case_images: PMC9500182_01
case_images: Clinical course of the patient during hospitalization (A) and in the outpatient setting (B).
case_images: fendo-13-997296-g001.jpg
case_images: PMC9500182_01_fendo-13-997296-g001.jpg
case_images: f1
case_images: His clinical course after admission is shown in  Figure 1A . Soft lean mass evaluated by bioelectrical impedance analysis was increased from 46.5 kg at baseline to 50.7 kg after his anti-insulin receptor antibodies became negative, suggesting an improvement in the catabolic state ( Figure 1B ). Platelets counts and hypocomplementemia were also recovered with an improvement of glycemic control and SLEDAI-2K became 1 point seven months after the initiation of therapy ( Figure 1B ).
case_images: Representative glucose profiles of CGM recordings. (A) Representative ambulatory glucose profile recorded by isCGM before treatment. (B) Two-week glucose profiles recorded by rtCGM one month after the initiation of treatment. (C) Two-week glucose profiles recorded by rtCGM nine months after the initiation of treatment.
case_images: fendo-13-997296-g002.jpg
case_images: PMC9500182_01_fendo-13-997296-g002.jpg
case_images: f2
case_images: Inc., CA, U.S.A.) revealed severe hyperglycemia throughout the day without evidence of hypoglycemia ( Figure 2A ). In addition to persistent ketosis, his body weight was progressively reduced, suggesting catabolic state. Figure 2B ) due to early detection of hypoglycemic event. Following these combined treatment strategies, hyperglycemia and ketosis improved, and he was discharged on his 71st admission day. Representative glucose profiling nine months after these treatments is shown in  Figure 2C .