Case Report |
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Toxoplasmosis Gondii Infection and Diabetes Mellitus Type 2 Treated by Using Autologous Peripheral Blood Stem Cells a Unique Case Re- port of a Caucasian 83 Year Old LadyCiro Gargiulo1*, Van Hung Pham2, Kieu C.D. Nguyen1, Ngan Duong Kim1, Thinh Nguyen Van1, An Luu Tuan1, Kenji Abe3, and Melvin Shiffman4. Abstract | | | | Introduction: Toxoplasma gondii is an intracellular protozoan responsible for up to one-third of the world's population infestation. Diabetes is one of the most silent and threatening disease of the modern time it is constantly in- creasing in both industrialized and developing countries. This is a case of clinically importance for two reason, firstly it will help clinicians save a broad differential diagnosis when attending to evaluate analogous cases and secondly, it may confirm the role of autologous peripheral blood stem cells (PB-SCs) in enhancing auto-immune response against parasitic infection and in regulating insulin uptake in diabetes mellitus type 2 (DM2). Case presentation: We present a unique case of 83- year-old woman from Argentina presenting with a widespread erythema and urticaria for 5 months and DM2 as underly- ing condition. She was initially diagnosed with unspecific skin auto-immune disorder. By the time of visit she was com- plaining of constant diarrhea-constipation and general mental and physical fatigue. Conclusion: This case illustrates that toxoplasmosis can present with just simple disseminated and generalized skin erythema with severe itching and, thus can be confused with similar infectious disease such as Epstein-Barr virus (EBV), cytomegalovirus, cat scratch disease or leishmaniasis. The report emphasizes the need of correct diagnostic procedure in confusing cases, and may help to increase the awareness about the identification of this disease. This case may open to the possibility of a different approach and me- thodology in treatment T gondii and DM2 through the use of PB-SCs.
Key words: Toxoplasma gondii, Human Peripheral Blood Stem cells, NK cells, CD3, CD4, CD8.
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