A 64-year-old man with a history of hypothyroidism and proven Hashimoto's thyroiditis presented with painless progressive asymmetric enlargement of the thyroid gland. Laboratory evaluation revealed an elevated erythrocyte sedimentation rate (ESR), elevated thyroid peroxidase antibody titer of 850 U/mL (normal <30 U/mL), free triiodothyronine (FT3) 2.34, free thyroxine (FT4) 0.97, and thyroid stimulating hormone (TSH) level of 22.11. A contrast enhanced CT (CECT) exam of the neck revealed a large heterogeneous mass lesion predominantly involving the left lobe of thyroid and partly involving the isthmus and anterior part of right lobe. A needle biopsy from the thyroid mass revealed features of non-Hodgkin's lymphoma (DLBCL) with the tumor cells staining positive for CD20, negative for cytokeratin (CK) and having a high proliferative index (MIB-1) of 35-40%. 18F-FDG PET/CT was performed for staging. It revealed a large heterogeneous mass lesion predominantly involving the left lobe of thyroid and partly involving the isthmus and anterior part of right lobe with intense radiotracer uptake in the thyroid mass (SUVmax-18.7) with no other abnormal identifiable areas [Figure –]. The patient underwent four cycles of combination chemotherapy (rituximab-cyclophosphamide, doxorubicin, vincristine, and prednisone) and was reevaluated with 18F-FDG PET/CT. Post therapy 18F-FDG PET/CT [Figure –] done 6 weeks after completion of chemotherapy revealed significant decrease in the size of the enlarged thyroid gland associated with no significant FDG avidity (SUVmax-2.0) of the residual thyroid mass (arrow), suggestive of complete metabolic response. The patient is in complete remission at 18 month follow-up.
A 70-year-old male presented a rapidly expanding mass of the neck associated with history of airway compression symptoms; progressive dyspnea and dysphonia lasting for 4 weeks, in a context of apyrexia and impairment of general condition. The patient was admitted to the hospital because of increasing dyspnea and urgently received a tracheostomy.\nA biopsy of the cervical mass was carried out and the histological examination showed diffuse infiltration of the thyroid gland by a monotonous population of atypical intermediate-sized lymphoid cells (Fig. ). These last possess scanty amphophilic to basophilic cytoplasm with centrally located nuclei of irregular shape, displaying dispersed basophilic chromatin, and frequent apoptotic figures (Fig. ). Scattered tingible body type macrophages were also present. Little residual thyroid follicles and some areas of necrosis was observed.\nImmunohistochemical staining was then performed and the tumour cells were positive for CD20, CD10 and BCL6. Ki-67 showed proliferation index approaching 100 %. CD3 and CD5 stained the background T cells (Fig. ). Immunoreactivity for Epstein-Barr virus (EBV) was negative. The diagnosis of BL was confirmed on fluorescence in situ hybridisation that showed tumour cell positivity for the t (8; 14) translocation. Bone marrow examination was normal.\nThe patient was transferred to the Clinical Haematology department. On physical examination, he was apyretic and hemodynamically stable with a cervical armouring by a huge mass of hard consistency. Neurological examination shows no sensorimotor deficits.\nOther systemic examinations were normal, without any palpable lymphadenopathy or organomegaly.\nThe computerized tomography (CT) scan showed a heterogeneous process of the thyroid gland measuring 10.5 × 8.2 × 6.5 cm in size, extending up towards the laryngeal region, infiltrating the right vocal cord and reducing the laryngeal lumen (Fig. ).\nThe thoraco-abdominal CT scan showed no other localization.\nThe examination of the cephalorachidian liquid showed no central nervous system involvement. The patient was diagnosed with thyroidal Burkitt lymphoma, stage I of Murphy [].\nAfter cardiac, renal and liver functions assessment, the patient received chemotherapy according to the LMBA02 protocol [], group A (Age > 60 years, no CNS nor bone marrow involvement), with a first course of COP (Cyclophosphamide, Vincristine and Prednisone) and intrathecal Methotrexate, followed a week after by a course of R-COPADEM (Rituximab at day 0 and day 6, Cyclophosphamide day 2,3 and 4, Prednisone from day 1 to 5, Doxorubicineat day 2, high dose Methotrexate at day 1 with folic acid rescue from day 2 to day 6 and intrathecal chemotherapy at day 2 and day 6).\nAt day 15 of chemotherapy, the patient developed febrile neutropenia, refractory to broad-spectrum antibiotics and antifungals. The evolution was marked by the installation of a septic shock with acute respiratory distress syndrome that led to his transfer to intensive care unit where he was intubated and ventilated. The patient died 2 days after.