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.
A 60-year-old man originally from China with no prior history of thyroid or autoimmune disease received a standard course of 48-week pegylated IFN-α and ribavirin therapy for chronic HCV (genotype 1b) with achievement of sustained virological response. He had compensated chronic liver disease with cirrhosis (Child-Pugh A) without other complications and no other reported medical problems. He denied previous use of amiodarone, lithium, medications, or supplements containing iodine or exposure to contrast. He was a nonsmoker and did not drink alcohol. Six months after commencing treatment, he reported fatigue, weight gain of 3 kg, and slowed cognition at a routine clinical visit. He denied changes to his skin, hair, or bowel habits. On examination, his vital signs were normal. His weight was 78 kg with a body mass index (BMI) of 26.8 kg/m2. There was no goitre and there were no signs of oedema, dermopathy, ophthalmopathy, or lymphadenopathy. Cardiac, respiratory, and gastrointestinal examinations were normal and in particular no stigmata of chronic liver disease was present. A peripheral neurological examination including reflexes was normal.\nSerum biochemistry including electrolytes, renal function, and full blood count were within normal limits, with no biochemical or serological evidence of decompensated liver disease. Alpha-fetoprotein (AFP) was normal at 3.5 kIU/L [normal, 0.0–6.0]. Pretreatment HCV quantitative RNA was >3,000,000 IU/mL and was undetectable 6 months after commencing treatment. A recent abdominal ultrasound revealed a radiologically normal liver with no signs of portal hypertension or hepatic lesions. His serum thyroid stimulating hormone (TSH) prior to therapy was 1.65 mIU/L [normal, 0.27–4.2] with a normal free T4 (fT4) of 14.5 pmol/L [normal, 12–25]. The TSH at the time of review (i.e., 6 months later) was 58.8 mIU/L, free T4 was 11.1 pmol/L, and free T3 was 4.2 pmol/L [normal, 2.5–6.0] (). Anti-TPO (983 IU/mL, normal <35) and anti-TG (733 U/mL, normal <80) antibodies were elevated ().\nGiven his symptoms and biochemical evidence of autoimmune hypothyroidism, the patient was commenced on standard adult thyroxine replacement therapy at 100 mcg daily. His symptoms improved and there was full clinical and biochemical resolution of his hypothyroid state. Fourteen months later, he returned for follow-up reporting symptoms of hyperthyroidism with weight loss, tremor, and palpitations. He had lost 5 kg of weight. At the time of review, serum TSH was suppressed at <0.02 mIU/L with elevated fT4 of 54.3 pmol/L, fT3 of 20.2 pmol/L, and an elevated TRAb of 4.0 U/L (normal <1.0), with anti-TPO (1,163 IU/mL) and anti-TG (114 U/mL) antibodies. Technetium scan revealed bilateral diffuse increased tracer uptake (5.9%, normal 0.5–3.5%), consistent with Graves' Disease ().\nThe patient's thyroxine was ceased and he was placed on antithyroid treatment with carbimazole 5 mg TDS. He self-ceased therapy 6 months later, with serendipitous clinical and biochemical remission. His serum TSH was 3.84 mIU/L, fT4 17 pmol/L, and fT3 4.5 pmol/L, but with persistently elevated anti-TPO at 383 IU/mL. Anti-TG 23 U/mL and TRAb < 1 U/L were normal. At the time of writing, the patient remained clinically and biochemically euthyroid.