Non-alcoholic fatty liver disease (NAFLD) is becoming increasingly prevalent worldwide, affecting up to 30% of the global population. NAFLD is closely associated with obesity and type 2 diabetes. While initially characterized by excess fat accumulation in the liver (steatosis), some patients can progress to develop more severe non-alcoholic steatohepatitis (NASH) and liver fibrosis. Accurate staging of fibrosis is important for predicting outcomes but liver biopsy is invasive and not always practical. Non-invasive tests (NITs) using blood tests or imaging can help stratify patients' risk of advanced fibrosis as an alternative to biopsy. Lifestyle modifications addressing diet and exercise are recommended for managing NAFL
This document discusses identifying and managing advanced fibrosis due to nonalcoholic steatohepatitis (NASH). It begins by outlining the impact of advanced fibrosis, including increased risk of liver-related morbidity and mortality as well as potential for rapid progression to cirrhosis in some patients. It then examines challenges with biopsy as the reference standard for identification given sampling error and limitations. Non-invasive tests are presented as an alternative, with sequential use of two tests recommended. The document concludes by emphasizing the importance of identifying advanced fibrosis patients to prevent cirrhosis and complications.
This document provides an overview of current treatment and updates on non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). It begins with definitions of NAFLD and NASH. It then discusses the prevalence of NAFLD globally and in Asian countries. Risk factors and the pathogenesis involving the gut microbiota and a potential role in lean NASH are reviewed. Current methods for diagnosis including laboratory tests, imaging, serum biomarkers, and liver biopsy are summarized. Current treatment options including lifestyle modifications, metformin, pioglitazone, and vitamin E are mentioned. Several newer potential treatment approaches are also listed. The role of transient elastography in management is
American Association of Clinical Endocrinology Clinical Practice [Autosaved]....vardhini14
This document provides clinical practice guidelines for the diagnosis and management of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) from the American Association of Clinical Endocrinology. It recommends screening high risk individuals, such as those with obesity or diabetes, for NAFLD. The fibrosis-4 index is the preferred initial blood test to assess liver fibrosis risk. Lifestyle modifications including 5-10% weight loss through diet and exercise are first-line management strategies. For patients with diabetes and NASH, treatment with pioglitazone, GLP-1 receptor agonists, or SGLT2 inhibitors may provide benefit. Referral to a specialist
Non-alcoholic fatty liver disease (NAFLD) is the most common liver disorder in Western countries, affecting 17-46% of adults. NAFLD often parallels metabolic syndrome and its risk factors like obesity and diabetes. The guidelines recommend screening individuals with metabolic risk factors or obesity for NAFLD through procedures to diagnose fatty liver. A liver biopsy is needed to diagnose non-alcoholic steatohepatitis (NASH) by identifying features like steatosis, lobular inflammation and ballooning. Non-invasive markers can help identify those at high risk of fibrosis and reduce the need for biopsies. NAFLD is closely associated with insulin resistance and metabolic syndrome.
Common liver Disease in Primary Care SettingChernHaoChong
- The document discusses common liver problems encountered in primary care, including abnormal liver function tests, abnormal findings on liver ultrasound, and viral hepatitis serology interpretations.
- Studies show that only a small percentage of abnormal liver function tests are actually due to liver disease, while the majority are caused by cancer, cardiovascular disease, or respiratory disease.
- Non-alcoholic fatty liver disease is increasingly common in Asia, with genetic factors playing a stronger role. Screening and management of metabolic complications is important when NAFLD/NASH is identified.
- Assessment for significant liver fibrosis or cirrhosis is important for high-risk NAFLD/NASH patients, while lifestyle modifications remain the first-line
The document discusses the proposal to change the name of non-alcoholic fatty liver disease (NAFLD) to metabolic associated fatty liver disease (MAFLD). It notes that NAFLD's name does not accurately capture the metabolic nature of the disease. The name change was proposed by an international panel of experts and aims to reduce stigmatization and increase consideration of the disease. If adopted, MAFLD would be used instead of NAFLD to describe fatty liver disease associated with metabolic dysfunction. The document supports the name change as a way to properly frame the growing epidemic of this liver disease.
Slides From Hot Topics in NASH:New Strategies for the Diagnosis of NASH.2019hivlifeinfo
Slides From Hot Topics in NASH: New Strategies for the Diagnosis of NASH
xpert faculty present key data on current and emerging NASH treatment options for your patients.
Rita Basu, MD
Wing-Kin Syn, MBChB, PhD, FACP, FRCP
Format: Microsoft PowerPoint (.ppt)
File Size: 3.84 MB
Released: February 11, 2019
Evidence based management of Non Alcoholic fatty liver diseaseJayastu Senapati
Non-Alcoholic Fatty Liver Disease (NAFLD) is a growing problem, with a prevalence of 9-32% in India. The document discusses the epidemiology, diagnosis, and treatment of NAFLD. For diagnosis, it recommends using diagnostic indices along with imaging and liver tests, with biopsy as a last resort. Treatment involves lifestyle changes like exercise and diet modification as the most important non-pharmacological approach. Pharmacological options and investigational therapies are also discussed.
This document discusses identifying and managing advanced fibrosis due to nonalcoholic steatohepatitis (NASH). It begins by outlining the impact of advanced fibrosis, including increased risk of liver-related morbidity and mortality as well as potential for rapid progression to cirrhosis in some patients. It then examines challenges with biopsy as the reference standard for identification given sampling error and limitations. Non-invasive tests are presented as an alternative, with sequential use of two tests recommended. The document concludes by emphasizing the importance of identifying advanced fibrosis patients to prevent cirrhosis and complications.
This document provides an overview of current treatment and updates on non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). It begins with definitions of NAFLD and NASH. It then discusses the prevalence of NAFLD globally and in Asian countries. Risk factors and the pathogenesis involving the gut microbiota and a potential role in lean NASH are reviewed. Current methods for diagnosis including laboratory tests, imaging, serum biomarkers, and liver biopsy are summarized. Current treatment options including lifestyle modifications, metformin, pioglitazone, and vitamin E are mentioned. Several newer potential treatment approaches are also listed. The role of transient elastography in management is
American Association of Clinical Endocrinology Clinical Practice [Autosaved]....vardhini14
This document provides clinical practice guidelines for the diagnosis and management of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) from the American Association of Clinical Endocrinology. It recommends screening high risk individuals, such as those with obesity or diabetes, for NAFLD. The fibrosis-4 index is the preferred initial blood test to assess liver fibrosis risk. Lifestyle modifications including 5-10% weight loss through diet and exercise are first-line management strategies. For patients with diabetes and NASH, treatment with pioglitazone, GLP-1 receptor agonists, or SGLT2 inhibitors may provide benefit. Referral to a specialist
Non-alcoholic fatty liver disease (NAFLD) is the most common liver disorder in Western countries, affecting 17-46% of adults. NAFLD often parallels metabolic syndrome and its risk factors like obesity and diabetes. The guidelines recommend screening individuals with metabolic risk factors or obesity for NAFLD through procedures to diagnose fatty liver. A liver biopsy is needed to diagnose non-alcoholic steatohepatitis (NASH) by identifying features like steatosis, lobular inflammation and ballooning. Non-invasive markers can help identify those at high risk of fibrosis and reduce the need for biopsies. NAFLD is closely associated with insulin resistance and metabolic syndrome.
Common liver Disease in Primary Care SettingChernHaoChong
- The document discusses common liver problems encountered in primary care, including abnormal liver function tests, abnormal findings on liver ultrasound, and viral hepatitis serology interpretations.
- Studies show that only a small percentage of abnormal liver function tests are actually due to liver disease, while the majority are caused by cancer, cardiovascular disease, or respiratory disease.
- Non-alcoholic fatty liver disease is increasingly common in Asia, with genetic factors playing a stronger role. Screening and management of metabolic complications is important when NAFLD/NASH is identified.
- Assessment for significant liver fibrosis or cirrhosis is important for high-risk NAFLD/NASH patients, while lifestyle modifications remain the first-line
The document discusses the proposal to change the name of non-alcoholic fatty liver disease (NAFLD) to metabolic associated fatty liver disease (MAFLD). It notes that NAFLD's name does not accurately capture the metabolic nature of the disease. The name change was proposed by an international panel of experts and aims to reduce stigmatization and increase consideration of the disease. If adopted, MAFLD would be used instead of NAFLD to describe fatty liver disease associated with metabolic dysfunction. The document supports the name change as a way to properly frame the growing epidemic of this liver disease.
Slides From Hot Topics in NASH:New Strategies for the Diagnosis of NASH.2019hivlifeinfo
Slides From Hot Topics in NASH: New Strategies for the Diagnosis of NASH
xpert faculty present key data on current and emerging NASH treatment options for your patients.
Rita Basu, MD
Wing-Kin Syn, MBChB, PhD, FACP, FRCP
Format: Microsoft PowerPoint (.ppt)
File Size: 3.84 MB
Released: February 11, 2019
Evidence based management of Non Alcoholic fatty liver diseaseJayastu Senapati
Non-Alcoholic Fatty Liver Disease (NAFLD) is a growing problem, with a prevalence of 9-32% in India. The document discusses the epidemiology, diagnosis, and treatment of NAFLD. For diagnosis, it recommends using diagnostic indices along with imaging and liver tests, with biopsy as a last resort. Treatment involves lifestyle changes like exercise and diet modification as the most important non-pharmacological approach. Pharmacological options and investigational therapies are also discussed.
This document provides an overview of non-alcoholic fatty liver disease (NAFLD) including its definitions, risk factors, pathogenesis, diagnosis, complications, screening recommendations, and treatment options. It discusses how NAFLD is the most common liver disease in Western countries, closely linked to metabolic syndrome. The key aspects are that lifestyle modifications targeting 7-10% weight loss are the first-line treatment. Pharmacotherapy with pioglitazone or vitamin E may be considered for patients with NASH, especially those with significant fibrosis. Ongoing research is exploring additional novel pharmacologic treatments.
The document discusses non-alcoholic fatty liver disease (NAFLD), which includes a spectrum of conditions from simple steatosis to non-alcoholic steatohepatitis (NASH) and cirrhosis. NAFLD is strongly associated with obesity and metabolic syndrome. The prevalence of NAFLD is increasing globally and varies from 5-30% in different regions. Diagnosis requires imaging and liver biopsy. Treatment focuses on lifestyle modifications and medications to improve insulin resistance.
This document summarizes non-alcoholic fatty liver disease (NAFLD) from an endocrinology perspective. It defines NAFLD and related terms, discusses the pathophysiology involving insulin resistance and lipotoxicity, epidemiology as a growing global problem, challenges in diagnosis and evaluation, and currently available treatment options focusing on lifestyle modification and insulin sensitizers. Key points covered include the need for accurate definitions to classify disease subtypes, the role of the adipose tissue-liver axis in disease progression, and limitations of non-invasive testing underscoring the continued need for liver biopsy in certain cases.
This document discusses the management of diabetes in patients with concomitant liver disease. It notes that about half of patients with cirrhosis have diabetes due to insulin resistance caused by the liver disease. Lifestyle changes and metformin are recommended initially if liver disease is mild. Insulin, sulfonylureas, meglitinides, alpha-glucosidase inhibitors, and thiazolidinediones may be used, with monitoring needed due to potential side effects or altered drug metabolism in liver disease. Insulin requirements can vary depending on the stage of liver disease.
Abstract— Non Alcoholic Fatty Liver Disease is also becoming public health impotance nowadays. So this study was aimed to determine the association of Non Alcoholic Fatty Liver Disease with metabolic syndrome and Cardio-Vascular disease along with assessment of degree of severity of NAFLD with respect to number of components of metabolic syndrome. This study includes a total of 222 subjects were enrolled as per the inclusion/exclusion criteria, out of which 110 cases who had NAFLD with hepatic steatosis on ultrasonography and 112 subjects who did not have NAFLD were considered control. These cases and controls were interrogated and investigated further. Observations were recorded and association of Non Alcoholic Fatty Liver Disease with metabolic syndrome and Cardio-Vascular disease along with assessment of degree of severity of NAFLD with respect to number of components of metabolic syndrome. Statistical methods used were unpaired student’s t-test for continuous variables, Fischer’s and chi-sq test for categorical variables using bivariate analysis by Graph Pad Instat Version 3.10. Risk was assessed in terms of Odd's Ratio. The patients with MS and NAFLD had a higher proportion of CVD compared with those who did not have NAFLD (29.1 vs 18.1 %). This study concludes that NAFLD is significantly associated with MS; most significant with WC, followed by TG and FBS and thus can be considered as hepatic component of MS. This needs more research with large multi-centric prospective studies to evaluate NAFLD as an independent risk factor for CVD.
- Screening for NAFLD is recommended for high-risk groups including those with obesity, metabolic syndrome, prediabetes or diabetes.
- Initial screening involves assessing metabolic risk factors and obtaining liver enzymes or biomarkers of steatosis. Abdominal ultrasound or serum fibrosis markers can then help determine risk of steatosis or fibrosis.
- For those at medium or high risk, referral to a specialist is recommended to further evaluate disease severity and need for biopsy. Low risk patients should be followed up every 2 years with repeat screening.
Non Alcoholic Fatty Liver Disease: A New Urban Epidemic.KETAN VAGHOLKAR
This document discusses non-alcoholic fatty liver disease (NAFLD), which has become very common in urban populations. NAFLD ranges from simple fatty liver to non-alcoholic steatohepatitis (NASH), which is characterized by fatty changes, inflammation, and fibrosis that can progress to cirrhosis. The main causes are obesity, insulin resistance, and dyslipidemia. Weight loss and improving insulin sensitivity through diet and exercise are the primary treatment approaches. Medications like vitamin E, pioglitazone, and metformin may also provide benefits, but more research is still needed on medical therapies for NAFLD.
- Non-alcoholic fatty liver disease (NAFLD) has been renamed to metabolic dysfunction associated steatotic liver disease (MASLD) to better reflect its pathogenesis.
- MASLD includes hepatic steatosis in the presence of cardiometabolic risk factors like obesity, diabetes, and dyslipidemia.
- Risk factors, pathogenesis, clinical features, diagnosis, and management of MASLD were discussed with emphasis on lifestyle modifications, weight loss, treatment of cardiometabolic conditions, and potential pharmacotherapy.
This document summarizes non-alcoholic fatty liver disease (NAFLD), which ranges from simple steatosis to non-alcoholic steatohepatitis (NASH) and cirrhosis. NAFLD is strongly associated with obesity, diabetes, and metabolic syndrome. While the pathogenesis is not fully understood, theories involve insulin resistance and interactions between the gut and liver. Diagnosis involves blood tests, ultrasound, or biopsy. Limited treatment options include weight loss, vitamin E (for NASH), and pioglitazone. Ongoing research is exploring new drug targets to treat NAFLD and prevent progression to end-stage liver disease.
An updated review on nonalcoholic steatohepatitis, epidemiology, pathology, diagnosis, treatment modalities and current clinical trials are reviewed.
New England Journal of Medicine review article from November 2017 entitled "Cause, Pathogenesis, and Treatment of Nonalcoholic Steatohepatitis" was extensively cited, please see references on the last slide (DOI: 10.1056/NEJMra1503519).
This is purely for educational purposes; I do not diagnose, treat, or offer patient-specific advice by sharing these slides.
Core Components of the Metabolic Syndrome in Nonalcohlic Fatty Liver DiseaseIOSR Journals
This study examined the association between nonalcoholic fatty liver disease (NAFLD) and metabolic syndrome (MetS) in Bangladeshi patients. The study included 67 patients diagnosed with NAFLD and 50 healthy controls matched for age and BMI. Results found that NAFLD patients had higher levels of insulin resistance, triglycerides, and central obesity compared to controls. However, no significant association was found between MetS and NAFLD when defined by common diagnostic criteria. Individual components of MetS like dyslipidemia, central obesity, and high postprandial glucose were significantly associated with NAFLD on logistic regression analysis. The study concludes that while various MetS components are linked to NAFLD in
Non-Alcoholic Fatty Liver Disease (NAFLD)Sariu Ali
Nonalcoholic fatty liver disease (NAFLD) is defined as hepatic steatosis without significant alcohol consumption or other known liver diseases. It includes nonalcoholic fatty liver (NAFL) characterized by hepatic fat accumulation without inflammation or fibrosis, and nonalcoholic steatohepatitis (NASH) characterized by fat accumulation with inflammation and hepatocyte injury. NAFLD is strongly associated with obesity and metabolic syndrome. Lifestyle interventions including weight loss and exercise are recommended first-line treatment, while pioglitazone and vitamin E may improve liver histology in non-diabetic adults with NASH. Liver biopsy is needed to distinguish NASH from NAFL and assess fibrosis to guide management.
This document discusses the epidemiology, pathogenesis, and histopathology of fatty liver disease. It covers both non-alcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD). For NAFLD, key points include its increasing prevalence due to the rise in obesity and diabetes. The pathogenesis involves insulin resistance leading to lipid accumulation in the liver. Histologically, NAFLD is graded based on steatosis, lobular inflammation, and hepatocyte ballooning. For ALD, heavy drinking can lead to steatosis in most people, while a subset develop alcoholic steatohepatitis. The pathogenesis of ALD also involves oxidative stress and cytokine pathways. Liver biopsy remains the gold standard
This journal club presentation summarized a study on the relationship between obesity and the severity of non-alcoholic fatty liver disease (NAFLD). The presentation included:
- An overview of the systematic review and meta-analysis that examined 13 studies with over 11,000 NAFLD patients to compare clinical features between non-obese and obese NAFLD.
- Key results showing obesity was associated with higher liver enzymes and inflammation scores, but not higher NAFLD activity scores or prevalence of NASH. Obesity was also correlated with increased liver fibrosis in NAFLD patients.
- The methodology involved assessing study quality, extracting data on patient characteristics and outcomes, and using statistical analyses to evaluate differences between
INTRODUCTION:
▶ Most common among all Liver disorders & the cause of CLD
▶ Commonest cause of asymptomatic abnormal LFTs
▶ Most common cause of End stage liver disease requiring liver transplantation
▶ Present in 75% of the individuals with Obesity and Type 2DM
▶ NAFLD exists as a spectrum from simple steatosis to cirrhosis
▶ Hepatic steatosis describes accumulation of fat >5% of liver weight
▶ Commonest cause of death in patients with NAFLD, NAFL and NASH is cardiovascular disease
NAFLD -DEFINITION:
Evidence of hepatic steatosis (Imaging/Histology)
No cause for secondary fat accumulation
(significant alcohol consumption, drugs, hereditary conditions)
Working Classification of NAFLD
NNFL(Non NASH Fatty Liver) Type 1 : Only steatosis
Type 2 : Steatosis + non specific lobular inflammation
NASH( Non alcoholic Steatohepatitis)
Type 3 : Steatosis + Inflammation +/- Fibrosis of variable levels
Type 4 : Steatosis + Inflammation + Hepatocyte ballooning + Fibrosis/Mallory Denk bodies
Nonalcoholic Fatty Liver Disease (NAFLD) Encompasses the entire spectrum of fatty liver disease in individuals without significant alcohol consumption, ranging from fatty liver to steatohepatitis and cirrhosis.
Nonalcoholic Fatty Liver (NAFL) Presence of hepatic steatosis with no evidence of hepatocellular injury in the form of ballooning of the hepatocytes or no evidence of fibrosis. The risk of progression to cirrhosis and liver failure is minimal.
Nonalcoholic steatohepatitis (NASH) Presence of hepatic steatosis and inflammation with hepatocyte injury (ballooning) with or without fibrosis. This can progress to cirrhosis, liver failure and rarely liver cancer.
NASH Cirrhosis Presence of cirrhosis with current or previous histological evidence of steatosis or
steatohepatitis
Cryptogenic Cirrhosis Presence of cirrhosis with no obvious etiology. Patients with cryptogenic cirrhosis are heavily enriched with metabolic risk factors such as obesity and metabolic syndrome.
DIAGNOSIS:
NAFLD/NASH is a diagnosis of exclusion, and liver biopsy will often be required to confirm the diagnosis, stage the disease, rule out other liver diseases, and determine the need for and urgency of aggressive therapy
DIAGNOSIS
WHEN TO SUSPECT NAFLD???
History : no symptoms ,fatigue, malaise and abdominal discomfort.
▶ The presence of any of the following, especially with a history of abnormal AST/ALT, should lead to a work-up for NAFLD/NASH:
Presence of obesity, especially morbid obesity (BMI > 35)
Diagnosis of type 2 diabetes mellitus
Diagnosis of metabolic syndrome
History of obstructive sleep apnea
Presence of insulin resistance
Chronic elevation of AST/ALT, otherwise unexplained
Detailed patient history of alcohol consumption—threshold < 20 g/day in women, < 30 g/day in men.
▶ Physical examination :
Central obesity correlates with severity of inflammation on biopsy
dorsocervical lipohypertrophy (buffalo hump) correlates with hepatocyte injury.
advanced liver disease: spider ang
NAFLD Patients have Limited Access to GLP1 Agonists and SGLT2 Inhibitors: NHA...JohnJulie1
This study analyzed medication use among patients with NAFLD and/or advanced fibrosis using NHANES 2017-2018 data. The following key points are summarized:
1. Patients with NAFLD or advanced fibrosis had higher rates of polypharmacy, with more medications and medication classes compared to those without these conditions.
2. While medication usage indicated higher risk of cardiovascular and metabolic issues associated with NAFLD, usage of GLP1 agonists and SGLT2 inhibitors was low among diabetics regardless of NAFLD status.
3. Diabetics with advanced fibrosis had fewer medications on average than those without advanced fibrosis, possibly due to disease progression effects, though access to beneficial therapies like G
This document discusses nonalcoholic fatty liver disease (NAFLD). It begins by explaining that NAFLD ranges from simple steatosis to nonalcoholic steatohepatitis (NASH), which can progress to cirrhosis. Insulin resistance plays a key role in the metabolic abnormalities seen in NAFLD. The pathogenesis of NASH is not fully understood. Currently, there are no approved therapies, so treatment focuses on lifestyle modifications like weight loss and exercise to improve comorbidities. The prevalence of NAFLD is increasing due to the rising obesity epidemic.
This document provides information on non-alcoholic fatty liver disease (NAFLD). It defines NAFLD and discusses its spectrum, including steatosis and non-alcoholic steatohepatitis (NASH). Risk factors, epidemiology, pathogenesis, diagnosis and treatment options are summarized. Liver biopsy remains the gold standard for diagnosing NASH, but transient elastography and biomarkers can help identify patients at risk of advanced fibrosis who may require biopsy. Lifestyle modifications targeting weight loss and insulin resistance are the primary treatment approach.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
This document provides an overview of non-alcoholic fatty liver disease (NAFLD) including its definitions, risk factors, pathogenesis, diagnosis, complications, screening recommendations, and treatment options. It discusses how NAFLD is the most common liver disease in Western countries, closely linked to metabolic syndrome. The key aspects are that lifestyle modifications targeting 7-10% weight loss are the first-line treatment. Pharmacotherapy with pioglitazone or vitamin E may be considered for patients with NASH, especially those with significant fibrosis. Ongoing research is exploring additional novel pharmacologic treatments.
The document discusses non-alcoholic fatty liver disease (NAFLD), which includes a spectrum of conditions from simple steatosis to non-alcoholic steatohepatitis (NASH) and cirrhosis. NAFLD is strongly associated with obesity and metabolic syndrome. The prevalence of NAFLD is increasing globally and varies from 5-30% in different regions. Diagnosis requires imaging and liver biopsy. Treatment focuses on lifestyle modifications and medications to improve insulin resistance.
This document summarizes non-alcoholic fatty liver disease (NAFLD) from an endocrinology perspective. It defines NAFLD and related terms, discusses the pathophysiology involving insulin resistance and lipotoxicity, epidemiology as a growing global problem, challenges in diagnosis and evaluation, and currently available treatment options focusing on lifestyle modification and insulin sensitizers. Key points covered include the need for accurate definitions to classify disease subtypes, the role of the adipose tissue-liver axis in disease progression, and limitations of non-invasive testing underscoring the continued need for liver biopsy in certain cases.
This document discusses the management of diabetes in patients with concomitant liver disease. It notes that about half of patients with cirrhosis have diabetes due to insulin resistance caused by the liver disease. Lifestyle changes and metformin are recommended initially if liver disease is mild. Insulin, sulfonylureas, meglitinides, alpha-glucosidase inhibitors, and thiazolidinediones may be used, with monitoring needed due to potential side effects or altered drug metabolism in liver disease. Insulin requirements can vary depending on the stage of liver disease.
Abstract— Non Alcoholic Fatty Liver Disease is also becoming public health impotance nowadays. So this study was aimed to determine the association of Non Alcoholic Fatty Liver Disease with metabolic syndrome and Cardio-Vascular disease along with assessment of degree of severity of NAFLD with respect to number of components of metabolic syndrome. This study includes a total of 222 subjects were enrolled as per the inclusion/exclusion criteria, out of which 110 cases who had NAFLD with hepatic steatosis on ultrasonography and 112 subjects who did not have NAFLD were considered control. These cases and controls were interrogated and investigated further. Observations were recorded and association of Non Alcoholic Fatty Liver Disease with metabolic syndrome and Cardio-Vascular disease along with assessment of degree of severity of NAFLD with respect to number of components of metabolic syndrome. Statistical methods used were unpaired student’s t-test for continuous variables, Fischer’s and chi-sq test for categorical variables using bivariate analysis by Graph Pad Instat Version 3.10. Risk was assessed in terms of Odd's Ratio. The patients with MS and NAFLD had a higher proportion of CVD compared with those who did not have NAFLD (29.1 vs 18.1 %). This study concludes that NAFLD is significantly associated with MS; most significant with WC, followed by TG and FBS and thus can be considered as hepatic component of MS. This needs more research with large multi-centric prospective studies to evaluate NAFLD as an independent risk factor for CVD.
- Screening for NAFLD is recommended for high-risk groups including those with obesity, metabolic syndrome, prediabetes or diabetes.
- Initial screening involves assessing metabolic risk factors and obtaining liver enzymes or biomarkers of steatosis. Abdominal ultrasound or serum fibrosis markers can then help determine risk of steatosis or fibrosis.
- For those at medium or high risk, referral to a specialist is recommended to further evaluate disease severity and need for biopsy. Low risk patients should be followed up every 2 years with repeat screening.
Non Alcoholic Fatty Liver Disease: A New Urban Epidemic.KETAN VAGHOLKAR
This document discusses non-alcoholic fatty liver disease (NAFLD), which has become very common in urban populations. NAFLD ranges from simple fatty liver to non-alcoholic steatohepatitis (NASH), which is characterized by fatty changes, inflammation, and fibrosis that can progress to cirrhosis. The main causes are obesity, insulin resistance, and dyslipidemia. Weight loss and improving insulin sensitivity through diet and exercise are the primary treatment approaches. Medications like vitamin E, pioglitazone, and metformin may also provide benefits, but more research is still needed on medical therapies for NAFLD.
- Non-alcoholic fatty liver disease (NAFLD) has been renamed to metabolic dysfunction associated steatotic liver disease (MASLD) to better reflect its pathogenesis.
- MASLD includes hepatic steatosis in the presence of cardiometabolic risk factors like obesity, diabetes, and dyslipidemia.
- Risk factors, pathogenesis, clinical features, diagnosis, and management of MASLD were discussed with emphasis on lifestyle modifications, weight loss, treatment of cardiometabolic conditions, and potential pharmacotherapy.
This document summarizes non-alcoholic fatty liver disease (NAFLD), which ranges from simple steatosis to non-alcoholic steatohepatitis (NASH) and cirrhosis. NAFLD is strongly associated with obesity, diabetes, and metabolic syndrome. While the pathogenesis is not fully understood, theories involve insulin resistance and interactions between the gut and liver. Diagnosis involves blood tests, ultrasound, or biopsy. Limited treatment options include weight loss, vitamin E (for NASH), and pioglitazone. Ongoing research is exploring new drug targets to treat NAFLD and prevent progression to end-stage liver disease.
An updated review on nonalcoholic steatohepatitis, epidemiology, pathology, diagnosis, treatment modalities and current clinical trials are reviewed.
New England Journal of Medicine review article from November 2017 entitled "Cause, Pathogenesis, and Treatment of Nonalcoholic Steatohepatitis" was extensively cited, please see references on the last slide (DOI: 10.1056/NEJMra1503519).
This is purely for educational purposes; I do not diagnose, treat, or offer patient-specific advice by sharing these slides.
Core Components of the Metabolic Syndrome in Nonalcohlic Fatty Liver DiseaseIOSR Journals
This study examined the association between nonalcoholic fatty liver disease (NAFLD) and metabolic syndrome (MetS) in Bangladeshi patients. The study included 67 patients diagnosed with NAFLD and 50 healthy controls matched for age and BMI. Results found that NAFLD patients had higher levels of insulin resistance, triglycerides, and central obesity compared to controls. However, no significant association was found between MetS and NAFLD when defined by common diagnostic criteria. Individual components of MetS like dyslipidemia, central obesity, and high postprandial glucose were significantly associated with NAFLD on logistic regression analysis. The study concludes that while various MetS components are linked to NAFLD in
Non-Alcoholic Fatty Liver Disease (NAFLD)Sariu Ali
Nonalcoholic fatty liver disease (NAFLD) is defined as hepatic steatosis without significant alcohol consumption or other known liver diseases. It includes nonalcoholic fatty liver (NAFL) characterized by hepatic fat accumulation without inflammation or fibrosis, and nonalcoholic steatohepatitis (NASH) characterized by fat accumulation with inflammation and hepatocyte injury. NAFLD is strongly associated with obesity and metabolic syndrome. Lifestyle interventions including weight loss and exercise are recommended first-line treatment, while pioglitazone and vitamin E may improve liver histology in non-diabetic adults with NASH. Liver biopsy is needed to distinguish NASH from NAFL and assess fibrosis to guide management.
This document discusses the epidemiology, pathogenesis, and histopathology of fatty liver disease. It covers both non-alcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD). For NAFLD, key points include its increasing prevalence due to the rise in obesity and diabetes. The pathogenesis involves insulin resistance leading to lipid accumulation in the liver. Histologically, NAFLD is graded based on steatosis, lobular inflammation, and hepatocyte ballooning. For ALD, heavy drinking can lead to steatosis in most people, while a subset develop alcoholic steatohepatitis. The pathogenesis of ALD also involves oxidative stress and cytokine pathways. Liver biopsy remains the gold standard
This journal club presentation summarized a study on the relationship between obesity and the severity of non-alcoholic fatty liver disease (NAFLD). The presentation included:
- An overview of the systematic review and meta-analysis that examined 13 studies with over 11,000 NAFLD patients to compare clinical features between non-obese and obese NAFLD.
- Key results showing obesity was associated with higher liver enzymes and inflammation scores, but not higher NAFLD activity scores or prevalence of NASH. Obesity was also correlated with increased liver fibrosis in NAFLD patients.
- The methodology involved assessing study quality, extracting data on patient characteristics and outcomes, and using statistical analyses to evaluate differences between
INTRODUCTION:
▶ Most common among all Liver disorders & the cause of CLD
▶ Commonest cause of asymptomatic abnormal LFTs
▶ Most common cause of End stage liver disease requiring liver transplantation
▶ Present in 75% of the individuals with Obesity and Type 2DM
▶ NAFLD exists as a spectrum from simple steatosis to cirrhosis
▶ Hepatic steatosis describes accumulation of fat >5% of liver weight
▶ Commonest cause of death in patients with NAFLD, NAFL and NASH is cardiovascular disease
NAFLD -DEFINITION:
Evidence of hepatic steatosis (Imaging/Histology)
No cause for secondary fat accumulation
(significant alcohol consumption, drugs, hereditary conditions)
Working Classification of NAFLD
NNFL(Non NASH Fatty Liver) Type 1 : Only steatosis
Type 2 : Steatosis + non specific lobular inflammation
NASH( Non alcoholic Steatohepatitis)
Type 3 : Steatosis + Inflammation +/- Fibrosis of variable levels
Type 4 : Steatosis + Inflammation + Hepatocyte ballooning + Fibrosis/Mallory Denk bodies
Nonalcoholic Fatty Liver Disease (NAFLD) Encompasses the entire spectrum of fatty liver disease in individuals without significant alcohol consumption, ranging from fatty liver to steatohepatitis and cirrhosis.
Nonalcoholic Fatty Liver (NAFL) Presence of hepatic steatosis with no evidence of hepatocellular injury in the form of ballooning of the hepatocytes or no evidence of fibrosis. The risk of progression to cirrhosis and liver failure is minimal.
Nonalcoholic steatohepatitis (NASH) Presence of hepatic steatosis and inflammation with hepatocyte injury (ballooning) with or without fibrosis. This can progress to cirrhosis, liver failure and rarely liver cancer.
NASH Cirrhosis Presence of cirrhosis with current or previous histological evidence of steatosis or
steatohepatitis
Cryptogenic Cirrhosis Presence of cirrhosis with no obvious etiology. Patients with cryptogenic cirrhosis are heavily enriched with metabolic risk factors such as obesity and metabolic syndrome.
DIAGNOSIS:
NAFLD/NASH is a diagnosis of exclusion, and liver biopsy will often be required to confirm the diagnosis, stage the disease, rule out other liver diseases, and determine the need for and urgency of aggressive therapy
DIAGNOSIS
WHEN TO SUSPECT NAFLD???
History : no symptoms ,fatigue, malaise and abdominal discomfort.
▶ The presence of any of the following, especially with a history of abnormal AST/ALT, should lead to a work-up for NAFLD/NASH:
Presence of obesity, especially morbid obesity (BMI > 35)
Diagnosis of type 2 diabetes mellitus
Diagnosis of metabolic syndrome
History of obstructive sleep apnea
Presence of insulin resistance
Chronic elevation of AST/ALT, otherwise unexplained
Detailed patient history of alcohol consumption—threshold < 20 g/day in women, < 30 g/day in men.
▶ Physical examination :
Central obesity correlates with severity of inflammation on biopsy
dorsocervical lipohypertrophy (buffalo hump) correlates with hepatocyte injury.
advanced liver disease: spider ang
NAFLD Patients have Limited Access to GLP1 Agonists and SGLT2 Inhibitors: NHA...JohnJulie1
This study analyzed medication use among patients with NAFLD and/or advanced fibrosis using NHANES 2017-2018 data. The following key points are summarized:
1. Patients with NAFLD or advanced fibrosis had higher rates of polypharmacy, with more medications and medication classes compared to those without these conditions.
2. While medication usage indicated higher risk of cardiovascular and metabolic issues associated with NAFLD, usage of GLP1 agonists and SGLT2 inhibitors was low among diabetics regardless of NAFLD status.
3. Diabetics with advanced fibrosis had fewer medications on average than those without advanced fibrosis, possibly due to disease progression effects, though access to beneficial therapies like G
This document discusses nonalcoholic fatty liver disease (NAFLD). It begins by explaining that NAFLD ranges from simple steatosis to nonalcoholic steatohepatitis (NASH), which can progress to cirrhosis. Insulin resistance plays a key role in the metabolic abnormalities seen in NAFLD. The pathogenesis of NASH is not fully understood. Currently, there are no approved therapies, so treatment focuses on lifestyle modifications like weight loss and exercise to improve comorbidities. The prevalence of NAFLD is increasing due to the rising obesity epidemic.
This document provides information on non-alcoholic fatty liver disease (NAFLD). It defines NAFLD and discusses its spectrum, including steatosis and non-alcoholic steatohepatitis (NASH). Risk factors, epidemiology, pathogenesis, diagnosis and treatment options are summarized. Liver biopsy remains the gold standard for diagnosing NASH, but transient elastography and biomarkers can help identify patients at risk of advanced fibrosis who may require biopsy. Lifestyle modifications targeting weight loss and insulin resistance are the primary treatment approach.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd...Donc Test
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8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Our backs are like superheroes, holding us up and helping us move around. But sometimes, even superheroes can get hurt. That’s where slip discs come in.
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4. SCOPE & DEFINITION
NAFLD
• Excessive hepatic fat accumulation with IR
• Steatosis in >5% of hepatocytes*
• Exclusion of secondary causes and AFLD†
NASH
NAFL
• Pure steatosis
• Steatosis and mild lobular inflammation
Cirrhotic
F4 fibrosis
Fibrotic
≥F2 to ≥F3 fibrosis
Early
F0/F1 fibrosis
HCC
5. Global prevalence estimated at 25% however it
is likely to have exceeded 30% prevalence in
most middle-income and high-income countries.
The most recent data are from Asia and suggest
that NAFLD affects 30% of the Asian population,
topping 40% in some territories.*
*Lancet Gastroenterol Hepatol 2019;4:389–98
6. NAFLD is closely linked with type 2 diabetes and
obesity.
NAFLD is not, however, confined to the obese
population. In the USA, 43% of people with
NAFLD are not obese, rising to 71% in Sweden.*
*Ye Q, Zou B, Yeo YH, et al. Global prevalence, incidence, and outcomes of non-obese or lean non-
alcoholic fatty liver disease: a systematic review and meta-analysis. Lancet Gastroenterol Hepatol
2020;5:739–52.
11. Non-alcoholic steatohepatitis is becoming the most
important aetiology for advanced liver disease.
AB, AbdYounossi ZM, Koenig elatif D, et al. Global epidemiology of nonalcoholic fatty liver disease-Meta-
Analytic assessment of prevalence, incidence, and outcomes. Hepatology 2016;64:73–84.
12. It is the fastest-growing indication for liver
transplantation in the USA, accounting for more
than 25% of transplants, compared with around
5% in 2002.
13. HCC is not the only cancer of concern. Studies
have found people with NAFLD have an
increased risk of colorectal cancers,
cholangiocarcinoma and cancers of the breast,
stomach, pancreas, prostate and oesophagus.*
*Liu S-S, Ma X-F, Zhao J, et al. Association between nonalcoholic fatty liver disease and extrahepatic cancers: a
systematic review and meta-analysis. Lipids Health Dis 2020;19:118.
14. NAFLD has an incremental adverse impact on
ASCVD risk over and above traditional risk
factors (up to double the risk).
NASH and its severity is also related to chronic
kidney disease (up to 3.5 times the risk). The
relationship of NAFLD with CVD and CKD is
independent of T2DM and obesity.*
*Papademetriou M, Athyros VG, Geladari E, Doumas M, Tsioufis C, Papademetriou V. The co-existence of NASH
and chronic kidney disease boosts cardiovascular risk: are there any common therapeutic options? Curr Vasc
Pharmacol 2018;16:254-68.
15. Despite limitations, liver biopsy results
are predictive of patient outcomes*1
15
Fibrosis stage
determined by
liver biopsy
predicts risk of all-
cause mortality in
NAFLD patients1
Kaplan-Meier survival estimates and fibrosis
stage1
F0
F2
F4
40
0 10 20 30
Years of follow-up
Proportion
alive
1.00
0.00
0.25
0.50
0.75
Log-rank <0.001
Controls
F1
F3
Adapted from Hagström H et al. J Hepatol 2017;67:1265 –
1273
*From a retrospective cohort study of 646 biopsy-proven NAFLD patients, each matched to 10 controls
NAFLD, nonalcoholic fatty liver disease
1. Hagström H et al. J Hepatol 2017;67:1265 –1273.
16. • In view of the foregoing findings & trends,
morbidity/mortality related to NAFLD are
bound to increase in the foreseeable future
and therefore increased awareness and
proactive screening is vital.
17. Pathophysiology of NAFLD
► NAFLD is a complex disease driven by
lipotoxicity, insulin resistance and activation of
inflammatory and immune pathways, closely
linked to metabolic disorders.
► There is increasing evidence of a link
between the gut microbiome and development
of both insulin resistance and NASH.
“Multiple Hit”
18. Pathogenesis: lifestyle and genes
1. Barrera F, George J. Clin Liver Dis 2014;18:91–112;
EASL–EASD–EASO CPG NAFLD. J Hepatol 2016;64:1388–402
• A Western diet/lifestyle has been associated with weight gain and obesity,
and NAFLD1
Recommendation
Unhealthy lifestyles play a role in the development and
progression of NAFLD.
The assessment of dietary and physical activity habits is part of
comprehensive NAFLD screening
A 1
Grade of evidence Grade of recommendation
Obesity
NAFLD
High calorie intake
Excess (saturated) fat
High fructose intake
Sedentary behaviour
19. Pathogenesis: lifestyle and genes
*Grade of evidence B, grade of recommendation 2
1. Anstee QM, et al. Nat Rev Gastroenterol Hepatol 2013;10:330–44;
EASL–EASD–EASO CPG NAFLD. J Hepatol 2016;64:1388–402
• Several genetic modifiers of NAFLD have been identified1
– A minority have been robustly validated
• PNPLA3 I148M and TM6SF2 E167K carriers have a higher liver fat content*
– Increased risk of NASH
– NAFLD not systematically associated with features of IR
Recommendation
Genotyping may be considered in selected patients and clinical
studies but is not recommended routinely
B 2
Grade of evidence Grade of recommendation
20.
21.
22. Gut microbiota and NAFLD
• Researchers have identified 8 species of gut
microbes which are twice as abundant in
advanced fibrosis, and 22 species which are
twice as abundant in mild or moderate
fibrosis.
• Research could pave the way for a non-
invasive stool test to identify the progression
from NAFLD to advanced fibrosis.
23. One hot question is whether the terminology of
NAFLD should be changed, given that many
people have liver damage from fatty liver
,alcohol and other aetiologies. A new name of
MAFLD—metabolic-associated liver disease—
has been proposed, to include people with fatty
liver and metabolic risk factors. The proposal is
under discussion by professional bodies
worldwide
24. Who Should Be Screened for NAFLD?
• The European guideline recommends that all
patients with obesity or the metabolic syndrome
be screened for NAFLD because of the prognostic
implications of progressive disease.
• The Asian guidelines: screening may be
considered in at-risk groups, such as patients with
diabetes and obesity. Lean NAFLD is prevalent in
Asia, where almost a quarter of patients with
NAFLD are not obese.
25. • AASLD: Routine Screening for NAFLD in high-
risk groups attending primary care, diabetes,
or obesity clinics is not advised at this time
because of uncertainties surrounding
diagnostic tests and treatment options, along
with lack of knowledge related to long-term
benefits and cost-effectiveness of screening.
26. How Should NAFLD Be Diagnosed, and How
Should It Be Monitored?
• Liver histology: Gold standard for differentiating
steatohepatitis from simple steatosis and for
assessing fibrosis staging. Due to its invasive nature
and associated costs, all guidelines agree that liver
biopsy should be considered only in select
individuals.
• All guidelines agree that NonInvasive Tools (NITs)
should be used to stratify patients as low or high risk
for advanced fibrosis.
27. Diagnosis: protocol for evaluation of
NAFLD
*According to a priori probability or clinical evaluation
EASL–EASD–EASO CPG NAFLD. J Hepatol 2016;64:1388–402
• Patients could be asymptomatic or complain of unexplained fatigue and RUQ
discomfort. Incidental discovery of steatosis also indicates comprehensive
evaluation
– Family and personal history of NAFLD-associated diseases
– Exclusion of secondary causes of steatosis
Level Variable
Initial
evaluation
1. Alcohol intake: <20 g/day (women), <30 g/day (men)
2. Personal and family history of diabetes, hypertension and CVD
3. BMI, waist circumference, change in body weight
4. Hepatitis B/hepatitis C virus infection
5. History of steatosis-associated drugs
6. Liver enzymes (ALT, AST, GGT)
7. Fasting blood glucose, HbA1c, OGTT, (fasting insulin [HOMA-IR])
8. Complete blood count
9. Serum total and HDL cholesterol, triacylglycerol, uric acid
10. Ultrasonography (if suspected for raised liver enzymes)
Extended*
evaluation
1. Ferritin and transferrin saturation
2. Tests for coeliac and thyroid diseases, polycystic ovary syndrome
3. Tests for rare liver diseases (Wilson, autoimmune disease, AATD)
28. NON-INVASIVE TESTS(NITs)
The diagnosis of NAFLD is usually made after excess liver fat is demonstrated
by ultrasound, MRI or other modality. These modalities only reveal NAFL and
not NASH/Fibrosis.
Liver biopsy may be the gold standard investigation for determining fibrosis
stage in NAFLD, but it is invasive, costly, carries a risk of complications and,
probably most importantly, is subject to sampling and inter- and intra-
observer variability.
NITs have prognostic value in predicting both mortality and liver related
complications in patients with NAFLD/NASH
29. Commonly used NITs
NITs, non-invasive tests
1. EASL. J Hepatol 2015;63:237–264; 2. Alkhouri N et al. Gastroenterol Hepatol (NY) 2012;8(10): 661–668; 3. Atay K et al. Biomedical Research 2017;28(2):565–570; 4. Chalasani N et al. Hepatology
2018;67(1):328–357.
• NITs use different approaches to determine liver fibrosis:1
• NITs are an area of active research and learning continues to evolve
29
ELFTM is a trademark of Siemens Healthineers
*ELFTM is not commercially available in the US, but used widely outside of the US
FibroScan® is a registered trademark of EchoSensTM, Paris
FibroTest® is a registered trademark of BioPredictive S.A.S, Paris; FibroSure® is distributed by LabCorp in the US
List of NITs provided above is not exhaustive
• FibroSure®
(FibroTest® outside of the
US)2
• ELFTM (Enhanced Liver
Fibrosis)2*
• NFS (NAFLD fibrosis
score)2
• FIB-4 (Fibrosis-4)2
• APRI (Aspartate
aminotransferase/ platelet
ratio index)3
• Simple Scores
•use information from
standard liver tests and
patient data1
Proprietary Serum Tests
test biomarkers
associated with fibrosis
stage1
• Transient elastography
(e.g. FibroScan®)2
• MRE (Magnetic resonance
elastography)4
Imaging techniques
focus on liver stiffness1
30. What makes a good NIT?
• A good NIT is both sensitive and specific in determining the presence or
absence of Advanced Fibrosis1
– Use of two cut-off values can maximize sensitivity and specificity compared to the use of a single cut-off value2
• An acceptable NIT also has an AUROC value closer to 1.0*1
30
*The AUROC (Area Under the Receiver Operating Characteristic curve) gives an average performance of a model (NIT) along all sensitivity thresholds. The higher the AUROC (or the closer to 1.0 or
similar) the better the model is at distinguishing between patients with disease and no disease1
AUROC, area under the receiver operating characteristic curve; NIT, non-invasive test
1. Bewick V et al. Crit Care 2004;8(6):508–512; 2. Anstee QM et al. Hepatology 2019; doi: 10.1002/hep.30842.
Indeterminate
Presence of Advanced
Fibrosis
Absence of Advanced
Fibrosis
Upper cut-off value
Lower cut-off value
Lower threshold
maximizes
sensitivity, ensuring
that patients with
Advanced Fibrosis are
not wrongly excluded2
Upper threshold
maximizes
specificity, ensuring
that patients without
Advanced Fibrosis are
not wrongly diagnosed2
31. Fibrosis 4 (FIB-4) can be easily calculated in office with a
simple blood test and online calculators1
31
FIB-4, fibrosis-4; URL, Uniform Resource Locator
1. Fibrosis-4 calculator. Available at: https://www.mdcalc.com/fibrosis-4-fib-4-index-liver-fibrosis. (Accessed September 2019); 2. Alkhouri N et al. Gastroenterol Hepatol (NY)
2012;8(10): 661–668.
• Based on age, platelet count, alanine aminotransferase (ALT) level and
aspartate aminotransferase (AST) level2
• Simple score that uses readily available patient data
FIB-4 =
32. FIB-4 can determine the presence of
Advanced Fibrosis1,2
32
• AUROC of 0.78 (95% CI:0.78–0.78)2
• Recognized by AASLD as clinically useful in identifying patients with a higher likelihood of F3
or F43
• LabCorpTM recently incorporated FIB-4, including these cut-off points, into its test report4
Indeterminate
Presence of Advanced
Fibrosis
Absence of Advanced
Fibrosis
Sensitivity of 82%
18% of patients with
Advanced Fibrosis are
missed
Specificity of 93%
7% of patients are wrongly
diagnosed with Advanced
Fibrosis
FIB-4 cut-off scores and accuracy for measurement of Advanced
Fibrosis*2
≥2.67
<1.3
*FIB-4 test results are based on age, hence the accuracy of the test may vary according to age
AASLD, American Association for the Study of Liver Diseases; AUROC, area under the receiver operating curve; CI, confidence interval; F3, stage 3 fibrosis; F4, stage 4 fibrosis; FIB-4, Fibrosis-4
1. Alkhouri N et al. Gastroenterol Hepatol (NY) 2012;8(10): 661–668; 2. Anstee QM et al. Hepatology 2019; doi: 10.1002/hep.30842; 3. Chalasani N et al. Hepatology 2018;67(1):328–357; 4. Available
from https://www.labcorp.com/test-menu/46291/fib-4#. (Accessed September 2019)
33. FIB-4 score may predict long-term
outcomes
33
FIB-4, fibrosis-4
1. Angulo P et al. Gastroenterology 2013;145:782–789.
Cumulative probability of death/liver transplantation
is related to FIB-4 score1
1.0
Survival
probability
(%)
Duration (years)
0.0
0.2
0.4
0.6
0.8
25
20
15
10
5
0
FIB-4: >2.67
FIB-4: 1.30 to 2.67
FIB-4: <1.30
Adapted from Angulo P et al. Gastroenterology 2013;145:782–789Adapted from Hagström H et al. J Hepatol 2017;67:1265 –1273
Liver biopsy
Years of follow-up
P = 0.03
FIB-4 Liver biopsy
Charts are illustrative and not comparative due to differing patient populations described in
the studies
34. Nonalcoholic Fatty Liver Disease and Recent Guideline Updates
Clinical Liver Disease, Volume: 17, Issue: 1, Pages: 23-28, First published: 01 February 2021, DOI: (10.1002/cld.1045)
35. NAFLD Fibrosis Score (NFS) can be easily calculated in
office
with a simple blood test and online calculators1
35
ALT, alanine aminotransferase; AST, aspartate aminotransferase; BMI, body mass index; NAFLD, nonalcoholic fatty liver disease; NFS, NAFLD fibrosis score; URL, Uniform Resource Locator
1. NAFLD fibrosis score. Available from https://www.mdcalc.com/nafld-non-alcoholic-fatty-liver-disease-fibrosis-score (Accessed September 2019); 2. Alkhouri N et al. Gastroenterol Hepatol (NY) 2012;8(10): 661–668.
• Based on age, hyperglycemia, BMI, platelet count, albumin level, and AST/ALT ratio2
• Simple score that uses readily available information
NFS =
Permission to use MDCalc logo and NAFLD URL has been kindly granted by Dr Graham Walker, Co-Creator of MDCalc
Calculator available at:
https://www.mdcalc.com
36. NFS can determine the presence of
Advanced Fibrosis
36
*NFS test results are based on age, hence the accuracy of the test may vary according to age
AASLD, American Association for the Study of Liver Diseases; AUROC, area under the receiver operating curve; CI, confidence interval; F3, stage 3 fibrosis; F4, stage 4 fibrosis; NAFLD, non-alcoholic
fatty liver disease; NFS, NAFLD fibrosis score
1. Anstee QM et al. Hepatology 2019; doi: 10.1002/hep.30842; 2. Chalasani N et al. Hepatology 2018;67(1):328–357.
• AUROC: 0.74 (95% CI:0.74–0.74)1
• Recognized by AASLD as clinically useful in identifying patients with a higher
likelihood of F3 or F42
Indeterminate
Presence of Advanced
Fibrosis
Absence of Advanced
Fibrosis
Sensitivity of 89%
11% of patients with
Advanced Fibrosis are
missed
Specificity of 89%
11% of patients are
wrongly diagnosed with
Advanced Fibrosis
NFS cut-off scores and accuracy for measurement of Advanced Fibrosis*1
≥0.676
<-1.455
37. NFS may predict long-term outcomes
37
NAFLD, nonalcoholic fatty liver disease; NFS, NAFLD fibrosis score
1. Angulo P et al. Gastroenterology 2013;145:782–789.
Cumulative probability of death/liver transplantation is related to NFS1
1.0
Survival
probability
(%)
0.0
0.2
0.4
0.6
0.8
25
20
15
10
5
0
NAFLD-FS: -1.455 to
0.676
NAFLD-FS: <-1.455
Duration (years)
NAFLD-FS:
>0.676
Adapted from Angulo P et al. Gastroenterology 2013;145:782–789Adapted from Hagström H et al. J Hepatol 2017;67:1265 –1273
Liver biopsy
Years of follow-up
P <0.001
NFS Liver biopsy
Charts are illustrative and not comparative due to differing patient populations described in
the studies
38. APRI (aspartate aminotransferase/platelet ratio index) can be easily
calculated in office with a simple blood test and online calculators1
• Based on AST and platelet count1
• Simple score that can be used at the bedside or in an outpatient setting1
APRI, aspartate aminotransferase/platelet ratio index; AST, aspartate aminotransferase; URL, Uniform Resource Locator
1. Kruger FC et al. S Afr Med J 2011;101:477-480.
U/L
AST
U/L
AST upper limit of normal
X109
/L
Platelet count
Norm: 1–40
40
Norm: 150–350
APRI
=
38
39. APRI can exclude Advanced Fibrosis
• AUROC: 0.76 (95% CI:0.74–0.79)1
APRI cut-off scores and accuracy for measurement of Advanced Fibrosis*1
Caution needed with false positives, particularly in patients with acute hepatitis2
May be more useful to exclude, rather than determine, Advanced Fibrosis3
*The study population included patients with histological findings consistent with NAFLD
APRI, aspartate aminotransferase/platelet ratio index; AUROC, area under the receiver operating curve; CI, confidence interval; NAFLD, nonalcoholic fatty liver disease
1. Siddiqui MS et al. Clin Gastroenterol Hepatol 2019; doi: 10.1016/j.cgh.2018.12.031; 2. EASL. J Hepatol 2015;63:237–264; 3. Atay K et al. Biomedical Research 2017;28(2):565–570.
Specificity of 65%
35% of patients are
wrongly diagnosed with
Advanced Fibrosis
Sensitivity of 90%
10% of patients with
Advanced Fibrosis are
missed
Absence of Advanced
Fibrosis
Presence of Advanced
Fibrosis
Indeterminate
>0.84
<0.57
39
40. Cumulative probability of death/liver transplantation is
related to APRI score1
Adapted from Angulo P et al. Gastroenterology 2013;145:782–789
Liver biopsy
Years of follow-up
Adapted from Hagström H et al. J Hepatol 2017;67:1265 –1273
APRI, aspartate aminotransferase/platelet ratio index
1. Angulo P et al. Gastroenterology 2013;145:782–789.
APRI may predict long term outcomes
Liver biopsy
Charts are illustrative and not comparative due to differing patient populations described in
the studies
40
1.0
Survival
probability
(%)
Duration (years)
0.0
0.2
0.4
0.6
0.8
25
20
15
10
5
0
APRI: <0.5
APRI: 0.5 to
1.5
APRI:
>1.5
APRI
41. FibroSure®
can determine the presence of Advanced Fibrosis
• Proprietary serum test that combines five biomarkers: haptoglobin, α2-
macroglobulin, apolipoprotein A1, total bilirubin and gamma glutamyl-
transferase*1
• AUROC: 0.832 (SE 0.01)
Specificity of 83%
17% of patients are
wrongly diagnosed with
Advanced Fibrosis
FibroTest® is a registered trademark of BioPredictive S.A.S, Paris; FibroSure® is distributed by LabCorpTM in the US
Sensitivity of 84%
16% of patients with
Advanced Fibrosis are
missed
Early or no Fibrosis
Presence of Advanced
Fibrosis
Moderate‡
*False positives can arise from haemolysis, Gilbert syndrome, cholestasis and inflammation due to increased levels of α2-macroglobulin and haptoglobin4
†In patients with hepatitis C
‡Moderate, F1–F2 and F2–bridging fibrosis with few septa3
AUROC, area under the receiver operating curve; SE, standard error
1. Alkhouri N et al. Gastroenterol Hepatol (NY) 2012;8(10): 661–668; 2. Poynard T et al. Comp Hepatol 2004;3:8; 3. LabCorp NASH FibroSure sample report. Available at: https://files.labcorp.com/testmenu/550140.pdf
(Accessed October 2019); 4. Lucero C and Brown RS. Gastroenterol Hepatol 2016;12(1):33–40.
>0.58
≤0.31
41
42. ELF (enhanced liver fibrosis) score can
determine
the presence of Advanced Fibrosis
• Combines three biomarkers of fibrosis: hyaluronic acid, tissue inhibitor of metalloproteinase 1
and amino-terminal peptide of procollagen III1
• AUROC for identifying Advanced Fibrosis (cut-off ≥9.8): 0.86 (95% CI: 0.83–0.89)2
• ELF is recommended by NICE for the diagnosis of Advanced Fibrosis in adults with NAFLD3
42
Moderate* Presence of Advanced
Fibrosis
Sensitivity of 85%
15% of patients with
Advanced Fibrosis are
missed
Specificity of 90%
10% of patients are wrongly
diagnosed with Advanced
Fibrosis
ELF cut-off scores and accuracy for measurement of Advanced
Fibrosis4
Early or no fibrosis
≥9.8
<7.7
*Moderate, categorized as mild–advanced fibrosis, ELF scores of 7.7–9.79
AUROC, area under the receiver operating curve; CI, confidence interval; ELF, enhanced liver fibrosis; NAFLD, nonalcoholic fatty liver disease; NICE, National Institute for Health and Care Excellence
1. Alkhouri N et al. Gastroenterol Hepatol (NY) 2012;8(10): 661–668; 2. Siemens Healthineers. ELF instructions for use. Available at: https://doclib.healthcare.siemens.com/ (Accessed October 2019);
3. NICE. Non-alcoholic fatty liver disease (NAFLD): assessment and management. NICE guideline NG49, July 2016. Available at: https://www.nice.org.uk/guidance/ng49 (Accessed October 2019); 4.
Day J et al. JALM 2019;DOI:10.1373/jalm.2018.027359.
43. ELF score may predict long-term liver-
related outcomes1
43
*Kaplan–Meier survival curves for survival free of liver-related events including complications of portal hypertension, liver cancer, liver transplantation, and death for patients with ELF scores in
the ranges <7.70, 7.7–9.79, 9.80–11.29, and ≥11.30
ELF, enhanced liver fibrosis; IFU, instructions for use
1. Day J et al. JALM 2019;DOI:10.1373/jalm.2018.027359.
Cumulative probability of liver-related events is related to ELF score*1
Liver biopsy
Years of follow-up
Adapted from Hagström H et al. J Hepatol 2017;67:1265 –1273
Liver biopsy
Charts are illustrative and not comparative due to differing patient populations described in
the studies
Adapted from Day J et al. JALM 2019;DOI:10.1373/jalm.2018.027359
Time to event (years)
Cumulative
survival
1.0
0.0
0.2
0.4
0.6
0.8
10
8
6
4
2
0
ELF
≥11.30
9.8–11.29
7.70–9.79
<7.70
ELF IFU cut-offs
44. Transient Elastography (e.g. FibroScan®) can
determine the presence of Advanced Fibrosis
• Imaging technique that evaluates both fibrosis and steatosis:1
– Liver stiffness expressed as kPa, correlates with fibrosis
– Controlled attenuation parameter, expressed in dB/m, correlates with steatosis
• Recognized by AASLD as clinically useful for the identification of
Advanced Fibrosis in patients with NAFLD2
Presence of Advanced
Fibrosis
Absence of Advanced
Fibrosis
Sensitivity of 91%
9% of patients with
Advanced Fibrosis are
missed
Specificity of 92%
8% of patients are wrongly
diagnosed with Advanced
Fibrosis
Indeterminate
AASLD, American Association for the Study of Liver Diseases; AUROC, area under the receiver operating curve; CI, confidence interval; kPa, kilopascal; NAFLD, nonalcoholic fatty
liver disease
1. Mikolasevic I et al. World J Gastroenterol 2016;22(32):7236–7251; 2. Chalasani N et al. Hepatology 2018 Jan;67(1):328–357; 3. Wong VWS et al. Hepatology 2010;51(2):454–462.
≥9.6 kPa
<7.9 kPa
44
45. Transient Elastography (e.g. FibroScan®)
measures
liver stiffness, which correlates with fibrosis1
45
BMI, body mass index
1. Grandison GA and Angulo P. Clin Liver Dis 2012;16(3):567–585; 2. Kemp W and Roberts S. Aust Fam Physician 2013;42(7):468–471.
Measures liver
stiffness over
an area
estimated to
be 100x
greater than
that of liver
biopsy1
Failure to obtain
readings is more
likely in patients
with a high BMI
(>30 kg/m2),
however, use of
XL probe may
help overcome
this limitation1
Over-estimation
of fibrosis can
occur in cases of
hepatitis,
cholestasis, liver
congestion and if
mass lesions are
present in the
liver2
FibroScan® is a registered trademark of EchoSensTM, Paris
• Liver stiffness is measured via a mechanically induced,
controlled 50 Hz frequency shear wave1
• The propagation speed of the shear wave is measured with
pulse echo ultrasound, with the results presented as
kilopascals (kPa)1
46. Fibrosis stage measured by
Transient Elastography is predictive of mortality
46
LSM, liver stiffness measurement; TE, transient elastography
1. Boursier J et al. J Hepatol 2016;65(3):570–578.
Cumulative probability of death is related to Transient Elastography
score1
Adapted from Boursier J et al. J Hepatol
2016;65(3):570–578
Adapted from Hagström H et al. J Hepatol
2017;67:1265 –1273
1.0
Overall
survival
Follow-up (years)
0.0
0.2
0.4
0.6
0.8
10
8
6
4
2
0
LSM fibrosis
classification:
LSM1 (F0/1)
LSM3 (F1/2)
LSM4 (F2/3)
LSM6 (F3/4)
LSM7 (F4)
P <0.001
Liver biopsy
TE
Years of follow-up
TE Liver biopsy
Charts are illustrative and not comparative due to differing patient populations described in
the studies
47. Magnetic resonance elastography (MRE) can
determine the presence of Advanced Fibrosis
*Moderate is classified as patients with fibrosis staging of F2
AUROC, area under the receiver operating curve; CI, confidence interval; F0–F2, stage 0–2 fibrosis; F2, stage 2 fibrosis; F3, stage 3 fibrosis; MRE, magnetic resonance elastography
1. Grandison GA and Angulo P. Clin Liver Dis 2012;16(3):567–585; 2. Hsu C et al. Clin Gastroenterol Hepatol 2019;17(4):630–637.e8.
• Imaging technique that assesses the propagation of mechanical waves through liver
tissue to estimate the degree of fibrosis1
• AUROC for identifying Advanced Fibrosis (≥F3) vs F0–2: 0.93 (95% CIs: 0.90–0.96)2
Moderate*
Presence of Advanced
Fibrosis
Sensitivity of 85%
15% of patients with
Advanced Fibrosis are
missed
Specificity of 83%
17% of patients are
wrongly diagnosed with
Advanced Fibrosis
MRE cut-off scores and accuracy for measurement of advanced
fibrosis2
Early or No Fibrosis
>3.62
<2.97
47
48. MRE in clinical practice
MRE has been
shown to be
both sensitive
and specific
when
identifying
different
stages of liver
fibrosis2
Unlike other
NITs and liver
biopsy, MRE
estimates the
average
degree of
fibrosis
throughout
the entire
liver2
Limitations
include the
high cost of the
equipment and
the level of
expertise
required to
interpret
results2
MRE is recognized by AASLD as “clinically useful” for the identification of Advanced
Fibrosis*1
Inflammat
ion/
fibrosis
Healthy
liver
†
*Identification of Advanced Fibrosis in patients NAFLD1
†MRE image indicates Advanced Fibrosis (F3) – liver stiffness 6.1 kPa. Adapted from Venkatesh SK et al. J Magn Reson Imaging 2013;37:544–555
AASLD, American Association for the Study of Liver Diseases; kPa, kilopascal; MRE, magnetic resonance elastography; NAFLD, nonalcoholic fatty liver disease; NIT, non-invasive test
1. Chalasani N et al. Hepatology 2018 Jan;67(1):328–357; 2. Grandison GA and Angulo P. Clin Liver Dis 2012;16(3):567–585. 48
49. Summary of common tests for
determining fibrosis stage*
Test AUROC Lower cut-off to rule
out Advanced Fibrosis
Sensitivity for lower
cut-off (%)
Upper cut-off to rule in
Advanced Fibrosis
Specificity for upper
cut-off (%)
Simple scores
FIB-41 0.78 <1.3 82 ≥2.67 93
NFS1 0.74 <-1.455 89 ≥0.676 89
APRI2 0.76 <0.57 90 >0.84 65
Proprietary serum tests
FibroSure®3 0.83 ≤0.31 84 >0.58 83
ELF4,5 0.86† <7.7 85 ≥9.8 90
Imaging techniques
FibroScan®6 0.93 <7.9 kPa 91 ≥9.6 kPa 92
MRE7 0.93‡ <2.97 kPa 85 >3.62 kPa 83
Histological tests
Liver biopsy8 0.87 ≤F2 85 ≥F3 89
*For informational purposes only – not intended for comparison
†AUROC is for upper cut-off of ≥9.6 to detect patients with Advanced Fibrosis
‡AUROC is for upper cut-off of >3.62 kPa to detect patients with ≥F3 fibrosis
APRI, aspartate aminotransferase/platelet ratio; AUROC, area under the receiver operating curve; ELF, enhanced liver fibrosis; FIB-4, fibrosis 4; kPa, kilopascal; MRE, magnetic resonance elastography; NAFLD,
nonalcoholic fatty liver disease; NFS, NAFLD fibrosis score
1. Anstee QM et al. Hepatology 2019; doi: 10.1002/hep.30842; 2. Siddiqui MS et al. Clin Gastroenterol Hepatol 2019; doi: 10.1016/j.cgh.2018.12.031; 3. Poynard T et al. Comp Hepatol 2004;3:8; 4. Siemens
Healthineers. ELF instructions for use. Available at: https://doclib.healthcare.siemens.com/ (Accessed October 2019); 5. Day J et al. JALM 2019;DOI:10.1373/jalm.2018.027359; 6. Wong VWS et al. Hepatology
2010;51(2):454–462; 7. Hsu C et al. Clin Gastroenterol Hepatol 2019;17(4):630–637.e8; 8. Ratzui V et al. Gastroenterology 2005;128:1898–1906. 49
50. • Plasma CytoKeratin(CK-18) -emerging as one
of the promising biomarkers for the
noninvasive detection of NASH.
52. For patients with Advanced Fibrosis without cirrhosis,
halting progression is an important goal1,2
1. Filozof C et al. Hepatol Commun 2017; 1(7): 577–585; 2. FDA Noncirrhotic Nonalcoholic Steatohepatitis With Liver Fibrosis: Developing Drugs
for Treatment Guidance for Industry. December 2018; 3. Angulo P et al. Gastroenterology 2015;149:389–397.
HALT/REVERSE
INFLAMMATION
FIBROSIS
• Preventing
progression to
cirrhosis is a principle
objective of
management1
PREVENT
Progression to
CIRRHOSIS
• Fibrosis stage is
associated with overall
survival and
liver-related
complications3
• Presence and severity
of fibrosis may predict
long-term outcomes3
52
53. With no indicated pharmacological treatments,
management options are currently limited1,2
EASD, European Association for the Study of Diabetes; EASL, European Association for the Study of the Liver; EASO, European Association for the Study of Obesity; FDA, Food and Drug
Administration; NASH, nonalcoholic steatohepatitis; US, United States
1. Chalasani N et al. Hepatology 2018;67(1):328–357; 2. EASL-EASD-EASO. J Hepatol 2016;64:1388–1402. 3. Oseini AM et al. Liver Int 2017;37 Suppl 1:97–103; 4. FDA
Noncirrhotic Nonalcoholic Steatohepatitis With Liver Fibrosis: Developing Drugs for Treatment Guidance for Industry, December 2018.
Lifestyle Modification
• Lifestyle modification, including
changes such as diet, weight loss,
and exercise, is recommended as a
first-line treatment3
• Lack of patient compliance may be a
key limitation of this approach1
• Non-indicated treatments, such as vitamin E or
pioglitazone, may be considered in select
patients1,2
• GLP1 Agonist
• Data are limited and risks and benefits should be
discussed with each patient before starting
therapy1
Non-indicated pharmacological
treatments
There is an urgent need for options for patients
with Advanced Fibrosis due to NASH3
53
60. The GLP1 RA semaglutide has completed a 72-
week phase II trial with 320 participants,
showing resolution of NASH with no worsening
of fibrosis for 56% of patients on 0.4 mg
compared with 20% on placebo.*
*Newsome PN, Buchholtz K, Cusi K, et al. A placebo-controlled trial of subcutaneous
Semaglutide in nonalcoholic steatohepatitis. N Engl J Med 2021;384:1113–24.
61. On the Horizon..
Five phase III studies are expected to complete the trial part
having surrogate, histological endpoints before the end of
2024 :
1. Aramchol
2. Resmetiron
3. Obeticholic acid
4. Belapectin
5. Lanifibranor
6. Efruxifermin.
62. Conclusion
The challenge of NASH remains to license a
treatment for this increasingly prevalent and
important condition. There is no shortage of
candidate drugs, but difficulties in diagnosis,
staging and monitoring the effects of
treatment have added unprecedented
complexity to the field.
Combination therapies seem promising.
IR, insulin resistance; NASH, non-alcoholic steatohepatitis
a process of multiple parallel ‘hits’ which put stress on the liver.19 External factors which raise the risk include unhealthy diet such as fructose
overconsumption20 and lack of exercise, while genetic factors also affect people’s chances of developing the condition.21
AATD, α1-antitrypsin deficiency; ALT, alanine aminotransferase; AST, aspartate aminotransferase; BMI, body mass index; CVD, cardiovascular disease; GGT, gamma-glutamyl transpeptidase; HbA1c, glycated haemoglobin; HDL, high-density lipoprotein; HOMA-IR, Homeostatic Model Assessment of Insulin Resistance; OGTT, oral glucose tolerance test
Proposed diagnostic and risk stratification algorithm for patients with suspected NAFLD. 1HBV and HCV serological workup should be completed in the primary care setting, with subsequent workup tailored to the individual patient by hepatology. Note that NAFLD may coexist with other chronic liver diseases. 2Evidence‐based optimal follow‐up of patients with NAFLD has not been established. The EASL recommends monitoring low‐risk patients with NAFLD without worsening metabolic risk factors every 2 to 3 years. 3Biopsy should also be considered in patients with increasing number of metabolic diseases who are at high risk for steatohepatitis.
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