A 65-year-old female was admitted in September 2020 for diabetic ketosis. She had a history of T2D for 16 years. Acarbose and metformin were initially prescribed but were switched to insulin Aspart 30 (20-15 units twice a day) because of poor glucose control since November 2019. She denied a history of using lipoic acid and any drug containing sulfur/sulfhydryl groups (eg, thiols with -SH) such as methimazole, captopril, D-penicillamine, hydralazine, glutathione, methionine, mercaptans, clopidogrel, aurothioglucose, imipenem, penicillin G, and diltiazem. Since June 2020, she had experienced polydipsia and a 10 kg weight loss without any symptoms of hypoglycemia. Her peripheral blood sugar concentrations increased to 20 mmol/L. The patient sought medical advice from our Endocrine Unit. Laboratory tests showed positive ketone body, hyperinsulinemia, and positive IAs. After being admitted to our hospital, her physical examination found her to be very thin, with a BMI of 17.71 kg/m2. Laboratory findings, the level of growth hormone, thyroid and adrenal function, and indexes of autoimmune antibodies were all normal except for hyperlipidemia. Thyroid B-ultrasound and abdominal CT scan were negative. The IAs test revealed that the class of immunoglobulins were strongly positive (3+): > 50 U/mL (average value: 0.00-0.40 U/mL, RBA). The HLA allele of this patient was DRB1*0403.
A 300-min OGTT 82.5g anhydrous glucose was carried out on 07:00 11/09/2020: the basal glucose level was 13.60 mmol/L, with a maximum level of 22.30 mmol/L at 180 min. The plasma insulin ranged from a basal level of 531.50 mIU/L to a peak of 973.00 mIU/L at 240 min, and C-peptide levels (average value: 0.37-1.47mmol/L) were 0.41 nmol/L at the baseline and 0.87 nmol/L at the peak. CGM was performed for 72 hours after admission, which revealed: TIR (3.9 mmol/L <PT <10 mmol/L) of 4.15% (2 h 59 min), TAR (PT > 13.9 mmol/L) of 95.85% (69 h 1 min), TBR (PT <3.9 mmol/L) of 0% (0 min). The patient was hospitalized due to an acute complication of diabetes (diabetic ketosis), and her pancreatic islet function was inferior. After hospitalization, she was continuously monitored for hyperglycemia instead of hypoglycemia. After an intravenous infusion of a small dose of insulin and a large amount of liquid supplement, the ketosis of the patient was relieved. Intensive insulin treatment was given to her after she turned negative for ketone bodies; however, the glucose did not drop significantly compared with that before treatment. Her treatment regimen was changed to acarbose (50 mg three times a day), metformin (0.5 g twice a day), and glargine (18 units once a day). In addition, prednisone was added (5 mg three times a day) for five days. Following this treatment, her glucose level improved gradually. The laboratory tests during follow-ups are shown in Table 2 and Figure 2.