MON-653 Rapid Progression of Steatotic Liver in Fulminant Type 1 Diabetes prior to Insulin Therapy

Abstract Disclosure: S. Sakagami: None. A. Uchiyama: None. S. Kiyobayashi: None. Y. Fujiwara: None. C. Son: None. Fulminant type 1 diabetes mellitus (FT1DM) is a subtype of type 1 diabetes, characterized by very rapid progression of islet destruction and absolute insulin deficiency.In FT1DM with diabetic ketoacidosis, steatotic liver sometimes progresses rapidly after insulin administration. We report a very rare case of FT1DM in which steatotic liver developed prior to insulin therapy.A woman in her 30s presented to her primary care physician with 3 days of abdominal pain. Blood tests revealed hyperamylasemia and an abdominal ultrasound demonstrated pancreatic enlargement. She was referred to our hospital on day 6 of the disease. A CT scan showed pancreatic enlargement and fluid collection in the left pararenal space. She was diagnosed with acute pancreatitis and admitted to the hospital. The postprandial blood glucose level was 257 mg/dL and no antidiabetic medication was started. On day 8, the second CT scan showed steatotic liver, which had not been detected in the first CT scan 2 days before. On day 11, Laboratory examination revealed the presence of urinary ketones, fasting hyperglycemia (259 mg/dL), and metabolic acidosis with anion gap level of 21.9 mEq/L. Plasma HbA1c level was 6.1%. Based on these findings, we diagnosed her with diabetic ketoacidosis due to FT1DM and started intravenous insulin infusion. The following day, the ketoacidosis resolved and we switched to subcutaneous insulin injection. Retrospectively measured serum fasting C-peptide levels were low at 1.4 ng/mL with a plasma glucose level of 257 mg/dL on day 6, and became undetectable on day 9 with a plasma glucose level of 350 mg/dL. In a glucose stimulatory test, her serum C-peptide was undetectable after glucagon injection. Islet autoantibodies were not detected. She was discharged on day 28 with a basal-bolus subcutaneous insulin regimen. MRI imaging demonstrated remission of the steatotic liver 4 months after discharge.In conclusion, we experienced a case of FT1DM with the rapid development of steatotic liver prior to insulin therapy, which was confirmed by sequential CT scans.In previous reports, rapid progression of steatotic liver was observed after the initiation of insulin therapy, suggesting that the acute increase in the lipogenic effects of insulin is involved in the accumulation of lipid in hepatocytes. However, in this case, steatotic liver developed prior to insulin treatment, indicating that other unknown mechanisms are involved in this pathophysiology. Presentation: Monday, July 14, 2025

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Journal of the Endocrine Society
Published
2025-10-01
DOI
https://doi.org/10.1210/jendso/bvaf149.1012
Primary Topic
Pancreatic function and diabetes
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article

MON-653 Rapid Progression of Steatotic Liver in Fulminant Type 1 Diabetes prior to Insulin Therapy

Aoi Uchiyama, Yuta Fujiwara, Sakura Kiyobayashi, Cheol Son et al.
Journal of the Endocrine Society
Pancreatic function and diabetes
article

MON-653 Rapid Progression of Steatotic Liver in Fulminant Type 1 Diabetes prior to Insulin Therapy

Aoi Uchiyama, Yuta Fujiwara, Sakura Kiyobayashi, Cheol Son, Satoru Sakagami
article en

Abstract

Abstract Disclosure: S. Sakagami: None. A. Uchiyama: None. S. Kiyobayashi: None. Y. Fujiwara: None. C. Son: None. Fulminant type 1 diabetes mellitus (FT1DM) is a subtype of type 1 diabetes, characterized by very rapid progression of islet destruction and absolute insulin deficiency.In FT1DM with diabetic ketoacidosis, steatotic liver sometimes progresses rapidly after insulin administration. We report a very rare case of FT1DM in which steatotic liver developed prior to insulin therapy.A woman in her 30s presented to her primary care physician with 3 days of abdominal pain. Blood tests revealed hyperamylasemia and an abdominal ultrasound demonstrated pancreatic enlargement. She was referred to our hospital on day 6 of the disease. A CT scan showed pancreatic enlargement and fluid collection in the left pararenal space. She was diagnosed with acute pancreatitis and admitted to the hospital. The postprandial blood glucose level was 257 mg/dL and no antidiabetic medication was started. On day 8, the second CT scan showed steatotic liver, which had not been detected in the first CT scan 2 days before. On day 11, Laboratory examination revealed the presence of urinary ketones, fasting hyperglycemia (259 mg/dL), and metabolic acidosis with anion gap level of 21.9 mEq/L. Plasma HbA1c level was 6.1%. Based on these findings, we diagnosed her with diabetic ketoacidosis due to FT1DM and started intravenous insulin infusion. The following day, the ketoacidosis resolved and we switched to subcutaneous insulin injection. Retrospectively measured serum fasting C-peptide levels were low at 1.4 ng/mL with a plasma glucose level of 257 mg/dL on day 6, and became undetectable on day 9 with a plasma glucose level of 350 mg/dL. In a glucose stimulatory test, her serum C-peptide was undetectable after glucagon injection. Islet autoantibodies were not detected. She was discharged on day 28 with a basal-bolus subcutaneous insulin regimen. MRI imaging demonstrated remission of the steatotic liver 4 months after discharge.In conclusion, we experienced a case of FT1DM with the rapid development of steatotic liver prior to insulin therapy, which was confirmed by sequential CT scans.In previous reports, rapid progression of steatotic liver was observed after the initiation of insulin therapy, suggesting that the acute increase in the lipogenic effects of insulin is involved in the accumulation of lipid in hepatocytes. However, in this case, steatotic liver developed prior to insulin treatment, indicating that other unknown mechanisms are involved in this pathophysiology. Presentation: Monday, July 14, 2025

Journal of the Endocrine SocietyVol. 9(Supplement_1)
Kobe City Nishi-Kobe Medical Center (JP)
Openalex Percentile: Top 52%
Pancreatic function and diabetes
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