAGE LEVEL

🚨 URGENT

DO NOT MISS — LIFE-THREATENING PRESENTATIONS

A rapidly enlarging, hard, fixed thyroid mass in a patient with longstanding Hashimoto thyroiditis raises concern for primary thyroid lymphoma and requires urgent specialist evaluation with fine-needle aspiration or core biopsy.
Severe hypothyroidism with altered mental status, hypothermia, bradycardia, or hypotension should prompt immediate evaluation for myxedema coma, which is a medical emergency requiring intensive care and parenteral thyroid hormone replacement.

URGENT EVALUATION TRIGGERS

Altered mental status, stupor, or coma in a patient with known or suspected hypothyroidism (possible myxedema coma).
Rapidly enlarging neck mass with stridor, dysphagia, or hoarseness (possible compressive goitre or thyroid lymphoma).
Severe bradycardia, hypotension, or hypothermia in a patient with hypothyroid features.
New-onset severe heart failure or pericardial effusion in a patient with untreated hypothyroidism.

Contraindications & Precautions

SPECIAL PRECAUTIONS

Monitor TSH and free T4 at appropriate intervals after initiating or adjusting levothyroxine
and avoid over-replacement
which can cause iatrogenic thyrotoxicosis
atrial fibrillation
and accelerated bone loss.
In pregnancy
thyroid function should be monitored each trimester (or more frequently) because levothyroxine requirements commonly increase and untreated maternal hypothyroidism carries risks to both mother and fetus.
Before treating subclinical hypothyroidism
confirm the persistence of TSH elevation on a repeat sample and consider the patient's age
symptoms
cardiovascular risk
and pregnancy status
as not all cases benefit from therapy.
Be alert to the possibility of coexisting autoimmune conditions (e.g.
coeliac disease
Addison disease
type 1 diabetes) when patients present with unexplained symptoms or poor response to standard therapy.

Complications

DOWNSTREAM CLINICAL COMPLICATIONS

Overt hypothyroidism — progressive thyroid destruction leads to deficient thyroid hormone production
causing fatigue
weight gain
cold intolerance
bradycardia
and cognitive slowing.
Cardiovascular complications — untreated hypothyroidism is associated with diastolic hypertension
dyslipidaemia
accelerated atherosclerosis
pericardial effusion
and
in severe cases
heart failure.
Myxedema coma — a rare but life-threatening decompensation of severe hypothyroidism characterised by impaired consciousness
hypothermia
bradycardia
and hypoventilation
requiring emergency treatment.
Goitre-related compressive symptoms — a large goitre may cause dysphagia
dyspnoea
or hoarseness due to oesophageal or tracheal compression.
Association with other autoimmune diseases — Hashimoto thyroiditis is associated with coeliac disease
autoimmune gastritis
type 1 diabetes mellitus
Addison disease
vitiligo
and pernicious anaemia.
Rarely
thyroid lymphoma — chronic lymphocytic thyroiditis is a risk factor for primary thyroid lymphoma
although the absolute risk is very low.

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Confused With (LASA & DDx) ★

LEXICAL (LASA) — SIMILAR NAMES

Hashimoto disease

Often used interchangeably, but 'Hashimoto disease' can occasionally refer more broadly to the autoimmune process; Hashimoto thyroiditis specifies the thyroid-targeted chronic inflammatory disease.

Graves disease

Both are autoimmune thyroid diseases, but Graves disease causes hyperthyroidism via TSH-receptor–stimulating antibodies, whereas Hashimoto thyroiditis typically causes hypothyroidism through destructive thyroiditis.

CLINICAL DIFFERENTIAL DIAGNOSES (DDx)

Graves disease

Key Distinguishing Feature: Graves disease presents with thyrotoxicosis, diffusely increased thyroid uptake on scintigraphy, and TSH-receptor–stimulating antibodies; Hashimoto thyroiditis usually causes hypothyroidism or euthyroidism with TPO antibodies.

Subacute (De Quervain) thyroiditis

Key Distinguishing Feature: Subacute thyroiditis is painful, post-viral, and self-limited, with a tender goitre and suppressed uptake on scintigraphy during the thyrotoxic phase; Hashimoto thyroiditis is painless and chronic.

Postpartum thyroiditis

Key Distinguishing Feature: Postpartum thyroiditis occurs within 12 months of delivery, often has a biphasic course (thyrotoxic followed by hypothyroid), and commonly remits; Hashimoto thyroiditis is chronic and not pregnancy-restricted.

Iodine deficiency or excess

Key Distinguishing Feature: Iodine-related thyroid dysfunction is corrected by adjusting iodine intake; in Hashimoto thyroiditis, TPO antibodies are typically positive and thyroid autoimmunity is the primary driver.

Drug-induced hypothyroidism

Key Distinguishing Feature: Drugs such as amiodarone, lithium, or interferon can cause hypothyroidism, but TPO antibodies are often negative and the dysfunction may resolve after the offending agent is withdrawn; Hashimoto thyroiditis is autoimmune and chronic.

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Clinical Pearls

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TPO antibodies are the most sensitive serological marker for Hashimoto thyroiditis and are present in over 90% of patients; thyroglobulin antibodies are less sensitive (50–80%) but can be useful when TPO antibodies are negative.

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A transient thyrotoxic phase (hashitoxicosis) can occur early in the disease due to release of preformed thyroid hormone from damaged follicles; this should not be mistaken for Graves disease, and antithyroid drugs are not indicated.

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The decision to treat with levothyroxine should be based on thyroid function status and clinical context, not on antibody positivity alone; euthyroid antibody-positive individuals generally do not require therapy.

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Hashimoto thyroiditis is associated with other autoimmune conditions, so a high index of suspicion for coeliac disease, Addison disease, type 1 diabetes, and pernicious anaemia is warranted when patients have unexplained symptoms or poor response to treatment.

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In pregnancy, TPO antibody positivity increases the risk of miscarriage and preterm birth, and levothyroxine should be initiated or dose-adjusted when TSH is elevated above pregnancy-specific reference ranges.

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Example Usage & SOAP

CLINICAL SENTENCE

""The patient is a 42-year-old woman with a 6-month history of fatigue, weight gain, and cold intolerance, found to have a diffusely enlarged, firm, non-tender goitre and a TSH of 8.2 mIU/L with positive TPO antibodies, consistent with Hashimoto thyroiditis and subclinical hypothyroidism.""

IN A SOAP NOTE

S: 42-year-old woman reports fatigue, 5-kg weight gain, cold intolerance, and constipation over 6 months. O: Diffusely enlarged, firm, non-tender thyroid gland; no ophthalmopathy. TSH 8.2 mIU/L (reference 0.4–4.0), free T4 11.5 pmol/L (reference 9–19), TPO antibodies 450 IU/mL (strongly positive). A: Hashimoto thyroiditis with subclinical hypothyroidism. P: Initiate levothyroxine 50 mcg daily; repeat TSH and free T4 in 6–8 weeks; counsel on lifelong therapy and monitoring.

DIFFERENTIAL DIAGNOSIS CONTEXT

Differential for Hashimoto thyroiditis: (1) Graves disease — exclude by absence of thyrotoxicosis, negative TSH-receptor antibodies, and lack of diffuse increased uptake on scintigraphy; (2) subacute thyroiditis — exclude by absence of neck pain, tenderness, and typical post-viral history; (3) postpartum thyroiditis — consider only in the postpartum period and note that it often remits; (4) drug-induced hypothyroidism — review amiodarone, lithium, interferon, and checkpoint inhibitor exposure; (5) iodine deficiency or excess — assess dietary and supplement history and urinary iodine if available.

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Prognosis

SHORT-TERM OUTCOME

With appropriate levothyroxine replacement, most patients achieve normal thyroid function tests within weeks to a few months, and symptoms typically improve gradually over several weeks; dose titration is guided by TSH monitoring every 6–8 weeks until stable.

LONG-TERM PROGNOSIS

The long-term prognosis is generally excellent: with adequate hormone replacement, life expectancy and quality of life are comparable to the general population, and progression to end-organ complications is prevented. However, the disease is chronic and usually requires lifelong therapy once overt hypothyroidism has developed; a small proportion of patients may have persistent symptoms despite biochemical euthyroidism.

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References & Coding

ICD-10 DIAGNOSTIC CODE

E06.3

LITERATURE CITATIONS & GUIDELINES

[1]Boucai L. Hashimoto Thyroiditis. Merck Manual Professional Edition. 2026.

[2]Kaur J, Jialal I. Hashimoto Thyroiditis. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2026 Jan-.

[3]Wiersinga WM. Hashimoto's thyroiditis. In: Endocrinology (Switzerland): Pathogenesis, Diagnosis, and Treatment. Springer; 2018:205-247.

[4]Jonklaas J, Bianco AC, Bauer AJ, et al. Guidelines for the treatment of hypothyroidism: prepared by the American Thyroid Association task force on thyroid hormone replacement. Thyroid. 2014;24(12):1670-1751.

MEDICAL DISCLAIMER — This content is intended for educational purposes and qualified healthcare professionals only. Always refer to current clinical diagnostic criteria, institutional protocols, and official guidelines. Medobo is not responsible for clinical decisions made based on this content.