In vivo confirmation of altered hepatic glucose metabolism in patients with liver fibrosis/cirrhosis by 18F-FDG PET/CT

Verloh, Niklas; Einspieler, Ingo; Utpatel, Kirsten; Menhart, Karin; Brunner, Stefan M.; Hofheinz, Frank; Hoff, Jörg van den; Wiggermann, Philipp; Evert, Matthias; Stroszczynski, Christian; Hellwig, Dirk; Grosse, Jirka

doi:10.1186/s13550-018-0452-y

Cited by 31 publications

(17 citation statements)

References 71 publications

(56 reference statements)

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“…In patients with NASH, the [ 18 F]FDG assessed using the SUV analysis showed little promise [ 23 ]. Nevertheless, the increased [ 18 F]FDG update in liver fibrosis observed in this study is in general agreement with the findings of the human study reported by Verloh et al [ 24 ] and the animal study reported by Su et al [ 25 ]. With BDL, GLUT-1 levels quantified by IHC demonstrated increased expression in this study ( Figure 5 ).…”

Section: Discussionsupporting

confidence: 94%

Comparison of ¹⁸F-FDG, ¹⁸F-Fluoroacetate, and ¹⁸F-FEPPA for Imaging Liver Fibrosis in a Bile Duct-Ligated Rat Model

Hsieh

Chu

et al. 2021

Mol Imaging

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Developing sensitive diagnostic methods for a longitudinal evaluation of the status of liver fibrosis is a priority. This study is aimed at assessing the significance of longitudinal positron emission tomography (PET) imaging with 18F-labeling tracers for assessing liver fibrosis in a rat model with bile duct ligation (BDL). Twenty-one 6-week-old Sprague-Dawley male rats were used in this study. Longitudinal PET images using [18F]N-2-(2-fluoroethoxy)benzyl)-N-(4-phenoxypyridin-3-yl)acetamide ([18F]FEPPA) ( n = 3 ), [18F]fluoroacetate ([18F]FAc) ( n = 3 ), and 18F-fluoro-2-deoxy-D-glucose ([18F]FDG) ( n = 3 ) were obtained at 0, 1, and 2 weeks after BDL. Biochemical assays, histological assays, immunohistochemical staining assays, and next generation sequencing analyses were also performed at 0 ( n = 3 ), 1 ( n = 3 ), 2 ( n = 3 ), and 3 ( n = 3 ) weeks after BDL, which demonstrated the severe damage in rat livers after BDL. Regarding [18F]FEPPA and [18F]FDG, there was a significantly higher uptake in the liver after BDL (both P < 0.05 ), which lasted until week 2. However, the uptake of [18F]FAc in the liver was not significantly different before and after BDL ( P = 0.28 ). Collectively, both [18F]FEPPA and [18F]FDG can serve as sensitive probes for detecting the liver fibrosis. However, [18F]FAc is not recommended to diagnose liver fibrosis.

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Section: Discussionsupporting

confidence: 94%

Comparison of ¹⁸F-FDG, ¹⁸F-Fluoroacetate, and ¹⁸F-FEPPA for Imaging Liver Fibrosis in a Bile Duct-Ligated Rat Model

Hsieh

Chu

et al. 2021

Mol Imaging

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“…3c–g ). Because glucose metabolism provides a reliable measure of liver inflammation 34 , we were able to further rule out liver inflammation prior to therapy as a predisposing cause of CD4 + T EM ≥21% hepatitis by estimating hepatic glucose uptake in patients who underwent 18 F-fluoro-2-deoxy- d -glucose ( 18 F-FDG) PET/CT studies as part of routine tumour staging shortly before starting immunotherapy (Fig. 3h ).…”

Section: Resultsmentioning

confidence: 99%

“…Hepatic glucose metabolism as a measure of liver inflammation 34 was analysed retrospectively in all 32 patients who underwent pretreatment 18 F-FDG positron emission tomography and computed tomography (PET-CT) imaging as part of routine tumour staging shortly before starting immunotherapy. After overnight fasting, whole-body PET acquisitions covering at least the trunk were started 60–90 min after i.v.…”

Section: Methodsmentioning

confidence: 99%

Virus-specific memory T cell responses unmasked by immune checkpoint blockade cause hepatitis

et al. 2021

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Treatment of advanced melanoma with combined PD-1/CTLA-4 blockade commonly causes serious immune-mediated complications. Here, we identify a subset of patients predisposed to immune checkpoint blockade-related hepatitis who are distinguished by chronic expansion of effector memory CD4+ T cells (TEM cells). Pre-therapy CD4+ TEM cell expansion occurs primarily during autumn or winter in patients with metastatic disease and high cytomegalovirus (CMV)-specific serum antibody titres. These clinical features implicate metastasis-dependent, compartmentalised CMV reactivation as the cause of CD4+ TEM expansion. Pre-therapy CD4+ TEM expansion predicts hepatitis in CMV-seropositive patients, opening possibilities for avoidance or prevention. 3 of 4 patients with pre-treatment CD4+ TEM expansion who received αPD-1 monotherapy instead of αPD-1/αCTLA-4 therapy remained hepatitis-free. 4 of 4 patients with baseline CD4+ TEM expansion given prophylactic valganciclovir and αPD-1/αCTLA-4 therapy remained hepatitis-free. Our findings exemplify how pathogen exposure can shape clinical reactions after cancer therapy and how this insight leads to therapeutic innovations.

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“…Although glucose levels in the blood of cirrhotic rats and humans in the postprandial period do not differ from the norm ( Table 1 and Table 2 ), the metabolism of glucose in the case of LC undergoes significant changes [ 8 , 31 , 32 , 33 ]. An important indicator of the state of glucose metabolism in the liver is the content of glycogen, the level of which depends on the rates of its synthesis and degradation.…”

Section: Discussionmentioning

confidence: 99%

Postprandial Glycogen Content Is Increased in the Hepatocytes of Human and Rat Cirrhotic Liver

Bezborodkina

Оковитый

Kudryavtsev

2021

Cells

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Chronic hepatitises of various etiologies are widespread liver diseases in humans. Their final stage, liver cirrhosis (LC), is considered to be one of the main causes of hepatocellular carcinoma (HCC). About 80–90% of all HCC cases develop in LC patients, which suggests that cirrhotic conditions play a crucial role in the process of hepatocarcinogenesis. Carbohydrate metabolism in LC undergoes profound disturbances characterized by altered glycogen metabolism. Unfortunately, data on the glycogen content in LC are few and contradictory. In this study, the material was obtained from liver biopsies of patients with LC of viral and alcohol etiology and from the liver tissue of rats with CCl4-induced LC. The activity of glycogen phosphorylase (GP), glycogen synthase (GS), and glucose-6-phosphatase (G6Pase) was investigated in human and rat liver tissue by biochemical methods. Total glycogen and its labile and stable fractions were measured in isolated individual hepatocytes, using the cytofluorometry technique of PAS reaction in situ. The development of LC in human and rat liver was accompanied by an increase in fibrous tissue (20- and 8.8-fold), an increase in the dry mass of hepatocytes (by 25.6% and 23.7%), and a decrease in the number of hepatocytes (by 50% and 28%), respectively. The rearrangement of the liver parenchyma was combined with changes in glycogen metabolism. The present study showed a significant increase in the glycogen content in the hepatocytes of the human and the rat cirrhotic liver, by 255% and 210%, respectively. An increased glycogen content in cells of the cirrhotic liver can be explained by a decrease in glycogenolysis due to a decreased activity of G6Pase and GP.

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In vivo confirmation of altered hepatic glucose metabolism in patients with liver fibrosis/cirrhosis by 18F-FDG PET/CT

Cited by 31 publications

References 71 publications

Comparison of ¹⁸F-FDG, ¹⁸F-Fluoroacetate, and ¹⁸F-FEPPA for Imaging Liver Fibrosis in a Bile Duct-Ligated Rat Model

Comparison of ¹⁸F-FDG, ¹⁸F-Fluoroacetate, and ¹⁸F-FEPPA for Imaging Liver Fibrosis in a Bile Duct-Ligated Rat Model

Virus-specific memory T cell responses unmasked by immune checkpoint blockade cause hepatitis

Postprandial Glycogen Content Is Increased in the Hepatocytes of Human and Rat Cirrhotic Liver

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In vivo confirmation of altered hepatic glucose metabolism in patients with liver fibrosis/cirrhosis by 18F-FDG PET/CT

Cited by 31 publications

References 71 publications

Comparison of 18F-FDG, 18F-Fluoroacetate, and 18F-FEPPA for Imaging Liver Fibrosis in a Bile Duct-Ligated Rat Model

Comparison of 18F-FDG, 18F-Fluoroacetate, and 18F-FEPPA for Imaging Liver Fibrosis in a Bile Duct-Ligated Rat Model

Virus-specific memory T cell responses unmasked by immune checkpoint blockade cause hepatitis

Postprandial Glycogen Content Is Increased in the Hepatocytes of Human and Rat Cirrhotic Liver

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Product

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Comparison of ¹⁸F-FDG, ¹⁸F-Fluoroacetate, and ¹⁸F-FEPPA for Imaging Liver Fibrosis in a Bile Duct-Ligated Rat Model

Comparison of ¹⁸F-FDG, ¹⁸F-Fluoroacetate, and ¹⁸F-FEPPA for Imaging Liver Fibrosis in a Bile Duct-Ligated Rat Model