Autologous bone marrow stem cell transplantation for the treatment of type 2 diabetes mellitus / 中华医学杂志(英文版)

ABSTRACT

<p><b>BACKGROUND</b>Autologous peripheral stem cell transplantation was first reported in 2007 to treat type 1 diabetes mellitus (DM) and achieved encouraging effect, but whether similar outcome can be achieved in type 2 DM is not well demonstrated. The objective of this study was to determine the effect of combination of autologous bone marrow stem cell transplantation (BMT) and hyperbaric oxygen treatment on type 2 DM.</p><p><b>METHODS</b>The study involved 31 patients with type 2 DM (aged 33 to 62 years) from January 2009 to January 2011 in the Central Hospital of Wuhan, China. Clinical variables (body mass index, duration of DM, insulin requirement, oral hypoglycemic drugs, time free from insulin, time free from oral drugs) and laboratory variables (hemoglobin A1c (HbA1c)), mononuclear cells infused, and C-peptide in four time points) were assessed. Purified bone marrow stem cells were infused into major pancreatic arteries. Follow-up was performed at the 30, 90, 180, 360, 540 and 720 days (mean 321 days) after BMT.</p><p><b>RESULTS</b>Mean HbA1c values showed a significant reduction during follow-up in all patients after BMT. It decreased by more than 1.5% (from 8.7% to 7.1%) as quickly as at 30 days after BMT. Afterwards mean HbA1c fluctuated between plus or minus 0.5% until 24 months rather than declined continuously. At 90 days after the combined therapy C-peptide increased significantly compared with baseline (P < 0.0001). But in other time points C-peptide was similar with baseline data (P > 0.3). All patients had insulin and/or oral hypoglycemic drugs reduced to different levels. The dose of insulin of 7 patients (7/26, 27%) reduced for a period of time after BMT.</p><p><b>CONCLUSIONS</b>Combined therapy of intrapancreatic BMT and hyperbaric oxygen treatment can improve glucose control and reduce the dose of insulin and/or oral hypoglycemic drugs in type 2 DM patients, but it only improve pancreatic β-cell function transiently. Further randomized controlled clinical trials involved more patients will be required to confirm these findings and the mechanism needs to be illustrated deeply.</p>