title: Metabolic effects of a corticosteroid-free immunosuppressive regimen in recipients of pancreatic transplant.
abstract: BACKGROUND
  A corticosteroid (CS)-free immunosuppressive regimen may be considered less diabetogenic than treatments including CSs principally after pancreas transplantation.
  
  
  METHODS
  To test whether a CS-free immunosuppressive treatment is metabolically superior to a regimen including CSs, we prospectively studied 19 CS-free simultaneous pancreas and kidney (SPK) transplant recipients (body mass index=22+/-1 kg/m2; cyclosporine dose=400+/-19 mg/kg/day; azathioprine dose=77+/-8 mg/day; basal plasma C-peptide=1.3+/-0.12 ng/mL) and 12 matched CS-treated SPK transplant recipients (prednisone dose=9+/-1 mg/day; basal C-peptide=2.2+/-0.2 ng/mL) by means of the 6,6-2H(2)-glucose infusion and the euglycemic insulin clamp (1 mU/kg/min, insulin infusion rate). In addition, six renal transplant recipients receiving a CS-free regimen were also studied as a control group.
  
  
  RESULTS
  In the postabsorptive state, CS-treated SPK transplant recipients demonstrated comparable plasma glucose levels but higher plasma insulin levels than CS-free SPK transplant recipients. Plasma triglyceride levels were significantly higher in CS-treated SPK patients than in CS-free SPK patients (1.16+/-0.16 mg/dL vs. 0.88+/-0.08; P<0.05). High-density lipoprotein and apoprotein A(1) levels were similar in both groups. No difference was observed in pyruvate, lactate, beta-OH-butyrate, and basal endogenous glucose production in all three groups of patients studied. During euglycemic hyperinsulinemia, the inhibition of endogenous glucose production and the stimulation of tissue glucose disposal were not statistically different among the three groups.
  
  
  CONCLUSIONS
  SPK recipients receiving chronic low-dose CS maintenance therapy do not present a lower glucose disposal than CS-free recipients. Nonetheless, this is obtained at the expense of a higher endogenous insulin secretion, which can cause an alteration of the triglyceride profile.
authors.affiliation: Department of Medicine, San Raffaele Scientific Institute, Milan, Italy. luzi.livio@hsr.it
authors.forename: Livio
authors.initials: L
authors.lastname: Luzi
authors.forename: Lucia
authors.initials: L
authors.lastname: Picena Sereni
authors.forename: Alberto
authors.initials: A
authors.lastname: Battezzati
authors.forename: Attilio
authors.initials: A
authors.lastname: Elli
authors.forename: Jean-Paul
authors.initials: JP
authors.lastname: Soulillou
authors.forename: Diego
authors.initials: D
authors.lastname: Cantarovich
mesh_terms: D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D000328:Adult; D001379:Azathioprine / Q000627:therapeutic use; D001786:Blood Glucose / Q000378:metabolism*; D002096:C-Peptide / Q000097:blood; D003520:Cyclophosphamide / Q000627:therapeutic use; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000601:surgery*; D004359:Drug Therapy, Combination; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D016030:Kidney Transplantation / Q000276:immunology / Q000502:physiology*; D007700:Kinetics; D008297:Male; D016035:Pancreas Transplantation / Q000276:immunology / Q000502:physiology*; D011241:Prednisone / Q000627:therapeutic use
chemical_list: D000305:Adrenal Cortex Hormones; D001786:Blood Glucose; D002096:C-Peptide; D007166:Immunosuppressive Agents; D003520:Cyclophosphamide; D001379:Azathioprine; D011241:Prednisone