Patients with Ketosis-prone type 2 diabetes appear more insulin resistant than patients with non-ketotic type 2 diabetes at the time of acute destabilisation

摘要

Aims: Ketosis-prone Type 2 diabetes (KPDM) describes an unusual form of diabetes: the occurrence of ketosis but negative autoantibodies and the ability to manage without long-term insulin therapy. KPDM is considered primarily a result of acute beta cell failure. We reviewed insulin-dose requirements at hospital discharge as a surrogate measure of acute insulin resistance in newly diagnosed antibody-negative diabetes, in patients with and without significant ketonuria. Methods: Data were collected from patients admitted with ketone-positive symptomatic hyperglycaemia at an urban hospital. All cases were treatment-na€ıve on admission with glucose >12mmol/l and subsequently proved to be negative for GAD and ICA antibody. KPDM had admission pH ≤ 7.30, bicarbonate ≤15mmol/l and urinary ketones ≥80mg/dl. Ketosis-only (KO) had ketones ≥80mg/dl but pH >7.30. Type 2 diabetes had ketones ≤40mg/dl. Data are mean SEM. Results: Over 30 months, 9 KPDM, 19 KO and 10 Type 2 diabetes were studied. There was no difference in age between the KPDM, KO and Type 2 diabetes groups (37.8 4.0, 47.8 2.4, 43.0 3.5 years) and a similar distribution of ethnicity. The admission glucose and HbA1c were no different between groups (glucose 37.2 3.2, 32.0 3.2, 34.9 4.1mmol/l; HbA1c 133 10, 120 7, 114 10mmol/mol). Groups had comparable body weight (87.3 3.7, 92.4 7.3, 100.5 6.7kg). There was a trend to greater total daily dose of insulin at discharge in the KPDM group (72.9 3.2 units/day) than the KO (52.0 6.3 units/day) or Type 2 diabetes (49.4 5.1 units/day) groups, p=0.06. This was significant when normalised per kilogram of body weight (0.85 0.04, 0.56 0.06, 0.51 0.07 units/kg/ day; p=0.01). Conclusion: KPDM appears to exhibit greater insulin resistance than other forms of diabetes at acute presentation. Along with beta cell dysfunction, this may be the precipitant for metabolic destabilisation and ketosis.