Experience sharing of glucose management in a patient with LADA

Medical history and basic diagnosis

The patient was diagnosed with T2DM one year ago in an outside hospital and had been hospitalized for diabetic ketosis. The patient was admitted to the hospital with “T2DM, diabetic ketosis” because of sudden onset of vomiting with no obvious cause.

Examination: HbA1c 11.7%, fasting glucose 10.2 mmol/L, OGTT 2 h postprandial glucose 22.9 mmol/L; C-peptide release test fasting, 1 h postprandial and 2 h levels 1.15 ng/ml, 1.50 ng/ml and 1.39 ng/ml respectively; blood ketones 2.1 mmol/L; diabetic autoantibodies: glutathione /L; diabetic autoantibodies: weakly positive for glutamic acid decarboxylase (GAD) antibody.

Admission diagnosis: LADA, diabetic ketosis, diabetic peripheral neuropathy.

Interpretation of treatment plan based on FGM

The patient was characterized as a young new-onset diabetic patient, staging to be determined, with markedly elevated blood glucose on admission, possible insulin sensitivity, and high blood glucose fluctuations. The treatment plan was to correct ketosis and use subcutaneous insulin pump to intensify glucose lowering, apply FGM to monitor blood glucose dynamically, and use dynamic glucose profile (AGP) to fine-tune glucose

The initial insulin pump basal rate was 0.7 u/h with three meals of 8u, 6u and 6u, and the dose was adjusted in combination with FGM monitoring (Figure 3)

On day 4, the FGM showed that the patient’s postprandial glucose was still high, especially after breakfast, so the basal rate of insulin pump was adjusted to 0.9 u/h and the amount of three meals was adjusted upward to 10u, 8u and 8u. On day 7, after the patient’s blood glucose stabilized, OGTT and insulin and C-peptide release tests were performed (Figure 4).

After the diagnosis of LADA, three short and one long glucose-lowering regimens (glargine insulin + menthol insulin before three meals) were adopted, and the dose regimen was adjusted in conjunction with the FGM blood glucose monitoring, and the patient’s blood glucose continued to reach the standard smoothly (Figure 5).

Treatment experience

Dr. Xiao concluded that the diagnosis of LADA was established because of the patient’s young age of onset (<40 years old), obvious symptoms of three excesses and one deficiency, ketosis onset, multiple positive diabetic antibodies, and other autoimmune diseases (Hashimoto’s disease), and poor islet function even after intensive glucose lowering. In the process of precise glucose regulation, stabilization and auxiliary diagnostic tests after admission, FGM monitoring played an important role, allowing the doctor to finely adjust the glucose-lowering plan and dose, and achieve satisfactory treatment results in a short period of Time.

This patient was admitted with such high blood glucose and ketosis. An OGTT should not be performed in this case, nor should a C-peptide release test be performed to understand B-cell function; it should wait until the blood glucose has stabilized.