Hashimoto Thyroiditis (Chronic Autoimmune Thyroiditis)
This patient has Hashimoto thyroiditis, the most common cause of primary hypothyroidism in iodine-sufficient areas, characterized by the classic triad of elevated TSH, low free thyroxine, and positive thyroid peroxidase antibodies in a patient with a diffusely enlarged, firm, nodular thyroid gland. 1
Diagnostic Confirmation
The diagnosis is definitively established by the following key features present in this case:
Elevated TSH (6.0) with low free thyroxine (0.8) confirms primary hypothyroidism, distinguishing this from central hypothyroidism where both TSH and free T4 would be low 2, 1
Positive thyroid peroxidase antibodies (TPO-Ab = 48) are the hallmark serologic marker of Hashimoto thyroiditis and are present in the vast majority of cases 1, 3
Diffusely enlarged, firm, nodular, non-tender thyroid gland represents the classic physical examination finding where lymphocytic infiltration creates an irregular texture on palpation 1, 4
Hypothyroid symptoms including fatigue, depressed mood, and hoarse voice are the most common clinical presentation as thyroid destruction progresses 1, 3
Key Distinguishing Features
This presentation clearly differentiates from other thyroid disorders:
Not Graves' disease: The patient has hypothyroid symptoms (fatigue, depression, hoarse voice) rather than hyperthyroid manifestations (heat intolerance, tachycardia, weight loss), and the thyroid is lumpy/nodular rather than smooth 1
Not toxic multinodular goiter: This would present with thyrotoxicosis, not hypothyroidism 1
Not drug-induced hypophysitis: While the patient takes lithium, the elevated TSH with low free T4 indicates primary thyroid failure, not central hypothyroidism (which would show low TSH with low free T4) 2
Important Clinical Context
Several factors in this patient's history are relevant:
Postpartum timing (14 months after delivery, recently weaned): Hashimoto thyroiditis can present as painless postpartum thyroiditis, though the persistent hypothyroidism at 14 months indicates chronic autoimmune thyroiditis rather than transient postpartum thyroiditis 4
Lithium use: While lithium can cause hypothyroidism, the positive TPO antibodies and classic thyroid examination findings confirm autoimmune etiology 1
Family history of hypothyroidism: Genetic susceptibility plays a significant role in Hashimoto thyroiditis development 3, 5
Depressed mood: This is both a symptom of hypothyroidism and potentially confounded by her bipolar disorder history, making thyroid hormone replacement particularly important 1, 3
Management Approach
Initiate levothyroxine replacement therapy at 1.6 mcg/kg/day based on lean body mass (note: with BMI 32.5, use ideal body weight for dosing calculation) 1, 6
Monitor TSH at 6-8 weeks after starting treatment and after any dose adjustment to achieve target TSH in normal range 1
Lifelong thyroid hormone replacement is required, as Hashimoto thyroiditis leads to progressive thyroid destruction 1, 6
Avoid T3 (triiodothyronine) therapy unless persistent symptoms despite optimal levothyroxine treatment, as evidence for combination therapy is limited 3, 6
Critical Monitoring Considerations
Evaluate for discrete thyroid nodules during follow-up, as Hashimoto thyroiditis carries 1.6 times higher risk of papillary thyroid cancer 6
Screen for other autoimmune disorders periodically, particularly given the 20-30% association with other organ-specific autoimmune conditions 2, 5
TPO antibody levels typically decline with levothyroxine treatment (mean 70% decrease after 5 years), though they rarely normalize completely (only 16% become negative) 7