Endothelium-derived Microparticles Are Increased in Teenagers With Cobalamin Deficiency.

INTRODUCTION: Vitamin B 12 (cobalamin) deficiency may be a significant cause of hyperhomocysteinemia, and high homocysteine (Hcy) levels are associated with an increased risk of cardiovascular disease. Endothelium-derived microparticles (EMPs) are a new marker in endothelial dysfunction and atherosclerosis, which play a role in cardiovascular diseases' pathogenesis. This study aimed to evaluate the EMPs, the markers of endothelial dysfunction and atherosclerosis, and lipid profile in teenagers with cobalamin deficiency. MATERIALS AND METHODS: This prospective study included 143 teenagers, 75 vitamin B 12 deficient patients and 68 healthy controls between 11 and 18 years of age. Routine laboratory tests, hemogram, vitamin B 12 , folic acid, ferritin, Hcy, lipid profile and EMPs were examined and compared. EMP subgroups were analyzed by flow cytometry method according to the expression of membrane-specific antigens. The microparticles released from the endothelium studied were VE-cadherin (CD144), S-endo1 (CD146), and Endoglin (CD105). RESULTS: The present study demonstrates that circulating CD105+ EMP, CD144+ EMP, CD146+ EMPs, and Hcy were increased, and high-density lipoprotein (HDL) cholesterol was reduced in teenagers with cobalamin deficiency. Vitamin B 12 showed a negative correlation with EMPs and Hcy, positive correlation with folate and HDL. All EMPs showed a significant positive correlation with triglyceride, vitamin B 12 , and HDL. CONCLUSION: Vitamin B 12 deficiency may predispose to endothelial damage and atherosclerosis by increasing EMPs and harms lipid metabolism in the long term.

Modulation of inflammation by mesenchymal stem cell transplantation in peritoneal dialysis in rats.

AIM: The purpose of this study was to determine the effect of mesenchymal stem cell (MSC) transplantation on the peritoneal morphology and inflammation markers in rat models of peritoneal dialysis (PD). MATERIALS AND METHODS: Wistar albino rats were divided into two groups: control (C) (n = 8) and experimental groups (n = 50). PD solution was given to the experimental group during 6 weeks. Then, experimental group was divided into three groups as PD, MSC, and placebo (P) groups. MSC group was treated with MSC (1.5 × 10(6) cells/kg) and P group was treated with phosphate buffer solution via intraperitoneal injection. Evaluation was performed to C and PD groups at the end of 6 weeks and to MSC and P groups at second and third week of the treatment (MSC-2, P-2, MSC-3, and P-3 groups). RESULTS: The submesothelial area was significantly thickened in PD and P groups compared to C and MSC groups. Peritoneal fibrosis was seen in P-3 group but not in MSC group. There were no significant differences between the MSC-3 and C groups according to morphological findings. Levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were significantly increased in MSC-2 group compared to the other groups (p-values ranged from 0.0001 to 0.04). TNF-α and IL-6 levels in MSC-3 and P-3 groups were lower than PD and C groups (p < 0.0001 for TNF-α and p = 0.0001-0.002 for IL-6). CONCLUSION: Giving MSC may protect the peritoneal membrane from the deleterious effect of PD and extend the life of the peritoneal membrane. Our study is the first on this issue and more detailed studies are needed.

A case of Turner syndrome associated with acute myeloid leukemia (M2).

A 9-year-old girl was diagnosed as acute myeloid leukemia-M2 according to the French-American-British classification. In addition, a diagnosis of Turner syndrome (TS) was made, on the basis of the presence of the chromosomal abnormality, ovarian failure, and abnormal physical features. In particular, children with Down syndrome have increased risk of developing acute myeloblastic leukemia especially M7. On the other hand, cases of myeloid leukemia that are complicated with TS are extremely rare. This is the first report of TS with acute myeloid leukemia of M2 subtype and t (8; 21) in children.