Manifold implications of forgotten hyperglycemia in clinical opiate dependence

Both chronic opiate dependence and diabetes are widespread public health problems. The historically causal relationship between opiate pharmacology and hyperglycemia would appear to have fallen from current medical knowledge. The aims of this study were to assess the severity of hyperglycemia in our opiate substance use disorder (SUD) patient population and review its pathophysiological basis. A review was undertaken of our clinical pathology database, comparing SUD patients and general medical controls (NSUD). A total of 1,602 SUD patients were compared with 2,858 NSUD patients 15-50 years of age. Mean ages were 31.29 ± 7.40 and 31.55 ± 9.17 years, respectively (P = 0.42) and were 68.60 and 52.76% male (P < 0.0001). The glycosylated hemoglobin (HbA1c) level in diabetics was 8.14 ± 2.76 and 6.29 ± 1.88 (P = 0.0032). In a nested case-control subset, random glucose, HbA1c, and fructosamine levels were all significantly elevated (P < 0.05). Adjusted for age, the HbA1c level was elevated among the SUD group (P < 0.0001) the age at addiction interaction was also significant (P < 0.0001). Serum glucose, HbA1c, fructosamine, and microalbumin levels were shown to be biomarkers of age. At multiple regression analysis, interactions between age, addictive status, glycemia, and the inflammatory markers, ethrocyte sedimentation rate and C-reactive protein, were significant (P < 0.05). At age 50, diabetic SUD patients had a HbA1c of 8.31%, which was equivalent to that of NSUD patients at age 140.54 years, a 181.07% elevation. These results confirm that hyperglycemia is higher in both an absolute and an age-dependent sense among diabetic SUD patients. These results are consistent with an acceleration of age-related and degenerative pathologies in many tissues and therefore carry far-reaching implications for the safety of indefinite opiate maintenance.