Hashimoto's Thyroiditis

Hashimoto's thyroiditis is an autoimmune condition in which lymphocytes infiltrate the thyroid and antibodies target thyroid peroxidase and thyroglobulin, the enzymes the gland uses to build hormone. Destruction is gradual, so most people move through years of normal thyroid function with positive antibodies, then subclinical hypothyroidism, before overt hypothyroidism appears. It is the leading cause of hypothyroidism wherever iodine intake is adequate, and it affects women roughly seven to ten times as often as men, most commonly between 30 and 50. Genetics, previous pregnancy, high iodine intake, radiation exposure and other autoimmune conditions all raise risk, and coeliac disease, type 1 diabetes, vitiligo and pernicious anaemia frequently travel with it. Treatment is straightforward once thyroid function falls: levothyroxine replaces what the gland can no longer make, titrated against TSH. The autoimmunity itself is not treated. Selenium at 200 mcg daily reduces TPO antibody titres in most randomised trials, though whether that changes symptoms or slows progression is unresolved. Vitamin D deficiency is common in this group and worth correcting. The key clinical point is that antibodies alone are not a disease to treat — thyroid function is what determines whether medication is needed.

• •Fatigue that does not improve with rest
• •Cold intolerance
• •Unexplained weight gain or difficulty losing weight
• •Dry skin, brittle nails and hair thinning
• •Constipation
• •Low mood, irritability or brain fog
• •Heavy or irregular periods
• •Muscle aches, cramps and joint stiffness
• •Goitre — a visible or palpable swelling at the front of the neck
• •Hoarseness or a feeling of fullness in the throat

• •Autoimmune attack on thyroid peroxidase and thyroglobulin
• •Genetic predisposition, including HLA and CTLA-4 variants
• •Female sex and postpartum immune shifts
• •Excessive iodine intake, including from kelp supplements or amiodarone
• •Previous neck irradiation
• •Coexisting autoimmune disease such as coeliac or type 1 diabetes
• •Possible viral triggers, though causation is unproven

A genetically primed immune system loses tolerance to thyroid antigens, most often triggered around a hormonal or immunological shift such as pregnancy. Chronic lymphocytic infiltration then destroys follicular cells faster than they regenerate. Because the thyroid holds reserve capacity, hormone output stays normal for years while the antibody titre climbs — which is why antibody positivity long precedes symptoms, and why the earliest measurable change is usually a rising TSH rather than a falling T4.