Non-Hodgkin's thyroid lymphoma associated with Hashimoto's thyroiditis.

We report two cases of thyroid lymphoma. First was of a 54-year-old lady who presented with a 10 year history of goiter. Examination revealed an enlarged thyroid gland extending sub-sternally, with no palpable lymph nodes. She had been on thyroxine for 4 months, due to a high TSH with positive antibodies. Fine needle aspiration cytology of thyroid showed Hashimoto thyroiditis (HT). A total thyroidectomy was done because of pressure symptoms. Histopathology revealed HT in right lobe and Diffuse Large B-cell Non-Hodgkin's lymphoma (DLBCL) in left lobe. Second case was of a 30 year-old man who presented with dyspnoea secondary to rapidly enlarging thyroid. On examination, thyroid was diffusely enlarged together with palpable lymph nodes. His TSH was elevated & Anti-TPO antibodies were positive suggesting an autoimmune etiology. Ultrasound showed, an ill-defined heterogeneous mass in the left lobe of thyroid gland with multiple enlarged lymph nodes. Ultrasound guided thyroid core biopsy revealed DLBCL.

Infusion of autologous retrodifferentiated stem cells into patients with beta-thalassemia.

Beta-thalassemia is a genetic, red blood cell disorder affecting the beta-globin chain of the adult hemoglobin gene. This results in excess accumulation of unpaired alpha-chain gene products leading to reduced red blood cell life span and the development of severe anemia. Current treatment of this disease involves regular blood transfusion and adjunct chelation therapy to lower blood transfusion-induced iron overload. Fetal hemoglobin switching agents have been proposed to treat genetic blood disorders, such as sickle cell anemia and beta-thalassemia, in an effort to compensate for the dysfunctional form of the beta-globin chain in adult hemoglobin. The rationale behind this approach is to pair the excess normal alpha-globin chain with the alternative fetal gamma-chain to promote red blood cell survival and ameliorate the anemia. Reprogramming of differentiation in intact, mature, adult white blood cells in response to inclusion of monoclonal antibody CR3/43 has been described. This form of retrograde development has been termed "retrodifferentiation", with the ability to re-express a variety of stem cell markers in a heterogeneous population of white blood cells. This form of reprogramming, or reontogeny, to a more pluripotent stem cell state ought to recapitulate early hematopoiesis and facilitate expression of a fetal and/or adult program of hemoglobin synthesis or regeneration on infusion and subsequent redifferentiation. Herein, the outcome of infusion of autologous retrodifferentiated stem cells (RSC) into 21 patients with beta-thalassemia is described. Over 6 months, Infusion of 3-h autologous RSC subjected to hematopoietic-conducive conditions into patients with beta-thalassemia reduced mean blood transfusion requirement, increased mean fetal hemoglobin synthesis, and significantly lowered mean serum ferritin. This was always accompanied by an increase in mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC) in such patients. No adverse side effects in response to the infusion of autologous RSC were noted. This novel clinical procedure may profoundly modify the devastating course of many genetic disorders in an autologous setting, thus paving the way to harnessing pluripotency from differentiated cells to regenerate transiently an otherwise genetically degenerate tissue such as thalassemic blood.