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Case Report
A 57 years old man with pulmonary tuberculosis,hepatocellular injury with a
false positive anti-HBc, Anemia of chronic disease
INTRODUCTION
Pulmonary Tuberculosis
Tuberculosis is an infectious disease caused by the bacteria directly TB (Mycobacterium
tuberculosis). The most of TB germs attacked the lungs, but can also on other organs. The TB
case definitions below are based on the level of certainty of the diagnosis and on whether or not
laboratory confirmation is available. Tuberculosis suspect. Any person who presents with symptoms or signs suggestive of
TB. The most common symptom of pulmonary TB is a productive cough for more than 2
weeks,1
which may be accompanied by other respiratory symptoms (shortness of breath,
chest pains, haemoptysis) and/or constitutional symptoms (loss of appetite, weight loss,
fever, night sweats, and fatigue).2
.
Case of tuberculosis. A definite case of TB (defined below) or one in which a health
worker (clinician or other medical practitioner) has diagnosed TB and has decided to treatthe patient with a full course of TB treatment.
Definite case of tuberculosis. A patient with Mycobacterium tuberculosis complex
identified from a clinical specimen, either by culture or by a newer method such as
molecular line probe assay.
Cases of TB are also classified according to the:
anatomical site of disease;
bacteriological results (including drug resistance);
history of previous treatment;
HIV status of the patient.
Pulmonary tuberculosis (PTB) refers to a case of TB (defined above) involving the lung
parenchyma. Miliary tuberculosis is classified as pulmonary TB because there are lesions in the
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lungs. Tuberculous intrathoracic lymphadenopathy (mediastinal and/or hilar) or tuberculous
pleural effusion, without radiographic abnormalities in the lungs, constitutes a case of
extrapulmonary TB. A patient with both pulmonary and extrapulmonary TB should be classified
as a case ofpulmonary TB.
Smear-negative PTB cases should either:
A. have sputum that is smear-negative but culture-positive forM. tuberculosis:
a case of pulmonary TB is considered to be smear-negative if at least two sputum
specimens at the start of treatment are negative for AFB1 in countries with a functional
EQA system.
in all settings with an HIV prevalence of >1% in pregnant women or 5% in TB patients,
sputum culture for M. tuberculosis should be performed in patients who are sputum
smear-negative to confirm the diagnosis of TB.
OR
B. meet the following diagnostic criteria:
decision by a clinician to treat with a full course of anti-TB therapy; and
radiographic abnormalities consistent with active pulmonary TB and
either:
laboratory or strong clinical evidence of HIV infection
or:
if HIV-negative (or unknown HIV status living in an area of low HIV prevalence), no
improvement in response to a course of broad-spectrum antibiotics (excluding anti-TB
drugs and fluoroquinolones and aminoglycosides).
Hepatocellular injury refers to a process that involves primarily the hepatocytes as
opposed to one that affects primarily the biliary tract (termed cholestatic disease) or
an infiltrative process. Hepatocellular injury usually results in the elevation of AST and ALT
with little or no elevation of alkaline phosphatase. The AST:ALT ratio is often useful in
determining the etiology of enzyme elevation. Acute hepatocellular injury is apparent in patients
who present with serum aminotransferase levels that are 10X the upper limits of normal and have
no known prior history of liver disease. When present, symptoms are usually non-specific with
flu-like symptoms: fatigue, nausea, vomiting, abdominal pain, arthralgias and occasionally
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diarrhea. Initial evaluation includes serologies for hepatitis A IgM, hepatitis B (core antibody
IgM), and hepatitis C.Acute infection with the hepatitis A virus (HAV) never leads to chronic
liver disease and
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PRESENTATION OF CASE
A 57-year-old man was admitted in Dr. Kariadi Hospital, referred from general municipal
Semarang hospital, complaining of 2 weeks shortness of breath. Patients were treated for 3 days
in general municipal Semarang hospital but had no improvement. He had no wheezes, and this
complaint were more pronounced during activity. Shortness of breath was not affected by
weather and emotion changes. He had productive cough for 2 weeks, with purulent sputum. The
patient also complained having multiple oral ulcer, so he was not eager to have eating and
drinking. There was no nocturnal awakening due to shortness of breath, no swollen of gums, no
nausea, no vomiting. His defecation and micturien were normal. The patient also complained of
continuous fever for two weeks. There were no chills noted, but he experienced significant
weight loss of approximately 3 kgs during last one month. He had history of smoking rolled
cigarettes, 12 cigarettes each day for approximately 30 years and had stopped since he got this
complaint. There were no history of tattoo, free sexual intercourse, and history of lung diseases.
History of family illness: No history of tuberculosis
No history of hepatitis
Past history :No history of tuberculosis
No history of hepatitis
He did not have diabetes.
Family history:
There were no member of his family having complain like this or history of lung
diseases.
There were no family members who had history of diabetes mellitus and high blood
pressure.
Social and Economy history:
The patient worked as a farmer before sick, with his wife. He had six children.
The hospital costs were financed by Jamkesmas.
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Physical examination:
On physical examination, he was alert, looked weak and pale, with GCS E4 M6 V5. His
body weight was 45 kg, her height was 160 centimeters with a body mass index of 18 kg/m
2
(underweight). His vital sign were noted: blood pressure was 100/60 mmHg, pulse rate was 90
times per minute regular, volume and tension enough, the body temperature was 38,5C
(axillary), and respiratory rate was 28 times per minute.
The palpebral conjunctivae looked pale, sclera was unicteric. Examination on the neck
showed no distention in jugular venous pressure, no enlargement of the lymph nodes and thyroid.
On the thorax examination was found no mass, no spider nevi, no axillary lymph nodes
enlargement. Examination on the chest: there was dullness on right lower hemithoraks, breathing
sound: bronchial, pathological sound: rough rales third pitch upper the right lung, and third basal
of the right and left lung. Examination on the heart was not found any enlargement of ventricle
and atrium, the heart sound was normal and heart rate was 90 times per minute.
On the abdominal examination, there was a flat contour with normal bowel sound. There
were no masses and renal ballottement. Liver and spleen were not palpable. Rectal toucher: no
external or internal hemorrhoid, good sphincter ani tone, ampulla rectum was not collapsed,
smooth mucosa, no fecal blood.
Extremities : Superior Inferior
- Pale +/+ +/+
- Cold -/- -/-
- Edema -/- -/-
- Clubbing finger -/- -/-
- White nail -/- -/-
- Eritema palmaris -/- -/-
- Physiological reflex +N/+N +N/+N
- Pathological reflex -/- -/-
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Laboratory Result
Laboratoryexamination
June 9th2012
Reference range
Hemoglobine (gr%) 7,82 1316
Hematocrit (%) 25,2 4054
RBC (million/ul) 3,62 4,56,5
MCH (pg) 21,62 2732
MCV (fL) 70,52 7696
MCHC (g/dL) 30,63 2936
WBC (thousand/ul) 23,34 411
Platelet (thousand/ul) 468,4 150400
Glucose /BSL (mg/dl) 77 80-110
Ureum (mg/dL) 59 1539
Creatinin (mg/dL) 1,6 0,601,3
Sodium (mmol/L) 130 136145
Potassium (mmol/L) 5,1 3,55,1
Chlorida (mmol/L) 98 98107
Calcium (mmol/L) 2,06 2,122,52
Laboratory Examination June 9t
2012 Reference range
Total protein (gr/dl) 6.0 6,4-8,2
Albumin (gr/dl) 2.4 3,4-5,0Globulin (gr/dl) 3.60 2,30-3,50
Total bilirubin (mg/dl) 0.60 0,00-1,00
Direct bilirubin (mg/dl) 0.36 0,00-0,30
SGOT (U/l) 3058 15-37
SGPT (U/l) 1877 30-65
Alkali phosphatase (U/l) 236. 50,0-136,0
Gamma GT (U/l) 170 5-85
Cor : The Apex shifted to laterokaudal, Aorta elongation
Pulmonary: vascular appearance increase accompanied by
blurring vascular. It looked infiltrates on the both lung field, it
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Chest X Ray June 9th
2012
Impression :
Cor : Cardiomegali (LV, Suspicious LA)
Aorta Elongation
Pulmonary : Pulmonary oedemaRight pleural effusion
looked homogeneous calcification on the basal right lung, It
showed blunted right costophrenic sinus.
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The aim of this case report was to establish diagnosis and the management of this case.
Problems :
1. Pulmonary Infiltrates DD/ Hospital Acquired Pneumonia
Pulmonary Tuberculosis
2. Hepatocellular injury DD/ Hepatitis Akut
Hepatitis Ischaemic
3. Hypochromic Microcytic Anemia DD/ Anemia of chronic diseases
4. Right pleural effusion
Treatment :
1. O 3 lt/minute
2. Normal saline infuse 0,9% 20 drops per minute
3. Soft diet 1700 kcal
4. Inj. Ceftriaxone 2 g once daily
5. Tablet Sistenol Oral 500 mg three times daily
6. Tablet ambroxol 30 mg oral three times daily
Rhytm: sinus, HR: 100 times/minute, Axis: normoaxis, Transition zone: V3-V4, P wave:
0.04 sec,PR-interval: 0.12 sec, QRS complex: 0.04 sec, ST segment: isoelectric,ratio R:S
in V1:
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Plans for Diagnosis and Monitoring
1. Blood culture, sputum culture
2. Sputum gram, acid fast bacilli three times, and fungus staining
3. Seromarker hepatitis
4. Abdominal Ultrasound
5. Liver function test repeated
6. complete blood count repeated
7. Peripheral blood smear, differential count
8. ESR I/II
9. Serum Fe, TIBC, Feritin
10.Tuberculin test
Progress Evaluation
Day 3 (Jun 12th
, 2012)
The patient did not have fever. He still looked pale and weak, composmentis.
Blood pressure was 100/70 mmHg; HR was 100 beat perminute; respiratory rate was 26 times
per/minute; the body temperature was 37,2C
Laboratory
examination
June
12th
2012
Reference range
Hemoglobine (gr%) 8,85 1316
Hematocrit (%) 29,1 4054
RBC (million/ul) 4,02 4,56,5
MCH (pg) 22,0 2732
MCV (fL) 72,50 7696
MCHC (g/dL) 30,4 2936
WBC (thousand/ul) 11,2 411
Platelet (thousand/ul) 333 150400
Glucose /BSL (mg/dl) 77 80-110
Ureum (mg/dL) 122 1539
Creatinine (mg/dL) 1,99 0,601,3
Sodium (mmol/L) 138 136145
Potassium (mmol/L) 4,5 3,55,1
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ESR 1 Jam (mm) 39.0 1,010
ESR 2 Jam (mm) 75.0
Fe serum (ug/dl) 11 50175
TIBC (ug/dl) 207 250450
Ferritin (ug/dl) 74,67 70435
Differential count
Peripheral blood smear
Erythrocytes
Platelets
Leukocytes
Eosinophils 0%, Basophils 0%, Stab neutrophils 1%, Segmented
neutrophils 87%, Lymphocytes 8%, Monocytes 3%, Myelosit 1 %
Normocytic, mild poikilocytosis (tear drop cell, eliptosit cell,
Normal in number and shape
Increased in number, neutrophilia +, toxic granulation +
Gram Staining
Negative rod gram bacili Positive
Streptococcus (+) Positive
Gram diplococcus (+) Positive
Ziehl Nielsen Staining
Acid Fast Bacili Negative
Leukocytes > 25/LPK
Fungus Staining
YEAST CELL Negative
Blood culture result : there was no bacteria growth
Sputum culture and antibiotic resistance result :
Chlorida (mmol/L) 100 98107
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Acinetobacter spp
Sensitive : Amikacin, Ampiciline-sulbactame, Ceftazidime, Ciprofloksasin, Cotrimoxazol,
Gentamicin, Piper tazobactom, Sulbactam Cefoperazone, Doripenam, Tigecyclin.
Resistance : Amoxyclav, Cefepime, Chloramphenicol, Fosfomycin, Cefoperazone.
Evaluation : Hospital Acquired Pneumonia
DD/ Pulmonary Tuberculosis
Anemia of chronic diseases
DD/ Fe deficiency Anemia
Plans: - Chest X-Ray repeated
-MGIT culture
Treatment :
1. O 3 lt/minute
2. Normal saline infuse 0,9% 20 drops per minute
3. Soft diet 1700 kcal
4. Inj. Ampiciline-sulbactame 500 mg three times daily
5. Tablet ambroxol 30 mg oral three times daily
Day 5 (Juni 14th
, 2012)
The patient had cough, shortness of breath and still weak.
Blood pressure: 100/60 mmHg; HR: 90 x/minute; RR: 27x/minute; temperature: 36,5C
The palpebral conjunctivae looked pale
Chest examination found crackles on lung auscultation.
Hb : 8,30 g/dl Creatinine : 1,40 mg/dl
Ht : 29,4 % Sodium : 143 mmol/l
Leukocyte : 10.800 /mm3
Potassium : 4,8 mmol/l
Platelet : 436.000 /mm3
Chloride : 107 mmol/l
Ureum : 71 mg/dl
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Laboratory Findings June 14t
2012 Reference range
HBsAg 0,00 (Negative) Negative
Anti HBc Total Positive Negative
Anti HCV 0,08 Negative
IGM Anti HAV 0,09 (Negiative) Negative
Evaluation : Hepatocellular injury with seromarker anti HBc positive
DD/ Resolved infection (most common)
False-positive anti-HBc, thus susceptible
Low level chronic infection
Resolving acute infection
- Plans : HBV DNA, Anti HBS, IgM anti HBC
USG Abdomen
Treatment :
1. Infusion Normal saline 30 drops/minute
2. Soft diet 1700 kcal
Laboratory Findings June 14t
2012 Reference range
Total protein (gr/dl) 5.3 6,4-8,2
Albumin (gr/dl) 2.6 3,4-5,0
Globulin (gr/dl) 2,7 2,30-3,50
SGOT (U/l) 42 15-37
SGPT (U/l) 212 30-65
Fosfatase Alkali (U/l) 93 50,0-136,0
Gamma GT (U/l) 652 5-85
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Day 17 (June 26th
, 2012)
The patient had fever again, cough, shortness of breath and still weak.
He still looked pale ,composmentis.
Blood pressure 110/60 mmHg; HR 108 x/minute; RR 28x/minute; temp 38,4C
Chest examination found crackles on lung auscultation.
Gram Staining
Negative rod gram bacili Positive
Streptococcus (+) Positive
Gram diplococcus (+) Positive
Ziehl Nielsen Staining
Acid Fast Bacili Negative
Leukocytes > 25/LPK
Laboratory
examination
July 8t
2012
Reference range
Hemoglobine (gr%) 10,4 1316
Hematocrit (%) 34,7 4054
RBC (million/ul) 4,3 4,56,5
MCH (pg) 24,2 2732
MCV (fL) 80,7 7696
MCHC (g/dL) 30,0 2936
WBC (thousand/ul) 10,5 411
Platelet (thousand/ul) 381 150400
Glucose /BSL (mg/dl) 110 80-110
Ureum (mg/dL) 11 1539
Creatinine (mg/dL) 0,6 0,601,3
Sodium (mmol/L) 132 136145
Potassium (mmol/L) 3,8 3,55,1
Chlorida (mmol/L) 100 98107
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. Chest X Ray June 20th 2012
Impression : compared to the previous X-ray picture is not visible changes
Laboratory results on June 26th
2012 :
- HBV DNA = viral not detectabled
- Ig M Anti HBC = non reactive
- Anti HBs = negative
USG Abdomen :
- Pleural effusion bilateral
- Minimally ascites
- Not found intraabdominal organ disorders with ultrasound technique
Tuberculin test : Negative ( Induration < 10 mm )
Evaluation : Hospital Acquired Pneumonia
DD/ Pulmonary Tuberculosis
Anemia of chronic disease
False-positive anti-HBc, thus susceptible
Treatment :
1. O 3 lt/minute.
2. Normal saline infuse 0,9% 20 drops per minute.
3. Soft diet 1700 kcal.
4. Inj. Ampiciline-sulbactame 500 mg three time daily
Cor : The Apex shifted to laterokaudal, Aorta elongation
Pulmonary: vascular appearance increase accompanied by blurring
vascular. It looked infiltrates on the both lung field, it looked
homogeneous calcification on the basal right lung, It showed
blunted right costophrenic sinus.
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5. Tablet ambroxol 30 mg oral three time daily
Plan : Bronchoscopy
MGIT culture
Day 28 (July 5th
, 2012)
The patient had shortness of breath and still weak.
He still looked pale ,somnolent.
Blood pressure 100/60 mmHg; HR 98 x/minute; RR 28x/minute; temp 36,4C
Chest examination found crackles on lung auscultation.
Laboratory
examination
August 14 t
2012
Reference range
SGOT 22 1537 U/l
SGPT 34 3065 U/l
Bronchoscopy :
- Results : Inflammation
MGIT culture : Positive .
Evaluation : Pulmonary Tuberculosis.
Treatment : 1. Tablet Rifampicyn 500 mg one time daily oral
2. Tablet Isoniazid 480 mg one time daily oral
3. Tablet Pyrazinamid 500 mg three time daily oral
4. Tablet Ethambutol 500 mg two time daily oral
5. Tablet B Complek Three time daily orall
Plan : Chest X-Ray repeated after two month treatment
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SGOT, SGPT repeated after two month treatment
After 2 mont treatment (August 28th
, 2012)
The patient had not shortness of breath and apparently healthy.
Blood pressure 110/60 mmHg; HR 88 x/minute; RR 20x/minute; temp 36,4C
Impression : compared to the previous X-ray picture is visible changes
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CLINICAL PATHWAY
A 57-year-old man was admitted in Dr. Kariadi Hospital, referred from general municipal Semarang
hospital, complaining of 2 weeks shortness of breath. Patients were treated for 3 days in general
municipal Semarang.He had productive cough for 2 weeks, with purulent sputum The patient also
complained of continuous fever for two weeks. There were no chills noted, but he experienced
significant weight loss of approximately 3 kgs during last one month. He had history of smoking
rolled cigarettes, 12 cigarettes each day for approximately 30 years and had stopped since he got this
complaint. There were no history of lung diseases.
Pulmonary
InfiltratesDD/-Hospital
Acquired
Pneumonia
-Pulmonary
Tuberculosis
Hepatocellular injury
DD/ Hepatitis akut
Hepatitis Ischaemic
Hypochromic Microcytic Anemia
DD/ Anemia of chronic diseases
Anemia defisiensi Fe
Physical examination : he was alert, looked weak and pale,body mass index of 18 kg/m
(underweight). Blood pressure was 100/60 mmHg, pulse rate was 90 times per minute regular,
volume and tension enough, the body temperature was 38,5C (axillary), and respiratory rate was
28 times per minute. The palpebral conjunctivae looked pale, sclera was unicteric..Examination
on the chest: there was dullness on right lower hemithoraks, breathing sound: bronchial,
pathological sound: rough rales third pitch upper the right lung, and third basal of the right and
left lung.
Laboratory : Hemoglobine level of 7,82 g/dl, Hematocrit 25,2 %,MCH 21,62 pg, MCV 70,52 fl,
His serum albumin level was low 2 gr/dl, Liver function tes was elevated ( SGOT 3058 U/l,SGPT 1877 U/l, Alkali phosphatase 236 U/l, Gamma GT 170 U/l), AChest radiograph showed
Pulmonary: vascular appearance increase accompanied by blurring vascular. It looked infiltrates
on the both lung field, it looked homogeneous calcification on the basal right lung, It showed
blunted right costophrenic sinus. Electrocardiography Conclusion : Sinus rhythm, and RBBB
incomplete
Pulmonary Tuberculosis
Hepatocellular injury with
a false positive Anti HBcAnemia of chronic
diseases
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DISCUSSION
A 57-year-old man was admitted in Dr. Kariadi Hospital, referred from general municipal
Semarang hospital, complaining of 2 weeks shortness of breath. Patients were treated for 3 daysin general municipal Semarang.He had productive cough for 2 weeks, with purulent sputum The
patient also complained of continuous fever for two weeks. There were no chills noted, but he
experienced significant weight loss of approximately 3 kgs during last one month. He had history
of smoking rolled cigarettes, 12 cigarettes each day for approximately 30 years and had stopped
since he got this complaint. There were no history of lung diseases. Physical examination : he
was alert, looked weak and pale,body mass index of 18 kg/m2
(underweight). Blood pressure was
100/60 mmHg, pulse rate was 90 times per minute regular, volume and tension enough, the
body temperature was 38,5C (axillary), and respiratory rate was 28 times per minute. The
palpebral conjunctivae looked pale, sclera was unicteric..Examination on the chest: there was
dullness on right lower hemithoraks, breathing sound: bronchial, pathological sound: rough rales
third pitch upper the right lung, and third basal of the right and left lung.
Laboratory : Hemoglobine level of 7,82 g/dl, Hematocrit 25,2 %,MCH 21,62 pg, MCV 70,52 fl,
His serum albumin level was low 2 gr/dl, Liver function tes was elevated ( SGOT 3058 U/l,
SGPT 1877 U/l, Alkali phosphatase 236 U/l, Gamma GT 170 U/l), AChest radiograph showed
Pulmonary: vascular appearance increase accompanied by blurring vascular. It looked infiltrates
on the both lung field, it looked homogeneous calcification on the basal right lung, It showed
blunted right costophrenic sinus. Electrocardiography Conclusion : Sinus rhythm, and RBBB
incomplete.Based on those subjective and objective data, the resume problem lists were as
follow : A 57 years old man with pulmonary tuberculosis,hepatocellular injury with a false
positive anti-HBc, Anemia of chronic disease.
Tuberculosis is an infectious disease caused by the bacteria directly TB (Mycobacterium
tuberculosis). The most of TB germs attacked the lungs, but can also on other organs. The TB
case definitions below are based on the level of certainty of the diagnosis and on whether or not
laboratory confirmation is available.2
Tuberculosis suspect. Any person who presents with symptoms or signs suggestive of
TB. The most common symptom of pulmonary TB is a productive cough for more than 2
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weeks,1
which may be accompanied by other respiratory symptoms (shortness of breath,
chest pains, haemoptysis) and/or constitutional symptoms (loss of appetite, weight loss,
fever, night sweats, and fatigue).2
.
Case of tuberculosis. A definite case of TB (defined below) or one in which a health
worker (clinician or other medical practitioner) has diagnosed TB and has decided to treat
the patient with a full course of TB treatment.
Definite case of tuberculosis. A patient with Mycobacterium tuberculosis complex
identified from a clinical specimen, either by culture or by a newer method such as
molecular line probe assay.
Cases of TB are also classified according to the:
anatomical site of disease;
bacteriological results (including drug resistance);
history of previous treatment;
HIV status of the patient.
Pulmonary tuberculosis (PTB) refers to a case of TB (defined above) involving the lung
parenchyma. Miliary tuberculosis is classified as pulmonary TB because there are lesions in the
lungs. Tuberculous intrathoracic lymphadenopathy (mediastinal and/or hilar) or tuberculous
pleural effusion, without radiographic abnormalities in the lungs, constitutes a case of
extrapulmonary TB. A patient with both pulmonary and extrapulmonary TB should be classified
as a case ofpulmonary TB.
Smear-negative PTB cases should either:
A. have sputum that is smear-negative but culture-positive forM. tuberculosis:
a case of pulmonary TB is considered to be smear-negative if at least two sputum
specimens at the start of treatment are negative for AFB1 in countries with a functional
EQA system.
in all settings with an HIV prevalence of >1% in pregnant women or 5% in TB patients,
sputum culture for M. tuberculosis should be performed in patients who are sputum
smear-negative to confirm the diagnosis of TB.
OR
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B. meet the following diagnostic criteria:
decision by a clinician to treat with a full course of anti-TB therapy; and
radiographic abnormalities consistent with active pulmonary TB and
either:
laboratory or strong clinical evidence of HIV infectionor:
if HIV-negative (or unknown HIV status living in an area of low HIV prevalence), no
improvement in response to a course of broad-spectrum antibiotics (excluding anti-TB
drugs and fluoroquinolones and aminoglycosides).
Hepatocellular injury refers to a process that involves primarily the hepatocytes as
opposed to one that affects primarily the biliary tract (termed cholestatic disease) or
an infiltrative process. Hepatocellular injury usually results in the elevation of AST and
ALT with little or no elevation of alkaline phosphatase3. The AST:ALT ratio is often
useful in determining the etiology of enzyme elevation. Acute hepatocellular injury is
apparent in patients who present with serum aminotransferase levels that are 10X the
upper limits of normal and have no known prior history of liver disease. When present,
symptoms are usually non-specific with flu-like symptoms: fatigue, nausea, vomiting,
abdominal pain, arthralgias and occasionally diarrhea. Initial evaluation includes
serologies for hepatitis A IgM, hepatitis B (core antibody IgM), and hepatitis C.Acute
infection with the hepatitis A virus (HAV) never leads to chronic liver disease and
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HBsAg
anti-HBc
anti-HBs
negative
positive
negative
Interpretation unclear; four possibilities
1. Resolved infection (most com2. False-positive anti-HBc, thus3. Low level chronic infection
4. Resolving acute infection
Anemia of chronic disease, the anemia that is the second most prevalent afteranemia caused by iron deficiency, occurs in patients with acute or chronic immune activation.
The condition has thus been termed anemia of inflammation.4
Underlying Causes of Anemia of Chronic Disease
Associated diseases estimated prevalence
Infections (acute and chronic) 1895 percent
Cancert 3077 percent
Autoimmune 871 percent
Chronic rejection after solid-organ transplantation 870 percent
Chronic kidney disease and inflammation 2350 percent
Acute HBV Infection
IgG anti-HBc Chronic HBV infection / recovery
anti-HBs Immunity against HBV infection
IgG anti-Hbc + anti-Hbs HBV infection passed
IgG anti-Hbc + HbsAg Infeksi kronik HBV
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Diagnosis
Anemia of Chonic Disease is typically mild (Hgb level 8-10) and normocytic, though
microcytosis sometimes occurs. The serum iron level is low in ACD, and this leads some
clinicians to misdiagnose it as iron deficiency. But, in ACD the low iron level reflects inability to
mobilize adequate iron stores from the reticuloendothelial system into the blood, rather than a
deficiency of iron. Body iron stores are actually adequate. A distinguishing feature between iron
deficiency and ACS is that in ACD, low serum iron levels are accompanied by low or low-
normal iron binding capacity (ie, low transferrin level). In iron deficiency, on the other hand, low
serum iron levels are accompanied by high iron binding capacity.
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REFERENCES
1. Guidelines for the Management of Adults with Hospital acquired, Ventilator-associated,and Healthcare-associated Pneumonia (ATS). Am J Respir Critical Care Med Vol 171,
2005:pg 388-416 (www.atsjournals.org)
2. Guidelines for Treatment of tuberculosisFourth edition WHO 2010 : pg 21-453. Pedoman Nasional Tuberkulosis Paru di Indonesia Departemen Kesehatan Republik
Indonesia 2007 : pg 13-33.
4. Guidline Diagnostic Standards and Classification of Tuberculosis in Adults and ChildrenAmerican Thoracic Societv 2000: pg 2 -20.
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