Article Text

  1. A Gaiero1,
  2. S Bonanomi2,
  3. A Rovelli2,
  4. G Fichera1,
  5. A Boscarini1,
  6. R Mulas1,
  7. S Zecca1,
  8. A Cohen1
  1. 1Department of Pediatrics, San Paolo Hospital, Savona, Italy,
  2. 2Department of Pediatrics, San Gerardo Hospital, Monza, Italy


Few studies deal with impaired glucose metabolism in patients after HSCT. Beta-cell damage was reported in relation to chemotherapy agents, irradiation, chronic GvHD, endocrinological disorders and hormone treatments. Seven patients out of 201 HSCT survivors, developed diabetes at a median time of 11.7 years after transplant performed during childhood. The prevalence of diabetes in the studied population is 3.48% and the median age at diagnosis 20.35 years (11.2–34.4). The onset of diabetes in all patients was insidious and none had diabetic ketoacidosis. Diagnosis was made on fasting glycemia more than 125 mg/dl in four patients, oral glucose tolerance test (OGTT) in the remaining three patients who had impaired fasting glycemia. Fasting insulinemia was normal in five patients and elevated in two. Specific beta-cell autoantibodies for type-1 diabetes were negative in all patients. Body-Mass Indexes (BMI) at diabetes diagnosis were normal in all patients except one, who was at risk for obesity (BMI above the 85th percentile). Four patients required insulin treatment (two at diagnosis and two during follow-up); the remaining three patients, recently diagnosed, are on diet therapy only. These data make difficult to classify our patients as having type-1 or type-2 diabetes: only two patients had typical type-2 diabetes features although one had normal BMI.

We recommend that clinicians carefully evaluate even slight elevation of fasting blood glucose in HSCT patients, performing OGTT in the presence of confirmed fasting glycemia above 100 mg/dl. Diabetes should be considered as one of the endocrinological late-effect complications after HCT.

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