Case Discussion: Gastroenterohepatology

Semester 4

HIGH CA 19-9 IN A 59 YEAR OLD

FEMALE WITH CARCINOMA
CAPUT PANCREAS
1
Denina Setya Ningtyas
Moderator : dr. Singgih Pudjo Wahono, Sp.PK
DATA BASE
 Female, 59 months old
 Chief complaint: abdominal pain
 Current medical history :
The patient complained of abdominal pain since about 3
weeks. The patient also complains of nausea and vomiting and
decreased appetite. Since 1 week the patient seems weak.
According to the patient's husband, the patient appeared
thinner in the last 1 month, but the body weight was not
weighed. There is no complained of fever, cough, and
shortness of breath.
2
DATA BASE
History of past illness:
HT (-), DM (-), disease with same symptom (-)

Social History:
Smoking (-), alcohol consumption (-), her husband is a smoker
  
Family Medical History:
Cancer (-), HT (-), DM (-)

3
PHYSICAL EXAMINATION
General Looked moderately ill, GCS: 4-5-6, BW: 52 kg, height: 156 cm,
appearance Nutritional status: normal
Vital sign HR: 120x/m, RR: 20x/m, Tax: 36.7oC, BP: 110/60 mmHg,
SpO2: 98% with 3 lpm nasal canule
Head and Anemic conjungtiva +/+ , icteric sclera -/-
neck
Thorax Cor: ictus invisible, palpable at ICS V 2 cm lateral MCL sinistra, LHM
≈ ictus, RHM≈SL dextra, S1S2 single, murmur, gallop (-)
Pulmo: Rh-/-, Wh -/-

Abdomen Convex, bowel sound (+) normal, liver span 9 cm, traube space:
timpani (+), shifting dullness (+)
Extremity Warm acral, CRT <3 second, leg edema +/+
4
Hematology 12/6 14/6 18/6 Reference
Hb 8.00 9.50 7.5 10.85-14.9 g/dL
NET
Post transfusi hematemesis
Erythrocyte 3.03 PRC
3.50 2.82 4.11-5.55 x 106/µL
Leukocyte 7.97 7.30 3.55 4.79-11.34 x 103/µL
Hct 25.9 30.00 24.1 34-45.1 %
Plt 333 198 36 216-451 x 103/µL
MCV 85.5 85.7 85.5 71.8-82.0 fL
MCH 26.4 27.1 26.6 22.6-31.01 pg
MCHC 30.9 31.7 31.1 30.8-35.2 g/dL
RDW 15.7 16.4 16.8 11.3-14.6 %
Eo/Ba/Neut/Ly/Mo 0/0/74/14 0/0/80/12 0/1/84/10 ≤4/≤1/51-67/25-33/2-5
/13 /9 /5
5
LABORATORY DATA
Coagulation test
Parameter 12/6/22 Reference

PPT
•Patient 12,4 9,4 – 11,3
•Control 11,4
•INR 1,2 < 1,5
APTT
•Patient 32,2 24,6-30,6
•Control 25,8

6
Clinical 12/6 14/6 15/6 18/6 Reference
Chemistry

Bilirubin total 0.58 < 1.0 mg/dL

Bilirubin direk 0.38 < 0.25 mg/dL
Bilirubin 0.20 < 0.75 mg/dL
indirek
AST 73 0-32 U/L
ALT 42 0-33 U/L
Albumin 2.20 2.36 2.7 1.96 3.5-5.5 g/dL
albumin hematemesis

7
Imunoserology 12/6 Reference
Procalcitonin > 100 ng/mL < 0,5 low risk of sepsis
HbsAg Non reactive COI< 0.9 non reactive
COI: 0.431
Anti HCV Non reactive COI< 0.9 non reactive
COI: 0.080
CEA 2.44 < 5.0 ng/mL
Ca 19-9 36.58 <27 U/mL

8
Clinical Chemistry 17/6 Reference

Urea 23.5 16.6-48.5 mg/dL

Creatinine 0.80 <1.2 mg/dL

eGFR 97.551 mL/menit/ 1.73 m2

RBG 99 <200 mg/dL

Calcium 7.9 7.6-11 mg/dL
Phospor 3.7 2.7-4.5 mg/dL

9
Serum Electrolyte 12/06 Reference

Na 135 136-145 mmol/L

K 2.56 3.5-5 mmol/L

Cl 102 98-106 mmol/L

Antigen 12/6 Reference

Rapid test Antigen SARS- Negatif Negatif
CoV2

10
 Blood Gas Analysis
12/6/22 Reference Range
pH 7,31 7,35-7,45
pCO2 33,9 35-45
pO2 43,5 80-100
Bikarbonat 17,1 21-28
(HCO3)
Base Excess -9,4 (-3)-(+3)

O2 Saturation 75,2 >95

Hb 8,6
Suhu 37,0

Conclusion: metabolic acidosis dd/ vein sample 11

CXR 19/6/22  Normal
12
ABDOMINAL CT-
SCAN
Carcinoma caput pancreas
with peripancreatic mass
Multiple nodul ec. Susp.
Inflamation

13
THERAPY
 IVFD PZ: D10 1:1
 Inj. Lansoprazol 1x1 iv
 Inj. Tranexamic acid 3x1 iv
 Inj. Ceftriaxone 2x1 iv
 Inj. Santagesik 3x1 iv
 Inj. Ondancetron 3x 8 mg iv

14
 The laboratory results showed: normochromic normocytic anemia,
thrombocytopenia and increased RDW, acidosis metabolic, increased AST
and ALT, hypoalbuminemia, hyponatremia, hypokalemia, with high
procalcitonin and Ca 19-9.
 Radiology results: normal
 History taking, physical examination and other examination showed:
1. Ca caput pancreas
2. Hypoalbuminemia d.t liver insufficiency DD hypercatabolic state
3. Sepsis d.t pancreatic cancer DD susp. UTI
4. Normochromic anisocytosis Anemia dt chronic disease (malignancy)
5. Electrolyte imbalance dt low intake DD metabolic acidosis

15
 Performing: blood smear, reticulocyte, amylase, lipase, ascites fluid
analysis, total protein, globulin, ALP, GGT, AFP, blood culture, lactic
acid, urinalisis
 Monitoring: CBC, albumin, AST/ALT, ureum, creatinine, bilirubin
TDI, AST/ALT, electrolyte serum, FH, CEA, Ca 19-9, BGA, SOFA
score, CXR, Vital sign

16
DISCUSSION
Establishment of
diagnosis

High Ca 19-9 in this

patient
17
1 Establishment of diagnosis

18
DISCUSSION

1 • Establishment of
the diagnosis

19
 PANCREATIC CANCER
Pancreatic cancer is the fourth leading cause of cancer deaths, being
responsible for about 7% of all cancer-related deaths.  
Approximately 75% of all pancreatic carcinomas occur within the head
or neck of the pancreas, 15-20% occur in the body of the pancreas, and 5-
10% occur in the tail.
The relative 1-year survival rate for pancreatic cancer is only 28%, and the
overall 5-year survival is 7%
Pancreatic cancer is notoriously difficult to diagnose in its early stages.
At the time of diagnosis, 52% of all patients have distant disease and 26%
have regional spread.

McGuigan, Andrew, et al. "Pancreatic cancer: A review of clinical diagnosis, epidemiology, treatment and outcomes."  World journal of gastroenterology 24.43 (2018): 4846.
https://emedicine.medscape.com/article/280605-overview
 PANCREATIC CANCER: SIGNS &
SYMPTOMS
▪ Anorexia, malaise, nausea, fatigue, ▪ Painless obstructive jaundice: Most
diarrhea characteristic sign of cancer of head
▪ Significant weight loss: of the pancreas
Characteristic feature of pancreatic ▪ Developing, advanced intra-
cancer abdominal disease: Presence of
ascites, a palpable abdominal mass,
▪ Midepigastric pain: Common
hepatomegaly from liver
symptom of pancreatic cancer,
metastases, or splenomegaly from
sometimes with radiation of the pain
portal vein obstruction
to the midback or lower-back region
▪ Ascites may result, and this has
an ominous prognosis.

https://emedicine.medscape.com/article/280605-overview
 PANCREATIC CANCER: RISK FACTORS
NON-MODIFIABLE RISK FACTORS: MODIFIABLE RISK FACTORS:
1. Age: 90% of newly diagnosed patients are a. Smoking
aged over 55 years of age, with the b. Alcohol
majority in their 7th and 8th decade of life c. Chronic pancreatitis
2. Sex: Male : female = 4:1 d. Obesity
3. Ethinicity e. Dietary factor
4. Blood group
5. Gut microbiota
6. Family history and genetic susceptibility
7. Diabetes mellitus

McGuigan, Andrew, et al. "Pancreatic cancer: A review of clinical diagnosis, epidemiology, treatment and outcomes."  World journal of gastroenterology 24.43 (2018): 4846.
PANCREATIC CANCER: LABORATORY
FINDINGS
CBC : a mild normochromic anemia, Thrombocytosis
Hepatobiliary tests: Patients with obstructive jaundice show significant elevations in
bilirubin (conjugated and total), ALP, GGT, and, to a lesser extent, AST and ALT
Serum amylase and/or lipase levels: Elevated in less than 50% of patients with
resectable pancreatic cancers and in only 25% of patients with unresectable tumors
Patients with advanced pancreatic cancers and weight loss may also have general
laboratory evidence of malnutrition (eg, low serum albumin or cholesterol level).
Tumor markers such as CA 19-9 antigen and CEA: 75-85% have elevated CA 19-9
levels; 40-45% have elevated CEA levels

https://emedicine.medscape.com/article/280605-guidelines#g1
DIAGNOSIS ALGORITHM

24
DIAGNOSIS ALGORITHM

25
AX : DX CA CAPUT
PANCREAS,

26
 DATA INTERPRETATION
 Female, 59 years
 Anamnesis : anorexia, weight - Carcinoma caput pancreas
loss, decrease appetite,
 Lab. Findings: Normochromic
anisocytosis anemia,
thrombocytopenia, increased
AST/ALT, high procalcitonin,
high Ca 19-9,
hyponatremia,hypokalemia • Performing: amylase, lipase, ascites fluid analysis,
hypoalbuminemia, SOFA score: SAAG, total protein, globulin, ALP, GGT, AFP,
6 SPE (if needed), USG? , sesuaikan algoritm
 Thorax Xray: normal • Monitoring: CBC, albumin, AST/ALT, bilirubin
 Abdominal CT-Scan: ca caput
TDI, AST/ALT
pancreas
SEPSIS
 Sepsis is defined as life-threatening organ dysfunction caused
by a dysregulated host response to infection.
 Organ dysfunction can be identified as an acute change in total
SOFA score ≥2 points consequent to the infection.
 Septic shock can be defined with a clinical construct of sepsis
with persisting hypotension requiring vasopressors to maintain
MAP≥65mmHg and having a serum lactate level>2mmol/L
(18mg/dL) despite adequate volume resuscitation.

28
 Sofa score: 3

29
 SEPSIS RELATED
30
ASSOCIATED
PANCREATIC
CANCER
31
UTI
Score: 2
 DATA INTERPRETATION
 Female, 59 years
 Anamnesis : anorexia, weight - Sepsis d t pancreatic cancer DD susp. UTI
loss, decrease appetite,
 Lab. Findings: Normochromic
anisocytosis anemia,
thrombocytopenia, increased
AST/ALT, high procalcitonin,
high Ca 19-9,
hyponatremia,hypokalemia • Performing: lactic acid, sesuai sofa, urine culture,
hypoalbuminemia, SOFA score: blood culture (if needed)
6 • Monitoring: Vital sign, SOFA score, CBC,
 Thorax Xray: normal albumin, AST/ALT, bilirubin TDI,
 Abdominal CT-Scan: ca caput
pancreas
 HYPOALBUMINEMIA
 Hypoalbuminaemia is one of the most prevalent disorders in
hospitalized and critically ill patients.
 Hypoalbuminaemia may be a result of decreased production (rare) of
albumin or increased loss of albumin via the kidneys, gastrointestinal
(GI) tract, skin, or extravascular space or increased catabolism of
albumin or a combination of 2 or more of these mechanisms.
 The prevalence of hypoalbuminemia is higher amongst hospitalized,
critically ill, and elderly patients. One report by Brock et al.
determined the prevalence to be greater than 70% of elderly
hospitalized patients.

Hypoalbuminemia. Gounden V, et al. StatPearls Publishing. Europe PMC Plus. 2018

34
CAUSES OF
HYPOALBUMINEMIA
Reduced synthesis

Genetic abnormalities
Cirrhosis
Acute liver failure
Acute and chronic hepatitis
Malabsorption syndromes
Nutritional deficiencies (low-protein diets)
Critical illnesses
Diabetes
Chronic metabolic acidosis
Increased catabolism

Infections, Sepsis
Angelo Gatta, et al (2017). Causes and mechanisms of
Cancer hypoalbuminemia. Springer. Intern Emerg Med 7:193-199 35
 CAUSES OF HYPOALBUMINEMIA
Alteration in distribution
 Hemodilution (e.g., pregnancy)
 Decreased lymphatic clearance (e.g., during major surgery)
 Increase in transcapillary escape rate (e.g., major surgery and trauma, heart
failure, fluid loss, vasculitis, diabetes, cardiopulmonary bypass surgery,
infections, sepsis, shock, ischemia/reperfusion, hypothyroidism, burns,
extensive skin diseases)
Increased loss
 Renal loss (nephrotic syndrome)
 Skin loss (extensive burns, extensive exudative skin lesion)
 Gastrointestinal loss (protein-losing enteropathies)

Angelo Gatta, et al (2017). Causes and mechanisms of

36
hypoalbuminemia. Springer. Intern Emerg Med 7:193-199
 DATA INTERPRETATION
 Female, 59 years Hypoalbuminemia d.t liver insufficiency DD
 Lab. Findings: Normochromic hypercatabolic state
anisocytosis anemia,
thrombocytopenia, increased
AST/ALT, high procalcitonin,
high Ca 19-9,
hyponatremia,hypokalemia
hypoalbuminemia, SOFA score:
6 • Performing: blood smear, reticulocyte, amylase,
lipase, ascites fluid analysis, total protein, globulin,
ALP, GGT, AFP, blood culture, lactic acid,
 Thorax Xray: normal
urinalysis, blood culture
 Abdominal CT-Scan: ca caput
• Monitoring: CBC, albumin, AST/ALT, bilirubin
pancreas
TDI, AST/ALT, electrolyte serum, FH, CEA, Ca 19-
9, BGA, SOFA score, CXR, Vital sign
 DATA INTERPRETATION
 Female, 59 years - Normochromic anisocytosis anemia dt chronic
 Lab. Findings: Normochromic disease DD acute blood loss
anisocytosis anemia, - Carcinoma caput pancreas
thrombocytopenia, increased - Sepsis d.t pancreatic cancer DD susp. UTI
AST/ALT, high procalcitonin, - Hypoalbuminemia d.t liver insufficiency DD
high Ca 19-9, hypercatabolic state
hyponatremia,hypokalemia
hypoalbuminemia, SOFA score:
6 • Performing: blood smear, reticulocyte, amylase,
lipase, ascites fluid analysis, total protein, globulin,
ALP, GGT, AFP, blood culture, lactic acid,
 Thorax Xray: normal
urinalysis, blood culture
 Abdominal CT-Scan: ca caput
• Monitoring: CBC, albumin, AST/ALT, bilirubin
pancreas
TDI, AST/ALT, electrolyte serum, FH, CEA, Ca 19-
9, BGA, SOFA score, CXR, Vital sign
 DATA INTERPRETATION
 Female, 59 years Diagnosis:
 Lab findings: • Hypoalbuminemia d.t liver
Hypoalbuminemia insufficiency DD hypercatabolic state
Increased AST/ALT
SOFA score: 6

Plan
• Suggest : total protein, globulin,
ALP/GGT, bilirubin
• Monitoring: CBC, AST/ALT,
albumin, SOFA score

39
DISCUSSION

• High Ca 19-9 in this

patient
2

40
 CA 19-9 BIOMARKER
CA19-9 is the most commonly used and best validated serum tumor
marker for pancreatic cancer diagnosis in symptomatic patients and for
monitoring therapy in patients with pancreatic adenocarcinoma.
Normally synthesized by normal human pancreatic and biliary ductal cells
and by gastric, colon, endometrial and salivary epithelia.
CA 19-9 is present in small amounts in serum

• McGuigan, Andrew, et al. "Pancreatic cancer: A review of clinical diagnosis, epidemiology, treatment and outcomes."  World journal of gastroenterology 24.43 (2018): 4846.
• Lin, Y. C., Lee, P. H., Yao, Y. T., Hsiao, J. K., Sheu, J. C., & Chen, C. H. (2007). Alpha-fetoprotein-producing pancreatic acinar cell carcinoma.  Journal of the Formosan
Medical Association, 106(8), 669-672.
 CA 19-9
Serum cancer antigen 19-9 (CA 19-9) is the only marker approved by the
United States Food and Drug Administration for use in the routine
management of pancreatic cancer
However, CA19-9 is not an ideal marker since its sensitivity is only 87%
and specificity only 86% for pancreatic cancers when the upper normal
limit is set to 37 U/mL.
CA 19-9 is not recommended for use as a screening test for pancreatic
cancer and is only appropriate to monitor response to treatment and as a
marker of recurrent disease

• McGuigan, Andrew, et al. "Pancreatic cancer: A review of clinical diagnosis, epidemiology, treatment and outcomes."  World journal of gastroenterology 24.43 (2018): 4846.
• Lin, Y. C., Lee, P. H., Yao, Y. T., Hsiao, J. K., Sheu, J. C., & Chen, C. H. (2007). Alpha-fetoprotein-producing pancreatic acinar cell carcinoma.  Journal of the Formosan
Medical Association, 106(8), 669-672.
CA 19-9 BIOMARKER
The diagnostic utility of CA 19.9 presents important limitations above all
related to a low sensitivity in symptomatic patients and a low PPV. In
particular for the following:
1. Lacking in CA 19-9 sensitivity for early or small-diameter pancreatic
cancers. Because of serum CA 19-9 concentration is highly correlated to
the tumor size in most, if not in all, patients with pancreatic cancer, just 50
% of patients with pancreatic cancers less than 3 cm in diameter presents
elevated levels of CA 19-9, thus it is difficult to use CA 19-9 as a marker
for early diagnosis of pancreatic cancer
CA 19-9 BIOMARKER
2. Poor correlation between the degree of cell differentiation of the tumor
and the serum level of CA 19-9. Poorly differentiated pancreatic cancers
appear to express less CA 19-9 than either moderately or well
differentiated cancers.
3. Impossibility to detect CA 19-9 in subjects that have a fucosyltransferase
deficiency, approximately of 5–10 % of the Caucasian population, who
cannot synthesize the Ca-19-9 epitope. Therefore, in these genotypically
Lewis a–b– patients, false negative results for CA 19-9 serum levels can
be obtained even in the presence of advanced pancreatic cancer.
CONCLUSION
It has been discussed patient with carcinoma caput pancreas
+ hypoalbuminemia+ electrolyte imbalance
CA 19-9 is the most commonly used and best validated
serum tumor marker for pancreatic cancer.
High CA 19-9 level in this patient due to her pancreatic
cancer
 Performing: blood smear, reticulocyte, amylase, lipase,
ascites fluid analysis, total protein, globulin, ALP, GGT, AFP,
urinalysis, blood culture, lactic acid
 Monitoring: CBC, albumin, AST/ALT, bilirubin TDI,
AST/ALT, electrolyte serum, FH, CEA, Ca 19-9, BGA, SOFA
score, CXR, GCS, Vital sign
47
THANK YOU
PCCL PL IDx PDx
1. Female/59 years Normocromic Normocromic Blood smear,
Anisocytosis Anisocytosis Reticulocyt
Physical Examination Anemia Anemia
- Anemic conjunctiva d.t: Monitoring:
1. Chronic CBC
Laboratory disease
- Hb ↓ 2. Acute blood
- HCT ↓ loss
- MCV N, MCH N
- High RDW

48
PCCL PL IDx PDx
2. Female/ 59 y.o Electrolyte Electrolyte Urine electrolyte
imbalance imbalance
Laboratory d.t low intake Monitoring:
- Hyponatremia DD metabolic - SE
- Hypokalemia acidosis - BGA

Anamnesis
• Low intake

49
PCCL PL Idx PDx
3. woman/ 59 years Hypoalbumine Hypoalbuminem Total Protein
mia ia Globulin
Laboratory: dt liver ALP/GGT
Hypoalbuminemia insufficiency bilirubin T/D/I
 ↑AST and ALT DD
hypercatabolic
state Monitoring:
CBC
Albumin
ALT
AST

50
PCCL PL IDx PDx
4. Female/54 years Sepsis Sepsis d.t − Urinalysis
1. Pancreatic − Blood culture and
Laboratory: cancer sensitivity test
- Elevated Procalcitonin 2. Susp. UTI
- Hypoalbuminemia Monitoring:
- SOFA score 6 CBC
Procalcitonin
CRP
SOFA score
Thorax photo

51
PCCL PL IDx PDx
7. Female/ 59 y.o ca caput pancreas ca caput - Ascites fluid analysis
pancreas - Amylase, lipase
Laboratory - Fecal analysis
• NN Anemia - Total protein, globulin,
• ↑AST and ALT 2-3x ULN ALP, GGT
• Hypoalbuminemia - AFP
• ↑ CA 19-9 Monitoring:
- Normal thrombocyte  - GCS
thrombocytopenia - Vital sign
- Urine output
- SOFA score: 6
- CBC
- Bilirubin T/D/I
- AST, ALT
- Albumin
- CEA, CA 19-9

52
PCCL PL IDx PDx
7. Female/ 59 y.o ca caput pancreas ca caput - Ascites fluid analysis
- Amylase, lipase
pancreas - Fecal analysis
Physical Examination - Total protein, globulin,
-Anemic conjunctiva ALP, GGT
-shifting dullness (+) - AFP
Anamnesis Monitoring:
- weakness - GCS
- Vital sign
- Abdominal pain - Urine output
- ↓appetite, ↓ body weight - CBC
- Bilirubin T/D/I
Abdominal CT scan: - AST, ALT
- Albumin
- Carcinoma caput pancreas, - CEA, CA 19-9

53
Score: 0

54
55
56
57
KRITERIA DIAGNOSIS AKI PADA DEWASA MENURUT KDIGO

58
DEFINISI AKI, CKD DAN AKD
(KDIGO)

59
PENDEKATAN DIAGNOSTIK

60
KLASIFIKASI CKD (NATIONAL KIDNEY FOUNDATION
KIDNEY DISEASE AND QUALITY INITIATIVE )

61
DEFINISI AKI (AKIN)

62
DEFINISI AKI (RIFLE)

63
AKI
 AKI is defined as an abrupt (within hours) decrease in kidney
function, which encompasses both injury (structural damage)
and impairment (loss of function).
 AKI is defined as any of the following (Not Graded):
 Increase in SCr by ≥0.3 mg/dl (≥26.5 μmol/l) within 48
hours; or
 Increase in SCr to ≥ 1.5 times baseline, which is known or
presumed to have occurred within the prior 7 days; or
 Urine volume < 0.5 ml/kg/h for 6 hours

64
SEPSIS
 Sepsis is defined as life-threatening organ dysfunction caused
by a dysregulated host response to infection.
 Organ dysfunction can be identified as an acute change in total
SOFA score ≥2 points consequent to the infection.
 Septic shock can be defined with a clinical construct of sepsis
with persisting hypotension requiring vasopressors to maintain
MAP≥65mmHg and having a serum lactate level>2mmol/L
(18mg/dL) despite adequate volume resuscitation.

66
 Sofa score:6

67
PROCALCITONIN
 Procalcitonin (PCT) is the precursor of the hormone
calcitonin, and it is produced by the C cells of the thyroids
gland as preprocalcitonin, then cleaved by proteolytic
enzymes into procalcitonin. Into the C cells, procalcitonin is
cleaved into calcitonin, katacalcin and a proteic residue, and
it is not released into the blood stream of healthy individuals.
 PCT is known as a good biological diagnostic marker for
severe sepsis, or septic shock in critically ill patients.

Picariello et all, Procalcitonin in patients with acute coronary syndromes and cardiogenic shock submitted to percutaneous coronary
Intervention, Intern Emerg Med (2009) 4:403–408 68
 Kafkas et al.  PCT concentrations are elevated from the time
of admission, and are detectable in serum earlier that CK-MB or
troponin I in most patients.
 PCT could be considered as a novel sensitive myocardial index
because its release in AMI is probably due to the inflammatory
process that occurs during AMI.
 Elevated concentrations of PCT have been reported in
patients with cardiogenic shock.
 CS patients show high-PCT concentrations, especially in the
presence of multiorgan failure and in the absence of signs of
infections (cultures and clinical findings).
 High-PCT concentrations (>2 ng/ml) are frequently found in
CS patients with multiorgan failure disease
Picariello et all, Procalcitonin in patients with acute coronary syndromes and cardiogenic shock submitted to percutaneous coronary
Intervention, Intern Emerg Med (2009) 4:403–408 70
71
 CARCINOEMBRYONIC ANTIGEN
CEA is a glycoprotein with a molecular weight of 180 kDa, with branched
oligosaccharide chains linked to a polypeptide chain. 
Carcinoembryonic Antigen (CEA) is most useful as a marker for colorectal,
gastrointestinal, lung, and breast carcinoma.
CEA is also useful for monitoring breast, lung, gastric, and pancreatic
carcinoma.
CEA is the second most common serum biomarker used clinically for
detecting pancreatic carcinoma. The mean sensitivity and specificity estimates
for CEA were 44.2% and 84.8% respectively.

• Tietz Fundamentals of Clinical Chemistry. 6th ed. 2008.

• Rückert, F., Pilarsky, C., & Grützmann, R. (2010). Serum tumor markers in pancreatic cancer—recent discoveries.  Cancers, 2(2), 1107-1124.
74
 ALPHA-FETOPROTEIN (AFP)
Alpha-fetoprotein (AFP) is a single-chain serum glycoprotein with a molecular weight of about
70,000 Dalton
It is produced mainly in the foetal liver, yolk sac and foetal gastrointestinal tract. AFP was initially
thought to be specific to hepatocellular carcinoma and embryonal cell carcinoma, and is usually
not detected in the sera of healthy adults. Its physiological function is unknown and it has a
biological half-life of approximately 4-5 days. AFP is widely used in diagnosis and in monitoring
therapy efficinecy.
AFP is rarely found in other malignancies such as pancreatic carcinoma

Mueller, S. B., Micke, O., Herbst, H., Schaefer, U., & Willich, N. (2005). Alpha-fetoprotein-positive carcinoma of the pancreas: a case report.  Anticancer research, 25(3A), 1671-
1674.
 The case of a 19-year-old male with an alpha-fetoprotein (AFP)-producing
acinar cell carcinoma of the pancreas. Tumour markers other than AFP were
normal (CA 19-9, CEA, CA-125, β-HCG).
The immunohistochemical staining indicated an AFP-producing pancreatic
tumor
After combined radio-chemotherapy, AFP levels declined from about 3000
ng/ml (reference area: 0-7 ng/ml) to 18 ng/ml, but increased when
widespread metastasis appeared.

Mueller, S. B., Micke, O., Herbst, H., Schaefer, U., & Willich, N. (2005). Alpha-fetoprotein-positive carcinoma of the pancreas: a case report.  Anticancer research, 25(3A), 1671-
1674.
A 47-year-old man with chronic hepatitis B had progressive elevated α-fetoprotein of 2 years’
duration.
A pancreatic tail tumor, instead of liver tumor, was detected. He underwent elective distal
pancreatectomy and splenectomy and the pathology turned out to be acinar cell carcinoma of the
pancreas.
Serum level of α-fetoprotein returned to normal soon after surgery. No cancer recurrence was
noted after 3 years of follow-up.
Alpha-fetoprotein is commonly used as a tumor marker to screen for hepatocellular carcinoma in
high-risk patients. However, elevated α-fetoprotein could occur in a much rarer disease, acinar cell
carcinoma of the pancreas.
DISCUSSION

• High
2 Procalcitonin in
this patient

78
PROCALCITONIN
 Procalcitonin (PCT) is the precursor of the hormone
calcitonin, and it is produced by the C cells of the thyroids
gland as preprocalcitonin, then cleaved by proteolytic
enzymes into procalcitonin. Into the C cells, procalcitonin is
cleaved into calcitonin, katacalcin and a proteic residue, and
it is not released into the blood stream of healthy individuals.
 PCT is known as a good biological diagnostic marker for
severe sepsis, or septic shock in critically ill patients.

Picariello et all, Procalcitonin in patients with acute coronary syndromes and cardiogenic shock submitted to percutaneous coronary
Intervention, Intern Emerg Med (2009) 4:403–408 79
81
 ACUTE CHOLANGITIS
❖ Acute cholangitis is a clinical entity caused by bacterial infection of the biliary
system, most commonly secondary to partial or complete obstruction of the bile
duct or hepatic ducts.
❖ The most frequently found pathogens  Escherechia coli (25%-50%), Klebsiella
species (15%-20%), Enterococcus species (10%-20%) and Enterobacter species
(5%-10%).
❖ Sometimes, anaerobic bacteria like Bacteroids fragilis and Clostridium perfringens
can also cause acute cholangitis, particularly in patients with previous biliary
surgery and in the elderly population
❖ It may present as a local biliary infection or progressive SIRS, or more rapidly
advancing sepsis with or without multi-organ dysfunction.

Ahmed, M. (2018). Acute cholangitis-an update. World journal of gastrointestinal pathophysiology, 9(1), 1.

Gupta, M., & Sachdev, A. (2016). Acute cholangitis-An overview of diagnosis and medical management.  Chandigarh, 6(2), 1.
ACUTE CHOLANGITIS
❖ Acute cholangitis can be diagnosed if the clinical manifestations of Charcot's triad, i.e.,
fever and/or chills, abdominal pain (right upper quadrant or epigastric), and jaundice
are present.
❖ When not all of the components of the triad are present, then a definite diagnosis can
be made if laboratory data and imaging findings supporting the evidence of
inflammation and biliary obstruction are obtained.
❖ Clinical features:
• Charcot’s Triad : RUQ pain + Jaundice + Fever  Present in 60-79%
• Reynolds’ Pentad : Charcot’s triad + Hypotension + altered mental status  Present
in 15%
• Medical emergency if fever > 40C, septic shock, peritoneal signs, or bilirubin>10

Ahmed, M. (2018). Acute cholangitis-an update. World journal of gastrointestinal pathophysiology, 9(1), 1.

Gupta, M., & Sachdev, A. (2016). Acute cholangitis-An overview of diagnosis and medical management.  Chandigarh, 6(2), 1.
POSSIBLE ETIOLOGY OF ACUTE CHOLANGITIS