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 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
1

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 of pulmonary TB. Smear-negative PTB cases should either: A. have sputum that is smear-negative but culture-positive for M. 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

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 <1% of cases result in acute liver failure. The serologic diagnosis of acute hepatitis A is made by a positive IgM antibody test to hepatitis A (IgM anti-HAV) which is detectable as early as 20 days after initial exposure. Hepatitis B is parenterally transmitted. Highrisk groups are persons who are sexually promiscuous, intravenous drug users and patients who have received blood transfusions. Hepatitis B viral DNA (HBV-DNA) is also present in the serum at this time followed by the appearance of the IgM antibody to the core antigen (IgM antiHBc).

Anemia of chronic disease, the anemia that is the second most prevalent after anemia caused by iron deficiency, occurs in patients with acute or chronic immune activation. The condition has thus been termed anemia of inflammation. Underlying Causes of Anemia of Chronic Disease Associated diseases Infections (acute and chronic) Cancert Autoimmune Chronic rejection after solid-organ transplantation Chronic kidney disease and inflammation estimated prevalence 1895 percent 3077 percent 871 percent 870 percent 2350 percent

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 lownormal 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

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/m2 (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 - Pale - Cold

Superior +/+ -/-/-/-/-/+N/+N -/-

Inferior +/+ -/-/-/-/-/+N/+N -/-

- Edema - Clubbing finger - White nail - Eritema palmaris - Physiological reflex - Pathological reflex

Laboratory Result
Laboratory examination Hemoglobine (gr%) Hematocrit (%) RBC (million/ul) MCH (pg) MCV (fL) MCHC (g/dL) WBC (thousand/ul) Platelet (thousand/ul) Glucose /BSL (mg/dl) Ureum (mg/dL) Creatinin (mg/dL) Sodium (mmol/L) Potassium (mmol/L) Chlorida (mmol/L) Calcium (mmol/L) Laboratory Examination Total protein (gr/dl) Albumin (gr/dl) Globulin (gr/dl) Total bilirubin (mg/dl) Direct bilirubin (mg/dl) SGOT (U/l) SGPT (U/l) Alkali phosphatase (U/l) Gamma GT (U/l) June 9 th 2012
7,82 25,2 3,62 21,62 70,52 30,63 23,34 468,4

Reference range 13 16 40 54 4,5 6,5 27 32 76 96 29 36 4 11 150 400 80-110 15 39 0,60 1,3 136 145 3,5 5,1 98 107 2,12 2,52 June 9 th 2012 6.0 2.4 3.60 0.60 0.36 3058 1877 236. 170 Reference range 6,4-8,2 3,4-5,0 2,30-3,50 0,00-1,00 0,00-0,30 15-37 30-65 50,0-136,0 5-85

77 59 1,6 130 5,1 98 2,06

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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looked homogeneous calcification on the basal right lung, It showed blunted right costophrenic sinus.

Chest X Ray June 9 th 2012 Impression Cor Pulmonary : : Cardiomegali (LV, Suspicious LA) Aorta Elongation : Pulmonary oedema Right pleural effusion

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: <1; S in V1 + R in V5: < 35 mm, T wave: inverted T: V1-V3, tall T (-).Rsr' V1-V2 Conclusion : Sinus rhythm, and RBBB incomplete

Color Specific gravity pH Reduction Urobilinogen Acetone Protein

clouded yellow 1,030 5,5

Negative

0,2 mg/dl Negative

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Urine analysis results Epitel sediment Erythrocytes sediment Leukocyte sediment RBC casts WBC casts Cast granule
Bacteria

Negative 1-2 /high powered field 0-1 /high powered field Negative Negative Negative
Negative

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
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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 Hemoglobine (gr%) Hematocrit (%) RBC (million/ul) MCH (pg) MCV (fL) MCHC (g/dL) WBC (thousand/ul) Platelet (thousand/ul) Glucose /BSL (mg/dl) Ureum (mg/dL) Creatinine (mg/dL) Sodium (mmol/L) Potassium (mmol/L) June 12th 2012
8,85 29,1 4,02 22,0 72,50 30,4 11,2

Reference range 13 16 40 54 4,5 6,5 27 32 76 96 29 36 4 11 150 400 80-110 15 39 0,60 1,3 136 145 3,5 5,1
9

333 77 122 1,99 138 4,5

Chlorida (mmol/L)

100

98 107

ESR 1 Jam (mm) ESR 2 Jam (mm) Fe serum (ug/dl) TIBC (ug/dl) Ferritin (ug/dl)

39.0 75.0

1,0 10 50 175 250 450 70 435

11 207 74,67

Differential count

Eosinophils 0%, Basophils 0%, Stab neutrophils 1%, Segmented neutrophils 87%, Lymphocytes 8%, Monocytes 3%, Myelosit 1 %

Peripheral blood smear Erythrocytes Normocytic, mild poikilocytosis (tear drop cell, eliptosit cell, Normal in number and shape Platelets Leukocytes Increased in number, neutrophilia +, toxic granulation +

Gram Staining Negative rod gram bacili Streptococcus (+) Gram diplococcus (+) Positive Positive Positive

Ziehl Nielsen Staining Acid Fast Bacili Leukocytes Negative > 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 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 Ht Leukocyte Platelet Ureum : 8,30 g/dl : 29,4 % : 10.800 /mm3 : 436.000 /mm : 71 mg/dl
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3

Creatinine Sodium Potassium Chloride

: 1,40 mg/dl : 143 mmol/l : 4,8 mmol/l : 107 mmol/l

Laboratory Findings Total protein (gr/dl) Albumin (gr/dl) Globulin (gr/dl) SGOT (U/l) SGPT (U/l) Fosfatase Alkali (U/l) Gamma GT (U/l)

June 14th 2012 5.3 2.6 2,7 42 212 93 652

Reference range 6,4-8,2 3,4-5,0 2,30-3,50 15-37 30-65 50,0-136,0 5-85

Laboratory Findings HBsAg Anti HBc Total Anti HCV IGM Anti HAV

June 14th 2012 0,00 (Negative) Positive 0,08 0,09 (Negiative)

Reference range Negative Negative Negative 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

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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. Laboratory examination Hemoglobine (gr%) Hematocrit (%) RBC (million/ul) MCH (pg) MCV (fL) MCHC (g/dL) WBC (thousand/ul) Platelet (thousand/ul) Glucose /BSL (mg/dl) Ureum (mg/dL) Creatinine (mg/dL) Sodium (mmol/L) Potassium (mmol/L) Chlorida (mmol/L) Gram Staining Negative rod gram bacili Streptococcus (+) Gram diplococcus (+) Positive Positive Positive July 8th 2012
10,4 34,7 4,3 24,2 80,7 30,0 10,5

Reference range 13 16 40 54 4,5 6,5 27 32 76 96 29 36 4 11 150 400 80-110 15 39 0,60 1,3 136 145 3,5 5,1 98 107

381 110 11 0,6 132 3,8 100

Ziehl Nielsen Staining Acid Fast Bacili Leukocytes Negative > 25/LPK

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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.

. 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
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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. August 14 th 2012 22 34 15 37 U/l 30 65 U/l

Laboratory examination SGOT SGPT

Reference range

Bronchoscopy : - Results : Inflammation MGIT culture : Positive . Evaluation Treatment : Pulmonary Tuberculosis. : 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.

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

Pulmonary Infiltrates DD/-Hospital Acquired Pneumonia -Pulmonary Tuberculosis

Hepatocellular injury DD/ Hepatitis akut Hepatitis Ischaemic

Hypochromic Microcytic Anemia DD/ Anemia of chronic diseases Anemia defisiensi Fe

Hepatocellular injury with a false positive Anti HBc

Anemia of chronic diseases

Pulmonary Tuberculosis

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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 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. 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
18

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 of pulmonary TB. Smear-negative PTB cases should either: A. have sputum that is smear-negative but culture-positive for M. 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 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 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 <1% of cases result in acute liver failure. The serologic diagnosis of acute hepatitis A is made by a positive IgM antibody test to hepatitis A (IgM anti-HAV) which is detectable as early as 20 days after initial exposure. Hepatitis B is parenterally transmitted. High-risk groups are persons who are sexually promiscuous, intravenous drug users and patients who have received blood transfusions. Hepatitis B viral DNA (HBV-DNA) is also present in the serum at this time followed by the appearance of the IgM antibody to the core antigen (IgM anti-HBc). 3 Interpretation of Hepatitis B Serology Test Results

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HBsAg anti-HBc anti-HBs

negative positive negative

Interpretation unclear; four possibilities: 1. Resolved infection (most common) 2. False-positive anti-HBc, thus suscep 3. Low level chronic infection 4. Resolving acute infection

Acute HBV Infection

IgG anti-HBc anti-HBs Chronic HBV infection / recovery Immunity against HBV infection

IgG anti-Hbc + anti-Hbs

HBV infection passed

IgG anti-Hbc + HbsAg

Infeksi kronik HBV

Anemia of chronic disease, the anemia that is the second most prevalent after anemia 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 Infections (acute and chronic) Cancert Autoimmune Chronic rejection after solid-organ transplantation Chronic kidney disease and inflammation

estimated prevalence 1895 percent 3077 percent 871 percent 870 percent 2350 percent

21

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 lownormal 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 tuberculosis Fourth edition WHO 2010 : pg 21-45 3. 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 Children American Thoracic Societv 2000: pg 2 -20. 5. Comparison between mycobacteria growth indicator tube (MGIT), BACTEC 460 TB system and Lowenstein Jensen Medium for detection of mycobacterium tuberculosis Egyptian journal bronchology.2002 6. Bakta M. Anemia hipokromik mikrositik . Hematologi klinik ringkas. EGC. 2006. 192219 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 Clinical Approach to Anemia Hematology in clinical practice pg 10 15. 9. Diagnosis and Monitoring Hepatosellular Injury Manual Gastroenterohepatologi Lippincott 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.

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