A 66-year-old woman with a history of Hashimoto's thyroiditis and thyroid nodules initially presented for fine needle biopsy (FNB). Patient had no symptoms of hypothyroidism or hyperthyroidism. Her initial TSH was 5.9 IU/L (ref 0.27–4.20) with FT4 1.2 ng/dL (ref 0.89–1.76) (Fig. ) and thyroperoxidase (TPO Ab) and thyroglobulin (TG Ab) antibodies were 18,290 IU/mL (ref 0–34) and >2,250.0 IU/mL (ref 0.0–0.9) (Fig. ), respectively. Additionally serum thyroid stimulating immunoglobulin (TSI) level was 88% (ref 0–139) and thyrotropin receptor blocking antibody (TBRAb) (Fig. ) was also in the normal range (<10%, ref <10). Physical examination revealed normal vital signs and patient had no evidence of thyroid orbitopathy. Examination of the thyroid gland confirmed a 2-cm right lower lobe thyroid nodule and a 6-cm left thyroid nodule almost replacing the left lobe. Thyroid ultrasound showed multiple thyroid nodules bilaterally with a dominant hypervascular left thyroid mass 5.9 × 2.7 × 4.4 cm (Fig. ) and a right lower lobe nodule 2.4 × 2.4 × 2.2 cm. Additionally an ultrasound of the neck confirmed bilateral abnormal cervical lymphadenopathy. FNB of the thyroid nodules revealed a population of large lymphocytes with irregular nuclei (Fig. ). Fluorescence in situ hybridization (FISH) revealed a translocation t(14;18), fusing the immunoglobulin heavy chain gene at chromosome 14q32 with BCL2 gene at chromosome 18q21.3. Positron emission tomography computerized axial scan (PET-CT) of the chest and abdomen revealed a large retroperitoneal and mesenteric soft tissue mass, measuring 16 × 14 cm in greatest trans-axial dimension. The retroperitoneal mass encased the aorta and inferior vena cava as well as mesenteric vessels and both renal arteries. The mass also displaced the kidneys peripherally (Fig. ). She was diagnosed with stage-IVE diffuse large B-cell lymphoma (DLBCL) and underwent six cycles of R-CHOP chemotherapy. Patient also received subdiaphragmatic external radiation directed to the retroperitoneal mass. Following chemotherapy, and radiation therapy, PET-CT scan showed resolution of retroperitoneal mass, resolution of fluorodeoxy-glucose (FDG) avid thyroid nodule (Fig. ) as well as no evidence of thyroid nodules on repeat ultrasound. Following chemotherapy her thyroid functions normalized (serum TSH 3.9 IU/L and free T4 1.4 ng/dL). A moderate decrease in thyroid peroxidase Ab (range 8,432 to 11,288 IU/mL) and thyroglobulin Ab (range 1,268 to 1,600 IU/mL) were noted. Additionally TSI 88% and TBRAb <10% (ref <10) (Fig. ) continue to remain in the normal range. She remained euthyroid without any symptoms of hypo or hyperthyroid and her serum TSH and free T4 remained normal for the next 2 years (Fig. ). Additionally she had no evidence of lymphoma recurrence.\nTwo years later, patient reported significant unintentional weight loss and persistent fatigue over the past couple months. Physical examination revealed a heart rate of 120/min, fine tremors of outstretched fingers, and no thyroid orbitopathy. Thyroid was 40 g in size with no palpable nodules and deep tendon reflexes were brisk. Repeat laboratory testing revealed: TSH 0.005 IU/L, FT4 6.73 ng/dL and TSI 535% (Fig. ). Serum TBRAb was also mildly elevated (28%). TPOAb and TGAb levels were 7,976 and 1,088 IU/mL respectively (Fig. ). Additionally, an HLA DQB1*03 was positive. Further evaluation confirmed the diffuse large B-cell lymphoma (DLBCL) lymphoma was in remission. A thyroid uptake and scan showed diffuse uptake with no photopenic areas and the I131 uptake was elevated (4 h: 61.0%, reference 5–15%, at 24 h 70.3%, reference 10–30%).\nSince patient received CAT scan with iodine load she was treated with methimazole for 3 months and following this, the patient was treated with 19.4 millicuries of radioactive iodine for thyroid ablation. Following radioactive iodine treatment patient developed hypothyroidism and this was treated with levothyroxine (Fig. ). Patient remained euthyroid for the next 4 years and during these 4 years the lymphoma continues to remain in remission.
Our patient is a twenty-four-year-old female with a sixteen-year history of HT-related hypothyroidism on oral levothyroxine 100 mcg once daily. She complained of occasional palpitations, nervousness, weight loss, and irregular menses. Thyrotoxicosis was confirmed with a thyroid function test, and levothyroxine dose was reduced. However, the patient continued to exhibit thyrotoxic symptoms even after completely stopping levothyroxine. On examination, the patient was calm but tachycardic and afebrile, and her blood pressure was 116/90 mmHg, weight was 58 kg, and BMI was 21.8. She was noted to have peripheral tremors. Her thyroid exam revealed the presence of diffuse nontender goiter, with no palpable nodules. Eye examination was only remarkable for mild exophthalmos, and there was no evidence of dermopathy.\nThyroid function revealed depressed TSH <0.01 mIU/L (0.3–4.2) and high T4 26.4 pmol/L (11.6–21.9) (). Based on the persistence of symptoms despite stopping thyroid hormone supplementations and the presence of ophthalmopathy elements, the rare shift to GD was suspected. Autoimmune workup revealed a strong positive Anti-TSH Receptor (Anti-TSHR) titer, in addition to persistent positivity of previously positive thyroid peroxidase antibody (TPO Ab) and an increasing titer of Antithyroglobulin Ab (). Thyroid ultrasound revealed slight enlargement of the right lobe and increased vascularity in both lobes. Radioactive iodine uptake scan (RAIU) showed diffuse radiotracer uptake more prominent in the right thyroid lobe (). Those findings kept with the shift to GD.\nThe patient received suppressive therapy with oral carbimazole 20 mg once daily and propranolol. A subsequent follow-up three months later showed normalization of thyroid function and improvement in clinical status.