Hashimoto’s Thyroiditis

HASHIMOTO’S THYROIDITIS

ETIOLOGY OF HASHIMOTO’S THYROIDITIS

It is an autoimmune disease –
It is thought to be initiated by activation of CD4+T (helper) lymphocytes which further recruit cytotoxic CD8+T cells.
Thyroid tissue is destroyed by cytotoxic T cells and autoantibodies

Autoantibodies are directed against following antigens.

Thyroglobulin (Tg) 60%
Thyroid peroxidase (TPO) 95%
TSH-R, 60%
Antibodies are directed less commonly against the sodium/iodine symporter (25%).

Apoptosis (programmed cell death) is also implicated in the pathogenesis of Hashimoto’s thyroiditis.

Genetic association has been noted with

HLA (B8, DR3, DR4 & DR5)
CTLA-4 (a T cell regulating gene)

Several chromosomal abnormalities have been associated with Hashimoto’s thyroiditis

Turner syndrome
Down syndrome

PATHOLOGY OF HASHIMOTO’S THYROIDITIS

1. Gross features

Diffuse symmetrically enlarged thyroid.
Capsule is intact

2. Microscopic features:

Diffuse lymphocytic infiltration with germinal center formation and obliteration of thyroid follicles by widespread apoptosis.
The thyroid follicles are atrophic, lined by Hurthle cells.
Hurthle cells or Askanazy cells are metaplastic transformation of follicular cells. They have abundant eosinophilic granular cytoplasm (eosinophilic appearance is due to abundance of mitochondria in the cytoplasm).
- Hurthle cells are virtually pathognomonic – scanty or no colloid within the follicle.
There is mild to moderate: fibrosis (but not to the extent seen in Riedel’s thyroiditis)
Presence of Hurthle cells and lymphocytes on FNAC is characteristic of Hashimoto thyroiditis.

Thyroid Bcell lymphoma is a rare but well recognized complication of Hashimoto’s thyroiditis..

Papillary thyroid carcinoma may also be occasionally associated.

CLINICAL PRESENTATION OF HASHIMOTO’S THYROIDITIS

Like other autoimmune disease, more common in women (Male female ratio 1:10)
Age :30-50 yrs.
Most common presentation is that of a minimally or moderately enlarged firm gland with tenderness20% of patients present with hypothyroidism, and 5% present with hyperthyroidism (hashitoxicosis)!

On examiantion an enlarged pyramidal lobe is often palpable.

Mild hyperthyroidism may be present initially (d/t destruction of thyroid tissue) but hypothyroidism is inevitable and usually permanent.
Thyroid-associated ophthalmopathy is rare in patients with chronic autoimmune thyroiditis

INVESTIGATIONS IN A CASE OF HASHIMOTO’S THYROIDITIS

Laboratory findings are:

Elevated TSH, reduced T4 & T3 levels.
presence of thyroid autoantibodies (particularly TPO antibody)

In cases of doubt, diagnosis is confirmed by FNA biopsy.

MANAGEMENT IN A CASE OF HASHIMOTO’S THYROIDITIS

Thyroid hormone replacement therapy for overtly hypothyroid patients or in euthyroid patients to shrink large goiters.
Surgery may occasionally be indicated for suspicion of malignancy or for goiters causing compressive symptoms or cosmetic deformity.

Exam Important

Follicular destruction ,Increase in lymphocytes ,Oncocytic metaplasia is seen in Hashimoto’s Thyroiditis.
Orphan Annie eye nuclei is not seen in Hashimoto’s Thyroiditis.
Thyroid follicular infiltration by lymphocytes along with the presence of Hurthle cells is characteristic of Hashimoto’s disease.
Hashimoto’s thyroiditis is an autoimmune disorder.
In case of an Autoimmune disease,following is present: T cells recognise self antigen , Hashimoto’s thyroiditis is an example, Polyclonal B cell activation.
Higher incidence among females is present in an Autoimmune disease.
In hashimoto’s disease serum antibodies are mainly against Thyroid follicles and thyroglobulin.
There is increased risk of developing B-cell lymphoma in Hashimoto’s thyroiditis.
‘Hurthle cells’ are seen in Hashimoto’s thyroiditis.
Most common cause of Thyroiditis is Hashimoto’s thyroiditis.
Antithyroid nuclear antibodies are not seen in Hashimoto’s thyroiditis.
Antithyroid microsomal antibodies ,Anti TSH receptor antibodies and Increased level of thyroid hormones may be seen in Hashimoto’s thyroiditis.
Enlargement of thyroid gland with tenderness is most commonly seen in Hashimoto’s thyroiditis.
Anti-TPO antibodies are present in Hashimoto’s thyroiditis.

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Hashimoto’s Thyroiditis