ECEESPE2025 Poster Presentations Diabetes and Insulin (143 abstracts)
Fibrosis and severe steatosis contribute to liver dysfunction in patients with insulin resistance after hematopoietic stem cell transplantation
Haruki Yamano 1 , Kei Takasawa 1 , Reiko Kagawa 2 , Yoko Saito 1 , Ryosei Iemura 1 , Eriko Adachi 1 , Maki Gau 1 , Takeru Yamauchi 1 , Ryuichi Nakagawa 1 , Akito Sutani 1 , Shigeru Takishima 1 , Fukiko Kitahata 3 , 4 , Miyako Murakawa 3 , Takeshi Isoda 1 , Takahiro Kamiya 1 , Tomohiro Morio 1 , Masatoshi Takagi 1 , Satoshi Okada 2 & Kenichi Kashimada & 5
1Institute of Science Tokyo, Department of Pediatrics and Developmental Biology, Tokyo, Japan; 2Hiroshima University, Department of Pediatrics, Hiroshima, Japan; 3Institute of Science Tokyo, Department of Gastroenterology and Hepatology, Tokyo, Japan; 4Institute of Science Tokyo Hospital, Clinical Laboratory, Tokyo, Japan; 5National Center for Child Health and Development, Division of Endocrinology and Metabolism, Tokyo, Japan
JOINT225
Background: Hematopoietic stem cell transplantation (HSCT) survivors can develop a unique form of diabetes mellitus (DM) characterized by severe insulin resistance (IR) and dyslipidemia, despite having a non-obese body habitus. These clinical features resemble those of partial lipodystrophy (PL), and have recently been conceptualized as HSCT-associated PL. In classic PL, liver fibrosis, notably metabolic dysfunction-associated steatohepatitis (MASH), is recognized as a crucial factor determining long-term outcomes. However, few studies have investigated the hepatic status of non-obese post-HSCT patients with DM, emphasizing the need for greater understanding of their underlying pathophysiology.
Methods: We examined 20 non-obese (BMI < 25) HSCT recipients at two Japanese institutions (Institute of Science Tokyo and Hiroshima University). To reduce confounding influences, we excluded patients receiving ongoing corticosteroids or immunosuppressants, as well as those with drug-induced liver injury or hepatic graft-vs-host disease (GVHD). Participants were divided into two groups: those who developed DM with IR (DM group) and those who had not yet manifested DM (DM(-) group). We compared serum markers of liver fibrosis (type IV collagen, hyaluronic acid) alongside hepatic steatosis and fibrosis scores measured by ultrasound elastography, FibroScan® (controlled attenuation parameter [CAP] and liver stiffness measurement [LSM], respectively).
Results: Between the two groups, we found no significant differences regarding age at evaluation, BMI, intensity of conditioning regimens, or serum liver fibrosis markers (type IV collagen and hyaluronic acid). However, time since HSCT was significantly longer in the DM group. Although there was no statistically significant difference in serum fibrosis markers, FibroScan® measurements revealed that both hepatic steatosis and fibrosis scores were significantly higher in the DM group. (CAP: DM group 307 [261–343. 5] dB/m vs. DM(-) group 237 [216. 5–271] dB/m, P = 0. 041, and LSM: DM group 6. 7 [5. 9–9. 9] kPa vs. 4. 1 [3. 5–4. 7] kPa, P = 0. 007)
Discussion: These findings suggest that non-obese HSCT survivors with DM show a pattern of hepatic steatosis and fibrosis consistent with PL. Based on our results, FibroScan® surveillance may be more sensitive than conventional serum markers for detecting early hepatic abnormalities in this population. In a certain case, liver biopsy highlighted a form of fibrosis differing from typical MASH, underscoring the need for further investigation into disease mechanisms.
Conslusion: HSCT survivors can develop not only abnormal glucose and lipid metabolism, but also hepatic dysfunction probably due to PL. FibroScan® is an effective non-invasive tool for assessing liver dysfunction in post-HSCT patients.
Volume 110
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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