Thyroid Disorders
Hashimoto’s Thyroiditis
The autoimmune cause of most underactive thyroid — how the immune system slowly lowers thyroid function, and how it is detected and managed.

Overview
Hashimoto’s thyroiditis is an autoimmune condition in which the immune system gradually attacks the thyroid gland, reducing its ability to make hormone over months to years. It is the most common cause of hypothyroidism and often runs in families alongside other autoimmune conditions. Many people have positive antibodies for years before the gland actually fails, and the condition can be detected and monitored well before symptoms appear.
This page explains the cause. For the resulting condition and its treatment, see Hypothyroidism and Subclinical Hypothyroidism; for the antibody test, see Abnormal Thyroid Function Tests.
How it develops
The immune system produces antibodies (anti-TPO) against the thyroid. Over time, inflammation and scarring reduce hormone output, so TSH rises as the pituitary tries to stimulate the failing gland. The process is usually slow and painless, though some people notice a transient overactive phase (hashitoxicosis) early on.
Symptoms and signs
Symptoms are those of an underactive thyroid once hormone levels fall — tiredness, weight gain, cold intolerance, dry skin and hair, constipation and low mood. A firm, painless enlargement of the thyroid may be felt. In the early antibody-positive stage there may be no symptoms at all.
Risk factors
- Family history of thyroid disease or other autoimmune conditions.
- Female sex — far more common in women.
- Middle age and beyond, though it can occur earlier.
- Other personal autoimmune disease (for example type 1 diabetes, vitiligo).
- Previous pregnancy (post-partum thyroiditis can precede it).
Evaluation and investigations
- TSH and free T4 to stage the function (normal, subclinical, or overt hypothyroidism).
- Anti-TPO antibodies — the hallmark marker.
- Thyroid ultrasound if the gland is enlarged or nodular.
- Cholesterol and blood sugar, as metabolic risk often clusters.
Management
Treatment is for the resulting hypothyroidism, not the antibodies themselves. If hormone levels are normal, monitoring with periodic TSH is enough. Once the gland fails, levothyroxine replaces the missing hormone for life, with the dose adjusted to a normal TSH. There is no benefit to treating antibody-positive but functionally normal thyroid with medication.
Follow-up
Even when no treatment is needed, annual TSH checks are advised because progression can occur. Once on levothyroxine, follow-up is the same as for hypothyroidism.
How we help
Dr. Nayak identifies the autoimmune cause, stages the current thyroid function, and advises whether treatment or monitoring is right for you — with structured follow-up to catch any progression early. Consultations are available in-clinic in Bhubaneswar and over teleconsultation.
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