Startling hyperglycaemia with transient beta cell stunning in a patient with type 2 diabetes.

Yuka Sato, Masaki Kakizawa, Shin-Ichi Aso, Masayuki Takayama,Koh Yamashita,Takahide Miyamoto,Toru Aizawa

ENDOCRINE JOURNAL(2020)

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摘要
A 59-year-old woman unaware of having diabetes was transferred due to coma. Upon discovery at home, her consciousness on the Glasgow Coma Scale was ElV2M4, BP 95/84 mmHg, body temperature 34.7 degrees C. On arrival at ER, height was 1.63 m, weight 97 kg, plasma glucose (PG) 1,897 mg/dL, HbA(1c) 13.6%, osmolality 421 mosm/kg, arterial pH 7.185, lactate 6.34 mmol/L, beta-hydroxybutyrate 7.93 mmol/L. With saline and regular insulin infusion, PG was lowered to 1,440 mg/dL at 2 hours and then to 250 mg/dL by Day 3, and consciousness normalized by Day 5. On admission, serum immunoreactive insulin (IRI) was undetectable (<0.03 U/mL), C-peptide immunoreactivity (CPR) undetectable (<0.003 ng/mL), and anti-glutamic acid decarboxylase antibody negative. Following the above-described treatment, fasting PG was 186 mg/dL and CPR 1.94 ng/mL, respectively, on Day 14; 2-h post-breakfast PG 239 mg/dL and CPR 628 ng/mL, respectively, on Day IS. The patient discharged on Day 18 with 1,800 kcal diet. 32 U insulin glargine and 40 mg gliclazide. Fifteen months later at outpatient clinic, her HbA(1c) was 6.9% and 2-h post-breakfast PG 123 mg/dL and CPR 5.30 nedt, with 750 mg metfonnin, 10 mg gliclazide and 18 U insulin glargine. Transient, but total cessation of insulin secretion was documented in a patient with type 2 diabetes under severe metabolic decompensation. Swift, sustained recovery of insulin release indicated that lack of insulin at the time of emergency was due to secretory failure, i.e., unresponsive exocytotic machinery or depletion of releasable insulin, rather than loss of beta cells.
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关键词
Insulin secretion in vivo,Ketoacidosis,Startling hyperglycaemia
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