Category: Thyroid

Monitor: 26


Saturday, Apr 27
10:30 AM – 11:00 AM

Objective : It is uncommon to encounter both Hashimoto’s Thyroiditis (HT) and Graves’ Disease (GD) in the same patient. We report two cases with hypothyroidism from HT followed by hyperthyroidism from GD.

Methods : n/a

Results :

Case 1
: A 53-year-old female on levothyroxine (LT4) treatment for hypothyroidism was noted to be hyperthyroid with a TSH of <0.005mIU/L (nl 0.1–5.0), FT4 6.3 ng/dL (nl 0.7–1.9) and FT3 of 23 pg/mL (nl 2.0– 4.4). She was symptomatic with tremors, atrial fibrillation and Graves’ orbitopathy. LT4 was stopped, yet her hormone levels were persistently elevated after four weeks with a repeat TSH of < 0.005 mIU/L, FT4 8 ng/dL and FT3 30 pg/mL. Thyroid ultrasound showed a diffusely enlarged gland with increased vascularity. Thyroid Stimulating Immunoglobulin (TSI) and TSH receptor antibody (TRAb) were positive at 22.7 IU/L (nl 0.0-0.55) and 23.9 IU/L (nl 0.0-1.7) respectively, consistent with a diagnosis of GD. Thyroid Peroxidase antibody was elevated at >1300 IU/mL (nl <0.9). She responded well to methimazole, and she awaits definitive radioiodine treatment.

Case 2:
A 48-year-old woman was on LT4 (50 mcg daily) for hypothyroidism due to HT. She presented with resting tremor, anxiety, heat intolerance and a diffusely enlarged, slightly tender thyroid. The LT4 dose was considered too low to cause hyperthyroidism. TSH was 0.02 mIU/L, FT4 6.0 ng/dL, FT3 19.6 pg/mL and TSI was 240 % of baseline (nl < 140%). Thyroid ultrasound showed an enlarged homogeneous gland with mild hypervascularity. LT4 was stopped, and the hyperthyroidism gradually resolved over three months. She later required resumption of LT4.

Discussion :

HT and GD are the most common presentations of autoimmune thyroid disease. In the above cases, there was conversion of autoimmune hypothyroidism to hyperthyroidism. This may be explained by the presence of Thyroid Blocking antibodies (TBAbs) and Thyroid Stimulating antibodies (TSAbs). TBAbs are present in about 20 % of patients with HT, and can play a role in the development of hypothyroidism. A potential mechanism for the conversion is that the TBAbs decline and the TSAbs increase to contribute to the pathogenesis of GD. Factors that initiate this process are unclear. A bioassay of blocking antibodies (TBAbs) was not available.

Conclusion :

Autoimmune thyroid disease with conversion from hypothyroidism to hyperthyroidism is uncommon. This phenomenon should be suspected when patients with known HT have persistently elevated thyroid hormone levels in spite of reduction of LT4. In such cases, clinicians should investigate further with antibody testing and imaging studies for GD.


Sandeep Kunwar

Internal Medicine Resident
Creighton University School of Medicine, Nebraska

I am Sandeep second year Internal medicine resident at Creighton University School of Medicine, Omaha, Nebraska. I did my Medical school from Universal college of Medical Sciences, Nepal.

Rama Priyanka Nagireddi

Endocrinology Fellow
Division of Endocrinology, Diabetes and Metabolism, Creighton University School of Medicine

Endocrinology fellow. Division of Endocrinology, Diabetes and Metabolism, Creighton University School of Medicine, Omaha, Nebraska

Robert J. Anderson

Program Director, Fellowship in Endocrinology, Diabetes and Metabolism
1. Creighton University School of Medicine 2. VA Nebraska-Western Iowa Healthcare System, Nebraska

Dr. Robert Anderson is an endocrinologist in Omaha, Nebraska and is affiliated with Creighton University Medical Center-Bergan Mercy. He received his medical degree from Northwestern University Feinberg School of Medicine. He finished his endocrinology fellowship in Mayo Clinic, Rochester, Minnesota. Currently, he is a chief, section of endocrinology in VA-Nebraska Western Iowa healthcare system and a program director of fellowship in endocrinology at Creighton University School of Medicine.

Mohsen Zena

Assistant Professor
Division of Endocrinology, Diabetes and Metabolism, Creighton University School of Medicine

Assistant Professor, Division of Endocrinology, Diabetes and Metabolism, Creighton University School of Medicine.