Hashimoto's thyroiditis
The autoimmune destruction of the thyroid gland, and the leading cause of hypothyroidism in iodine-sufficient countries. Slowly progressive; managed lifelong with thyroxine replacement.
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Upload your lab report - freeWhat it is
Hashimoto's thyroiditis is an autoimmune disease in which the immune system attacks the thyroid gland, gradually replacing follicles with lymphocytic infiltrate and fibrosis. It is 7–10× commoner in women than men, peaks in middle age, and clusters with other autoimmune conditions (coeliac, type 1 diabetes, vitiligo, Sjögren's). The biochemical course typically runs: anti-TPO antibodies positive → subclinical hypothyroidism (raised TSH, normal Free T4) → overt hypothyroidism (raised TSH, low Free T4). Once overt, treatment with levothyroxine is straightforward and effective, but lifelong.
Key lab markers
- TSH — the most sensitive screen; rises early as the gland struggles.
- Free T4 — falls in overt disease; normal in subclinical phase.
- Anti-TPO antibodies — positive in 90–95% of cases, confirming autoimmune mechanism.
- Lipid panel — cholesterol often rises with untreated hypothyroidism.
Symptoms
Often slow and easily missed:
- Fatigue, sluggishness
- Weight gain despite stable appetite
- Cold intolerance
- Dry skin, hair thinning
- Constipation
- Heavy or irregular periods
- Goitre (visible neck swelling) in early phases
- Cognitive slowing, low mood
Related symptoms
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When to discuss with a doctor
Sustained TSH above the lab reference range with positive anti-TPO is the diagnostic picture. Subclinical hypothyroidism (TSH 5–10, normal Free T4) is often monitored before starting replacement; TSH >10 or symptomatic patients are usually treated. Annual TSH and a once-only anti-TPO are the typical monitoring approach. Mediora.AI surfaces the thyroid panel; dosing of levothyroxine belongs with a primary-care or endocrine physician.