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Kia Saeian
Reza Shaker
Editors
Liver Disorders
A Point of
Care Clinical Guide
123
Liver Disorders
Kia Saeian • Reza Shaker
Editors
Liver Disorders
A Point of Care Clinical Guide
Editors
Kia Saeian Reza Shaker
Division of Gastroenterology and Hepatology Division of Gastroenterology and Hepatology
Medical College of Wisconsin Medical College of Wisconsin
Milwaukee, WI, USA Milwaukee, WI, USA
ISBN 978-3-319-30101-3 ISBN 978-3-319-30103-7 (eBook)

DOI 10.1007/978-3-319-30103-7
Library of Congress Control Number: 2016935856
© Springer International Publishing Switzerland 2017

This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of
the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation,
broadcasting, reproduction on microfilms or in any other physical way, and transmission or information
storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology
now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication
does not imply, even in the absence of a specific statement, that such names are exempt from the relevant
protective laws and regulations and therefore free for general use.
The publisher, the authors and the editors are safe to assume that the advice and information in this book
are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the
editors give a warranty, express or implied, with respect to the material contained herein or for any errors
or omissions that may have been made.
Printed on acid-free paper
This Springer imprint is published by Springer Nature

The registered company is Springer International Publishing AG
The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland
Preface
Patients with liver disease may be fearful of the diagnosis particularly since once
they are told they have liver disease, they envision having cirrhosis and its associ-
ated ominous implications. Moreover, patients often receive confusing and at times
contradictory responses. Beyond the typical questions of why and how they are
affected by the disease, liver patients may be concerned about their long-term prog-
nosis, whether they can drink alcohol and if so, how much, if there is truly a best
approach for management moving forward, and what lifestyle changes they should
undertake. The unique aspect of this handbook on liver disease is its patient-based
perspective. World-class experts in the field provide cogent responses to everyday
questions often posed by patients with liver disease followed by a succinct and
evidence-based summary of a particular disorder. The summaries are not intended
to be exhaustive but rather intended to provide the reader with a manageable and
clinically relevant basis with which to care for patients with liver disease.
Disorders of the liver affect an increasingly large number of individuals, and the
emergence of myriad new therapeutic options including the new direct-acting anti-
viral agents used in the treatment of chronic hepatitis C has changed the landscape
of the management of chronic liver disease. In addition to covering the spectrum of
identified liver diseases, this handbook also provides insights into appropriate test-
ing and disease monitoring of patients, use of medications, supplements, alternative
therapies and alcohol, operative risk assessment, implementation of health mainte-
nance for patients with chronic liver disease and cirrhosis, identification and man-
agement of particular complications of cirrhosis and appropriate referral for liver
transplantation, as well as management of special populations.
It is often the case that questions posed by patients are seemingly straightforward
but require the provider to synthesize and distill complex and nuanced hepatology
literature into a simple answer that the patient can comprehend. Each chapter will
begin with patient questions followed by answers offered by the world-class experts.
The answers and evidence-based summary will guide the nonhepatologist (gastro-
enterologists, internists, physician extenders) liver provider as well as hepatologists
to easily and quickly answer common patient questions and address their medical
needs. Our guiding principles have been brevity and maintenance of a very clinical
v
vi Preface
focus such that the provider can derive insight into the particular disorder by reading
for just a few minutes during a busy clinic day.
We are grateful to the world-class experts who kindly agreed to offer their
insights and authored the chapters in this handbook and feel honored to have been
able to bring together such an outstanding group.
Milwaukee, WI Kia Saeian

Milwaukee, WI Reza Shaker
Contents
1 What Do Abnormal Liver Tests Mean?................................................. 1

Miguel Malespin and Rebecca Tsang
2 General Care of the Liver Patient.......................................................... 17
Sanjay Bhandari
3 Do I Need a Liver Biopsy?....................................................................... 27
Kiyoko Oshima
Part I What to Do with Tumors in the Liver?

4 Incidental Hepatic Lesions...................................................................... 43
Syed Rizvi
5 Benign Liver Lesions............................................................................... 51
Syed Rizvi
6 Malignant Liver Lesions.......................................................................... 71
Michael Loudin, Ranjan Mascarenhas, and Barry Schlansky
7 Health Maintenance in Liver Disease and Cirrhosis............................ 89
Veronica Loy
8 Preoperative and Postoperative Care of the Liver Patient.................. 99
Malcolm M. Wells and Thomas D. Schiano
Part II Distinct Liver Disorders

9 Viral Hepatitis: Hepatitis A and E.......................................................... 121
Adnan Said and Amanda DeVoss
10 Viral Hepatitis: Hepatitis B (& D).......................................................... 133
Tatyana Taranukha and Venelin Kounev
11 Viral Hepatitis: Hepatitis C.................................................................... 143
Chalermrat Bunchorntavakul and K. Rajender Reddy
vii
viii Contents
12 Viral Hepatitis: Other Viral Hepatides.................................................. 165

Adnan Said and Aiman Ghufran
13 Alcoholic Liver Disease............................................................................ 173
Ashutosh Barve, Luis S. Marsano, Dipendra Parajuli,
Matthew Cave, and Craig J. McClain
14 Nonalcoholic Fatty Liver Disease........................................................... 199
Samer Gawrieh
15 Autoimmune Liver Diseases: Autoimmune Hepatitis.......................... 217
Albert J. Czaja
16 Autoimmune Liver Diseases: Primary Biliary Cholangitits................ 251
Ahmad H. Ali, Elizabeth J. Carey, and Keith D. Lindor
17 Autoimmune Liver Diseases: Primary Sclerosing Cholangitis............ 289
José Franco
18 Autoimmune Liver Diseases: Overlap Syndromes............................... 307
Albert J. Czaja
19 Metabolic and Genetic Liver Diseases:
Alpha-1 Anti-trypsin Deficiency............................................................. 329
Helen S. Te
20 Metabolic and Genetic Liver Diseases: Hemochromatosis.................. 339
Matthew J. Stotts and Bruce R. Bacon
21 Metabolic and Genetic Liver Diseases: Wilson’s Disease..................... 355
Syed Rahman and Kia Saeian
22 Metabolic and Genetic Liver Diseases:
Glycogen Storage Diseases...................................................................... 369
Grzegorz W. Telega
23 Metabolic and Genetic Liver Diseases: Urea Cycle Defects................. 375
Grzegorz W. Telega
24 Metabolic and Genetic Liver Diseases: Porphyrias.............................. 381
Grzegorz W. Telega
25 Drug-Induced Liver Injury..................................................................... 389
Raj Vuppalanchi
26 Miscellaneous Disorders: Pregnancy-Associated Liver
Disorders, Vascular Disorders, Granulomatous Diseases,
and Amyloidosis....................................................................................... 405
Eric F. Martin
Contents ix
Part III Care of the Cirrhotic Patient

27 Portal Hypertension................................................................................. 455
Douglas A. Simonetto and Vijay H. Shah
28 Endoscopic Management of Portal Hypertension................................ 469
Murad Aburajab
29 Portosystemic Encephalopathy............................................................... 481
Jawaid Shaw and Jasmohan S. Bajaj
30 Ascites........................................................................................................ 507
Adam J. Schiro
31 Spontaneous Bacterial Peritonitis (SBP)............................................... 519
Adam J. Schiro
32 Hepatorenal Syndrome............................................................................ 531
Michael M. Yeboah
33 Hepatopulmonary Syndrome.................................................................. 545
Rahul Sudhir Nanchal and Tessa Damm
34 Endoscopy and the Liver Patient............................................................ 555
Abdul H. Khan
35 Liver Resection......................................................................................... 583
Amir H. Fathi and T. Clark Gamblin
36 Liver Transplantation: An Overview..................................................... 599
Joohyun Kim and Johnny C. Hong
Index.................................................................................................................. 621
Contributors
Murad Aburajab, M.D. Division of Gastroenterology and Hepatology, Medical

College of Wisconsin, Milwaukee, WI, USA
Ahmad H. Ali, M.B.B.S. Division of Gastroenterology and Hepatology, Mayo
Clinic, Phoenix, AZ, USA
Bruce R. Bacon, M.D. Division of Gastroenterology & Hepatology, St. Louis
University, Saint Louis, MO, USA
Jasmohan S. Bajaj, M.D. Division of Gastroenterology, Hepatology and Nutrition,
Virginia Commonwealth University, Richmond, VA, USA
McGuire VA Medical Center, Richmond, VA, USA
Ashutosh Barve, M.D. Division of Gastroenterology, Hepatology and Nutrition,
Department of Medicine, University of Louisville School of Medicine, Louisville,
KY, USA
Robley Rex Louisville VAMC, Louisville, KY, USA
Sanjay Bhandari, M.D. Department of General Internal Medicine, Medical
Chalermrat Bunchorntavakul, M.D. Division of Gastroenterology and
Hepatology, Department of Medicine, Hospital of the University of Pennsylvania,
Philadelphia, PA, USA
Department of Medicine, Rajavithi Hospital, College of Medicine, Rangsit
University, Bangkok, Thailand
Elizabeth J. Carey, M.D. Division of Gastroenterology and Hepatology, Mayo
xi
xii Contributors
Matthew Cave, M.D. Division of Gastroenterology, Hepatology and Nutrition,

KY, USA
Department of Pharmacology and Toxicology, University of Louisville School of
Medicine, Louisville, KY, USA
Department of Biochemistry and Molecular Biology, University of Louisville
School of Medicine, Louisville, KY, USA
Albert J. Czaja, M.D. Division of Gastroenterology and Hepatology, Mayo Clinic
College of Medicine, Rochester, MN, USA
Tessa Damm, M.D. Department of Critical Care Medicine, Aurora St. Luke’s
Medical Center, Milwaukee, WI, USA
Amanda DeVoss, M.M.S., PA-C Division of Gastroenterology and Hepatology,
Department of Medicine, William S. Middleton VAMC, University of Wisconsin
School of Medicine and Public Health, Madison, WI, USA
Amir H. Fathi, M.D. Division of Surgical Oncology, Medical College of
Wisconsin, Milwaukee, WI, USA
José Franco, M.D. Division of Gastroenterology and Hepatology, Medical College
of Wisconsin, Milwaukee, WI, USA
T. Clark Gamblin, M.D., M.S. Division of Surgical Oncology, Medical College
Samer Gawrieh, M.D. Division of Gastroenterology and Hepatology, Indiana
University School of Medicine, Indianapolis, IN, USA
Aiman Ghufran, M.D. Division of Gastroenterology and Hepatology, William
S. Middleton VA Medical Center, University of Wisconsin School of Medicine and
Public Health, Madison, WI, USA
Johnny C. Hong, M.D., F.A.C.S. Division of Transplant Surgery, Department of
Surgery, Medical College of Wisconsin, Milwaukee, WI, USA
A Joint Program of Froedtert & Medical College of Wisconsin, Children’s Hospital
of Wisconsin & Blood Center of Wisconsin, Milwaukee, WI, USA
Abdul H. Khan, M.D. Division of Gastroenterology, Gastroenterology and
Hepatology – Froedtert, Medical College of Wisconsin, Milwaukee, WI, USA
Joohyun Kim, M.D., Ph.D. Division of Transplant Surgery, Department of
Surgery, Medical College of Wisconsin, Milwaukee, WI, USA
Venelin Kounev, M.D. Division of Gastroenterology & Hepatology, Medical
Contributors xiii
Keith D. Lindor, M.D. Division of Gastroenterology and Hepatology, Mayo

College of Health Solutions, Arizona State University, Phoenix, AZ, USA
Michael Loudin, M.D. Division of Gastroenterology and Hepatology, Department
of Medicine, Oregon Health and Science University, Portland, OR, USA
Veronica Loy, D.O. Division of Hepatology, Loyola University of College,
Maywood, IL, USA
Miguel Malespin, M.D. Division of Gastroenterology and Hepatology, University
of Florida Health, Jacksonville, FL, USA
Luis S. Marsano, M.D. Division of Gastroenterology, Hepatology and Nutrition,
KY, USA
Eric F. Martin, M.D. Division of Hepatology, Miami University Miller School of
Medicine, Miami, FL, USA
Ranjan Mascarenhas, M.D. Austin Outpatient Clinic, Central Texas Veterans
Health Care System, Austin, TX, USA
Craig J. McClain, M.D. Division of Gastroenterology, Hepatology & Nutrition,
KY, USA
Department of Pharmacology and Toxicology, University of Louisville School of
Medicine, Louisville, KY, USA
Rahul Sudhir Nanchal, M.D. Division of Pulmonary & Critical Care, Medical
Kiyoko Oshima, M.D., Dr.Sc. Department of Pathology, Medical College of
Dipendra Parajuli, M.D. Division of Gastroenterology, Hepatology and Nutrition,
KY, USA
Syed Rahman, M.D. Division of Gastroenterology & Hepatology, Division of
Gastroenterology and Hepatology, Department of Medicine, Medical College of
K. Rajender Reddy, M.D. Division of Gastroenterology and Hepatology,
Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia,
PA, USA
xiv Contributors
Syed Rizvi, M.D. Division of Gastroenterology & Hepatology, Medical College of

Kia Saeian, M.D., M.Sc., Epi Division of Gastroenterology and Hepatology,
Medical College of Wisconsin, Milwaukee, WI, USA
Adnan Said, M.D., M.S. Division of Gastroenterology and Hepatology,
Department of Medicine, William S. Middleton VAMC, University of Wisconsin
School of Medicine and Public Health, Madison, WI, USA
Thomas D. Schiano, M.D. Icahn School of Medicine at Mount Sinai, The Mount
Sinai Medical Center, Recanati/Miller Transplantation Institute, New York, NY,
USA
Adam J. Schiro, M.D. Division of Gastroenterology & Hepatology, Department
of Medicine, Medical College of Wisconsin, Milwaukee, WI, USA
Barry Schlansky, M.D. Division of Gastroenterology and Hepatology, Department
of Medicine, Oregon Health and Science University, Portland, OR, USA
Vijay H. Shah, M.D. Department of Gastroenterology and Hepatology, Mayo
Clinic Hospital, Rochester, MN, USA
Jawaid Shaw, M.D. Department of Medicine, McGuire VA Medical Center,
Richmond, VA, USA
Douglas A. Simonetto, M.D. Department of Gastroenterology and Hepatology,
Mayo Clinic Hospital, Rochester, MN, USA
Matthew J. Stotts, M.D. Banner Health Greely, Colorado, St. Louis, MO, USA
Tatyana Taranukha, M.D. Division of Gastroenterology & Hepatology, Medical
Helen S. Te, M.D. Center for Liver Diseases, University of Chicago Medicine,
Chicago, IL, USA
Grzegorz W. Telega, M.D., M.S. Department of Pediatric Gastroenterology,
Hepatology and Nutrition, Medical College of Wisconsin, Milwaukee, WI, USA
Rebecca Tsang, M.D., M.P.H. Division of Gastroenterology, Loyola University
Medical Center, Maywood, IL, USA
Raj Vuppalanchi, M.D. Division of Gastroenterology and Hepatology, Indiana
University School of Medicine, Indianapolis, IN, USA
Malcolm M. Wells, M.D., F.R.C.P.C. Icahn School of Medicine at Mount Sinai,
The Mount Sinai Medical Center, New York, NY, USA
Michael M. Yeboah, M.B.Ch.B., Ph.D. Division of Nephrology, Medical College
Chapter 1
What Do Abnormal Liver Tests Mean?
Miguel Malespin and Rebecca Tsang
Commonly Posed Patient Questions
1. What are common causes of abnormal liver tests?

The initial step when evaluating abnormalities in liver panel testing is to
determine whether these changes reflect an acute or chronic process. An acute
process is typically suspected in an individual lacking a prior history or risk fac-
tors for the development of chronic liver disease. Once chronicity has been
established, a differential diagnosis can then be formulated on the basis of the
pattern, degree, and rapidity of liver enzyme elevation. Common acute causes of
elevated liver enzymes include drug toxicity (i.e., over-the-counter, prescribed,
and herbal therapy), alcohol abuse, acute viral disease (i.e., hepatitis A and B),
autoimmune diseases of the liver, benign or malignant liver tumors, thrombosis
of hepatic vasculature, and global hepatic hypoperfusion.
A chronic elevation in liver panel testing can either reflect states of persis-
tent hepatic inflammation that occur for greater than 6 months and/or hepatic
dysfunction from a cirrhotic liver’s inability to carry out its basic cellular
processes. Common etiologies include chronic liver disease from viral hepa-
titis (i.e., hepatitis B and C), alcohol abuse, nonalcoholic steatohepatitis
(NASH), hereditary hemochromatosis, and chronic autoimmune diseases of
the liver. The initial evaluation of both the acute and chronic liver disease
involves acquisition of a thorough but focused history, physical examination,
M. Malespin, M.D. (*)

Division of Gastroenterology and Hepatology, University of Florida Health,
Jacksonville, FL, USA
4555 Emerson St. Ste. 300, Jacksonville, FL 32207, USA
e-mail: miguel.malespin@jax.ufl.edu
R. Tsang, M.D., M.P.H.
Division of Gastroenterology, Loyola University Medical Center, Maywood, IL, USA
© Springer International Publishing Switzerland 2017 1

K. Saeian, R. Shaker (eds.), Liver Disorders,
DOI 10.1007/978-3-319-30103-7_1
2 M. Malespin and R. Tsang
serologic analysis, and liver-focused imaging with either ultrasound or com-

puted-tomography (CT) scan. A liver biopsy may be warranted in cases where
the diagnosis remains elusive.
It is important to consider that some patients may also have multiple causes of
liver disease. As in the case of coexisting chronic hepatitis C (HCV) and alcohol-
related liver disease, a second insult can potentiate viral replication, inflamma-
tion, and fibrosis. Given the unspecific nature of certain lab abnormalities, a
practitioner should remain attuned to nonhepatic causes of elevated liver enzymes.
Such examples include elevated total bilirubin levels secondary to hemolytic ane-
mia and increased levels of circulating levels of alanine aminotransferase (ALT)
and aspartate aminotransferase (AST) from skeletal muscle injury.
2. How long will it take for my AST/ALT to return to normal?
Hepatocyte inflammation is expressed serologically through an elevation in
levels of the transaminases, AST and ALT. The peak of injury after the insult
and time to laboratory normalization are dependent on the presence of preexist-
ing liver disease and the etiology of hepatic insult. For example, severe injury
secondary to acetaminophen toxicity typically resolves within weeks while cases
of penicillin or alcohol related hepatitis could take several months to normalize.
On the other hand, patients being treated with antiviral therapy for hepatitis B or
C demonstrate normalization of liver enzymes upon viral suppression or clear-
ance to undetectable levels. Treatment of NASH focuses on weight loss through
dietary modifications and exercise [2]. Studies have demonstrated that approxi-
mately 10 % of weight loss can lead to improvement in hepatocyte inflammation
and thus improvement in liver enzymes. The time to normalization of AST/ALT
can occur early but will typically vary between individuals.
3. What does it mean if my ALT and AST is low?
When evaluating laboratory values, the reported reference range signifies the
parameters that include the mean 95 % of the population. Thus, there will be a
reported abnormal value for liver enzymes above and below this normal range.
Low values do not represent a clinically significant abnormality and thus have no
repercussions. This principle also holds true for alkaline phosphatase and biliru-
bin levels in a normal patient with no prior history of liver disease.
Components of a Liver Profile
The term, liver function tests, is often used in the medical community to describe
the serologic measurements ordered to evaluate for liver disease. As part of the liver
function tests, aminotransferases are most commonly ordered as the initial test to
detect liver disease. The term liver function tests is a misnomer and do not necessar-
ily reflect liver function, but more so are biochemical tests that reflect inflammation.
In addition to the serum aminotransferases AST and ALT, the complete liver profile
also includes total and direct bilirubin, albumin, alkaline phosphatase, and occa-
sionally gamma glutamyl transpeptidase (GGT).
1 What Do Abnormal Liver Tests Mean? 3
It has been found that elevated aminotransferase levels are present in 7.9 % of the
population when sampling asymptomatic individuals [3]. As medical providers, it is
important to know how to interpret these tests to better assess and manage these
patients, as there is a mortality risk associated with acute and chronic liver diseases
and their complications.
Aminotransferases
Serum aminotransferases, also known as transaminases, include AST and ALT, and
are good indicators of acute hepatocellular injury. Formerly known as serum glu-
tamic oxaloacetic transaminase (SGOT), AST is located in the cytosol and mito-
chondria and catalyzes the transfer of the α-amino groups of the L-aspartic acid to
the α-keto group of ketoglutaric acid. Though most commonly found in the liver,
this enzyme is also present in striated muscle, the kidney, brain, pancreas, lung,
leukocytes, and erythrocytes. Formerly known as serum glutamic pyruvic transami-
nases (SGPT), ALT lies in the cytosol and catalyzes the transfer of the α-amino
groups of alanine to the α-keto group of ketoglutaric acid. This enzyme is also
found throughout the body, but is a more specific indicator of liver injury compared
to AST because it is significantly more concentrated in the liver. In hepatocellular
injury, damage to tissues rich in aminotransferases causes them to leak into the
serum, resulting in increased serum levels of ALT and/or AST. The absolute value
of serum levels does not necessarily reflect the degree of damage, and it cannot be
assumed that the higher the serum aminotransferase level, the more severe the liver
injury. These enzymes have a half-life measured in days, but AST is cleared more
rapidly than ALT.
Normal Range
NHANES III criteria for upper limit reference of the normal range for amino-
transferases were listed as AST >37 IU/L or ALT >40 IU/L for men and AST or
ALT >31 IU/L for women [4]. However, normal values for aminotransferases in
serum vary widely among laboratories due to technical issues. In addition, the
normal range varies between different population groups and so there is no uni-
versal definition. Similar to most clinical laboratory tests, the normal range for a
particular laboratory test is established as within two standard deviations from
the mean of a healthy population, which includes 95 % of a uniformly distributed
population. As mentioned earlier, serum aminotransferase level below the lower
reference limit is of no clinical importance, although lower levels have been seen
in hemodialysis patients thought to be partly due to B6 deficiency. Therefore, it is
only when the aminotransferase level exceeds the upper reference limit that it is
considered abnormal.
Aminotransferase levels vary according to age and gender. For instance, elevated
aminotransferases are more common for people between ages 30 and 40 years old,
and it seems to decrease after the age of 60. In a study of 975 healthy children aged
7–18 years old, the upper reference limit of ALT was 30 IU/L for boys and 21 IU/L
for girls [5], which is comparatively less than adults as evidenced by NHANES III
mentioned earlier. With respect to gender differences, overall the normal range for
males is higher than females [3, 5].
In addition, it has been shown that ALT levels correlated strongly with BMI, as
evidenced by the Prati et al. study in which 6835 healthy blood donors were
screened [2]. This could be a reflection of the increased prevalence of NAFLD in
patients with a higher BMI. There is also a significant prevalence of NAFLD in
overweight and obese patients with diabetes mellitus type II despite normal amino-
transferases [6]. This suggests that perhaps in this population, there should be a
higher index of suspicion in the lower-than-normal threshold aminotransferase
level in suspecting NAFLD.
Furthermore, there are ethnic differences for normal values of aminotransferases.
There are higher serum levels of aminotransferases in non-Hispanic blacks and
Mexican Americans compared to non-Hispanic whites [3]. In addition, serum ami-
notransferases for healthy Asians are significantly lower, as shown by the Wu et al.
study in Taipei with the upper limit reference of the normal range found to be
21 IU/L for men and 17 IU/L for women [7].
Of note, there have been some studies that have shown slightly increase in AST/
ALT during normal pregnancy, especially in the third trimester [8, 9]. However, the
majority of studies support the presence of normal aminotransferases during uncom-
plicated pregnancy [10, 11], and therefore elevated aminotransferases continue to
be excellent markers for liver diseases during pregnancy.
Common Causes of Elevated Aminotransferases
As previously noted, elevated aminotransferases are suggestive of hepatocellular

injury. The challenge of identifying a sole etiology was highlighted in one study,
illustrating that one or more causes were determined in only 31 % of patients with
elevated aminotransferases, leaving 69 % of cases unexplained [3]. Some of the most
common identifiable causes include alcohol use (13.5 %), hepatitis C (7.0 %), hemo-
chromatosis (3.4 %), hepatitis B (0.9 %), or a combination of causes (6.1 %).
Alterations in aminotransferase levels can be classified as: mild (<5 times the upper
limit of normal), moderate (5–10 times the upper limit of normal), and marked (>10
times the upper limit of normal). Though somewhat arbitrary, different etiologies
should be considered depending on magnitude of aminotransferase alteration.
Table 1.1 includes common causes of elevated aminotransferases based on the degree
of elevation [12].
Table 1.1 Causes of elevated aminotransferases

Moderate-to-marked elevation in aminotransferases Mild elevation in aminotransferases
Ischemic injurya, b Nonalcoholic fatty liver disease
Toxic injurya, b Alcoholic hepatitis
Acute viral hepatitisa, c, d Pharmacology
Acute biliary obstructiona, d, e Chronic viral hepatitis (B, C)
Alcoholic hepatitisa, d, e Hereditary hemochromatosis
Autoimmune hepatitis
Wilson’s disease
α-1-Antitripsin deficiency
Celiac disease
Extrahepatic causes
a
Aminotransferase level increase of 5–10 × upper limit of normal
b
Bilirubin increase of <5 × upper reference limit
c
Aminotransferase level increase of >10 × upper limit of normal
d
Bilirubin increase of 5–10 × upper limit of normal
e
Bilirubin increase of >10 × upper limit of normal
Initial Evaluation of Elevated Aminotransferases
The work-up for abnormal aminotransferases differs according to the degree of

alteration, since different etiologies are considered for mild elevations compared to
moderate–severe elevations. However, as mentioned earlier, the degree of elevation
does not necessarily reflect the extent of liver damage. Moderate–severe elevations
are more suggestive of an acute liver injury, whereas when mild elevations in ami-
notransferases are encountered, chronic liver diseases should also be considered in
addition to acute liver injury.
Mild alterations are commonly encountered by primary care physicians. Though
some expert recommendations include repeating transaminases 6 months before
initiating a work-up, the clinical scenario will likely dictate the urgency of further
clinical evaluation. However, if repeat transaminases are normal, this does not
entirely exclude liver diseases since aminotransferases fluctuate in liver disease.
The importance of a thorough history cannot be overstated. Also, there should be a
focus on identifying risk factors, family history, and possible exposures to over-the-
counter medications, supplements, and alcohol. If there is clear exposure such as a
medication and/or the pattern of aminotransferases is typical of alcohol use
(AST:ALT >2), then it is reasonable to repeat transaminases after discontinuing the
exposure. Initial testing for anti-HCV and HBsAg testing should be considered,
especially in patients with IV drug use, exposure to nonsterile needles, or sexual
exposure to an infected person with further consideration of anti-HCV testing in the
age-based cohort of persons born between 1945 and 1965 and HBsAg testing in
those of Asian descent.
Additional testing includes acquisition of ferritin, iron, and total iron-binding

capacity (TIBC) to screen for hereditary hemochromatosis, and if both ferritin and
transferrin saturation (iron/TIBC × 100) are increased, then it is reasonable to test
for HFE gene mutation. Furthermore, it is reasonable to test for antinuclear antibod-
ies (ANA), antismooth body antibodies (ASMA), immunoglobulin levels, and
occasionally anti-LKM (liver–kidney microsomes) to rule out autoimmune hepati-
tis, especially in young or middle-aged women with concomitant autoimmune dis-
eases. If the earlier tests are unrevealing, further serologic work-up to consider
include alpha-1 antitrypsin levels to rule out alpha-1 antitrypsin deficiency, tissue
transglutaminase antibodies to rule out celiac disease, and serum ceruloplasmin lev-
els in patients under the age of 50 to evaluate for Wilson’s disease. In the absence
of serological findings and a history of alcohol abuse, one shoulder consider the
presence of nonalcoholic fatty liver disease (NAFLD), particularly in patients with
conditions linked to metabolic syndrome and insulin resistance (i.e., increased BMI,
diabetes, hyperlipidemia, hypertension). However, lack of the above-mentioned
risk factors does not exclude the possibility of NAFLD. Despite the commonality
and increasing prevalence of fatty liver disease [13], the lack of disease-specific
serology can make the diagnosis challenging in the absence of histology.
Moderate-to-marked elevations in aminotransferases are usually more typical of
acute compared to chronic liver disease. A moderate increase in aminotransferase
levels has a higher sensitivity and specificity for identifying acute injury compared
to mild elevations in aminotransferases. Studies have shown a sensitivity of 91 %
and specificity of 95 % with an AST ≥ 200 IU/L while ALT levels ≥ 300 IU/L offer
sensitivity of 96 % and specificity of 94 % [14]. Although there are certain liver
injuries that are associated with markedly elevated aminotransferases, these same
etiologies should be considered in mild elevations as well.
Certain patterns of liver injury are indicative of specific disease etiologies. For
example, aminotransferases levels >75 times the upper limit of normal (ULN) are
indicative of ischemic or toxic liver injury [15] with a subsequent rise in bilirubin levels
3–5 days after the insult. Acute viral hepatitis usually present with a more modest ele-
vation of aminotransferases. Patients with moderate-to-marked increases (>10–
20 × ULN) in aminotransferases should be tested for IgM antibodies to hepatitis A, IgM
to hepatitis B core antigen, hepatitis B surface antigen, and hepatitis C antibody. If
these are negative, it is reasonable to test for HCV RNA particularly in the setting of
risk factors. Other considerations include acetaminophen-induced hepatic damage as it
causes 54 and 16 % of acute liver failure in the United Kingdom and United States [16].
Another etiology of moderate elevations is alcohol-induced acute hepatitis dam-
age. This can present as both acute and acute-on-chronic liver injury. The increase
in AST levels is reported to be less than six to seven times the ULN in 98 % of the
patients with alcoholic liver disease, and the AST:ALT ratio >1 in 92 % and >2 in
70 % of patients [17]. After these common causes have been excluded, other less
common causes such as nonhepatotropic viruses such as Epstein–Barr virus, cyto-
megalovirus, and herpes simplex virus, as well as other infiltrative, autoimmune,
extrahepatic, and congenital causes should be considered. Imaging modalities can
point to extrahepatic causes by demonstrating a dilated biliary system particularly
in the setting of biliary colic and/or known gallstones (Fig. 1.1).
Elevated
aminotransferases
Exposure
(alcohol, drugs)
Chronic, mild Acute, moderate-

severe elevations
Extrahepatic elevations
(5-10xULN,
(<5xULN) >10xULN)
Hereditary
Biliary obstruction hemochromatosis Ischemic injury
Ultrasound, CT ferritin, Fe, TIBC if hypotensive
(HFE mutation)
Alpha-1 antitrypsin Acute viral

Celiac
deficiency anti-HAV IgM,
anti-tTG
A1AT levels HBsAg, HBcAg IgM
Autoimmune
Rhabdomylosis Chronic viral
ANA, ASMA
CK HBsAg, anti-HCV
(anti-LKM)
Acetaminophen
Autoimmune
Thyroid disease toxicity
ANA, ASMA
TSH acetaminophen
(anti-LKM)
levels
Wilson's disease
ceruloplasmin
Liver biopsy if still

unclear
NAFLD
no serum test
Fig. 1.1 Evaluation of transaminase elevation. ULN upper limit of normal, Anti-tTG tissue trans-
glutaminase antibodies, CK creatine kinase, Fe iron, TIBC total iron binding capacity, HBV hepa-
titis B, HCV hepatitis C, HBsAg hepatitis B surface antigen, anti-HCV hepatitis C antibody, ANA
antinuclear antibodies, ASMA antismooth body antibodies, anti-LKM antibodies to liver–kidney
microsomes, NAFLD nonalcoholic fatty liver disease. Initially, if there is an obvious offending
agent (i.e., drug or alcohol), liver function tests can be repeated after discontinuation of offending
agent. If there is no offending agent or if no improvement in aminotransferases despite removal of
offending agent, work-up should be initiated. Moderate–severe elevations are more suggestive of
an acute process. Although mild elevations are more suggestive of a chronic process, acute etiolo-
gies should also be considered, especially if the chronicity of aminotransferase elevation is unclear
Alkaline Phosphatase and Gamma Glutamyl

Transpeptide (GGT)
Despite being produced predominantly in the liver and bone, alkaline phosphatase
isoenzymes can be found in renal, intestinal, placental tissue, or within leukocytes.
In the liver, alkaline phosphatase is located on the canalicular membrane of hepato-
cytes and an increase in serum levels usually indicates osseous or hepatobiliary
pathology. With a half-life of approximately 6 days, an increase in alkaline phos-
phatase levels occurs secondary to increased synthesis with leakage of the serum
and not due to decreased clearance.
GGT is a microsomal enzyme located throughout the body, including hepato-
cytes and cholangiocytes in the liver, kidney, pancreas, spleen, heart, brain, and
seminal vesicles. It has a high sensitivity for hepatobiliary disease but lacks speci-
ficity. Levels can become elevated in patients taking certain classes of medications,
including anticonvulsants, oral contraceptives, barbiturates, antiretroviral therapy,
as well as patients with comorbidities, such as chronic obstructive pulmonary dis-
ease, renal failure, and acute myocardial infarctions. GGT is clinically useful to
identify the etiology of an isolated increase in alkaline phosphatase, as it is not
elevated in bone disease. Elevated GGT levels also occur in alcohol-related liver
disease, even in patients with normal alkaline phosphatase levels. Because of its
high sensitivity, some physicians advocate acquisition of GGT levels as an indirect
marker of current alcohol consumption [18]. Beyond alcohol liver disease, GGT
levels may also be two to three times greater in more than 50 % of patients with
NAFLD [19]. Because elevated GGT levels are frequently elevated in most forms
of liver disease, it is most useful when evaluating patients with an elevated alkaline
phosphatase levels with otherwise normal liver enzymes and bilirubin levels.
Variations
There is some physiologic variation of serum alkaline phosphatase levels in certain

populations, including certain physiologic circumstance in which the intestinal
alkaline phosphatase can be proportionately elevated and result in elevated serum
levels. For instance, because patients with blood type O and B have increased intes-
tinal alkaline phosphatase after a fatty meal [20], some physicians recommend
obtaining fasting alkaline phosphatase levels. Also, elevated intestinal alkaline
phosphatase can be indicative of certain benign familial conditions, including
familial intrahepatic cholestasis or benign recurrent intrahepatic cholestasis, which
are typically characterized by elevations in the alkaline phosphatase despite a nor-
mal GGT with occasional elevations in the bilirubin level. The age of the individual
also has an impact on the serum alkaline phosphatase levels with levels being twice
as high in adolescents compared with adults due to increased bone growth. In addi-
tion, there is an unexplained increase in levels after age 30 years old, but the increase
is greater in women compared to men [21].
Clinical Significance of Low Alkaline Phosphatase
Patients with Wilson’s disease may have a low serum alkaline phosphatase, especially when
the patient presents with fulminant hepatitis and hemolysis. It is thought that this is due to
reduced activity of the enzyme, owing to displacement of the cofactor zinc by copper.
Common Causes of Elevated Alkaline Phosphatase
Table 1.2 lists the common causes of elevated levels [12]. When patients have an
isolated elevated alkaline phosphatase or if the alkaline phosphatase is elevated out
of proportion to the other liver enzymes, one should consider cholestatic disorders.
Table 1.2 Common causes of elevated alkaline phosphatase

Intrahepatic
Drugs Anabolic steroids, estrogens, ACE-I, antimicrobials, NSAIDS,
allopurinol, antiepileptics, hydralazine, procainamide, quinidine,
phenylbutazone
Primary biliary cirrhosis Predominantly middle-aged women with median age of 50 years
old, 95 % of patients have + AMA
Primary sclerosing Strongly associated with IBD, commonly in younger men,
cholangitis diagnosed by ERCP/MRCP
Granulomatous liver Sarcoidosis, TB, fungal infections, brucellosis, Q fever,
disease schistosomiasis
Viral hepatitis EBV, CMV, Hepatitis A, B, C, E
Genetic conditions Benign recurrent intrahepatic cholestasis type 1,2
Malignancy HCC, metastatic disease, paraneoplastic syndrome
Infiltrative liver disease Amyloidosis, lymphoma
Intrahepatic cholestasis
of pregnancy
Total parent nutrition
Graft-versus-host disease
Extrahepatic
Intrinsic
Immune-mediated duct Autoimmune pancreatitis, primary sclerosing cholangitis
injury
Malignancy Ampullary cancer, cholangiocarcinoma
Infections AIDS cholangiopathy, CMV, cryptosporidiosis, microsporidosis,
parasitic infections
Extrinsic
Malignancy Gallbladder cancer, metastases, portal adenopathy, pancreatic
cancer
Mirizzi syndrome Compression of common hepatic duct by stone in neck of gallbladder
Pancreatitis Also includes pancreatic pseudocyst
Initial Evaluation of Elevated Alkaline Phosphatase
If there is an elevated isolated alkaline phosphatase level in an asymptomatic patient,

a cholestatic disorder should be considered if GGT levels are elevated or if there is
elevated liver alkaline phosphatase when it is fractionated. This is particularly the
case for patients in whom the elevated alkaline phosphatase levels are elevated out
of proportion to aminotransferases. Initial evaluation with imaging of biliary tree
help discern between intrahepatic and extrahepatic etiologies. Initial imaging is
typically recommended with ultrasound to evaluate for biliary dilatation or mass
lesions, but of course CT or MRI may be more definitive albeit at a higher cost and
potential risk. When dilated ducts are seen on imaging, this is suggestive of an
extrahepatic cause of the cholestasis. This can occur secondary to an intrinsic or
extrinsic process causing biliary obstruction. Further work-up and/or management
may include magnetic resonance imaging including magnetic resonance cholangio-
pancreatography (MRCP), endoscopic retrograde cholangiopancreatography
(ERCP), and endoscopic ultrasound. In the absence of dilated ducts, further work-
up should focus on intrahepatic etiologies. Part of this includes a thorough history
of medications since some medications can cause a cholestatic picture. Liver biopsy
is useful for evaluating hepatic disease including primary biliary cirrhosis, drug-
induced liver injury, and small duct primary sclerosing cholangitis (Fig. 1.2).
Bilirubin Metabolism
Unconjugated bilirubin represents the product of the heme breakdown within the
reticuloendothelial system. This unsoluble form is then bound to albumin and trans-
ported to the liver. Once it reaches the hepatic sinusoids, the albumin complex dis-
sociates and within hepatocytes uridine-5′-diphosphate (UDP) glycuronylransferase
conjugates bilirubin to glucuronic acid. The now conjugated bilirubin is then excreted
into bile and travels to the distal ileum and colon where bacteria hydrolyze conju-
gated bilirubin to the unconjugated form. This is further reduced by bacteria to color-
less urobilinogen, which is excreted or absorbed by the intestine into the portal
system as urobilinogen. A minority of urobilinogen is excreted into urine while the
remainder enters the enterohepatic circulation, in which the liver reexcretes it.
Laboratory Assays for Bilirubin
The laboratory tests, direct and indirect bilirubin, are the components of total biliru-
bin and provide rough measurements of conjugated and unconjugated bilirubin lev-
els. This is determined by the van den Bergh reaction in which bilirubin reacts with
diazotized sulfanilic acid. The conjugated fraction reacts immediately, or “directly,”
and can be measured within 30–60 s. The total bilirubin is measured 30–60 min
Elevated ALP
Biliary pain Asymptomatic
Isolated Concurrent
elevated elevated
RUQ ALP AST, ALT
ultrasound
GGT normal GGT high

Hepatocellular
injury (Fig 1)
Cholestasis
Bone, renal, Biliary obstruction or

cardiac, extraheaptic malignancies
endocrine ultrasound
etiologies or
malignancies
Medications/Alcohol
Hepatitis B, C
HBsAg, anti-HCV
PBC
AMA
If etiology still unclear, consider
MRCP, ERCP, EUS, or liver PSC
biopsy
MRCP, ERCP
Autoimmune cholangitis
IgG4
Fig. 1.2 Evaluation of alkaline phosphatase elevation. ALP alkaline phosphatase, GGT gamma
glutamyl transpeptide, HBsAg hepatitis B surface antigen, anti-HCV hepatitis C antibody, PBC
primary biliary cirrhosis, AMA antimitochondrial antibody, PSC primary sclerosing cholangitis,
MRCP magnetic resonance cholangiopancreatography, ERCP endoscopic retrograde
cholangiopancreatography
after adding an accelerant. Subsequently, the unconjugated, or indirect, bilirubin is

the result of subtracting the direct bilirubin from the total bilirubin.
Normal Range
The normal range for total and indirect bilirubin falls between 1.0 to 1.5 and 0.8 to
1.2 mg/dL, respectively [22].
Table 1.3 Common causes of elevated bilirubin

Type Cause
Unconjugated hyperbilirubinemia Hemolysis
Gilbert’s syndrome
Hematoma reabsorption
Ineffective erythropoiesis
Conjugated hyperbilirubinemia Bile duct obstruction
Hepatitis
Cirrhosis
Autoimmune cholestatic diseases (PBC, PSC)
Total parenteral nutrition
Drug toxins
Vanishing bile duct syndrome
Common Causes of Elevated Bilirubin
Findings of an elevated bilirubin can be very nonspecific and must be evaluated in the
context of the other liver tests. When an elevation in bilirubin is associated with an
elevation in aminotransferases and/or alkaline phosphatase, the work-up for hepato-
cellular injury and/or cholestatic diseases should be performed. Findings of isolated
hyperbilirubinemia can reflect conditions associated with conjugated or unconju-
gated bilirubinemia. The most common causes of unconjugated hyperbilirubinemia
are hemolysis and Gilbert’s syndrome. Other causes are listed in Table 1.3.
Initial Evaluation of Elevated Bilirubin
As noted earlier, it is important to first determine whether the hyperbilirubine-

mia occurs in conjunction with other liver test abnormalities (i.e. aminotransfer-
ases, alkaline phosphatase). If this is the case, the evaluation should focus on
investigation of common hepatocellular (Table 1.1) or cholestatic diseases
(Table 1.2). However, in patients with isolated elevated bilirubin, it is important
to fractionate and determine if there is a predominance of conjugated or
unconjugated bilirubin. Findings of <15 % conjugated bilirubin suggest a hemo-
lytic process, an inability to conjugate heme, or an impairment of hepatic uptake.
Medications should also be reviewed to investigate for drug reactions leading to
impairment of hepatocellular bilirubin uptake. If none are identified, then
genetic deficiencies that impair conjugation of bilirubin should be considered,
which include Gilbert’s syndrome and Crigler–Najjar syndrome. Gilbert’s
syndrome has a reported incidence of 6–12 % in the population and occurs when
due to a mutation of the UDP glycuronyl transferase gene, resulting in reduction
in enzyme activity thus limiting conjugation. Gilbert’s syndrome is benign,
Elevated
bilirubin
Isolated Elevated
bilirubin AST/ALT
+/- ALP
<15% direct >15% direct
Hemolysis
LDH, haptoglobin,
peripheral smear Dubin-Johnson or
Rotor's syndrome Hepatocellular
and
Drugs cholestatic
causes
Gilbert's or Crigler-
Najjar syndrome
Fig. 1.3 Evaluation of bilirubin elevation. LDH lactate dehydrogenase. When the bilirubin is
elevated in conjunction with elevated transaminases and/or alkaline phosphatase, work-up for
hepatocellular and/or cholestatic etiologies should be considered (Figs. 1.1 and 1.2). For isolated
bilirubin, different causes are considered depending on the fractionation of the bilirubin
unlike Crigler–Najjar syndrome which is a rare disorder related to a mutation

resulting in reduced UDP glucuronyl transferase activity (<10 % in type II and
absence of activity in type I). Crigler–Najjar patients are at risk for neurotoxic-
ity secondary to hyperbilirubinemia, known as kernicterus.
Patients with isolated conjugated hyperbilirubinemia may have Dubin–Johnson
syndrome or Rotor’s syndrome, both uncommon, which is related to impaired
excretion of conjugated bilirubin across the bile canalicular membrane. Both of
these syndromes are not associated with adverse clinic outcomes (Fig. 1.3).
Albumin
Albumin is a plasma protein that is exclusively made by in the liver and accounts for
75 % of the plasma colloid pressure. The average adult procedure approximately
15 g/day and the half-life is 14–21 days [23]. This long half-life limits its reliability
in acute liver injury, but is clinically helpful in chronic liver disease since hepatic
synthesis of albumin is impaired in patients with advanced liver disease. However,
this is not specific to liver diseases, and low serum levels can be seen in patients with
nephrotic syndrome, malabsorption, protein-losing enteropathy, chronic systemic
inflammatory conditions, hormonal imbalances, or malnutrition. Therefore, it is not
necessarily a good screening test. It is important to interpret low albumin in the clini-
cal context and look for other markers of liver disease. Even in patients with liver
disease, if they are overloaded, the low serum albumin can be a reflection of the
increased volume of distribution instead of impaired hepatic synthetic function.
Prothrombin Time
Prothrombin time is a measurement of the rate at which prothrombin is converted to

thrombin, the extrinsic pathway of coagulation and depends on the activity of clot-
ting factors II, V, VII, and X—all of which are synthesized in the liver. Therefore,
prothrombin time is a reflection of liver dysfunction. Of note, factor V is sometimes
checked when trying to decide if abnormal prothrombin time is due to liver disease.
In chronic liver diseases, prolonged prothrombin time is a sign of advanced liver
disease. In acute liver diseases, it is a more reliable indicator of immediate synthetic
function since the half-life of the clotting factors are much shorter (approximately a
day). International normalized ratio (INR) standardizes prothrombin time measure-
ments based on the thromboplastin reagent used in the laboratory. It is used in a
similar fashion to prothrombin time. Other etiologies of prolonged prothrombin
time may be warfarin, deficiency in vitamin K, disseminated intravascular coagu-
lopathy. Of note, obstructive jaundice can decrease absorption of vitamin K and
may prolong prothrombin time but will respond to parental supplementation.
Conclusion
Interpretation of laboratory values in patients with abnormalities in liver panel test-

ing is critical to developing a differential diagnosis and initiation an adequate work-
up. The initial step when evaluating a patient with abnormalities in hepatic
transaminases is to first determine whether the clinical scenario represents an acute,
chronic, or acute-on-chronic process. Establishing disease chronicity is reliant on a
combination of laboratory, radiologic, physical exam, and histologic findings.
Clues suggesting the presence of advanced liver disease and/or cirrhosis include the
presence of hypoalbuminemia, elevation in prothrombin time, or elevated bilirubin lev-
els. Thrombocytopenia can be used as an indirect marker of portal hypertension, particu-
larly in the presence of splenomegaly, ascites, and portal hypertension. Other typical
physical exam findings encountered in cirrhotic patients include spider angiomata, pal-
mar erythema, gynecomastia, testicular atrophy, asterixis, and fetor hepaticus.
Acquisition of histology can be used to confirm a suspected diagnosis, rule out
hepatic disease, and stage the degree of fibrosis. This procedure can be performed
percutaneously with ultrasound guidance or through a transvenous approach where
access to the hepatic parenchyma is obtained by introduction of a cannula through
the jugular vein and into a hepatic venous system. The transvenous approach offers
an added benefit of assessing for the presence of portal hypertension.
Upon establishment of chronicity, the role of the practitioner is to establish the

severity of hepatic dysfunction, potential for reversibility, and the need for escala-
tion of care. Noncirrhotic patients without a preexisting history of liver disease who
develop severe hepatic injury in conjunction with encephalopathy and an elevation
in INR ≥ 1.5 are classified as having acute liver failure. Given the increase in mortality
associated with acute liver failure, transfer to a liver transplant center and intensive
care unit management is recommended upon diagnosis [24].
Acknowledgements Miguel Malespin: Has served as a consultant for Gilead Pharmaceuticals

Conflict of interest: None of the authors have a conflict of interest.
Financial support/funding: None
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The Project Gutenberg eBook of Respectfully
mine
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Title: Respectfully mine
Author: Randall Garrett
Illustrator: John Schoenherr
Release date: November 17, 2023 [eBook #72147]
Language: English
Original publication: New York, NY: Royal Publications, Inc, 1958
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*** START OF THE PROJECT GUTENBERG EBOOK

RESPECTFULLY MINE ***
Respectfully Mine
By RANDALL GARRETT
Illustrated by JOHN SCHOENHERR
Leland Hale was undoubtedly the cleverest

crook in the universe. But how could even he
crack that closely-guarded time capsule?
[Transcriber's Note: This etext was produced from

Infinity August 1958.
Extensive research did not uncover any evidence that
the U.S. copyright on this publication was renewed.]
Thieves respect property. They merely wish the
property to become their property, that they may more
perfectly respect it.—The Man Who Was Thursday, by
G. K. Chesterton.
Tracing the path of a human being over a million parsecs of space
and a half century of time isn't easy, even when the subject makes no
effort to conceal his route or confuse his contemporaries. The
difficulty increases by a factor of at least ten when the subject is a
wily, clever, and thoroughly ruthless scoundrel like Leland Hale. If it
was difficult for the Interstellar Police to track down Hale a century
ago, it is easy to see why it would be almost impossible today. The
records are too sketchy.
But while it is virtually impossible to give any coherent chronological
account of the life of Leland Hale, it is certainly possible to deduce
what did happen during those periods of his life which are accurately
documented. Modern psychometric analysis enables us to pinpoint
his character down to the seventieth decimal place, and that, in turn,
enables us to see what he must have done in a given circumstance,
being the kind of man he was.
Folk legend has a tendency to make heroes of even the vilest of
villains, provided they are colorful enough, and no amount of fact ever
quite smothers the romantic legend. Such mythical or semi-mythical
characters as Robin Hood, Jesse James, Billy the Kid, John Dillinger,
Captain Hamling Fox III, and Hilary Boone were all rascals to the
core, but even today they have their practicing cults. But the cultus
peculiar to Leland Hale seems to outshine them all, and for the
singularly perverse reason that he was worse than all the rest rolled
together. Indeed, he has been touted throughout the galaxy as a sort
of super Simon Templar, who "robbed from the rich and gave to the
poor." Rob from the rich he did, but the recipient was Leland Hale,
who was rarely, if ever, in penurious circumstances.
If there is any way in which the legends of Leland Hale do not
exaggerate, it is in the descriptions of his physical size. Here, there is
no need to exaggerate; Hale stood six feet six in his bare feet and
had an absolute mass of some one hundred thirty-eight kilograms—
very little of it fat. His hair was black and his skin was deeply tanned;
his face was hard, blocky, and handsome. Mentally, he was brilliant;
morally, he had one philosophy—"Leland Hale deserves to own the
galaxy." He knew the goal was unobtainable, but he worked steadily
at it.
What he wanted, he took, and if it wasn't available, he took the next
best thing—all of which brings us around to the peculiar incident on
the planet Apfahl.
A century ago, Apfahl was just one of those little backwater planets
that cluttered the fringes of the main streams of galactic trade. During
the early colonization of the planet, the great southern continent was
the only section of the new world that seemed worth colonizing. By
the end of the first three centuries, it was fairly well covered with
people, and those people had divided themselves into two groups.
The southernmost part of the continent, being closer to the pole, and
higher in altitude, was occupied by semi-nomadic herdsmen who kept
animals that could graze on the almost untillable tundra. The northern
peoples, on the other hand, became farmers.
As a result, the Apfahlians quarrelled over the rightful seat of the
colony government, and, after much strife, two capitals were set up,
and the country of Sudapfahl and the country of Nordapfahl glared at
each other across the boundary that separated them.
Just where the name Apfahl came from, no one is quite sure. Since it
was originally colonized by people from Vega IV, which in turn was
colonized directly from Earth by people of Old Germanic stock, an
attempt has been made to trace the name through that language. The
attempt has resulted in two schools of thought.
One school contends that the word comes from the Old Earth
German word Apfel, which means "apple"; the other school, with an
equally sound basis, insists that the name is derived from Abfall,
meaning "garbage." Which school of thought one follows seems to be
entirely dependent on whether one is an inhabitant of the planet or
has merely visited there.
Leland Hale was, perhaps, an exception to that rule; the first time he
saw it, hanging in the blackness a couple of hundred thousand miles
out of the forward plate of his expensive private ship, the planet
looked very much like an apple—ripe and ready for plucking.
Naturally.
Now, about all the average galactic citizen knows about Apfahl these
days is that it was the birthplace of Dachboden; as a matter of fact,
that's all anybody thought of it as a hundred years ago. Someone
says: "R. Philipp Dachboden, the Painter of Apfahl," and everyone
nods knowingly. But it would be worth your while to give five-to-one
odds against any given person being able to tell you what sector it's
in. And, actually, that's as it should be; aside from the fact that R.
Philipp Dachboden was born there, Apfahl has no claim whatever to
galactic prominence.
But it almost did. If it hadn't been for Leland Hale—
In order to understand exactly what happened, we'll have to look over

our cast of main characters. Aside from Leland Hale himself, there
are two gentlemen who played no small part in the Apfahlian farce.
Hinrik Fonshliezen was a tall, dark, lean specimen with a corvine
nose, a vulpine mind, and a porcine greed. Lest this list of
characteristics smack too much of the animalistic, let it be said that
Fonshliezen's memory was not elephantine, which was too bad for
him.
Hinrik's great grandfather, one Villim Fonshliezen, had managed,
through dint of much hard labor and much underhanded business, to
amass one of the biggest ranches in Sudapfahl. By the time Hinrik's
generation rolled around, the Fonshliezen holdings were great
enough to make it worth Hinrik's while to enter politics—which, of
course, he did. In what is known as due time, he reached the position
of State Portfolio, a chancellorship second only to the Prime
Chancellor himself.
It is easily understandable that his ambitions included the Primacy
itself. He knew, however, that his chances of actually getting the
office were slim. He was efficient; he could handle any of the
Portfolios in the File with ease. He had been elected to the File from
his own country because he had financial control of that country, but
winning a General Election was something else again, because he
was not a popular man.
That is not to say he was unpopular; probably he was no more
generally disliked than any other politician. But he simply didn't have
the knack of attracting favorable attention to himself; he was not, to
put it bluntly, a lovable man. He had very carefully avoided doing
anything that would make the public angry with him, but avoiding
hatred is not the same thing as attracting love.
Having come to this realization, Hinrik Fonshliezen found himself
looking for either a good deed to do or a good press agent—or both.
Let's leave him looking for the moment, and skip up above the border
into the country of Nordapfahl. In the city of Grosstat, we will find the
Museum of Cultural History, and within that museum, seated in a
comfortable, book-lined office, we find the museum's director, Dr.
Rudolf Mier.
Physically, Dr. Mier was easily distinguishable from Fonshliezen. To
parallel the previous trope, Mier was porcine in build, bovine in
manner, and lupine in business matters.
Mier liked the good things of life—food, liquor, women, fine art, good
music, and well-tailored clothes. He overindulged in all of them
except liquor and women. He was moderate in his use of the former
because he found drunkenness repulsive, and of the latter because
women found him repulsive.
The Museum of Cultural History was his great love, however; as long
as he had it and his work, he could dispense with many of life's little
luxuries—if it became absolutely necessary to dispense with them.
The Museum wasn't much by galactic standards. It had only been in
existence for a couple of centuries, and, in a scanty civilization such
as that of Apfahl, two hundred years isn't much time to pick up a
museum full of really valuable and worthwhile exhibits. The faded
uniform of Field Marshal So-and-so might excite the beating, patriotic
heart of an Apfahlian, but it was of very little worth as a cultural relic.
But to Dr. Mier, the Museum was one of the great landmarks of
human history. He envisaged a day, not too far distant, when his
small collection would be known as the Apfahlian Division of the
Interstellar Museum of Natural and Cultural History. According to the
records of the Interstellar Museum, Dr. Rudolf Mier actually made
tactful, cautious reaches toward such a goal. He was tactfully
reminded that it would be necessary to "improve the general
standards" of the Apfahlian museum before any such recognition
could be granted.
Dr. Mier did not actually think that such recognition would come in his
own lifetime; he was somewhat of an idealist, and we must give him
credit for that. But one day certain papers—very old-looking and
yellowed papers—came to his attention, and he sent off a hurried
spacegram to the Board of the Interstellar Museum.
In view of the fact that the Interstellar Museum's directors did not get
around to considering the spacegram for nearly two months, it is
unusual that Mier got an immediate reply to his communication. But
Mier didn't know that, and he was very pleased to hear that an art
expert, Dr. Allen H. Dale, was being dispatched immediately to
appraise the situation.
The eminent Dr. Dale had some trouble in reaching the planet; big
space liners did not—and still do not—make regular stops at Apfahl.
Dr. Dale did, however, manage to get the captain of the I.S.S.
Belvedere to veer aside from his predetermined course and drop his
passenger to Apfahl in a small flitter. It cost Dr. Dale a goodly sum,
but it was worth it.
When they were near the planet, the Belvedere stopped, and Dr. Dale
went aboard the flitter with the pilot.
Dr. Dale, the art expert, had a full, graying beard that covered half his
face, and a large shock of graying hair. He might have been a
muscular man, but the cut of his clothes made his six and a half feet
of body seem fat and clumsy. He gave the impression of a man who
could neither fight nor run, but who depended on superior pomposity
to stare down his opponents.
The flitter pilot strapped himself down and said: "Not much money on
Apfahl. Still, I hear there's something stirring." He adjusted Dr. Dale's
seat. "Something about art, eh?" He looked at his passenger as if
expecting some comment.
He was not disappointed. Dr. Dale cleared his throat and said: "Yes.
There has been some excitement in artistic circles of late. Of course,
the news only came out a few weeks ago, and it takes time for
anything like that to spread around the galaxy, even among the
civilized planets."
The pilot twiddled switches and control knobs as he eased the little
ship into a landing orbit. "Well, whatever it is, it must be important for
a man to lay out all the extra cash it costs to get Captain Gremp to
stop the Belvedere and drop you off." Again he glanced at his
passenger.
"Young man," said Dr. Dale, "if you are trying to pump me for
information, that is no way to go about it; on the other hand, if you are
merely trying to keep a conversation going, there is no need to be
coy. I am not on a secret mission for the Interstellar Police, nor am I
normally a close-mouthed man. If you are curious, say so; I can give
you a full explanation before we land."
The pilot reddened a little. "Well—uh—yes. I was sort of wondering
what's supposed to be so important about a piece of wood." Gingerly,
he applied power as the ship dropped toward the cloud-flecked
surface of Apfahl.
"Piece of wood!" Dr. Dale seemed in agony. His gray beard bristled in
indignation. "Young man, I presume you have heard of R. Philipp
Dachboden?"
The sarcasm in his voice was light, but even so the pilot reddened
more deeply. A hundred years ago, the brilliant genius of Dachboden
was perhaps not quite as widely appreciated as it is today, but even
then, two centuries after his death, the name of R. Philipp Dachboden
ranked with those of Da Vinci and Matisse.
"You are aware, I think," continued the pompous doctor, "that
Dachboden did all his sculpture in the wood of the dynak tree, which
is native to Apfahl?"
"Sculpture?" asked the pilot. "I thought he was a painter."
"He was," said Dr. Dale sourly. "His paintings are worth tens of
thousands. But his carvings are worth hundreds of thousands. There
are only eighteen examples of his work known to be in existence.
Now there is reason to believe there may be a nineteenth."
"Oh yeah," said the pilot. "He left one in the time capsule, eh?"
"Presumably. We'll know in a few weeks."
"I guess there'll be a lot of art experts coming in pretty soon, then,
huh?" the pilot asked.
"I expect my colleagues to arrive on the Quinsen, out of Denebola.
It's the next scheduled liner to make a stop here at Apfahl. I, however,
wanted to get the jump on them. Get in on the ground floor, so to
speak," the doctor told him.
"I getcha," said the pilot. It didn't occur to him to wonder what good it
would do to get in early when the time capsule wouldn't open until the
scheduled time, anyway, and by then all the art experts for a
thousand parsecs around would be clustered on the spot.
When the flitter landed, the self-important Dr. Allen H. Dale

supervised the unloading of his luggage at the third-rate little
spaceport near the city of Grosstat, a few miles from the shores of the
Kaltvosser Sea. It hadn't been grounded ten minutes before a big,
black, newly-made automobile of quaintly antique design rolled up to
the edge of the landing pit. Two uniformed men got out and stood at
attention at the rear door, which opened to disgorge a third man, a
civilian. The civilian was almost as broad as Dr. Dale, but not nearly
so tall; he looked well-fed, almost oily, and he had a smug expression
on his round face.
Flanked by the two uniformed men, the portly civilian moved
ponderously toward the heap of traveling bags and the gray-bearded
man who was standing beside them.
"Dr. Allen Dale?" he asked respectfully.
If, by this time, the astute reader has begun to suspect that Leland
Hale might perhaps be lurking behind that gray beard and that
anagrammatical alias, that reader may give himself a small pat on his
back. Leland Hale was perfectly capable of posing as an art expert
for the very simple reason that he was an art expert. Therefore, it was
with perfect and utter aplomb that he turned to the fat civilian, evinced
moderate surprise, and said: "I am Dr. Dale, sir. And whom have I the
honor of addressing?"
The civilian bowed very slightly, a mere angling of the spine and a
slight bob of the head. "I have," said the chubby one in slightly
accented Standard, "the honor to be the director of the Grosstat
Museum of Cultural History, Dr. Rudolf Mier."
Leland Hale looked pleasantly surprised. "Ah! Dr. Mier! A very great
pleasure to meet you, sir."
"We received your subradiogram, Doctor," said Mier. "Naturally, I,
myself, came to meet you."
"Naturally," agreed Leland Hale.
"We get very few extra-planetary visitors here," Dr. Mier continued
apologetically. "Apfahl is, I fear, a little off the—ah—beaten path. Of
course, we expect—"
"—to be more widely recognized after the opening of the time
capsule," Leland Hale finished for him. "Of course. And it's only right.
The galaxy must give due respect to the birthplace of the great
Dachboden—and they shall, never fear."
The Director looked like a freshly-petted cocker spaniel.
"We have arranged for your stay here, Dr. Dale. The Kayser Hotel is
holding a suite for you. Your instruments—" He gestured toward the
pile of luggage. "—will be taken there. I wonder if you would honor
me with your presence at lunch?"
"By all means, my dear Director—but the honor will be entirely mine."
Within three minutes, Leland Hale was firmly planted in the rear seat
of the car beside the Director of the Museum of Cultural History, while
the uniformed men sat in front, one of them tooling the vehicle off
down the narrow concrete roadway toward the city of Grosstat.
"Tell me," said Leland Hale, "how did all this come about? The news
releases were very sketchy."
Rudolf Mier leaned back comfortably in his seat and allowed a look of
semi-concentration to envelope his face.
"Well, it all began a couple of centuries ago—back during
Dachboden's lifetime. That's when the Museum was founded, you
know." Then he stopped and looked at Hale. "Ah—do you know? I
mean, are you acquainted with the history of Apfahl?"
Hale looked properly embarrassed, "I'm afraid I know very little,
Doctor. In spite of Dachboden's fame, Apfahl has not shared that
fame as it properly should. Let us say that, although Apfahl basks in
the glory of her renowned son, she doesn't reflect too much of it. You
will have to assume I know absolutely nothing, I'm afraid."
"I see," said Mier. "Well, then, at any rate, the Museum was founded
by a group of our forefathers for the purpose of preserving the unique
heritage that is Apfahl's. In accordance with this ideal, they proposed
to bury a time capsule containing contemporary artifacts. You are
acquainted with the practice, I assume?"
"It's quite common," said Hale.
"As it should be. Each age should take pains to be sure that the
ensuing age does not lose its heritage."
"Of course." Hale honestly didn't see why it should—if Hale could
ever be said to do anything honestly. Anything worth preserving was
not the sort of junk that was usually put in a time capsule. Oh, well—
"The capsule is of the standard type," Mier continued. "Hermetically
sealed, with a tamper-proof time lock activated by a radio-decay
clock. It's set to open at ——" He rattled off a string of numbers, and
then went on to explain the Apfahlian calendar, winding it up with:
"Our calendar is very scientific."
"Very," said Hale.
"At any rate, the capsule was buried underneath the Museum and
then practically forgotten. Oh, we knew it was there, but little notice
has been taken of the fact over the past century and more. We don't
even know what is in it—that is, not in detail. The official list, for
instance, simply says that 'various objects of art' are included, but it
makes no mention of Dachboden. That's not too strange, really, since
the great man's contemporaries didn't recognize his genius.
"But recently we have uncovered a book—a very old book, which we
believe was owned by Dachboden himself. Inside it, there was the
beginning of a letter addressed to a friend, in which Dachboden
mentioned that one of his dynak-wood statues had been picked to be
put in the time capsule, and had been sealed in just the day before
the letter was written.
"Naturally, as soon as we heard of that, we of the Museum exhumed
the time capsule to check again the exact date upon which it is due to
reopen. It is now under careful guard within the Museum itself."
As the car rolled into the outskirts of Grosstat, Hale looked around
and remarked: "So this is the birthplace of the famous Dachboden."
The expression on the face of the Director changed slightly; he
looked a little flustered.
"Well, not exactly," he said.
Hale turned on him, surprise showing in his eyes. "Not exactly? Oh,
come now, my dear Director; either it is or it isn't—eh?"
"Ah—well, yes. It isn't. Uh—what I mean to say is that, although
Dachboden spent most of his life in Grosstat, he was actually born in
Grunfelt."
"Oh?"
"Yes." He waved a hand in a little nervous circle. "You must
understand that Apfahl is, as I said, a rather—ah—well, backward is
too strong a word, but—" He stopped, swallowed, began again. "You
see, Dr. Dale, Apfahl does not yet have a united planetary
government. We have—ah—two sectors, each independently
governed. Of course, we who are more enlightened deplore such a
state of affairs, but—" He stopped again and smiled weakly.
"However that may be, Dr. Dale, it so happens that R. Philipp
Dachboden was born, not in this nation of Nordapfahl, but in the
country of Sudapfahl."
"But he came here to work, eh?"
Mier bobbed his head in an emphatic yes. "Of course! No man of his
brilliance could have been expected to stay in the art-smothering
atmosphere of Sudapfahl as it was two hundred years ago. Or even,
for that matter, as it is today."
"Well, well," boomed Leland Hale with pompous heartiness, "you are
certainly fortunate. Very fortunate indeed, Dr. Mier. To think that there,
in your museum, you have an art treasure worth many hundreds of
thousands of stellors—possibly a million. Marvelous!"
Dr. Rudolf Mier positively glowed. "Well—yes—I suppose we are
pretty lucky at that." A slight frown came over his face. "It has always
been—ah—somewhat of a thorn in the side of Apfahl—especially
Nordapfahl—that Dachboden was a little ungrateful in not allowing us
to keep at least one example of his art."
Leland Hale placidly refrained from pointing out that Dachboden
would have starved to death trying to sell his material on Apfahl two
centuries before. In the first place, no one there appreciated him, and
in the second place, there wasn't much money to be spent on art.
Even the little amount Dachboden got for his work off-planet was a
tremendous sum as far as Apfahl's economy was concerned.
The luncheon was typically Apfahlian fare—rough, tasteless, but

nourishing. Hale ate it stolidly, neither liking nor disliking it; he was
merely indifferent to it. Dr. Mier on the other hand, complained that it
wasn't properly cooked and still managed to put away enough for
three men.
"Tell me, Doctor," said Hale, when he found a lull between courses,
"have you considered the idea that someone might steal such a
valuable object?"
Mier finished chewing a bite, swallowed it, and shook his head.
"There is not much chance of that, Dr. Dale. In the first place, it is
locked within the capsule. Oh, I'll admit that the entire capsule could
be stolen; it is big, but not so big that it couldn't be taken by someone
with the proper equipment.
"However, that kind of equipment isn't available to the average man
here on Apfahl. And besides, it is thoroughly guarded. After we dug it
up from the basement, our government provided the Museum with a
full battalion of armed troops to surround the building day and night.
No unauthorized person can get in, and they certainly couldn't get the
time capsule out."
"Wouldn't it be possible to break into the capsule?"
Dr. Mier chuckled deeply. "You have not seen this capsule. Oh, I'll
grant that it might be broken into, but doing so would involve so much
damage that the contents would be ruined, rendering the attempt
useless. No, Dr. Dale; no one will steal our little treasure." He
chuckled again, and, as the next course was brought on, he began
shoveling it in. The silence was unbroken save for the sounds of
eating.
After a few moments, Leland Hale glanced casually at his watch and
compared it with the big mechanical clock on the wall of the hotel
cafe. He hoped his timing was correct.
It was. Seven minutes later, a man wearing the uniform of a Museum
guard scuttled into the room as though he were being followed by a
fleet of hornets. He stopped near the door, glanced rapidly over all
the diners, located Dr. Mier, and made his way hurriedly toward the
table.
"Dr. Mier! Dr. Mier!" His rasping voice was about as secretive as a
stage whisper. The other diners swiveled their heads to look.
Mier, startled, glanced up at the messenger.
"Yes, Mooler? Speak up, man; what is it?"
The uniformed man put a single sheet of paper on the table. "This just
came over the teletype wire from our correspondent in Sudapfahl, sir!
Read it!"
Dr. Mier read, and, as he did so, his eyes widened. "Good Heavens!"
he said at last, "This is terrible!"
"What?" asked Leland Hale, in all innocence.
"This!" Mier shoved the teletype sheet across the table.
Grunfelt, Sudapfahl: The excellent Hinrik
Fonshliezen, Portfolio of State, announced
today the discovery of a time capsule similar to
that in the Museum of Grosstat, Nordapfahl. The
capsule, set for a date approximately one day
later than that of the northern capsule, is said
to be buried beneath the capitol building,
according to official records disclosed to the
public this morning. Excavations will begin
immediately, according to his excellency's
statement, it is expected that the capsule may
contain some examples of the work of R. Philipp
Dachboden.
Leland Hale read it carefully and shook his head. "Dear me," he said
mildly.
"It may mean nothing to you, an outsider," said Dr. Mier bitterly, "but
do you realize that to us this is a matter of national honor and
prestige?"
"Oh, yes. Of course. Naturally. Believe me, Dr. Mier, I certainly
appreciate your position." He spread his hands slightly. "But, of
course, you realize that, as a representative of the Interstellar
Museum, I will have to check on the Sudapfahlian claim." Before Mier
could voice any objections, Leland Hale silenced him with a wave of
his hand. "You have nothing to worry about, Dr. Mier; as you know,
the Interstellar Museum only allows one branch to a planet. Naturally,
your museum would certainly have priority over that of Sudapfahl."
"Sudapfahl doesn't even have a museum," Mier said, looking fatly
superior.
"Besides," Hale continued mollifyingly, "I shan't go there until after I
have seen what your own time capsule has to offer. It seems to me
that the Sudapfahlian government actually doesn't know what's inside
their capsule. Their statements seem to be made out of pure
jealousy."
"You're probably quite right, Dr. Dale," said Mier.
"Oh, I know I'm right," said Leland Hale truthfully.
After lunch, Dr. Allen H. Dale informed Dr. Mier that, as he was a bit
fatigued from his trip, he would like to rest for a few hours. Mier
agreed whole-heartedly, and the two men made an appointment to
meet later in the afternoon for a tour of the Grosstat Museum of
Cultural History, and perhaps dinner and a few drinks afterwards.
After seeing his guest into his room, Dr. Mier strolled out of the hotel,
stepped into his car, and ordered the driver to take him to the
Museum. There were big things to be done. This new threat from the
south was not to be taken too lightly.
At the Museum—a huge, cold-looking, blocky granite structure—Mier
climbed out of his car, toiled up the broad stairs to the entrance, and
strolled rollingly in. On every side, flunkies, both in uniform and out,
bowed and scraped as the Great Man passed by. Dr. Mier reached
his book-lined office just as the telephone rang.
He picked up the instrument, a mechanism of ancient design
possessing no vision equipment, and announced that he was Dr.
Rudolf Mier.
"This is Lieutenant-Marshal Dilon, State Police. You have just
returned from lunch with a Dr. Allen H. Dale, purporting to be from the
Galactic Museum?"
"Why, yes; I just—What do you mean, purporting?"

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Liver Disorders A Point of Care Clinical

Guide 1st Edition Kia Saeian

Pocket Psych Drugs Point of Care Clinical Guide Darlene

Clinical Guide to Assessment and Treatment of

Point of Care Ultrasound 2nd Edition Nilam Soni

Perinatal Palliative Care A Clinical Guide Erin M.

Practical Point-of-Care Medical Ultrasound 1st Edition

Point of Care Ultrasound Made Easy 1st Edition John

Liver Disease in Clinical Practice 1st Edition Tim

Immunodiagnostic Technologies from Laboratory to Point

ISBN 978-3-319-30101-3 ISBN 978-3-319-30103-7 (eBook)

Library of Congress Control Number: 2016935856

© Springer International Publishing Switzerland 2017

Printed on acid-free paper

This Springer imprint is published by Springer Nature

Milwaukee, WI Kia Saeian

1 What Do Abnormal Liver Tests Mean?................................................. 1

Part I What to Do with Tumors in the Liver?

Part II Distinct Liver Disorders

12 Viral Hepatitis: Other Viral Hepatides.................................................. 165

Part III Care of the Cirrhotic Patient

Murad Aburajab, M.D. Division of Gastroenterology and Hepatology, Medical

Matthew Cave, M.D. Division of Gastroenterology, Hepatology and Nutrition,

Keith D. Lindor, M.D. Division of Gastroenterology and Hepatology, Mayo

Syed Rizvi, M.D. Division of Gastroenterology & Hepatology, Medical College of

Miguel Malespin and Rebecca Tsang

Commonly Posed Patient Questions

1. What are common causes of abnormal liver tests?

M. Malespin, M.D. (*)

© Springer International Publishing Switzerland 2017 1

serologic analysis, and liver-focused imaging with either ultrasound or com-

Components of a Liver Profile

Common Causes of Elevated Aminotransferases

As previously noted, elevated aminotransferases are suggestive of hepatocellular

Table 1.1 Causes of elevated aminotransferases

Initial Evaluation of Elevated Aminotransferases

The work-up for abnormal aminotransferases differs according to the degree of

Additional testing includes acquisition of ferritin, iron, and total iron-binding

Chronic, mild Acute, moderate-

Alpha-1 antitrypsin Acute viral

Liver biopsy if still

Alkaline Phosphatase and Gamma Glutamyl

There is some physiologic variation of serum alkaline phosphatase levels in certain

Clinical Significance of Low Alkaline Phosphatase

Common Causes of Elevated Alkaline Phosphatase

Table 1.2 Common causes of elevated alkaline phosphatase

Initial Evaluation of Elevated Alkaline Phosphatase

If there is an elevated isolated alkaline phosphatase level in an asymptomatic patient,

Laboratory Assays for Bilirubin

Biliary pain Asymptomatic

GGT normal GGT high

Bone, renal, Biliary obstruction or

after adding an accelerant. Subsequently, the unconjugated, or indirect, bilirubin is

Table 1.3 Common causes of elevated bilirubin

Common Causes of Elevated Bilirubin

Initial Evaluation of Elevated Bilirubin

As noted earlier, it is important to first determine whether the hyperbilirubine-

<15% direct >15% direct

unlike Crigler–Najjar syndrome which is a rare disorder related to a mutation

Prothrombin time is a measurement of the rate at which prothrombin is converted to

Interpretation of laboratory values in patients with abnormalities in liver panel test-

Upon establishment of chronicity, the role of the practitioner is to establish the

Acknowledgements Miguel Malespin: Has served as a consultant for Gilead Pharmaceuticals

Milwaukee, WI Kia Saeian