Case Report

Kepada Yth.
Acute lymphoblastic Leukemia FAB L1
Presenter

: Fitra Ali Alatas

Andri Winata S.

Day/Date

: April 22nd 2014

Supervisor

: dr. Hj. Tiangsa Br Sembiring, Sp.A(K)

Introduction
Acute leukemia is defined as a malignant disease of blood cells derived from
bone marrow, characterized by proliferation of white blood cells, with the
manifestation of abnormal cells in the peripheral blood. Proliferating blood leukocytes
in an irregular manner, uncontrolled and function becomes abnormal. Therefore the
process, other functions of normal blood cells also disrupted to cause the symptoms of
leukemia.1
Leukemia is classified based on the type of cells, both in cell maturity and cell
lineage. Based on the maturity of cells, divided into acute and chronic leukemia. If
malignant cells are mostly immature (blast) then classified acute leukemia, while if
the dominant is a mature cell then classified as chronic leukemia.2
In this case report, we want to explain about Acute Lymphoblastic Leukemia
one of two types acute leukemia which one of them is Acute myeloblastic leukemia.
The incidence Acute Lymphoblastic Leukemia (ALL) 82% more than Acute
myeloblastic leukemia (AML) 18%, and under reported that the proportion of male
patients is greater than in women. Acute Lymphoblastic Leukemia is a cancer that
often occurs in children and new cases per year occur by about 3000 in the U.S., 5000
in Europe and an estimated 2000-3000 cases in Indonesian.3
Classification Acute Lymphoblastic Leukemia can be performed based on
morphological or immunological markers, groups of French-American-British (FAB)
divided Acute Lymphoblastic Leukemia into three types subclassification.
1. FAB-L1: Small cells with homogeneous nuclear chromatin, a regular nuclear
shape, small or no nucleoli, scanty cytoplasm, and mild to moderate basophilia
2. FAB-L2: Large, heterogeneous cells with variable nuclear chromatin, an irregular
nuclear shape, 1 or more nucleoli, a variable amount of cytoplasm, and variable
basophilia

3. FAB-L3: Large, homogeneous cells with fine, stippled chromatin; regular nuclei;
prominent nucleoli; and abundant, deeply basophilic cytoplasm. The most
distinguishing feature is prominent cytoplasmic vacuolation.6
The following tests and procedures may be used to diagnose Acute
Lymphoblastic Leukemia and find out if leukemia cells have spread to other parts of
the body such as the brain or testicles.4
Physical exam for checking signs of disease, such as lumps or anything else
that seems unusual. A history of the patient's health habits and past illnesses and
treatments will also be taken.4
In the physical exam we can find out, fever, signs and symptoms of anemia,
palpable lymphadenopathy, rashes from skin infiltration with leukemic cells, mild
hepatomegaly may be found and left upper quadrant fullness and early satiety due to
splenemegaly (about 10-20% of cases).5
Bleeding manifestations are most often found in the form of petechiae,
purpura or ecchymosis, which occurs in 40-70% of patients with acute leukemia at the
time of diagnosis. The most frequent site of bleeding is to the skin, eyes, mucosal
membranes of the nose, gingival and gastrointestinal tract..2
Diagnosis Acute Lymphoblastic Leukemia is made by examination of bone
marrow aspiration, from bone marrow we can obtained component containing 30% of
immature cells (blast).7
Examination from peripheral blood smear in patient Acute Lymphoblastic
Leukemia from obtained normochromic normocytic anemia, sometimes can be found
normoblas. In counts type limfoblas, limfoblas number can be up to 100,
thrombocytopenia was also found.3
Treatment for Acute Lymphoblastic Leukemia can be classified into two type,
specific therapy, in the form of chemotherapy and supportive therapy, to treat bone
marrow failure, either because of the leukemia itself or as a result of therapy.8 And we
will explain on the next page.
Acute leukemia is a leukemia with rapid clinical manifestation, and for own
prognosis Acute Lymphoblastic Leukemia without treatment, the patient can be died
within an average of 3-4 months. However, it turns out with good treatment of acute
leukemia were cured more than chronic leukemia.8

Objective
1. Reported a case of men aged 17 years with a diagnosis of Acute Lymphoblastic
Leukemia
2. Explaining about the symptoms, signs and clinical manifestation of Acute
Lymphoblastic Leukemia
3. Explaining the stages of Acute Lymphoblastic Leukemia and its treatment.
4. Explaining the prognosis of Acute Lymphoblastic Leukemia.
The aim of this paper is to report a case Acute Lymphoblastic Leukemia in a 17
years old male.
Case
JY, male, 17 years, Indonesian, admitted to H. Adam Malik hospital, on 25 March
2014 to continue chemotherapy, patient is former patient division hemato-oncology
with a diagnosis of acute lymphoblastic leukemia FAB L1 phase Induction and getting
chemotherapy, os before coming to the Hospital H. Adam Malik on 13 February 2014
referenced from Sinar Husni hospital with diagnosis blood disorders. From anamnesis
have found of bleeding in the gums frequently during the night and pale lips, bleeding
already experienced approximately 2 months, pallor, difficulty swallowing on 2 days
ago, found headache, os also have a fever with chills, dont have history of recurrent
fever, night sweats tend intermittent and on his right elbow also found red spots
experienced one day in the past. On 19 February 2014, conducted Bone Marrow
Aspiration and concluded in bone marrow showed cells limfoblast >25% and other
systems hypoplasia, impression Acute Lymphoblastic Leukemia FAB L1.
Physical examination
Consciousness was clear, body weight (BW): 48 kg, body length (BL): 155 cm, body
temperature: 36,9 0C. General condition were moderate, and nutritional status was
mild malnutrition.
Head

: Eyes Light reflexes (+/+), pupils were isochoric

No pale on lower eyelid conjunctives and lips. Ears and nose were
normal

Neck

: Lymph nodes enlargement was not found

Chest

: Symmetrical fusiform, no retraction

HR : 90 bpm, regular, no murmur
RR : 20 tpm, regular, no rales

Abdomen

: Soepel, peristaltic normal, liver and spleen were not palpable

Extremities

: Pulse : 90 bpm, regular, P/V was good. CRT <3

Laboratory finding on March 25th 2014:

Hemoglobin 9.50 gr/dL, Hematocrite 27.80%, Leucocytes 8.58x10 3/mm3, Platelet 12
x103/mm3. SGPT 15 U/L. SGPT 33 U/L. ALP 91 U/L. Ureum 33,70 mg/dl. Kreatinin
0.80 mg/dl
Working Diagnosis: Acute lymphoblastic leukemia FAB L1 phase Induction
Therapy :
-

Cotrimoxazole 2x480 mg
Plain Chemotherapy
o IT MTX 12 mg
o Vincristine 1,5 mg/m2 = 2.04 mg
o Doxorubicin 20 mg/m2 = 27.3 mg
Diet Mb 2060 kkal + 96 gr protein
Platelet transfusion 5 units

Follow up on March 26th2014

S
O

: Fever (-), Pale (-), Bleeding (-)

: Sens : CM
T : 37 C

Head

BW: 48 kg

BSA: 1,36 m2

: Eyes Light reflexes (+/+), pupils were isochoric

No pale on lower eyelid conjunctives and lips. Ears and nose were normal

Neck

: Lymph nodes enlargement was not found

Chest

: Symmetrical fusiform, no retraction

HR : 80 bpm, regular, no murmur
RR : 20 tpm, regular, no rales

Abdomen

: Soepel, peristaltic normal, liver and spleen were not palpable

Extremities

: Pulse : 80 bpm, regular, P/V was good. CRT <3, petechiae +/+ on

the upper arm

: Acute lymphoblastic leukemia FAB L1 phase Induction
:

A
P

Cotrimoxazole 2x480 mg
Dexamethason 2-2-1
Transfusion PRC I 175 cc
Diet Mb 2060 kkal + 96 gr protein

Plain Chemotherapy
o IT MTX 12 mg
o Vincristine 1,5 mg/m2 = 2.04 mg
o Doxorubicin 20 mg/m2 = 27.3 mg
Laboratory finding on March 26th 2014:
Hemoglobin 7.90 gr/dL, Hematocrite 23.60%, Leucocytes 4.17x10 3/mm3, Platelet 30
x103/mm3.
Follow up on March 27th2014
S
O

: Fever (-), Pale (-), Bleeding (-)

: Sens : CM
T : 37 C

Head

BW: 48 kg

BSA: 1,36 m2

: Eyes Light reflexes (+/+), pupils were isochoric

No pale on lower eyelid conjunctives and lips. Ears and nose were normal

Neck

: Lymph nodes enlargement was not found

Chest

: Symmetrical fusiform, no retraction

HR : 82 bpm, regular, no murmur
RR : 24 tpm, regular, no rales

Abdomen

: Soepel, peristaltic normal, liver and spleen were not palpable

Extremities

: Pulse : 80 bpm, regular, P/V was good. CRT <3, petechiae +/+ on

the upper arm

: Acute lymphoblastic leukemia FAB L1 phase Induction
:

A
P

Cotrimoxazole 2x480 mg
Dexamethason 2-2-1
Transfusion PRC II 200 cc
Diet Mb 2060 kkal + 96 gr protein
Plain Chemotherapy
o IT MTX 12 mg
o Vincristine 1,5 mg/m2 = 2.04 mg
o Doxorubicin 20 mg/m2 = 27.3 mg

Follow up on March 28th 2014

S
O
Head

: Fever (-), Pale (-), Nousea (-)

: Sens : CM
T : 36.8 C

BW: 48 kg

BSA: 1,36 m2

: Eyes Light reflexes (+/+), pupils were isochoric

No pale on lower eyelid conjunctives and lips. Ears and nose were normal

Neck

: Lymph nodes enlargement was not found

Chest

: Symmetrical fusiform, no retraction

HR : 82 bpm, regular, no murmur

RR : 24 tpm, regular, no rales
Abdomen

: Soepel, peristaltic normal, liver and spleen were not palpable

Extremities

: Pulse : 80 bpm, regular, P/V was good. CRT <3, petechiae +/+ on

the upper arm

: Acute lymphoblastic leukemia FAB L1 phase Induction
:

A
P

Cotrimoxazole 2x480 mg
Dexamethason 2-2-1
Transfusion PRC III 250 cc
Diet Mb 2060 kkal + 96 gr protein
Plain Chemotherapy
o IT MTX 12 mg
o Vincristine 1,5 mg/m2 = 2.04 mg
o Doxorubicin 20 mg/m2 = 27.3 mg

Follow up on March 29th 2014

S
O

: Fever (-), Pale (-)

: Sens : CM

Head

T : 37.2 C

BW: 48 kg

BSA: 1,36 m2

: Eyes Light reflexes (+/+), pupils were isochoric

No pale on lower eyelid conjunctives and lips. Ears and nose were normal

Neck

: Lymph nodes enlargement was not found

Chest

: Symmetrical fusiform, no retraction

HR : 82 bpm, regular, no murmur
RR : 24 tpm, regular, no rales

Abdomen

: Soepel, peristaltic normal, liver and spleen were not palpable

Extremities

: Pulse : 80 bpm, regular, P/V was good. CRT <3, petechiae +/+ on

the upper arm

: Acute lymphoblastic leukemia FAB L1 phase Induction
:

A
P

Cotrimoxazole 2x480 mg
Dexamethason 2-2-1
Diet Mb 2060 kkal + 96 gr protein
Plain Chemotherapy
o IT MTX 12 mg
o Vincristine 1,5 mg/m2 = 2.04 mg
o Doxorubicin 20 mg/m2 = 27.3 mg

Laboratory finding on March 29th 2014:

Hemoglobin 12.30 gr/dL, Hematocrite 34.2%, Leucocytes 4.63x103/mm3, Platelet
19x103/mm3.
Follow up on March 30th 2014
S
O

: Fever (-), Pale (-), Nousea (-)

: Sens : CM
T : 36.7 C

Head

BW: 48 kg

BSA: 1,36 m2

: Eyes Light reflexes (+/+), pupils were isochoric

No pale on lower eyelid conjunctives and lips. Ears and nose were normal

Neck

: Lymph nodes enlargement was not found

Chest

: Symmetrical fusiform, no retraction

HR : 82 bpm, regular, no murmur
RR : 24 tpm, regular, no rales

Abdomen

: Soepel, peristaltic normal, liver and spleen were not palpable

Extremities

: Pulse : 80 bpm, regular, P/V was good. CRT <3, petechiae +/+ on

the upper arm

: Acute lymphoblastic leukemia FAB L1 phase Induction
:

A
P

Inj. Vincristine 1,5 mg/m2 = 2.04 mg

Inj. Doxorubicin 20 mg/m2 = 27.3 mg 20 gtt/i micro, finished within 24 hours (started

date 30-3-2014, 12.00 am- ended date 31-3-2014, 12.00 am)

Cotrimoxazole 2x480 mg
Dexamethason 2-2-1
Diet Mb 2060 kkal + 96 gr protein

Laboratory finding on March 30th 2014:

Hemoglobin 12.4 gr/dL, Hematocrite 35.5%, Leucocytes 5.60x103/mm3, Platelet 21
x103/mm3.
Follow up on March 31th 2014
S
O
Head

: Fever (-), Pale (-), Nousea (-)

: Sens : CM
T : 36.7 C

BW: 48 kg

BSA: 1,36 m2

: Eyes Light reflexes (+/+), pupils were isochoric

No pale on lower eyelid conjunctives and lips. Ears and nose were normal

Neck

: Lymph nodes enlargement was not found

Chest

: Symmetrical fusiform, no retraction

HR : 82 bpm, regular, no murmur
RR : 24 tpm, regular, no rales

Abdomen

: Soepel, peristaltic normal, liver and spleen were not palpable

Extremities

: Pulse : 80 bpm, regular, P/V was good. CRT <3, petechiae +/+ on

the upper arm

: Acute lymphoblastic leukemia FAB L1 phase Induction
:

A
P

Inj. Doxorubicin 20 mg/m2 = 27.3 mg 20 gtt/i micro, finished within 24 hours (started

date 30-3-2014, 12.00 am- ended date 31-3-2014, 12.00 am)

Cotrimoxazole 2x480 mg
Dexamethason 2-2-1
Diet Mb 2060 kkal + 96 gr protein

Discussion
Acute Lymphoblastic Leukemia is a cancer that often occurs in children and
under reported that the proportion of male patients is greater than in women. 3 In a
healthy child, the bone marrow makes blood stem cells (immature cells) that become
mature blood cells over time. A blood stem cell may become a myeloid stem cell or a
lymphoid stem cell.
A myeloid stem cell becomes one of three types of mature blood cells:
1. Red blood cells that carry oxygen and other substances to all tissues of the
body.
2. Platelets that form blood clots to stop bleeding.
3. White blood cells that fight infection and disease.
A lymphoid stem cell becomes a lymphoblast cell and then one of three types
of lymphocytes (white blood cells):
1. B lymphocytes that make antibodies to help fight infection.
2. T lymphocytes that help B lymphocytes make the antibodies that help fight
infection.
3. Natural killer cells that attack cancer cells and viruses.

In a child with Acute Lymphoblastic Leukemia, too many stem cells become
lymphoblasts, B lymphocytes, or T lymphocytes. These cells are cancer (leukemia)
cells. The leukemia cells do not work like normal lymphocytes and are not able to
fight infection very well. Also, as the number of leukemia cells increases in the blood
and bone marrow, there is less room for healthy white blood cells, red blood cells, and
platelets. This may lead to infection, anemia, and easy bleeding.4
Risk factor Acute Lymphoblastic Leukemia is anything that increases your
risk of getting a disease but having a risk factor does not mean that you will get
cancer and not having risk factors doesnt mean that you will not get cancer.
Possible risk factors for Acute Lymphoblastic Leukemia include the following:
1.
2.
3.
4.

Being exposed to x-rays before birth.

Being exposed to radiation.
Past treatment with chemotherapy.
Having certain changes in the genes.

Having certain genetic conditions, such as:

1.
2.
3.
4.
5.

Down syndrome.
Neurofibromatosis type 1 (NF1).
Shwachman syndrome.
Bloom syndrome.
Ataxia-telangiectasia.4

Sign and symptom in physical exam we can find out, fever, signs and
symptoms of anemia, palpable lymphadenopathy, rashes from skin infiltration with
leukemic cells, mild hepatomegaly may be found and left upper quadrant fullness and
early satiety due to splenemegaly (about 10-20% of cases).5
Bleeding manifestations are most often found in the form of petechiae,
purpura or ecchymosis, which occurs in 40-70% of patients with acute leukemia at the
time of diagnosis. The most frequent site of bleeding is to the skin, eyes, mucosal
membranes of the nose, gingival and gastrointestinal tract..2
Diagnosis is based Bone marrow aspiration/biopsy, The removal of bone
marrow and a small piece of bone by inserting a hollow needle into the hipbone or
breastbone. A pathologist views the bone marrow and bone under a microscope to
look for signs of cancer.4

Lumbar puncture

Lumbar puncture may also be done, a procedure used to collect a sample of

cerebrospinal fluid from the spinal column. This is done by Placing a needle into the
spinal column. The sample of fluid is checked for leukemia cells. This procedure is
also called an LP or spinal tap.

This procedure is done after Leukemia is diagnosed to find out if leukemia

cells have spread to the brain and spinal cord. Intrathecal chemotherapy is given after
the sample of fluid is removed to treat any leukemia cells that may have spread to the
brain and spinal cord.4
The treatment of childhood Acute Lymphoblastic Leukemia is done in phases:
1. Remission induction: This is the first phase of treatment. The goal is to kill the
leukemia cells in the blood and bone marrow. This puts the leukemia into
remission.
2. Consolidation / intensification: This is the second phase of treatment. It begins
once the leukemia is in remission. The goal of consolidation / intensification
therapy is to kill any leukemia cells that remain in the body and may cause a
relapse.
3. Maintenance: This is the third phase of treatment. The goal is to kill any
remaining leukemia cells that may regrow and cause a relapse. Often the cancer
treatments are given in lower doses than those used during the remission induction
and consolidation / intensification phases. Not taking medication as ordered by the
doctor during maintenance therapy increases the chance the cancer will come
back. This is also called the continuation therapy phase. 4

Treatment for Acute Lymphoblastic Leukemia can be classified into two type,
specific therapy, in the form of chemotherapy and supportive therapy, to treat bone
marrow failure, either because of the leukemia itself or as a result of therapy.8
Stage of chemotherapy treatment consists of:
1. Remission induction phase form of intensive chemotherapy to achieve remission,
ie a state where the clinical symptoms disappeared, accompanied by a blast in the
bone marrow is less than 5%. Morphologic examination can not dijumpain
leukemia cells in the bone marrow and peripheral blood.
2. Phases posttremisi a phase of treatment to maintain remission as long as possible,
which in turn will lead to a cure. this is achieved by:
a. Continued chemotherapy, consisting of:
- Consolidation therapy
- Maintenance therapy
- Late intensification
b. Bone marrow transplant: a consolidation therapy that provides a permanent
cure in some patients, especially patients aged under 40 years.8
Chemotherapy for all the most basic consists of an alloy of drugs (regimens):
1. Induction of remission:
1) Drugs in use consists of:
o vincristine (VCR)
1.5 mg/m2 / week
o prednisone (Pred)
6 mg/m2/day, oral
o L asparaginase (L asp)
10.000 U/m2
o daunorubicin
25 mg/m2/week 4 week
2) Regimens for ALL with standard risk consists of:
o Prednisone + VCR.
o Prednisone + VCR + L asp.
3) Regimen for all high-risk or ALL in adults include:
o Pred + VCR + DNR + with or without L asp.
o Group GIMEMA from Italian gives DNR + VCR + pred + L asp with
or without cyclophosphamide.8

2. Postremisi therapy
a. therapy for santuary phase (eradicate leukemia cells hide in the CNS and
testes)
o IT triple consisting of: intrahecal methotrexate (MTX) ara C (cytosine
arabinoside), and dexamenthason
o Cranial radiotherapy (CTR)

b. Intensive therapy / consolidation noncrossresistent regimen on remission

induction regimen
c. Maintenance therapy (maintenance) commonly used 6 mercaptopurine (6
MP) and MTX orally every week. given for 2-3 years with interspersed
consolidation or intensification therapy.8
Suporatif therapy in patients with leukemia is important, with the specific therapy
it will determine the success rate of therapy . Chemotherapy intensive should be
supported by intensive supportive therapy , if not then the patient may die from the
side effects of the drug , an iatrogenic death. Supportive therapy serves to overcome
the effects caused of by leukemia itself and also to overcome the side effects of the
drug . Supportive therapy be given are:
1. Therapies to treat anemia : PRC transfusion to maintain hemoglobin around
9-10 g/dl . for potential bone marrow transplant , blood transfusion should be
avoided .
2. Therapies to treat the infection , the same as in the case of aplastic anemia
consists of:
a. Adequate antibiotic
b. Transfusion of granulocyte concentrates
c. Special care (Isolation)
d. hemopietic growth factor ( G - CSF or GM - CSF )
3. Therapies to treat bleeding consists of :
a. Platelet transfusions to maintain platelet concentrates 10x10/ml
minimum, ideally above 20x20/ml .
b. In M3 given heparin for DIC overcome
4. Therapies to address other things, that
a. Management leukostasis: performed with intravenous hydration and
leukapheresis. immediately do the induction of remission to decrease the
number of leukocytes.
b. Management of syndrome lysis: with adequate hydration, administration
of allopurinol and alkalinization of urine.
Prognosis of patients with acute leukemia are very varied and individualistic, and
results for treatment of Acute Lymphoblastic Leukemia is excellent, with intensive
therapy achieved a cure in 70-90% cases in children with Acute Lymphoblastic
Leukemia and 40-50% cases in adult with Acute Lymphoblastic Leukemia, but at the
age of over 65 years the result is dropped to 5% .8

Conclusion
This paper reports a case of a 17 years old male diagnosed with Acute
Lymphoblastic Leukemia. A comprehensive work up had been done to confirm the
diagnosis.

References
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hematologi onkologi anak. First Edition. IDAI: 2005.h.236-47.
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Andalas. 2012.
3. Pinontoan, Eunike, etc. Pengaruh Kemoterapi Terhadap Profil Hematologi pada
Penderita Leukemia Limfoblastik Akut, Jurnal Unsrat Vol.1. 2013.

4. Childhood

Acute

Lymphoblastic

Leukemia

Treatment.

Acces

from:

http://www.cancer.gov/cancertopics/pdq/treatment/childALL/Patient/page1
5. Seiter, Karen, etc. Acute Lymphoblastic Leukemia. Acces from:
http://emedicine.medscape.com/article/207631-overview
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Sari Pediatri, Vol.12, No.2, August 2010.
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