Is Your Liver Well?

Total Page:16

File Type:pdf, Size:1020Kb

Is Your Liver Well? 10/15/2020 Is Your Liver Well? Marina Roytman MD, FACP Liver Program Director, UCSF Fresno Clinical Professor of Medicine, UCSF October 10, 2020 1 What shall we learn today? What does the liver do? What can damage my liver? What is fatty liver disease? What is Hepatitis C? Who is at risk for liver disease? How can I find out if I have it? What can I do to take improve the health of my liver? 2 1 10/15/2020 Where is My Liver? Liver is located on the right side of your abdomen Healthy liver is completely hidden under the ribs It is about the size of a football 3 What Does My Liver Do? Liver is the body’s factory ◦ It makes proteins that help your blood clot ◦ It makes proteins that help your body be nourished It removes toxic substances from your body 4 2 10/15/2020 What Happens If My Liver Is Damaged? Initially liver may get swollen It may be felt below the ribs More serious or ongoing damage will lead to liver scarring and becoming small and hard This is called CIRRHOSIS = a LOT of scarring 5 What are the Physical Signs of Liver Disease? 6 3 10/15/2020 What Can Damage My Liver? Alcohol: #1 cause of liver damage Viral Hepatitis: infection of the liver ◦ “hepa” = liver ◦ “itis” = inflammation ◦ Types of viral hepatitis A, B, C, D, E Excess weight: may lead to liver damage similar to viral hepatitis or alcoholism 7 Non-alcoholic Fatty Liver Disease: Alphabet soup? NAFLD: Fat in the liver without a good alternative explanation NAFL: NASH: Fat in the liver without Fat in the liver resulting any signs of injury in inflammation and +/- scarring 8 4 10/15/2020 9 Non-alcoholic Fatty Liver Disease: An Emerging American Epidemic 1 in 3 Americans has fatty liver Ultrasound data estimates 50% Up to 50% in diabetics Up to 90% in patients undergoing weight loss surgery 3-10 times more common then Hepatitis C 10 5 10/15/2020 Age-adjusted Prevalence of Obesity and Diagnosed Obesity BMIDiabetes ≥30 kg/m Among2) US Adults 2000 2015 1994 No Data <14.0% 14.0%–17.9% 18.0%–21.9% 22.0%–25.9% > 26.0% Diabetes 2000 2015 1994 No Data <4.5% 4.5%–5.9% 6.0%–7.4% 7.5%–8.9% >9.0% CDC’s Division of Diabetes Translation. United States Surveillance System available at http://www.cdc.gov/diabetes/data 11 Who is at Risk for Fatty Liver Disease? Wong RJ, World J Hepatol 2014;6:263-273 12 6 10/15/2020 Who is at Risk for Fatty Liver Disease? Metabolic syndrome ◦ Diabetes or high blood sugar ◦ High blood pressure ◦ High cholesterol and or triglycerides ◦ Excess fat around the waist line 13 Does Genetics Play a Role? Multiethnic cohort of >59,000 adults in Ontario comparing race, BMI and prevalence of diabetes Chiu M, Diabetes Care 34:1741-48;2011 14 7 10/15/2020 Does Genetics Play a Role? Median hepatic fat content and PNPLA3 rs738409 genotypes in European Americans, African Americans and Hispanics in the Dallas Heart Study (0.23) (0.17) (0.49) Allele Frequency Patients of Hispanic and Asian origin may develop fatty liver disease at a lower weight and a lesser burden of risk factors. Romeo S, Nat Genet 2008 15 What Happens in Fatty Liver Disease? NAFLD NASH NASH with fibrosis ~70 million (25% ) NASH-related cirrhosis 10% of NAFLD NASH- (~7 million) HCC 1% (~700,000) ~4,000 cases/yr 16 8 10/15/2020 Who is at the highest risk of complications of fatty liver disease? Liver Scarring Patients with more severe fibrosis have markedly worse outcomes Controls F0-F2 F3-F4 Prognostic hierarchy from Loomba, et al. Gastroenterology. 2015; Ekstedt et al. Gastroenterology 2015. 17 18 9 10/15/2020 Weight Loss Works! 293 patients with NASH were encouraged to adopt recommended lifestyle changes to reduce their weight over 52 weeks 261 had biopsies at the beginning and at the end of the study 88 (30%) lost >5% body weight Vilar-Gomez, et al. Gastroenterology. 2015. 19 Weight Loss Leads to Reduction in Liver Scarring! Vilar-Gomez, et al. Gastroenterology. 2015 20 10 10/15/2020 21 Eat Yogurt and Drink Coffee! Both improve the health of the bacteria in your gut Healthier gut bacteria decrease inflammation in the liver (that leads to scarring) Coffee is also an appetite suppressant Coffee = black! Yogurt = plain! Avoid probiotics in pill form! 22 11 10/15/2020 Future Therapeutic Targets Thyroid receptor beta agonist Fibroblast growth factor 21 Glucagon-like peptide-1 Combination therapies Duodenal mucosal ablation 23 Do We Have Clinical Trials In Fresno and Can I Participate? Yes! Trials for fatty liver disease are currently running at UCSF Fresno If interested, contact: ◦ Sonia Garcia, Clinical Research Coordinator 559-499-6637 [email protected] 24 12 10/15/2020 What Else Can Damage My Liver? Hepatitis C (+) single stranded linear RNA virus Mimics the cellular mRNA (messenger RNA) molecule Exploits host cellular apparatus to synthesize proteins during replication 25 HCV is Underdiagnosed and Undertreated Cascade of Care in 2018 in the United States 3.0 2,710,935 2.5 2.0 1.5 24% 5% (millions) 1.0 656,007 Number of Individuals Individuals ofNumber 0.5 132,572 125,670 0.0 Viremic Aware Treated in 2018 Cured in 2018 1. Chhatwal J et al. APT. 2019; 2. Zibbell JE, et al. Am J Public Health. 2018;108(2):175-181. 2. Data on file 3. Zibbell JE, et al. Am J Public Health. 2018;108(2):175-181. 26 13 10/15/2020 Chronic Hepatitis C Is a Progressive Disease HEALTHY LIVER FIBROTIC LIVER CIRRHOTIC LIVER Few or no symptoms; can progress without signs for decades Most pts asymptomatic until serious liver complications arise 1. CDC. MMWR Morb Mortal Wkly Rep. 1998;47(RR-19):1-39. 2. Heidelbaugh JJ, et al. Am Fam Physician. 2006;74:756-762. 27 Why is Hepatitis C Curable? • Unlike some other viruses, HCV RNA is only present in the cytoplasm (not in the nucleus) of the host cell1 • Without the stable, genetic-material reservoir of the nucleus created by other viruses, the possibility exists for HCV cure by treatment1 a a cccDNA = covalently closed circular DNA 1. Soriano V, Perelson AS, Zoulim F. Why are there different dynamics in the selection of drug resistance in HIV and hepatitis B and C viruses? J Antimicrob Chemother. 2008;62(1):1-4. 9 28 14 10/15/2020 Age Distribution of New HCV Infections in the US Skews Toward Adolescents and Young Adults 29 Hot off the Press: CDC Update Universal hepatitis C screening: Hepatitis C screening at least once in a lifetime for all adults aged 18 years and older Hepatitis C screening for all pregnant women during each pregnancy 30 15 10/15/2020 How to Diagnose Hepatitis C: Antibody Test It looks for footprints of the virus in your blood If it is positive, patient had been exposed to the virus at some point 15-25% of patients clear the virus on their own Further testing is necessary to determine active infection 31 Hepatitis C RNA: Do I Have Live Virus in Me? Viral Load = PCR Presence of virus = chronic Hepatitis C Viral load DOES NOT correlate to the severity of inflammation, progression of liver disease or chance of cure. 32 16 10/15/2020 What if I am Diagnosed with Hepatitis C? You can be cured with a simple, oral regimen (pills) in as little as 8 to12 weeks! 98% chance of cure! Cure will stop progression of liver disease and allow you liver to heal! 33 SVR Associated With a Reduction in HCC, Liver-Related Mortality, Transplantation, and All-Cause Mortality 30 Hepatocellular Liver-Related Mortality All-Cause Carcinoma or Liver Transplantation Mortality P <0.001 P <0.001 P <0.001 20 Without SVR Without SVR Without SVR 10 Cumulative Incidence (%) Incidence Cumulative With SVR With SVR With SVR 0 012345678910 012345678910 012345678910 Time (y) Time (y) Time (y) International, multicenter, long-term follow-up study of 530 consecutive CHC patients with advanced hepatic fibrosis or cirrhosis, who started an IFN-based treatment regimen between 1990 and 2003. Median follow-up duration 8.4 years Significant reduction of 10-year cumulative incidence of HCC, liver-related mortality or transplantation, and all-cause mortality in patients who achieved SVR van der Meer AJ, et al. JAMA. 2012;308:2584-2593. 34 17 10/15/2020 How do I find out if I have scarring or fat in my liver? 35 The FibroScan Probe Ultrasound “Crystal” (Shear wave speed measurement) Actuator (Shear wave generator) 36 18 10/15/2020 FibroScan = No Needles Needed to Measure Liver Scarring Probe mechanically induces shear wave … Shear Wave 37 Results Disease Significant Cirrhosis F0-F1 F2 Fibrosis F3 F4 HBV < 6.0 > 6.0 > 9.0 > 12.0 HCV < 7.0 > 7.0 > 9.5 > 12.0 HCV-HIV < 7.0 < 10.0 > 11.0 > 14.0 Cholestatic < 7.0 > 7.5 > 10.0 > 17.0 NAFLD/NASH < 7.0 > 7.5 > 10.0 > 14.0 Utilization of FibroScan in Clinical Practice; Bonder S, Afdhal N; Current Gastroenterology Rep, 2014 16-372 38 19 10/15/2020 FibroScan = No Needles Needed to Measure Liver Fat CAP 1 2 Acoustic Impedance 39 Ultrasound Attenuation Rate CAP 40 20 10/15/2020 Results 19 Study Meta-Analysis / 2735 Subjects Grade CAP Cutoff Sensitivity Specificity AUC dB/M S0 vs S1-S3 248 0.69 0.82 0.82 S0-S1 vs S2-S3 268 0.77 0.81 0.86 S0-S2 vs S3 280 0.88 0.78 0.88 Steatosis Grade Affected Hepatocytes CAP Range: 100-400 dB/m S1 < 33 % S2 33 – 66 % S3 > 66 % Karlas et al, 2016 41 What Have We Learnt? Fatty Liver Disease Hepatitis C Exercise! Hepatitis C is Eat healthy! common Eat yogurt! It often does not Drink coffee! cause symptoms Maintain healthy Everyone should be weight! tested! Hepatitis C can be cured in 8-12 weeks! Ask your doctor to check your liver tests! 42 21 10/15/2020 43 22.
Recommended publications
  • Primary Biliary Cholangitis: a Brief Overview Justin S
    REVIEW Primary Biliary Cholangitis: A Brief Overview Justin S. Louie,* Sirisha Grandhe,* Karen Matsukuma,† and Christopher L. Bowlus* Primary biliary cholangitis (PBC), previously referred to supported by the higher concordance of PBC in monozy- as primary biliary cirrhosis, is the most common chronic gotic compared with dizygotic twins.4 In addition, certain cholestatic autoimmune disease affecting adults in the human leukocyte antigen haplotypes have been associ- United States.1 It is characterized by a hallmark serologic ated with PBC, as well as variants at loci along the inter- signature, antimitochondrial antibody (AMA), and specific leukin-12 (IL-12) immunoregulatory pathway (IL-12A and bile duct pathology with progressive intrahepatic duct de- IL-12RB2 loci).5 struction leading to cholestasis. PBC is potentially fatal and can have both intrahepatic and extrahepatic complications. PATHOGENESIS EPIDEMIOLOGY The primary disease mechanism in PBC is thought to be T cell lymphocyte–mediated injury against intralobu- PBC affects all races and ethnicities; however, it is best lar biliary epithelial cells. This causes progressive destruc- studied in the Caucasian population. The condition pre- tion and eventual disappearance of the intralobular bile dominantly affects women older than 40 years, with a ducts. Molecular mimicry has been proposed as the ini- female/male ratio of 9:1.2 Although the incidence of PBC tiating event in the loss of tolerance primarily to mito- appears to be stable, the overall prevalence of the disease chondrial pyruvate dehydrogenase complex, E2, during is increasing.3 An individual’s genetic susceptibility, epige- which exogenous antigens evoke an immune response netic factors, and certain environmental triggers seem to that recognizes an endogenous (self) antigen inciting an play important roles.
    [Show full text]
  • Non-Alcoholic Fatty Liver Disease
    Non-alcoholic fatty liver disease Description Non-alcoholic fatty liver disease (NAFLD) is a buildup of excessive fat in the liver that can lead to liver damage resembling the damage caused by alcohol abuse, but that occurs in people who do not drink heavily. The liver is a part of the digestive system that helps break down food, store energy, and remove waste products, including toxins. The liver normally contains some fat; an individual is considered to have a fatty liver (hepatic steatosis) if the liver contains more than 5 to 10 percent fat. The fat deposits in the liver associated with NAFLD usually cause no symptoms, although they may cause increased levels of liver enzymes that are detected in routine blood tests. Some affected individuals have abdominal pain or fatigue. During a physical examination, the liver may be found to be slightly enlarged. Between 7 and 30 percent of people with NAFLD develop inflammation of the liver (non- alcoholic steatohepatitis, also known as NASH), leading to liver damage. Minor damage to the liver can be repaired by the body. However, severe or long-term damage can lead to the replacement of normal liver tissue with scar tissue (fibrosis), resulting in irreversible liver disease (cirrhosis) that causes the liver to stop working properly. Signs and symptoms of cirrhosis, which get worse as fibrosis affects more of the liver, include fatigue, weakness, loss of appetite, weight loss, nausea, swelling (edema), and yellowing of the skin and whites of the eyes (jaundice). Scarring in the vein that carries blood into the liver from the other digestive organs (the portal vein) can lead to increased pressure in that blood vessel (portal hypertension), resulting in swollen blood vessels (varices) within the digestive system.
    [Show full text]
  • Non-Alcoholic Fatty Liver Disease Information for Patients
    April 2021 | www.hepatitis.va.gov Non-Alcoholic Fatty Liver Disease Information for Patients What is Non-Alcoholic Fatty Liver Disease? Losing more than 10% of your body weight can improve liver inflammation and scarring. Make a weight loss plan Non-alcoholic fatty liver disease or NAFLD is when fat is with your provider— and exercise to keep weight off. increased in the liver and there is not a clear cause such as excessive alcohol use. The fat deposits can cause liver damage. Exercise NAFLD is divided into two types: simple fatty liver and non- Start small, with a 5-10 minute brisk walk for example, alcoholic steatohepatitis (NASH). Most people with NAFLD and gradually build up. Aim for 30 minutes of moderate have simple fatty liver, however 25-30% have NASH. With intensity exercise on most days of the week (150 minutes/ NASH, there is inflammation and scarring of the liver. A small week). The MOVE! Program is a free VA program to help number of people will develop significant scarring in their lose weight and keep it off. liver, called cirrhosis. Avoid Alcohol People with NAFLD often have one or more features of Minimize alcohol as much as possible. If you do drink, do metabolic syndrome: obesity, high blood pressure, low HDL not drink more than 1-2 drinks a day. Patients with cirrhosis cholesterol, insulin resistance or diabetes. of the liver should not drink alcohol at all. NAFLD increases the risk for diabetes, cardiovascular disease, Treat high blood sugar and high cholesterol and kidney disease. Ask your provider if you have high blood sugar or high Most people feel fine and have no symptoms.
    [Show full text]
  • Diet and Fatty Liver Disease
    10/15/2020 Diet and Fatty Liver Disease KRISTEN COLEMAN RD CNSC CRMC LIVER EXPO 2020 1 Fatty Liver Disease Importance of liver health and liver functions of digestion Fatty Liver Disease and Pediatrics Nutrition tips for a healthy liver Foods that cause Fatty Liver What foods to eat to with Fatty Liver Disease 2 1 10/15/2020 Liver Function Removes toxicants from the body Metabolizes / Digests protein, carbohydrates, and fat Glycogen Storage Controls / Regulates neuro-hormonal mechanisms 3 Fatty Liver and Children Fatty liver disease is the most common cause of chronic liver disease in children ◦ Simple Fatty Liver Disease – fat accumulated on live but no cell damage or inflammation ◦ Non-Alcoholic Steatohepatitis (NASH) – fat accumulation with inflammation and cell damage which can lead to cirrhosis or liver cancer Effects 1 in 10 kids ◦ Fatty liver disease in children has doubled in the last 20 years ◦ Why? ◦ Increase in pediatric obesity ◦ Poor nutrition ◦ Limited activity 4 2 10/15/2020 Fatty Liver and Children Children and Diet ◦ Fruit Juice, sports drinks, soda ◦ High carbohydrate snacks – crackers, chips ◦ High fructose corn syrup intake - fruit snacks, sugary yogurts, canned fruits, granola bars ◦ High intake of processed foods – chicken nuggets,- French fries ◦ Limited intake of fiber and water intake ◦ Grazing / frequent snacking Diet treatment for fatty liver in kids is the same as adults 5 How does diet effect/cause Fatty Liver? All carbohydrates are broken down into glucose Glucose travels though the blood stream and delivers energy to our cells If the cells do not need energy the glucose molecule is sent back to the liver for storage.
    [Show full text]
  • Non-Alcoholic Fatty Liver Disease Sonogram
    The Sonographic Progression of Non-Alcoholic Fatty Liver Disease into Non- Alcoholic Cirrhosis of the Liver Student Researcher: Giana Tondora Faculty Advisor: Karen L. Klimas, MS, R.T.(R), RDMS Reversal of Non-alcoholic Cirrhosis Introduction Once non-alcoholic cirrhosis is present, it most • Within the past 20 years, sonography has Types of Liver Cirrhosis Sonographic Liver Elastography likely cannot be reversed and only treatments can become the modality of choice for • Alcoholic be given to slow the disease's process depending evaluation of the liver. Both alcoholic and what caused the cirrhosis. If the cirrhosis was non-alcoholic fatty infiltration and cirrhosis Alcoholic liver cirrhosis occurs after alcohol caused by hepatitis B or C, antiviral drugs can be cases have become more prevalent at this has been heavily consumed over many years prescribed in order to suppress the immune time and it is crucial for the sonographer to and the liver replaces healthy tissue with scar system. If the cirrhosis is caused by diabetes or tissue. Alcoholic cirrhosis presents itself in the obesity, insulin will be given to the patient and it provide the best diagnostic images will be recommended that the patient maintains a possible. “Non-alcoholic fatty liver disease early stages as fatty liver disease. After fatty liver disease it progressed to alcoholic nutritional diet and refrain from any alcohol. This (NAFLD) is the most common liver disease nutritional diet should consist of cutting back on hepatitis and then finally alcoholic cirrhosis. in the United States” (Khov, Sharma & carbs and including foods and drinks in their diets Riley, 2014).
    [Show full text]
  • Patterns of Abnormal Lfts and Their Differential Diagnosis
    Patterns of abnormal LFTs and their differential diagnosis Professor Matthew Cramp South West Liver Unit and Peninsula Schools of Medicine and Dentistry, Plymouth Outline • liver function tests / tests of liver function • sources of various liver enzymes • patterns of liver enzyme abnormality • major causes of abnormal liver function • Assess liver disease severity • Form a differential diagnosis on the basis of LFTs and limited history Liver function tests • AST • ALT • alkaline phosphatase • GGT • Bilirubin • Albumin, total protein. – ie mostly indicators of liver damage Tests of liver function • Synthetic functions: – Albumin – Clotting factors – prothrombin time • Excretory function – bilirubin Interpretation of LFTs • AST / ALT – hepatocellular enzymes • AST – mitochondrial • ALT – cytosolic • AST / ALT ratio – ALT > AST – hepatitis – AST > ALT – alcohol or in advanced fibrosis / cirrhosis Interpretation of LFTs • Alkaline phosphatase – biliary epithelium – also comes from bone • GGT – also biliary • Alk P GGT - biliary source – Obstruction – Infiltration – congestion • Alk Phos GGT normal - think bones • Isoenzymes – rarely needed Interpretation of LFTs • Albumin • Total protein / globulin fraction Other tests: • PT / INR • Alpha-foetoprotein (AFP) • Full blood count Causes of chronic liver disease • Non-alcoholic fatty liver disease • Alcohol • Viral • Immunological • Genetic / Metabolic Investigation of abnormal LFTs • History • Non-invasive liver disease screen • Imaging – typically ultrasound Investigation of abnormal LFTs
    [Show full text]
  • Acute Severe Transaminitis As a Unique Presentation of Chronic Cholecystitis
    Open Access Case Report DOI: 10.7759/cureus.16102 Acute Severe Transaminitis as a Unique Presentation of Chronic Cholecystitis Huda Fatima 1 , Deepti Avasthi 1 1. Internal Medicine, St. Vincent Mercy Medical Center, Toledo, USA Corresponding author: Huda Fatima, [email protected] Abstract The hepatocellular function can be evaluated using aspartate aminotransferase (AST) and alanine aminotransferase (ALT) which are biochemical markers of the liver. Whenever there is an ischemic, toxic, or inflammatory injury to the liver, necrosis of the hepatocytes occurs and these biochemical markers are released into the circulation, showing an acute elevation in serum levels. In this case report, we discuss the unique clinical presentation of a female patient who came to the Emergency Room (ER) with acute onset chest pain with laboratory findings of elevated serum aminotransferases and cholestatic markers and was ultimately diagnosed with chronic cholecystitis. The usual clinical presentation associated with extremely elevated levels of liver enzymes can be one of three cases: acute viral hepatitis, toxin-induced liver injury, or acute ischemic insult to the liver. However, our patient was diagnosed with chronic cholecystitis despite her unique initial presentation of acute, severe transaminitis. While one may find elevated liver enzyme levels in acute cholecystitis, owing to the sudden nature of the inflammatory process, chronic cholecystitis is not known to cause high levels of serum amino transaminases or fulminant liver failure. Our case report indicates a diverse phenotype of chronic cholecystitis with an unusual presentation of acute, severe transaminitis. It helps expand the differential diagnoses of acute elevation of liver function tests (LFTs). Further studies are needed to explore the pathology behind chronic cholecystitis in order to understand its impact on liver damage.
    [Show full text]
  • Complications of Non-Alcoholic Fatty Liver Disease in Extrahepatic Organs
    diagnostics Review Complications of Non-Alcoholic Fatty Liver Disease in Extrahepatic Organs Wataru Tomeno 1,2, Kento Imajo 2 , Takuya Takayanagi 1,2, Yu Ebisawa 1,2, Kosuke Seita 1,2, Tsuneyuki Takimoto 1,2, Kanami Honda 1,2, Takashi Kobayashi 2 , Asako Nogami 2, Takayuki Kato 1,2, Yasushi Honda 2 , Takaomi Kessoku 2, Yuji Ogawa 2, Hiroyuki Kirikoshi 3, Yasunari Sakamoto 1,2, Masato Yoneda 2, Satoru Saito 2 and Atsushi Nakajima 2,* 1 Department of Gastroenterology, International University of Health and Welfare Atami Hospital, 13-1 Higashikaigancho, Atami-shi, Shizuoka 413-0012, Japan; [email protected] (W.T.); [email protected] (T.T.); [email protected] (Y.E.); [email protected] (K.S.); [email protected] (T.T.); [email protected] (K.H.); [email protected] (T.K.); [email protected] (Y.S.) 2 Department of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama 236-0004, Japan; [email protected] (K.I.); [email protected] (T.K.); [email protected] (A.N.); [email protected] (Y.H.); [email protected] (T.K.); [email protected] (Y.O.); [email protected] (M.Y.); [email protected] (S.S.) 3 Department of Clinical Laboratory, Yokohama City University Hospital, 3-9 Fukuura, Kanazawa-ku, Yokohama 236-0004, Japan; [email protected] * Correspondence: [email protected]; Tel.: +81-45-787-2640 Received: 8 October 2020; Accepted: 6 November 2020; Published: 7 November 2020 Abstract: Non-alcoholic fatty liver disease (NAFLD) is now recognized as the most common chronic liver disease worldwide, along with the concurrent epidemics of metabolic syndrome and obesity.
    [Show full text]
  • A New Endemic of Concomitant Nonalcoholic Fatty Liver Disease and Chronic Hepatitis B
    microorganisms Review A New Endemic of Concomitant Nonalcoholic Fatty Liver Disease and Chronic Hepatitis B 1, 1, 1 1,2 1 Hira Hanif y , Muzammil M. Khan y, Mukarram J. Ali , Pir A. Shah , Jinendra Satiya , Daryl T.Y. Lau 1,* and Aysha Aslam 3,* 1 Liver Center, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA; [email protected] (H.H.); [email protected] (M.M.K.); [email protected] (M.J.A.); [email protected] (P.A.S.); [email protected] (J.S.) 2 Department of Internal Medicine, University of Texas, San Antonio, TX 78229, USA 3 Department of Medicine, Louis A Weiss Memorial Hospital, Chicago, IL 60640, USA * Correspondence: [email protected] (D.T.Y.L.); [email protected] (A.A.) Equal first author contribution. y Received: 16 September 2020; Accepted: 30 September 2020; Published: 4 October 2020 Abstract: Hepatitis B virus (HBV) infection remains a global public problem despite the availability of an effective vaccine. In the past decades, nonalcoholic fatty liver disease (NAFLD) has surpassed HBV as the most common cause of chronic liver disease worldwide. The prevalence of concomitant chronic hepatitis B (CHB) and NAFLD thus reaches endemic proportions in geographic regions where both conditions are common. Patients with CHB and NAFLD are at increased risk of liver disease progression to cirrhosis and hepatocellular carcinoma. Due to the complexity of the pathogenesis, accurate diagnosis of NAFLD in CHB patients can be challenging. Liver biopsy is considered the gold standard for diagnosing and determining disease severity, but it is an invasive procedure with potential complications.
    [Show full text]
  • Clinical Analysis on Gall Bladder Disease Cholecystitis And
    DOI: 10.21276/sjams.2016.4.7.36 Scholars Journal of Applied Medical Sciences (SJAMS) ISSN 2320-6691 (Online) Sch. J. App. Med. Sci., 2016; 4(7C):2480-2483 ISSN 2347-954X (Print) ©Scholars Academic and Scientific Publisher (An International Publisher for Academic and Scientific Resources) www.saspublisher.com Original Research Article Clinical analysis on Gall Bladder Disease Cholecystitis and Cholelitheasis Bhanumati Giridharan1, Madhivadhanam2 1,2Assosicate professor Department of General surgery, ESIC PGIMSR, KK Nagar, Chennai, Tamilnadu, India *Corresponding author Bhanumati Giridharan Abstract: Cholecystitis is a recurrent problem, a disease of hepato Biliary system. The risk factor, predispositioning for gall bladder disease includes obesity, DM, oestrogen and pregnancy, hemolytic disease and cirrohotic liver diseases. Apart from studying the epidemiology and demographic factors dietary habitats, clinical presentation diagnostic tools and management it also looks into the stone analysis and the culture of blood to formulate the antibiotic treatment proper. Acute cholecystitis occurs when bile becomes trapped in the gallbladder. This often happens because a gallstone blocks the cystic duct, the tube through which bile travels into and out of the gallbladder. When a stone blocks this duct, bile builds up, causing irritation and pressure in the gallbladder. This can lead to swelling and infection. To identify the risk factor of the gallstone disease more commonly epidemiological studies now use the ultrasonography inpatients with clinical evidence of pain in the abdomen with radiation , fever, and positive Murphys sign, following imaging ultrasonography evidences the gall baldder disease status and the other associated diseases. Asymptomatic gall stones Majority will not develop symptoms upto 80% have never experienced biliary pain or complications as acute cholecystitis, cholangitis or pancreatitis such asymptamatic gallstones develop 1.2% major complication.
    [Show full text]
  • Chronic Hepatitis C
    Chronic Hepatitis C AUGUST | 2018 Introduction Briefings such as this one are prepared in response to petitions to add new conditions to the list of qualifying conditions for the Minnesota medical cannabis program. The intention of these briefings is to present to the Commissioner of Health, to members of the Medical Cannabis Review Panel, and to interested members of the public scientific studies of cannabis products as therapy for the petitioned condition. Brief information on the condition and its current treatment is provided to help give context to the studies. The primary focus is on clinical trials and observational studies, but for many conditions there are few of these. A selection of articles on pre-clinical studies (typically laboratory and animal model studies) will be included, especially if there are few clinical trials or observational studies. Though interpretation of surveys is usually difficult because it is unclear whether responders represent the population of interest and because of unknown validity of responses, when published in peer-reviewed journals surveys will be included for completeness. When found, published recommendations or opinions of national organizations medical organizations will be included. Searches for published clinical trials and observational studies are performed using the National Library of Medicine’s MEDLINE database using key words appropriate for the petitioned condition. Articles that appeared to be results of clinical trials, observational studies, or review articles of such studies, were accessed for examination. References in the articles were studied to identify additional articles that were not found on the initial search. This continued in an iterative fashion until no additional relevant articles were found.
    [Show full text]
  • Gastrointestinal Complications of Diabetes Mellitus
    Diabetes Mellitus: Management of Gastrointestinal Complications BETH CAREYVA, MD, and BRIAN STELLO, MD, Lehigh Valley Health Network/University of South Florida Morsani School of Medicine, Allentown, Pennsylvania Gastrointestinal disorders are common complications of diabetes mellitus and include gastroparesis, nonalcoholic fatty liver disease, gastroesophageal reflux disease, and chronic diarrhea. Symptoms of gastroparesis include early satiety, postprandial fullness, nausea, vomiting of undigested food, bloating, and abdominal pain. Gastroparesis is diagnosed based on clinical symptoms and a delay in gastric emptying in the absence of mechanical obstruction. Gastric empty- ing scintigraphy is the preferred diagnostic test. Treatment involves glucose control, dietary changes, and prokinetic medications when needed. Nonalcoholic fatty liver disease and its more severe variant, nonalcoholic steatohepatitis, are becoming increasingly prevalent in persons with diabetes. Screening for nonalcoholic fatty liver disease is not recom- mended, and most cases are diagnosed when steatosis is found incidentally on imaging or from liver function testing followed by diagnostic ultrasonography. Liver biopsy is the preferred diagnostic test for nonalcoholic steatohepatitis. Clinical scoring systems are being developed that, when used in conjunction with less invasive imaging, can more accu- rately predict which patients have severe fibrosis requiring biopsy. Treatment of nonalcoholic fatty liver disease involves weight loss and improved glycemic control; no medications have been approved for treatment of this condition. Diabe- tes is also a risk factor for gastroesophageal reflux disease. Patients may be asymptomatic or present with atypical symp- toms, including globus sensation and dysphagia. Diabetes also may exacerbate hepatitis C and pancreatitis, resulting in more severe complications. Glycemic control improves or reverses most gastrointestinal complications of diabetes.
    [Show full text]