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346 BASIC SKILLS IN INTERPRETING LABORATORY DATA
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is converted to direct bilirubin by glucuronyl transferase. Thus,
an elevated level of indirect bilirubin may result from increased
breakdown of red blood cells (hemolysis) or reduced hepatic conversion of indirect bilirubin to direct bilirubin. Common causes
include hemolysis, Gilbert syndrome, and drugs, such as proben
ecid or rifampin.
Increased direct bilirubin usually implies hepatic disease,
which interferes with secretion of bilirubin from the hepato
cytes or clearance of bile from the liver. There are exceptions
to this, Dubin-Johnson syndrome and Rotor syndrome being
two benign abnormalities of bilirubin metabolism and excre
tion. Direct hyper-
bilirubinemia, especially in the presence of
other abnormalities in the LFT prole, is generally classied as
reecting hepatic cholestasis, although it may also be due to
a hepatocellular process. In cholestatic disease, the bilirubin is
primarily conjugated, whereas in hepatocellular processes, signicant increases in both conjugated and unconjugated bilirubin may result. Cholestasis may be intrahepatic or extrahepatic.
Intrahepatic cholestasis may be due to viral hepatitis, reactions
to different medications, alcoholic hepatitis or cirrhosis, pregnancy, severe infection, or PBC. Extrahepatic cholestasis involves
obstruction of the larger bile ducts either inside or outside of the
liver, which can be due to strictures, stones, or tumors.
3.
What is the relative importance of AST and ALT tests in
terms of diagnosing hepatocellular disease?
ANSWER: Elevations of AST and ALT generally reect inamma-
tion in the liver. However, they are not associated with prognosis
(higher levels do not suggest a worse prognosis) or with etiology.
Although there is value in assessing the ratios of these two (for
example an AST/ALT ratio of over two may suggest alcoholic
liver disease), these tests do not “tell the whole story.” Evaluating a patient with suspected liver disease is a complex undertaking. The history must be obtained in d etail, including present and
past medications, supplements, vitamins, occupational exposure,
underlying diseases, history of surgical procedures, history of
transfusions, and drug use.
4. How is acute pancreatitis diagnosed?
ANSWER: The clinical presentation of acute pancreatitis gener-
ally consists of epigastric pain, often radiating to the back. There
can be associated nausea, vomiting, diaphoresis, and fever. The
challenge here is that these symptoms are not specic at all.
Similar complaints can be seen with biliary disease, ulcers, gastritis, small bowel problems, or compromised blood supply to the
gut. At times there can be overlap. Gallstones can migrate down
the common bile duct, causing pancreatitis. Ulcers can penetrate
the duodenum and invade the pancreas also causing pancreatitis. To establish a diagnosis of pancreatitis one looks for three
things. First, the clinical picture should be consistent with this
diagnosis. Second, a serum lipase or amylase should be over three
times normal (realizing that these tests are not specic). Third,
it is often of value (especially if the rst two criteria are not both
present) to have an advanced imaging study, either MRI or CT,
showing pancreatitis. Generally, two of the three criteria should
be present before diagnosing acute pancreatitis.
REFERENCES
1. Kwo PK, Cohen SM, Lim JK. ACG clinical guideline: evaluation of
abnormal liver chemistries. Am J Gastroenterol. 2017;112:18-25.
2. Kasper DL, Fauci AS, Hauser SL, etal. Harrison’s Principles of Internal
-
-
-
Medicine. 19th ed. New York, NY: McGraw Hill; 2015.
3. Chopra S, Grin PH. Laboratory tests and diagnostic procedures in
evaluation of liver disease. Am J Med. 1985;79:221-230.
4.
Neyra NR, Hakim RM, Shyr Y, etal. Serum transferrin and serum
prealbumin are early predictors of serum albumin in chronic
hemodialysis patients. J Ren Nutr. 2000;10:184-190.
5.
Spiekerman AM. Nutritional assessment (protein nutriture). Anal Chem.
1995;67:429R-436R.
6.
Mittman N, Avram MM, Oo KK, etal. Serum prealbumin predicts
survival in hemodialysis and peritoneal dialysis: 10 years of prospective
observation. Am J Kidney Dis. 2001;38:1358-1364.
7.
Giannini EG, Testa R, Savarino V. Liver enzyme alteration: a guide for
clinicians. CMAJ. 2005;172:367-379.
Green RM, Flamm S. AGA technical review on the evaluation of liver
8.
chemistry tests. Gastroenterology. 2002;123:1367-1384.
9.
Birkett DJ, Done J, Neale FC, etal. Serum alkaline phosphatase in
pregnancy: an immunologic study. Br Med J. 1966;1:1210-212.
10.
Wilson JW. Inherited elevation of alkaline phosphatase activity in the
absence of disease. N Engl J Med. 1979;301:983-984.
11.
Pratt DS, Kaplan MM. Evaluation of abnormal liver- enzyme results in
asymptomatic patients. N Engl J Med. 2000;342:1266-1271.
Kaplan MM, Matlo DS, Selinger MJ, etal. Biochemical basis for serum
12.
enzyme abnormalities in alcoholic liver disease. In: Chang NC, Chan
NM, eds. Early Identication of Alcohol Abuse. NIAAA Research
Monograph 17. Rockville, MD, US Department of Health and Human
Services; 1985:186-198.
13. Friedman LS, Keefee EB. Handbook of Liver Disease. 3rd ed. Philadelphia,
PA: Elsevier Saunders; 2012.
14. Dukes GE, Sanders SW, Russo J, etal. Transaminase elevations in patients
receiving bovine or porcine heparin. Ann Intern Med. 1984;100:646-650.
15. Chalasani N, Younossi Z, Lavine JE, etal. e diagnosis and management
of nonalcoholic fatty liver disease: practice guideline from the American
Association for the Study of Liver Diseases. Hepatology. 2018;67(1):328-357.
16. Diehl A, Boitnott J, Van Duyn M, etal. Relationship between pyridoxal
5′- phosphate deciency and aminotransferase levels in alcoholic hepatitis.
Gastroenterology. 1984;86:632-636.
17. Cohen GA, Gonet JA, Donabedian RK, etal. Observations on
decreased serum glutamic oxaloacetic transaminase (SGOT) activity in
azotemic patients. Ann Intern Med. 1976;84:275-280.
18. Chtioui H, Mauerhofer O, Gunther B, etal. Macro-AST in an
asymptomatic young patient. Ann Hepatol. 2010;9:93-95.
19.
Vilstrup H, Amodio P, Bajaj J, etal. Hepatic encephalopathy in chronic
liver disease: 2014 practice guideline by the American Association for the
Study of Liver Diseases and the European Association for the Study of the
Liver. Hepatology. 2014 60:715-733.
20. Chtioui H, Mauerhofer O, Gunther B, etal. Macro-AST in an asymptomatic
young patient. Ann Hepatol. 2010;9:93-95.
21. Ong JP, Aggarwal A, Krieger D, etal. Correlation between ammonia levels
and the severity of hepatic encephalopathy. Am J Med. 2003;114:188-193.
22. Haj M, Rockey DC. Ammonia levels do not guide clinical management
of patients with hepatic encephalopathy caused by cirrhosis. Am J
Gastroenterol. 2020;115:723-728.
23. Bhatia V, Singh R, Acharya SK. Predictive value of arterial ammonia for
complications and outcome of acute liver failure. Gut. 2006;55:98-104.
24. Foster MA, Hofmeister MG, Kupronis BA, etal. Increase in hepatitis
Avirus infections, United States, 2013-2018. MMWR Morb Mortal Wkly
Rep. 2019;68:413.
CHAPTER 15 • LivER And GAsTRoEnTERoLoGy TEsTs 347
https://t.me/med1917
25. Pawlotsky JM. Molecular diagnosis of viral hepatitis. Gastroenterology.
2002;122:554-568.
26. AASLD-ISDA Hepatitis C Guidance Panel. Hepatitis C Guidance 2019
Update: American Association for the Study of Liver Disease-Infectious
Disease Society of America recommendations for testing, managing, and
treating hepatitis C virus infection. Hepatology. 2019;71:686-709.
27. Lindor K, Bowlus CL, Boyer J, etal. Primary biliary cholangitis: 2018
practice guidance from the American Association for the Study of Liver
Diseases. Hepatology. 2019;69(1):394-419.
28. Kowdley KV, Brown KE, Ahn J, etal. ACG clinical guideline: hereditary
hemochromatosis. Am J Gastroenterol. 2019;114:1202-1208.
29. Siddique A, Kowdley K. Review article: the iron overload syndromes.
Aliment Pharmacol er. 2012; 35:876-893.
30. Cherfane C, Hollenbeck R, Go J, etal. Hereditary hemochromatosis:
missed diagnosis or misdiagnosis? Am J Med. 2013;126:1010-1015.
31. Bacon B, Adams P, Kowdley K, etal. Diagnosis and management of
hemochromatosis: 2011 practice guideline by the American Association
for the Study of Liver Disease. Hepatology. 2011;54(1):328-343.
32. Salgia R, Brown K. Diagnosis and management of hereditary
hemochromatosis. Clin Liver Dis. 2015;19:187-198.
33. Tenner S, Baillie J, DeWitt J, etal. American College of Gastroenterology
guideline: management of acute pancreatitis. Am J Gastroenterol. 2013;
108(9):1400-1415.
Frossardl JL, Steer ML, Pastor CM. Acute pancreatitis. Lancet. 2008;371:
34.
143-152.
35.
Frank B, Gottlieb K. Amylase normal, lipase elevated: Is it pancreatitis?
Am J Gastroenterol. 1999;94:463-469.
36. Bode C, Riederer J, Brauner B, etal. Macrolipasemia: a rare cause of
persistently elevated serum lipase. Am J Gastroenterol. 1990;85:412-416.
37. Chey WD, Leontiadis GI, Howden CW, etal. ACG clinical guideline:
treatment of Helicobacter pylori infection. Am J Gastroenterol. 2017;112:
212-238.
38. Logan RP, Walker MM. Epidemiology and diagnosis of Helicobacter pylori
infection. Br Med J. 2001;323:920-922.
39. Pan L, Mu M, Yang P, etal. Clinical characteristics of COVID-19 patients
with digestive symptoms in Hubei, China: a descriptive cross- sectional,
multicenter study. Am J Gastroenterol. 2020;115(5):766-733.
40. Surawicz CM, Brandt L, Binion DG, Ananthakrishnan AN. Guidelines
for diagnosis, treatment, and prevention of Clostridium dicile
infections. Am J Gastroenterol. 2013; 108(4):478-489.
41. Lee VR. Clostridium dicile infection in older adults: a review and update
on its management. Am J Geriatr Pharmacother. 2012;10:14-24.
42. Kelly CP, LaMont JT. Clostridium dicile: more dicult than ever.
NEngl J Med. 2008;359:1932-1940.
43. Louie TJ, Miller MA, Mullane KM, etal. Fidaxomicin vs vancomycin for
Clostridium dicile infection. N Engl J Med. 2011;364:422-432.
44. Bababy NE, Stiles J, Ruggiero,P etal. Evaluation of the Cephoid Xpert
Clostridium dicile Epi assay for diagnosis of Clostridium dicile
infection and typing of the NAP1 strain at a cancer hospital. J Clin
Microbiol. 2010;48:4519-4524.
348 BASIC SKILLS IN INTERPRETING LABORATORY DATA
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QUICKVIEW | Albumin
PARAMETER DESCRIPTION COMMENTS
Common reference ranges
Adults 4–5 g/dL (40–50 g/L)
Pediatrics 1.9–4.9 g/dL (19–49 g/L) <1 yr old
3.4–4.2 g/dL (34–42 g/L) 1–3 yr old
Critical value <2.5 g/dL (<25 g/L) In adults
Natural substance? Yes Blood protein
Inherent activity? Increases oncotic pressure of
plasma; carrier protein
Location
Production Liver
Storage Serum
Secretion/excretion Catabolized in liver Half-
Major causes of…
High or positive results Dehydration
Anabolic steroids (rare)
Iatrogenic (administration of
albumin)
Associated signs and symptoms Limited to underlying disorder No toxicological activity
Low results Decreased hepatic synthesis Seen in liver disease
Malnutrition or malabsorption Substrate deciency
Protein losses
Pregnancy or chronic illness
Associated signs and symptoms Edema, pulmonary edema, ascites At levels <2–2.5 g/dL or <20–25 g/L
After insult, time to…
Initial depression or positive
result
Lowest values Weeks Half- life, approximately 20 days
Normalization Weeks Assumes insult removed and no
Days
life, approximately 20 days
Via kidney in nephrotic syndrome or via
gut in protein- losing enteropathy
permanent damage
Drugs often monitored with test Parenteral nutrition Goal is increased levels
Causes of spurious results
Falsely elevated Ampicillin and heparin
Falsely lowered Supine patients, icterus, penicillin
CHAPTER 15 • LivER And GAsTRoEnTERoLoGy TEsTs 349
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QUICKVIEW | Prothrombin Time/International Normalized Ratio
PARAMETER DESCRIPTION COMMENTS
Common reference ranges
Adults and pediatrics INR: 0.9–1.1
PT: 12.7–15.4 sec
Critical value
Natural substance? Yes
Inherent activity? Indirect measurement of coagulation
Location
Production Coagulation factors produced in liver
Storage Carried in bloodstream
Secretion/excretion None
Major causes of…
Prolonged elevation
INR: >5
factors
Liver failure Liver unable to produce coagulation
Malabsorption or malnutrition Vitamin K aids in activation of
Warfarin Corrects with vitamin K
Unless on warfarin
factors; prolonged PT or increased
INR does not correct with vitamin K
coagulation factors and is not
absorbed; defect corrects with
parenteral vitamin K supplementation
supplementation
Antibiotics Interfere with vitamin K production by
bacteria in the GI tract or metabolism
or activation of clotting factors
Associated signs and symptoms Increased risk of bleeding and ecchymosis Easy bruising
Low results None
After insult, time to…
Initial elevation or positive result 6–12 hr
Peak values Days to weeks Depends on etiology
Normalization 4 hr if vitamin K responsive (due
to malabsorption, maldigestion,
warfarin) but 2–4 days if due to liver
disease and liver disease reverses
Drugs often monitored with test Warfarin
Causes of spurious results Improper specimen collection
350 BASIC SKILLS IN INTERPRETING LABORATORY DATA
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QUICKVIEW | Alkaline Phosphatase
PARAMETER DESCRIPTION COMMENTS
Common reference ranges
Adults 33–96 units/L
0.56–1.63 ukat/L
Pediatrics Varies; can be 2-
higher than in adults
Natural substance? Yes Metabolic enzyme (intracellular)
Inherent activity? Elevation alone causes no
symptoms
Location
Production Intracellular enzyme
Storage Liver, placenta, bone, small
intestine, leukocytes
Secretion/excretion None
Major causes of…
High or positive results
Cholestasis Hepatic; associated with elevation of GGT
Bone disease Paget disease, bone tumors, rickets,
Pregnancy Placental ALP
Childhood Related to bone formation
fold to 3- fold
Varies with assay
Elevated in pregnancy
Elevated with developing bone
Intracellular activity only
These tissues are rich in ALP
osteomalacia, healing fracture
Associated signs and symptoms Limited to underlying disorder Reects tissue or organ damage
Low results Vitamin D intoxication
Scurvy
Hypothyroidism
Associated signs and symptoms Limited to underlying disorder
After insult, time to…
Initial elevation or positive result Hours
Peak values Days
Normalization Days Assumes insult removed and no ongoing
damage
Drugs often monitored with test None
Causes of spurious results Blood drawn after fatty meal and
prolonged serum storage
CHAPTER 15 • LivER And GAsTRoEnTERoLoGy TEsTs 351
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QUICKVIEW | Aspartate Aminotransferase
PARAMETER DESCRIPTION COMMENTS
Common reference ranges
Adults 12–38 International Units/L
Varies with assay
(0.2–0.64 µkat/L)
Newborns/infants 30–100 International Units/L
Varies with assay
(0.5–1.67 µkat/L)
Critical value
>80 International Units/L (1.34 µkat/L)
Two times upper limit of normal
Natural substance? Yes Metabolic enzyme
Inherent activity? None in serum Intracellular activity only
Location
Production Intracellular enzyme
Storage Liver, cardiac muscle, kidneys, brain,
These tissues are rich in AST
pancreas, lungs
Secretion/excretion None
Major causes of…
High or positive results Hepatitis Elevated in any disease with
hepatocyte inammation (liver cells)
Hemolysis Elevated in any disease with damage
to tissues rich in enzyme
Muscular diseases
Myocardial infarction
Renal infarction
Pulmonary infarction
Necrotic tumors
Associated signs and symptoms Varies with underlying disease Reects tissue or organ damage
Low results None
After insult, time to…
Initial elevation or positive result 2–6 hr
Peak values 24–48 hr (without further cell damage) With extensive liver or cellular
damage, levels can go up to thousands
Normalization 24–48 hr Assumes insult removed and no
ongoing damage
Drugs often monitored with test Isoniazid, statins, allopurinol,
Monitoring frequency varies with drug
methotrexate, ketoconazole, and
valproic acid
Causes of spurious results
Falsely elevated Heparin, levodopa, methyldopa,
tolbutamide, para- aminosalicylic acid,
erythromycin, diabetic ketoacidosis
Falsely lowered Metronidazole, triuoperazine,
vitamin B
HMG-CoA = 3- hydroxy-3- methylglutaryl-CoA lyase.
deciency
6
352 BASIC SKILLS IN INTERPRETING LABORATORY DATA
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QUICKVIEW | Alanine Aminotransferase
PARAMETER DESCRIPTION COMMENTS
Common reference ranges
Adults 7–41 International Units/L
(0.12–0.68 µkat/L)
Newborns/infants 6–40 International Units/L
(0.1–0.67 µkat/L)
Critical value
Natural substance? Yes Metabolic enzyme
Inherent activity? None in serum Intracellular activity only
Location
Production Intracellular enzyme
Storage Liver, muscle, heart, kidneys These tissues are rich in ALT
Secretion/excretion Normally contained intracellularly,
Major causes of…
High or positive results
>60 International Units/L (>1 µkat/L) >2 times normal limit
Hepatitis Elevated in any disease with
Hemolysis Elevated in any disease with damage to
Varies with assay
Decreases to adult values within a few
months
but with cell damage, serum
concentrations increase
hepatocyte inammation (liver cells)
tissues rich in enzymes
Muscular diseases
Myocardial infarction
Renal infarction
Associated signs and symptoms Varies with underlying disease Reects tissue or organ damage
Low results Patients decient in vitamin B
Associated signs and symptoms None
After insult, time to…
Initial elevation or positive result 2–6 hr
Peak values 24–48 hr (without further cell damage) With extensive liver or cellular
Normalization 24–48 hr Assumes insult removed and no
Drugs often monitored with test Isoniazid and cholesterol- lowering
agents (eg, statins, allopurinol,
ketoconazole, valproic acid, and
methotrexate)
Causes of spurious results Heparin (false elevation)
6
damage, levels can go up to thousands
ongoing damage
Monitoring frequency varies with drug
CHAPTER 15 • LivER And GAsTRoEnTERoLoGy TEsTs 353
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QUICKVIEW | Bilirubin
PARAMETER DESCRIPTION COMMENTS
Common reference ranges
Adults Total: 0.3–1.3 mg/dL (5.1–22.2 µmol/L)
Indirect: 0.2–0.9 mg/dL
Direct: 0.1–0.4 mg/dL
Children 2–4 mg/dL (34.2–68.4 µmol/L) 24-
5–6 mg/dL (85.5–102.6 µmol/L) 48-
0.3–1.3 mg/dL (5.1–22.2 µmol/L)
Critical value
Natural substance? Yes Byproduct of Hgb metabolism
Inherent activity? Yes CNS irritant or toxin in high levels
Location
Production Liver
Storage Gallbladder Excreted into bile
Secretion/excretion Stool and urine Bilirubin and urobilinogen
Major causes of…
High or positive results
>4 mg/dL (>68.4 µmol/L)
Liver disease, both hepatocellular and
cholestatic
Varies slightly with assay
hr infant
hr infant
>1 mo old
In adults
in newborn (not adult)
Hemolysis
Metabolic abnormalities (eg, Gilbert
syndrome)
Associated signs and symptoms Jaundice
Low results No important causes
After insult, time to…
Initial elevation or positive result Hours
Peak values 3–5 days Assumes insult not removed
Normalization Days Assumes insult removed and no
evolving damage
Drugs often monitored with test None
Causes of spurious results Fasting, levodopa, phenelzine,
methyldopa, ascorbic acid (false
elevation)
354 BASIC SKILLS IN INTERPRETING LABORATORY DATA
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QUICKVIEW | Ammonia
PARAMETER DESCRIPTION COMMENTS
Common reference ranges
Adults and pediatrics 19–60 mcg/dL (11–35 µmol/L) Varies with assay
Newborns
Critical value Varies, generally 1.5 upper limit of
Natural substance? Yes Product of bacterial metabolism of
Inherent activity? Probably Progressive deterioration in neurologic
Location
Production In gut (by bacteria)
Storage None
Secretion/excretion Liver metabolizes to urea Urea cycle; diminished in cirrhosis
Major causes of…
High or positive results
Associated signs and symptoms Hepatic encephalopathy
Low results No important causes
<100 mcg/dL (71.4 µmol/L)
normal
Liver failure
Reye syndrome
Metabolic abnormalities (urea cycle)
Varies with assay
protein (in the gut)
function
After insult, time to…
Initial elevation or positive result Hours
Peak values No peak value; rises progressively
Normalization Days After appropriate therapy or resolution
of underlying liver disease
Drugs often monitored with test Valproic acid
Causes of spurious results Sensitive test (discussed in text)
Hematology: Red and White
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BloodCell Tests
16
OBJECTIVES
After completing this chapter, the
reader should be able to
•
Describe the physiology of blood
cell development and bone marrow
function
•
Discuss the interpretation and
alterations of hemoglobin,
hematocrit, and various red blood
cell indices in the evaluation
of macrocytic, microcytic, and
normocytic anemias
•
Describe the signicance of abnormal
erythrocyte morphology, including
sickling, anisocytosis, and nucleated
erythrocytes
•
Name the different types of
leukocytes and describe their primary
functions
•
Calculate the absolute number of
various types of leukocytes from
the white blood cell count and
differential
•
Interpret alterations in the white
blood cell count, differential, and CD4
lymphocyte count in acute bacterial
infections, parasitic infections, and
human immunodeciency virus
infection
•
Identify potential causes of
neutropenia and neutrophilia
Michael D. Katz and Timothy C. Jacisin
is chapter reviews the basic functions and expected laboratory values of erythrocytes (red blood cells [RBCs]) and leukocytes (white blood cells [WBCs]). It also
discusses, in an introductory manner, selected disorders of these two cellular components of blood. It must be remembered that the ability of laboratory medicine to
discriminate between leukocytes is increasing, and many methods considered investigational in this edition may become routine components of blood examination in
the future.
PHYSIOLOGY OF BLOOD CELLS AND
BONEMARROW
e cellular components of blood are derived from pluripotential stem cells located in
the bone marrow that can dierentiate into RBCs, WBCs, and platelets (Figure16-1).
Bone marrow is a highly structured and metabolically active organ that normally produces 2.5 billion RBCs, 1 billion granulocytes, and 2.5 billion platelets/kilogram of
body weight daily.1 Production can vary greatly from nearly 0 to 5 to 10 times normal. Usually, however, levels of circulating cells remain in a relatively narrow range
(Table16-1).
In a fetus and child, blood cell formation or hematopoiesis occurs in the marrow of virtually all bones as well as in liver, spleen, and other visceral organs. With
maturation, the task of hematopoiesis ceases in the liver and shis to at bones of the
axial skeleton, such as the skull, ribs, pelvis, and vertebrae. e long bones, such as
the femur and humerus, do not produce a large amount of blood cells in adulthood
2
DOI 10.37573/9781585286423.016
FIGURE 16-1. Schematic diagram of hematopoiesis.
355
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