Browsing by Author "Lakhal, Amel"
Now showing 1 - 2 of 2
- Results Per Page
- Sort Options
Item Autoimmune Polyglandular Syndrome Type II After Bone Marrow Transplant: Real Transfer or Acceleration of a Programmed Disease?(Başkent Üniversitesi, 2012-02) Mellouli, Fethi; Béjaoui, Mohamed; Hmida, Slama; Othman, Tarek Ben; Ladeb, Saloua; Torjmen, Lamia; Lakhal, Amel; Ksouri, HabibWe report a case of autoimmune polyglandular syndrome type II that developed in an 11-year-old boy with homozygous sickle cell disease after allogeneic bone marrow transplant; the donor was his father, who was human leukocyte antigen identical and had vitiligo. On day 24 after transplant, the patient developed grade 1 acute graft-versus-host disease, which was controlled over a period of 3 months with corticosteroid-induced immunosuppression. Full donor engraftment was documented on day 31 after transplant, and this was further confirmed on days 59, 231, 321, 472, 549, and 720. Three months after transplant, the recipient developed adrenal insufficiency, and at 13 months, he developed vitiligo. Seventeen months after transplant, autoimmune thyroid disease, positive for thyroid peroxidase and thyroglobulin autoantibodies, was diagnosed. At the same time, we identified adrenal insufficiency in the donor. We analyzed a serum sample from the recipient for autoantibody markers for type 1 autoimmune diabetes mellitus. The sample was positive for antiglutamic acid decarboxylase. Antibody against 21-hydroxylase enzyme was also found (261 U/mL; normal value, < 1 U/mL). We conclude that the recipient developed autoimmune polyglandular syndrome type II after bone marrow transplant from his father, who was probably affected by the same syndrome.Item Switch From Beta-Thalassemia Major to Beta-Thalassemia Intermedia After Secondary Graft Failure(Başkent Üniversitesi, 2010-09) Mellouli, Fethi; Béjaoui, Mohamed; Othman, Tarek Ben; Hmida, Slama; Ladeb, Saloua; Abdelkefi, Abderrahman; Torjmen, Lamia; Lakhal, Amel; Ksouri, HabibIn this article, we report a switch of β-thalassemia major to intermedia β-thalassemia after allogeneic bone marrow transplant of a 6-year-old girl from her HLA-matched brother. After stable mixed chimerism, the patient had a secondary graft rejection and returned to total recipient chimerism as assessed by real-time polymerase chain reaction assay. Nonetheless, with a medium hemoglobin rate of 89 g/L, she did not need further transfusions for 60 months after rejection. We conclude that complete loss of donor cells after bone marrow transplant for β-thalassemia major is compatible with a stable clinical state, probably due to a γ-globin gene demethylation that enhances γ-globin chain production and further allows constitution of a fetal hemoglobin rate compatible with free transfusion survival.