Case report english bagas revisi (Repaired).docx

7/29/2019 Case report english bagas revisi (Repaired).docx

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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


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




MCH (pg) 22,0 2732

MCV (fL) 72,50 7696

MCHC (g/dL) 30,4 2936


Platelet (thousand/ul) 333 150400



Creatinine (mg/dL) 1,99 0,601,3




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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 :



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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


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


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


Laboratory Findings June 14t


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


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




MCH (pg) 24,2 2732

MCV (fL) 80,7 7696

MCHC (g/dL) 30,0 2936


Platelet (thousand/ul) 381 150400



Creatinine (mg/dL) 0,6 0,601,3





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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.



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.


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


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.

5. Comparison between mycobacteria growth indicator tube (MGIT), BACTEC 460 TBsystem and LowensteinJensen Medium for detection of mycobacterium tuberculosis

Egyptian journal bronchology.2002

6. Bakta M. Anemia hipokromik mikrositik . Hematologi klinik ringkas. EGC. 2006. 192-219

7. Guenter Weiss, M.D., and Lawrence T. Goodnough, M.D Anemia of Chronic Disease( NEJM ) 2005 pg 1- 13.

8. Robert s Haliner, Kenneth A Ault, Michael lepotrosier, Henry M Rainder In ClinicalApproach to Anemia Hematology in clinical practice pg 1015.

9. Diagnosis and Monitoring Hepatosellular Injury Manual GastroenterohepatologiLippincott Williams & Wilkins 2002.

10.D. Robert Dufour, John A. Lott FredericS. Nolte, David R. Gretch, Raymond S. Koff,

and Leonard B. Seeff Diagnosis and Monitoring of Hepatic Injury. II.Recommendations

for Use of Laboratory Tests in Screening, Diagnosis, and Monitoring 2000 pg 2050-2068.

11.Colin W. Shepard, Edgar P. Simard, Lyn Finelli, Anthony E. Fiore, and Beth P.

BellHepatitis B Virus Infection: Epidemiology and Vaccination 2006 pg 1- 26.
http://www.atsjournals.org/http://www.atsjournals.org/http://www.atsjournals.org/http://www.atsjournals.org/


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