OUR WORK
FOCUS AREAS
To achieve our mission, we are actively investigating a number of areas in NAFLD and chronic liver disease including:
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Novel therapies for the treatment of NAFLD:
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Growth hormone-releasing hormone analog, tesamorelin (NIDDK R01 DK114144, Co-PI KEC)
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Aspirin (NIDDK K23 DK122104, PI:TGS)
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Site for industry sponsored clinical trials for adults with NASH and NASH-related cirrhosis
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Biomarker research for hepatic fibrosis in NAFLD and cardiovascular disease in NAFLD (NIDDK R03 DK113349, PI:KEC)
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Prevalence of and biomarkers for NAFLD in persons with HIV (NIDDK R01 DK112293, Co-I, KEC)
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Hepatocellular carcinoma risk factors and chemoprophylaxis
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Cirrhosis: Prospective longitudinal cohort in cirrhosis of all etiologies (Dana Farber Cancer Institute, PI: TGS)
OUR PUBLICATIONS
Effect of combined tobacco use and type 2 diabetes mellitus on prevalent fibrosis in patients with MASLD
Lisa Mun
Jack Bertman
Cheryl A. Rogen
Maryam K. Ibrahim
Madeline Berschback
Eugenia Uche-Anya
Robert Wilechansky
Tracey G. Simon
Kathleen E. Corey
Hepatology Communications
Nov 2023
Several studies have investigated the independent effect of cigarette smoking or type 2 diabetes mellitus (T2DM) on MASLD. However, the interaction effect between tobacco consumption and T2DM on MASLD severity remains underexplored. In this study, we assessed the combined effect of tobacco use and T2DM on hepatic fibrosis in MASLD. We conducted a single-center retrospective cross-sectional analysis of eligible participants from the Mass General Brigham Fibroscan database. The participants were divided into 3 groups: those with T2DM and history of tobacco use (primary exposure group), those with T2DM but no history of tobacco use (secondary exposure group), and those without T2DM and no history of tobacco use (reference group). An additional model was developed, which included a fourth group, participants with a history of tobacco use but no T2DM. The likelihood of fibrosis was determined using a defined fibrosis-4 index cutoff value of 1.3. In addition, we computed the estimated marginal means for liver stiffness measurement and compared the values among the exposure groups. Bivariable and multivariable logistic regression models were used to explore the associations between the exposure groups and the risk for hepatic fibrosis. Overall, 598 individuals were enrolled in the study. The bivariable logistic regression model revealed a significant independent association between T2DM, combined smoking and T2DM, and the outcome of interest, fibrosis. Age, sex, metabolic syndrome, aspirin use, statin use, hemoglobin A1C (A1C), and total bilirubin level were also significantly associated with fibrosis. In the adjusted fibrosis-4 multivariable model (comparing exposure groups to controls), cigarette smoking and T2DM interaction had higher odds of prevalent fibrosis (aOR, 3.04; 95% CI, 1.62-5.76), compared to those with T2DM alone (aOR 2.28; 95% CI, 1.37-3.85). The continuous liver stiffness measurement comparison across the exposure group showed an estimated marginal means of 6.26 (95% CL: 5.58-6.94), 7.54 (95% CL: 6.78-8.30), and 7.88 (6.78-8.99) for reference group, T2DM only group, and tobacco-T2DM group, respectively. The diabetes-only group and the combined tobacco-T2DM group had statistically significant associations with liver stiffness measurement (p values: 0.013 and 0.014, respectively).
Conclusion: Although diabetes is independently associated with hepatic fibrosis in patients with MASLD, the combination of tobacco consumption and diabetes is associated with a higher prevalence of fibrosis. Therefore, lifestyle change through tobacco use cessation in patients with diabetes could be beneficial in reducing the incidence of liver fibrosis among individuals with MASLD.
Aspirin for Metabolic Dysfunction-Associated Steatotic Liver Disease Without Cirrhosis: A Randomized Clinical Trial
Robert Wilechansky
Alessandra Grossman
Laura E Dichtel
Georg M Lauer
Karen K Miller
Yujin Hoshida
Kathleen E. Corey
Rohit Loomba
Raymond T Chung
Andrew T Chan
JAMA Network
Mar 2024
Importance: Aspirin may reduce severity of metabolic dysfunction-associated steatotic liver disease (MASLD) and lower the incidence of end-stage liver disease and hepatocellular carcinoma, in patients with MASLD. However, the effect of aspirin on MASLD is unknown.
Objective: To test whether low-dose aspirin reduces liver fat content, compared with placebo, in adults with MASLD.
Design, setting, and participants: This 6-month, phase 2, randomized, double-blind, placebo-controlled clinical trial was conducted at a single hospital in Boston, Massachusetts. Participants were ages 18 to 70 years with established MASLD without cirrhosis. Enrollment occurred between August 20, 2019, and July 19, 2022, with final follow-up on February 23, 2023.
Interventions: Participants were randomized (1:1) to receive either once-daily aspirin, 81 mg (n=40) or identical placebo pills (n=40) for 6 months.
Main outcomes and measures: The primary end point was mean absolute change in hepatic fat content, measured by proton magnetic resonance spectroscopy (MRS) at 6-month follow-up. The 4 key secondary outcomes included mean percentage change in hepatic fat content by MRS, the proportion achieving at least 30% reduction in hepatic fat, and the mean absolute and relative reductions in hepatic fat content, measured by magnetic resonance imaging proton density dat fraction (MRI-PDFF). Analyses adjusted for the baseline value of the corresponding outcome. Minimal clinically important differences for study outcomes were not prespecified.
Results: Among 80 randomized participants (mean age, 48 years; 44 [55%] women; mean hepatic fat content, 35% [indicating moderate steatosis]), 71 (89%) completed 6-month follow-up. The mean absolute change in hepatic fat content by MRS was -6.6% with aspirin vs 3.6% with placebo (difference, -10.2% [95% CI, -27.7% to -2.6%]; P=.009). Compared with placebo, aspirin treatment significantly reduced relative hepatic fat content (-8.8 vs 30.0 percentage points; mean difference, -38.8 percentage points [95% CI, -66.7 to -10.8]; P=.007), increased the proportion of patients with 30% or greater relative reduction in hepatic fat (42.5% vs 12.5%; mean difference, 30.0% [95% CI, -6.1% to -1.2%]; P=.004]), and reduced relative hepatic fat content by MRI-PDFF (-11.7 vs 15.7 percentage points; mean difference, -27.3 percentage points [95% CI, -45.2 to -9.4]; P=.003). Thirteen participants (32.5%) in each group experienced an adverse event, most commonly upper respiratory tract infections (10.0% in each group) or arthralgias (5.0% for aspirin vs 7.5% for placebo). One participant randomized to aspirin (2.5%) experienced drug-related heartburn.
Conclusions and relevance: In this preliminary randomized clinical trial of patients with MASLD, 6 months of daily low-dose aspirin significantly reduced hepatic fat quantity compared with placebo. Further study in a larger sample size is necessary to confirm these findings.
Prevalence of steatotic liver disease, MASLD, MetALD and significant fibrosis in people with HIV in the United States
Eduardo Vilar-Gomez
Tinsay A Woreta
Jordan E Lake
Laura A Wilson
Jennifer C Price
Susanna Naggie
Richard K Sterling
Sonya Heath
Edward R Cachay
Veeral Ajmera
James Tonascia
Mark S Sulkowski
Naga Chalasani
Rohit Loomba
Alimentary Pharmacology and Therapeutics
Mar 2024
Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) has recently been proposed as a replacement term for NAFLD
Aims: To assess the effects of this new nomenclature on the prevalence and distribution of different SLD categories in people with HIV (PWH) and identified factors associated with MASLD and clinically significant fibrosis (CSF).
Methods: PWH were prospectively enrolled from 9 US centres and underwent clinical evaluation and vibration-controlled transient elastography for controlled attenuation parameter (CAP) and liver stiffness measurement (LSM). SLD was defined as CAP ≥ 263 dB/m, CSF as LSM of ≥8 kPa, and advanced fibrosis (AF) as LSM ≥ 12 kPa. The prevalence of SLD, MASLD, metabolic dysfunstion and alcohol-associated liver disease (MetALD), ALD, cryptogenic (cSLD), CSF and AF were determined. Uni- and multivariate logistic regression models were used to assess factors associated with MASLD and CSF risk.
Results: Of 1065 participants, 74% were male, mean (SD) age 51.6 ± 11.9 years, 46% non-Hispanic Black and 74% with undetectable HIV RNA. The prevalence of SLD was 52%, MASLD 39%, MetALD 10%, ALD 3%, CSF 15% and AF 4%. Only 0.6% had cSLD. Black race was protective whereas obesity, ALT and AST levels were associated with increased risk of MASLD and CSF in MASLD. HIV or antiretroviral therapy did not affect MASLD risk.
Conclusions: MASLD and MetALD are the dominant causes of SLD in PWH, affecting almost half. Application of the new nomenclature resulted in minimal change in the proportion of patients with MASLD who would have been diagnosed previously with NAFLD.
CT Texture Analysis in Nonalcoholic Fatty Liver Disease (NAFLD)
Azadeh Tabari
Nataniel D Mercaldo
Kathleen E. Corey
Jad Husseini
Stephanie A Osganian
Mark L Chicote
Elizabeth M Rao
Karen K Miller
Miriam A Bredella
Journal of Clinical and Experimental Hepatology
Apr 2023
Background: Nonalcoholic fatty liver disease (NAFLD) is the most common form of liver disease worldwide. There are limited biomarkers that can detect progression from simple steatosis to nonalcoholic steatohepatitis (NASH). The purpose of our study was to utilize CT texture analysis to distinguish steatosis from NASH.
Methods: 16 patients with NAFLD (38% male, median (interquartile range): age 57 (48-64) years, BMI 37.5 (35.0-46.8) kg/m^2) underwent liver biopsy and abdominal non-contract CT. CT texture analysis was performed to quantify gray-level tissue summaries (e.g., entropy, kurtosis, skewness, and attenuation) using commercially available software (TexRad, Cambridge England). Logistic regression analyses were performed to quantify the association between steatosis/NASH status and CT texture. ROC curve analysis was performed to determine sensitivity, specificity, AUC, 95% CIs, and cutoff values of texture parameters to differentiate steatosis from NASH.
Results: By histology, 6/16 (37%) of patients had simple steatosis and 10/16 (63%) had NASH. Patients with NASH had lower entropy (median, interquartile range (IQR): 4.3 (4.1, 4.8) vs 5.0 (4.9, 5.2), P=0.013) and lower mean value of positive pixels (MPP) (34.4 (21.8, 52.2) vs 66.5 (57.0, 70.7), P=0.009) than those with simple steatosis. Entropy values below 4.73 predict NASH with 100% (95%CI: 67-100%) specificity and 80% (50-100%) sensitivity, AUC: 0.88. MPP values below 54.0 predict NASH with 100% (67-100%) specificity and 100% (50-100%) sensitivity, AUC 0.90.
Conclusion: Our study provides preliminary evidence that CT texture analysis may serve as a novel imaging biomarker for disease activity in NAFLD and the discrimination of steatosis and NASH.
Growth Hormone Administration Improves Nonalcoholic Fatty Liver Disease in Overweight/Obesity: A Randomized Trial
Kathleen E. Corey
Melanie S Haines
Mark L Chicote
Hang Lee
Allison Kimball
Caitlin Colling
Tracey G Simon
Michelle T Long
Jad Husseini
Miriam A Bredella
Karen K Miller
The Journal of Clinical Endocrinology & Metabolism
Nov 2023
Context: Overweight and obesity are associated with relative growth hormone (GH) deficiency, which has been implicated in the development of nonalcoholic fatty liver disease (NAFLD). NAFLD is a progressive disease without effective treatments.
Objective: We hypothesized that GH administration would reduce hepatic steatosis in individuals with overweight/obesity and NAFLD.
Methods: In this 6-month randomized, double-blind, placebo-controlled trial of low dose GH administration, 53 adults aged 18 to 65 years with BMI ≥ 25 kg/m2 and NAFLD without diabetes were randomized to daily subcutaneous GH or placebo, targeting insulin-like growth factor 1 (IGF-1) to the upper normal quartile. The primary endpoint was intrahepatic lipid content (IHL) by proton magnetic resonance spectroscopy (1H-MRS) assessed before treatment and at 6 months.
Results: Subjects were randomly assigned to a treatment group (27 GH; 26 placebo), with 41 completers (20 GH and 21 placebo) at 6 months. Reduction in absolute % IHL by 1H-MRS was significantly greater in the GH vs placebo group (mean ± SD: -5.2 ± 10.5% vs 3.8 ± 6.9%; P=0.009), resulting in a net mean treatment effect of -8.9% (95% CI, -14.5 to -3.3%). All side effects were similar between groups, except for non-clinically significant lower extremity edema, which was more frequent in the GH vs placebo group (21% vs 0%, P=.02). There were no study discontinuations due to worsening of glycemic status, and there were no significant differences in change in glycemic measures or insulin resistance between the GH and placebo groups.
Conclusion: GH administration reduces hepatic steatosis in adults with overweight/obesity and NAFLD without worsening glycemic measures. The GH/IGF-1 axis may lead to future therapeutic targets for NAFLD.
ADAMTSL2 protein and a soluble biomarker signature identify at-risk non-alcoholic steatohepatitis and fibrosis in adults with NAFLD
Kathleen E. Corey
Rebecca Pitts
Michelle Lai
Joseph Loureiro
Ricard Masia
Stephanie A Osganian
Jenna L Gustafson
Matthew M Hutter
Denise W Gee
Ozanan R Meireles
Elan R Witkowski
Shola M Richards
Jaison Jacob
Nancy Finkel
Debby Ngo
Thomas J Wang
Robert E Gerszten
Chinweike Ukomadu
Lori L Jennings
Journal of Hepatology
Jan 2022
Background & aims: Identifying fibrosis in non-alcoholic fatty liver disease (NAFLD) is essential to predict liver-related outcomes and guide treatment decisions. A protein-based signature of fibrosis could serve as a valuable, non-invasive diagnostic tool. This study sought to identify circulating proteins associated with fibrosis in NAFLD.
Methods: We used aptamer-based proteomics to measure 4,783 proteins in 2 cohorts (Cohort A and B). Targeted, quantitative assays coupling aptamer-based protein pull down and mass spectrometry (SPMS) validated the profiling results in a bariatric and NAFLD cohort (Cohort C and D, respectively). Generalized linear modeling-logistic regression assessed the ability of candidate proteins to classify fibrosis.
Results: From the multiplex profiling, 16 proteins differed significantly by fibrosis in cohorts A (n=62) and B (n=98). Quantitative and robust SPMS assays were developed for 8 proteins and validated in Cohorts C (n=71) and D (n=84). The A disintegrin and metalloproteinase with thrombospondin motifs like 2 (ADAMTSL2) protein accurately distinguished non-alcoholic fatty liver (NAFL)/non-alcoholic steatohepatitis (NASH) with fibrosis stage 0-1 (F0-1) from at-risk NASH with fibrosis stage 2-4, with AUROCs of 0.83 and 0.86 in Cohorts C and D, respectively, and from NASH with significant fibrosis (F2-3), with AUROCs of 0.80 and 0.83 in Cohorts C and D, respectively. An 8-protein panel distinguished NAFL/NASH F0-1 from at-risk NASH (AUROCs 0.90 and 0.87 in Cohort C and D, respectively) and NASH F2-3 (AUROCs 0.89 and 0.83 in Cohorts C and D, respectively). The 8-protein panel and ADAMTSL2 protein had superior performance to the NAFLD fibrosis score and fibrosis-4 score.
Conclusion: The ADAMTSL2 protein and an 8-protein soluble biomarker panel are highly associated with at-risk NASH and significant fibrosis; they exhibited superior diagnostic performance compared to standard of care fibrosis scores.
Lay summary: Non-alcoholic fatty liver disease (NAFLD) is one of the most common causes of liver disease worldwide. Diagnosing NAFLD and identifying fibrosis (scarring of the liver) currently requires a liver biopsy. Our study identified novel proteins found in the blood which may identify fibrosis without the need for a liver biopsy.
Expression of IGF-1 receptor and GH receptor in hepatic tissue of patients with nonalcoholic fatty liver disease and nonalcoholic steatohepatitis
Stephanie A Osganian
Sonu Subudhi
Ricard Masia
Hannah K Drescher
Lea M Bartsch
Mark L Chicote
Raymond T Chung
Denise W Gee
Elan R Witkowski
Miriam A Bredella
Georg M Lauer
Kathleen E. Corey
Growth Hormone & IGF Research
Aug 2022
Objective: The GH and IGF-1 axis is a candidate disease-modifying target in nonalcoholic fatty liver disease (NAFLD) given its lipolytic, anti-inflammatory and anti-fibrotic properties. IGF-1 receptor (IGF-1R) and GH receptor (GHR) expression in adult, human hepatic tissue is not well understood across the spectrum of NAFLD severity. Therefore, we sought to investigate hepatic IGF-1R and GHR expression in subjects with NAFLD utilizing gene expression analysis (GEA) and immunohistochemistry (IHC).
Design: GEA (n=318) and IHC (n=30) cohorts were identified from the Massachusetts General Hospital NAFLD Tissue Repository. GEA subjects were categorized based on histopathology as normal liver histology (NLH), steatosis only (Steatosis), nonalcoholic steatohepatitis (NASH) without fibrosis (NASH F0), and NASH with fibrosis (NASH F1-4) with GEA by the Nanostring nCounter assay. IHC subjects were matched for age, body mass index (BMI), sex, and diabetic status across three groups (n=10 each): NLH, Steatosis, and NASH with fibrosis (NASH F1-3). IHC for IGF-1R, IGF-1 and GHR was performed on formalin-fixed, paraffin-embedded hepatic tissue samples.
Results: IGF-1R gene expression did not differ across NAFLD severity while IGF-1 gene expression decreased with increasing NAFLD severity, including when controlled for BMI and age. GHR expression did not differ by severity of NAFLD based on GEA or IHC.
Conclusions: IGF-1R and GHR expression levels were not significantly different across NAFLD disease severity. However, expression of IGF-1 was lower with increasing severity of NAFLD. Additional research is needed regarding the contribution of the GH/IGF-1 axis to the pathophysiology of NAFLD and NASH.
Risk of Cardiovascular Disease in Individuals With Nonobese Nonalcoholic Fatty Liver Disease
Ashwini Arvind
Jacqueline B Henson
Stephanie A Osganian
Cheryl Nath
Lara M Steinhagen
Zoe N Memel
Arley Donovan
Oluwafemi Balogun
Raymond T Chung
Tracey G Simon
Kathleen E. Corey
Hepatology Communications
Feb 2022
Nonalcoholic fatty liver disease (NAFLD) is independently associated with obesity and cardiovascular disease (CVD). CVD is the primary cause of mortality in the predominantly obese population of adults with NAFLD. NAFLD is increasingly seen in individuals who are lean and overweight (i.e., nonobese), but it is unclear whether their risk of CVD is comparable to those with NAFLD and obesity. Using a prospective cohort of patients with NAFLD, we compared the prevalence and incidence of CVD in individuals with and without obesity. NAFLD was diagnosed by biopsy or imaging after excluding other chronic liver disease etiologies. Logistic regression was used to compare the odds of baseline CVD by obesity status. Cox proportional hazards regression was used to evaluate obesity as a predictor of incident CVD and to identify predictors of CVD in subjects with and without obesity. At baseline, adults with obesity had a higher prevalence of CVD compared to those without obesity (12.0% vs 5.0%, P=0.02). During follow-up, however, obesity did not predict incident CVD (hazard ratio [HR], 1.24; 95% confidence interval [CI], 0.69-2.22) or other metabolic diseases. Findings were consistent when considering body mass index as a continuous variable and after excluding subjects who were overweight. Age (adjusted HR [aHR], 1.05; 95% CI, 1.03-1.08), smoking (aHR, 4.61; 95% CI, 1.89-11.22), and decreased low-density lipoprotein levels (aHR, 0.98; 95% CI, 0.96-1.00) independently predicted incident CVD in the entire cohort, in subjects with obesity, and in those without obesity, respectively. Conclusion: Individuals with overweight or lean NAFLD are not protected from incident CVD compared to those with NAFLD and obesity, although CVD predictors appear to vary between these groups. Patients without obesity also shoudl undergo rigorous risk stratification and treatment.
Aspirin Use Is Associated with a Reduced Incidence of Hepatocellular Carcinoma: A Systematic Review and Meta‐analysis
Hepatology Communications
Nov 13, 2020
Hepatocellular carcinoma (HCC) is the third‐leading cause of cancer‐related death worldwide, with a growing incidence and poor prognosis. While some recent studies suggest an inverse association between aspirin use and reduced HCC incidence, other data are conflicting. To date, the precise magnitude of risk reduction—and whether there are dose‐dependent and duration‐dependent associations—remains unclear. To provide an updated and comprehensive assessment of the association between aspirin use and incident HCC risk, we conducted a systematic review and meta‐analysis of all observational studies published through September 2020. Using random‐effects meta‐analysis, we calculated the pooled relative risks (RRs) and 95% confidence intervals (CIs) for the association between aspirin use and incident HCC risk. Where data were available, we evaluated HCC risk according to the defined daily dose of aspirin use. Among 2,389,019 participants, and 20,479 cases of incident HCC, aspirin use was associated with significantly lower HCC risk (adjusted RR, 0.61; 95% CI, 0.51‐0.73; P ≤ 0.001; I2 = 90.4%). In subgroup analyses, the magnitude of benefit associated with aspirin was significantly stronger in studies that adjusted for concurrent statin and/or metformin use (RR, 0.45; 95% CI, 0.28‐0.64) versus those that did not (Pheterogeneity = 0.02), studies that accounted for cirrhosis (RR, 0.49; 95% CI, 0.45‐0.52) versus those that did not (Pheterogeneity = 0.02), and studies that confirmed HCC through imaging/biopsy (RR, 0.30; 95% CI, 0.15‐0.58) compared with billing codes (Pheterogeneity < 0.001). In four studies, each defined daily dose was associated with significantly lower HCC risk (RR, 0.98; 95% CI, 0.97‐0.98), corresponding to an 8.4% risk reduction per year of aspirin use. Conclusion: In this comprehensive systematic review and meta‐analysis, aspirin use was associated with a significant reduction in HCC risk. These benefits appeared to increase with increasing dose and duration of aspirin use.
Expert Panel Review on Non-Alcoholic Fatty Liver Disease in Persons with HIV
Jordan E Lake,
Turner Overton,
Susanna Naggie,
Mark Sulkowski,
Rohit Loomba,
David E Kleiner,
Jennifer C Price,
Kara W Chew,
Raymond T Chung,
Kathleen E Corey
Clinical Gastroenterology and Hepatology
Oct 15, 2020
Non-alcoholic fatty liver disease (NAFLD) affects 25% of adults in the general population and is a disease spectrum ranging from steatosis to non-alcoholic steatohepatitis (NASH) to end-stage liver disease. NAFLD is an independent risk factor for cardiovascular disease, diabetes mellitus and all-cause mortality, and NASH cirrhosis is a frequent indication for liver transplantation. In persons with HIV (PWH), chronic liver disease is the second leading cause of non-HIV-related mortality. Between 20-63% of PWH have NASH, and 14-63% have NASH with fibrosis. However, little is known about the optimal diagnostic strategies, risk factors for and treatment of NAFLD in PWH. Here we review current data on and identify knowledge gaps in the epidemiology, pathophysiology, diagnosis and management of NAFLD in PWH and highlight priorities for research.
Mortality in biopsy-confirmed nonalcoholic fatty liver disease: results from a nationwide cohort
Gut
Oct 9, 2020
This nationwide, matched cohort study included all individuals in Sweden with biopsy-confirmed NAFLD (1966 to 2017; n=10 568) to assess the risk of overall and cause-specific mortality across the spectrum of NAFLD histology. Over a median of 14.2 years, 4,338 NAFLD patients died. Compared with controls, NAFLD patients had significantly increased overall mortality (16.9 vs 28.6/1000 PY; aHR=1.93, 95% CI=1.86 to 2.00). Compared with controls, significant excess mortality risk was observed with simple steatosis (8.3/1000 PY, aHR=1.71, 95% CI=1.64 to 1.79), non-fibrotic NASH (13.4/1000 PY, aHR=2.14, 95% CI=1.93 to 2.38), non-cirrhotic fibrosis (18.4/1000 PY, aHR=2.44, 95% CI=2.22 to 2.69) and cirrhosis (53.6/1000 PY, aHR=3.79, 95% CI=3.34 to 4.30)( ptrend <0.01). Excess mortality associated with NAFLD was primarily from extrahepatic cancer (4.5/1000 PY, aHR=2.16, 95% CI=2.03 to 2.30), cirrhosis (2.7/1000 PY, aHR=18.15, 95% CI=14.78 to 22.30), cardiovascular disease (1.4/1000 PY, aHR=1.35, 95% CI=1.26 to 1.44) and hepatocellular carcinoma (HCC) (1.2/1000 PY, aHR=11.12, 95% CI=8.65 to 14.30).
Conclusion: All NAFLD histological stages were associated with significantly increased overall mortality, and this risk increased with worsening histology. Most of this excess mortality was from extrahepatic cancer and cirrhosis.
OUR POSTERS
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Clinical Process Improvement Leadership Program (CPIP)
Our Project:
"Early detection, reporting, and evaluation of incidentally identified hepatic steatosis".
Nonalcoholic fatty liver disease (NAFLD) is emerging as the most prevalent cause of chronic liver disease in the United States (US). The incidence of NAFLD is rising and has contributed to an increased number of incidental findings of hepatic steatosis on abdominal imaging. Late detection and management of the progressive form of NAFLD, nonalcoholic steatohepatitis (NASH), pose an increased risk of developing fibrosis, cirrhosis, and hepatocellular carcinoma. Furthermore, a lack of adequate support and early clinical intervention can also promote the risk of liver-related death and all-cause mortality. Therefore, early identification and appropriate etiology evaluation are crucial considering the deleterious effect of fatty liver sequelae.
Overall Hypothesis:
We hypothesize that the proposed intervention will lead to an increase in the number and proportion of documentation, referral, and evaluation of incidentally discovered hepatic steatosis.
To quantitatively assess the impact of the intervention, both baseline and follow-up abdominal imaging data would be obtained from the Massachusetts General Hospital (MGH) radiology department database. The baseline data would comprise radiology reports from January 2021 to December 2021. In the event of low reports (in contrast to the expected), the evaluation period would be adjusted to January – December 2019 (to account for the possible reduced radiology visits on account of the pandemic). In addition, a random survey of a proportion of the extracted reports would be selected (1 – 6-month period depending on the feasibility). The selection would be restricted to newly identified hepatic steatosis at the time of reporting.