Hashimoto's thyroiditis is the most common cause of hypothyroidism in iodine-sufficient regions. Named after Dr. Hakaru Hashimoto, this autoimmune disorder is characterized by chronic inflammation and destruction of the thyroid gland, often progressing silently until symptoms manifest over time.
To aid in understanding and remembering key clinical aspects of this condition, medical students often use the mnemonic “HASHIMOTO”, where each letter represents an important feature or association of the disease.
What is Hashimoto’s Thyroiditis?
Hashimoto’s thyroiditis, also known as chronic lymphocytic thyroiditis, is an autoimmune condition in which the body’s immune system mistakenly attacks thyroid tissue. Over time, this leads to progressive hypothyroidism as thyroid hormone production declines.
Epidemiology
- More common in women (10:1 female-to-male ratio)
- Peak incidence: Ages 30–50
- Often familial (genetic predisposition)
- Frequently coexists with other autoimmune diseases (e.g., type 1 diabetes, celiac disease)
Mnemonic: “HASHIMOTO”
Let’s decode this mnemonic to uncover the essentials of this disease.
H – Hypothyroidism Features
Hashimoto’s thyroiditis is the leading cause of primary hypothyroidism. The disease begins with a gradual, painless destruction of the thyroid gland, leading to underproduction of thyroid hormones—T3 and T4.
Common Hypothyroid Symptoms:
- Fatigue and lethargy
- Intolerance to cold
- Weight gain despite poor appetite
- Constipation
- Bradycardia
- Menstrual irregularities (menorrhagia, amenorrhea)
- Puffy face, dry skin, brittle nails
- Depression and slowed thinking
- Muscle weakness and cramps
- Edema in feet (non-pitting, myxedema)
Physical Signs:
- Dry, coarse skin
- Cold extremities
- Delayed reflexes
- Bradycardia
- Goitre (diffuse or nodular)
A – Autoimmune Etiology
Hashimoto’s thyroiditis is an autoimmune disease. The body produces autoantibodies against components of thyroid tissue.
Key Autoantibodies:
- Anti-thyroid peroxidase (Anti-TPO)
- Anti-thyroglobulin antibodies
These antibodies recruit lymphocytes and cause chronic inflammation, fibrosis, and atrophy of thyroid follicles.
Associated Autoimmune Conditions:
- Type 1 Diabetes
- Addison’s disease (part of polyglandular autoimmune syndrome)
- Pernicious anemia
- Rheumatoid arthritis
- Vitiligo
- Systemic lupus erythematosus (SLE)
S – Synthroid Treatment (Levothyroxine)
Treatment of Hashimoto’s involves thyroid hormone replacement, typically with levothyroxine (Synthroid).
Treatment Goals:
- Normalize TSH levels
- Alleviate hypothyroid symptoms
- Prevent goitre progression
Dosage:
- Average adult dose: 1.6 µg/kg/day
- Start low in elderly or cardiac patients
- Monitor TSH every 6–8 weeks when adjusting
Important Considerations:
- Take on empty stomach
- Avoid co-ingestion with calcium/iron
- Life-long treatment in most cases
H – Hurthle Cell Changes
Histopathological hallmark of Hashimoto’s is the presence of Hurthle cells.
Hurthle Cells:
- Enlarged epithelial cells with abundant eosinophilic, granular cytoplasm
- Originate from follicular cells
- Found on fine needle aspiration (FNA) cytology
Other Histological Features:
- Lymphocytic infiltration
- Germinal centers
- Follicular atrophy
- Fibrosis in late-stage disease
I – Initial Hashitoxicosis
In early stages, patients may present with transient hyperthyroid symptoms, a phase known as Hashitoxicosis.
Mechanism:
- Damaged thyroid follicles release stored T3 and T4 into circulation.
Symptoms of Hashitoxicosis:
- Palpitations
- Anxiety
- Heat intolerance
- Weight loss
- Tremors
Distinguishing Feature:
Unlike Graves’ disease, Hashitoxicosis is not due to increased hormone synthesis, and there is no TSH receptor antibody elevation.
This phase is self-limiting and followed by hypothyroidism.
M – Marginal Zone Lymphoma (NHL)
Chronic inflammation in Hashimoto’s patients increases the risk of thyroid lymphoma, particularly mucosa-associated lymphoid tissue (MALT) lymphoma, a subtype of non-Hodgkin lymphoma.
Clinical Clues:
- Rapid thyroid enlargement
- Compressive symptoms (dysphagia, hoarseness)
- Painful thyroid (unusual for Hashimoto’s alone)
Diagnosis:
- Ultrasound
- Core needle biopsy
- PET-CT for staging
Management:
- Chemotherapy and/or radiotherapy
- Surgery not usually preferred
O – Other: Goitre (Thyroid Enlargement)
Goitre in Hashimoto’s is usually:
- Diffuse and painless
- Firm and rubbery
- May fluctuate in size over time
- Sometimes nodular in late stages
Why Goitre Develops:
- Chronic inflammation
- TSH stimulation due to hormone deficiency
- Fibrotic tissue changes
Investigations:
- Ultrasound thyroid: Heterogeneous echotexture, pseudonodules
- Thyroid scan (RAIU): Low uptake
- FNAC: To rule out malignancy in suspicious nodules
T – TPO & Anti-Thyroglobulin Antibodies
These thyroid autoantibodies are hallmarks of autoimmune thyroiditis.
| Antibody | Sensitivity | Associated With |
|---|---|---|
| Anti-TPO | 90–95% | Hashimoto’s, Graves' |
| Anti-thyroglobulin (anti-Tg) | 50–60% | Hashimoto’s |
Note: Antibody levels are not required for treatment monitoring but are helpful in diagnosis, screening in families, and predicting hypothyroidism progression.
O – Lymphocytic Infiltrate
Histologically, Hashimoto’s thyroiditis shows:
- Dense lymphocytic infiltrates
- Formation of germinal centers
- Atrophy of thyroid follicles
- Scarring and fibrosis in late stages
These changes reflect the immune destruction and chronicity of the condition.
Clinical Features of Hashimoto’s Thyroiditis
Symptoms:
- Fatigue
- Depression
- Dry skin
- Hair thinning
- Memory impairment
- Hoarseness
- Menstrual irregularities
- Infertility
- Puffy face
Signs:
- Cold intolerance
- Constipation
- Weight gain
- Bradycardia
- Myxedema
- Delayed reflexes
- Periorbital puffiness
Investigations
| Test | Result in Hashimoto’s |
|---|---|
| TSH | Elevated |
| Free T4 | Low |
| Anti-TPO antibodies | Positive |
| Anti-thyroglobulin Ab | Positive |
| Thyroid ultrasound | Heterogeneous echotexture |
| Fine needle aspiration | Hurthle cells, lymphocytes |
| Radioiodine uptake scan | Low uptake |
Differential Diagnosis
| Condition | Antibody Profile | Radioiodine Uptake | Goitre |
|---|---|---|---|
| Hashimoto’s | Anti-TPO, anti-Tg ↑ | ↓ | Diffuse |
| Graves’ Disease | TSH receptor Ab ↑ | ↑↑ | Diffuse |
| Subacute Thyroiditis | ESR ↑, Ab negative | ↓ | Tender |
| Thyroid cancer | None specific | Variable | Nodular |
Management
1. Levothyroxine Replacement
- Start low and titrate up
- Reassess TSH every 6–8 weeks
- Monitor for over-replacement (AFib, osteoporosis)
2. Monitoring
- Yearly TSH in stable patients
- Watch for signs of overtreatment
3. Surgical Intervention
Rarely required, unless:
- Large goitre compressing trachea/esophagus
- Suspicious nodules
- Cosmetic concerns
Complications
- Myxedema coma (life-threatening hypothyroidism)
- Infertility
- Depression and cognitive impairment
- Thyroid lymphoma
- Goitre complications (compression, tracheomalacia)
Hashimoto’s and Pregnancy
Pregnant women with Hashimoto’s are at higher risk for:
- Miscarriage
- Preeclampsia
- Preterm birth
Target TSH: <2.5 mIU/L in 1st trimester
Levothyroxine dose often increases in pregnancy
Screening advised in women with:
- Family history
- Type 1 diabetes
- Previous miscarriage
Hashimoto’s vs Other Thyroid Disorders
| Feature | Hashimoto’s | Graves’ Disease |
|---|---|---|
| TSH | ↑ | ↓ |
| T3/T4 | ↓ | ↑ |
| Antibodies | Anti-TPO, anti-Tg | TSH receptor Ab |
| Eye involvement | Absent | Prominent (exophthalmos) |
| Goitre | Firm, painless | Soft, vascular |
| Treatment | Levothyroxine | Antithyroid drugs, RAI |
Summary Table: “HASHIMOTO” Mnemonic
| Letter | Feature | Explanation |
|---|---|---|
| H | Hypothyroidism features | Fatigue, cold intolerance, constipation, weight gain |
| A | Autoimmune | Autoantibodies against thyroid tissue |
| S | Synthroid (levothyroxine) treatment | Hormone replacement therapy |
| H | Hurthle cell changes | Histological finding in thyroid biopsy |
| I | Initial Hashitoxicosis | Early hyperthyroidism due to follicular destruction |
| M | Marginal zone lymphoma | Rare complication of chronic thyroid inflammation |
| O | Other: Goitre | Thyroid enlargement—diffuse or nodular |
| T | TPO and thyroglobulin antibodies | Diagnostic antibodies in Hashimoto’s |
| O | Lymphocytic infiltrate | Chronic inflammation seen on pathology |
Frequently Asked Questions (FAQs)
What is the most reliable test for Hashimoto's thyroiditis?
The most specific test is Anti-TPO antibodies along with elevated TSH and low T4 levels.
Can Hashimoto’s be cured?
There is no cure, but symptoms can be fully managed with lifelong thyroid hormone replacement.
Is goitre always present in Hashimoto’s?
Not always. Some patients may not have palpable thyroid enlargement, especially in late fibrotic stages.
Can Hashimoto’s thyroiditis cause hyperthyroidism?
Yes, temporarily. This is known as Hashitoxicosis, due to release of preformed hormones.
Does Hashimoto’s increase cancer risk?
It increases the risk of thyroid lymphoma, though thyroid carcinoma risk is only slightly elevated.
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