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.
What 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
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.