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An 8 year old boy has acute lymphoblastic leukemia (ALL). What info from his CBC show that he has (ALL).

hematocrit = 36%
hemoglobin = 8 g/dL
RBC count = 2.5 x 10 to the sixth power/ uL
WBC count = 20,000/ uL
Neutrophil count = 7,500/ uL
Basophil count= 200/ uL
Eosinophil count= 400/ uL
Monocyte count= 1,800/ uL
Lymphocyte count= 4,700/ uL
Platelet count= 15,000/ uL
Lymphoblast count= 46% of marrow cells

Answer 1

just look at the values that aren't normal
another thing to look at in ALL is the size of the WBC, they'll be VERY large

hematocrit is very low at 36%, normal should be between 42-48% depending on if you're a male or female

hemoglobin is very low at 8g/dL, normal is about 12-15 depending on if you're male of female

WBC count is very high, normal amount is about 12,000
neutrophil count should be 65% of WBC count or about 7500
basophil count should be <1% of WBC count or about 200
eosinophil count should be 4% of WBC count or about 400
monocyte count should be 6% of WBC count or about 700, so THAT is VERY HIGH at 1,800
lymphocyte count should be 25% of WBC count or about 3000 so that is VERY HIGH at 4,700

platelet count should be about 150,000-300,000 so it's VERY LOW

Answer 2

I'm by no means an expert but due to a childhood leukemia I learned that in cases of leukemia the tell all is a low platelet count and a high white blood cell count. In the above example, the platelet count is 15,000 which below the normal counts of 200,000 to 400,000. At the same time, the white cell count is 20,000 when the norm should be between 4,300 and 10,800. A low platelet count indicates that one of two things: platelets are being destroyed after production in the bone marrow or that they are not being produced in the bone marrow. High white cell counts indicate that there is an infection in the body or that they are being produced at abnormal amounts. In this case, the first step would be to perform a bone marrow biopsy to determine what is happening at the root of blood cell production process. I'm not a physician by any means, but I speak as person who battled illness for 7 years and has been in remission for almost 10. Eventually, you pick up a thing or two. Hope this helps!

Answer 3

Acute Lymphoblastic Leukemia Cbc

Answer 4

The only requirement for a leukemia to be classified as acute is that there should be more than 30% blasts in the bone marroe, if u look at the last line it says
Lymphoblast count= 46% of marrow cells
so this leukemia is acute, now acute leukemias are of 2 types lymphoblastic or myeloblastic, depending on whether the blasts are lymphoid or myeloid,in this case Lymphoblast count is raised, hence this Leukemia is Acute Lymphoblastic Leukemia

Answer 5

I don't have anything new to add, just a few excerpts from some reputable sources that may help.

From emedicine --Acute Lymphoblastic Leukemia
(written by 2 MDs, last updated 2006)
http://www.emedicine.com/ped/topic2587.htm
"Lab Studies:

Basic laboratory tests
On initial evaluation, obtain a CBC. A hematologist or hematopathologist must evaluate the peripheral smear for the presence and morphology of lymphoblasts. An elevated leukocyte count of >10 X 109/L (>10 X 103/µL) occurs in one half of patients with ALL. The degree of leukocytic elevation (blasts) at diagnosis remains the most important predictor of the patient's prognosis. Neutropenia, anemia, and thrombocytopenia may be observed secondary to inhibition of normal hematopoiesis by leukemic infiltration. Rare cases of ALL may initially manifest with pancytopenia.
Various metabolic abnormalities may include increased serum levels of uric acid, potassium, phosphorus, and calcium, and lactate dehydrogenase (LDH). The degree of abnormality reflects the leukemic cell burden and destruction (lysis). Although not universally performed, coagulation studies can be helpful, including tests of the prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen level, and D-dimer level to assess for disseminated intravascular coagulation; these studies are particularly important in a child who is acutely toxic.
Immunophenotyping
Complete morphologic, immunologic, and genetic examination of the bone marrow is necessary to establish the diagnosis of ALL.
An important advancement in the classification of ALL was the observation that malignant lymphoblasts share many of the features of normal lymphoid progenitors. ALL cells rearrange their immunoglobulin and T-cell receptor (TCR) genes and express antigen receptor molecules in ways that correspond to such processes in normal developing B and T lymphocytes. However, lymphoblasts can also have aberrant gene expression with resultant phenotypes that differ from those of normal lymphocyte progenitors. Nevertheless, ALL can be classified broadly as B- or T-lineage ALL.
The diagnosis of B-cell leukemia, which accounts for only about 3% of ALLs, depends on the detection of surface immunoglobulin on leukemic blasts. Lymphoblasts with this phenotype have a distinctive morphology, with deeply basophilic cytoplasm containing prominent vacuoles. This morphologic pattern is designated L3 in the French-American-British (FAB) system (see Histologic Findings below). Prominent clinical features include extramedullary lymphomatous masses in the abdomen or head and neck and frequent involve the CNS.
Approximately 80% of childhood ALLs involve lymphoblasts with phenotypes that correspond to those of B-cell progenitors. These cases can be identified by their cell-surface expression of 2 or more B-lineage–associated antigens, ie, CD19, CD20, CD24, CD22, CD21, or CD79. Only CD79 is specific for B-lineage ALL. In addition, about one fourth of B-cell precursor cases express cytoplasmic immunoglobulin µ heavy-chain proteins and are designated pre–B-cell ALL. Cases related to B-cell precursors can be subclassified as early pre–B-cell, pre–B-cell, or transitional pre–B-cell cases. Although mature B-cell ALL should be differentiated from B-precursor cases, distinguishing the subtypes of B-precursor ALL is probably not clinically relevant.
T-cell ALL is identified by the expression of T-cell–associated surface antigens, of which cytoplasmic CD3 is specific. T-cell ALL cases can be classified by early, mid, or late thymocytes. Clinical features most closely associated with T-cell ALL are high blood leukocyte counts and CNS involvement. About one half of patients have a mediastinal mass at the time of diagnosis. The prognosis of patients with T-cell ALL has historically been worse than that of patients with B-lineage ALL. However, the outlook for patients with T-cell leukemia appears to improve with intensive chemotherapy."

The following information comes from an online medical book
(which is only available by subscription, it is not free on the internet)..Chapter 91-Acute Lymphoblastic Leukemia [from
Williams Hematology, 7th edition]

"Laboratory Features
Anemia, neutropenia, and thrombocytopenia are common in patients with newly diagnosed ALL. The severity reflects the degree of marrow replacement by leukemic lymphoblasts (Table 91-3).59,60,61,62,63,64 Presenting leukocyte counts range widely, from 0.1 to 1500 x 109/liter (median 10–12 x 109/liter). Hyperleukocytosis (>100 x 109/liter) is seen in 10 to 16 percent of patients. Profound neutropenia (<0.5 x 109/liter) is found in 20 to 40 percent of patients, rendering them at high risk for infection. Most patients have circulating leukemic blast cells. Hypereosinophilia, generally reactive, may precede the diagnosis of ALL by several months.70 Some patients, principally male, have ALL with the t(5;14)(q31;q32) chromosomal abnormality and a hypereosinophilic syndrome (pulmonary infiltration, cardiomegaly, and congestive heart failure). These patients often do not have circulating leukemic blasts or other cytopenias and have a relatively low percentage of blasts in the bone marrow.71 Activation of the interleukin-3 gene on chromosome 5 by the enhancer element of the immunoglobulin heavy-chain gene on chromosome 14 is thought to play a central role in leukemogenesis and the associated eosinophilia in these cases.71 In patients with anemia, a strong inverse relationship exists between the hemoglobin level and age at diagnosis.62 Occasionally, a child with ALL has a hemoglobin level as low as 1 g/dl.

Table 91–3. Presenting Laboratory Features in Children and Adults with Acute Lymphoblastic Leukemia

Decreased platelet counts often are seen at diagnosis (median, 48–52 x 109/liter). This finding differs from immune thrombocytopenia because the decreased platelet counts almost always are accompanied by anemia, leukocyte abnormalities, or both.72 Severe bleeding is uncommon, even when platelet counts are as low as 20 x 109/liter, provided infection and fever are absent.73 Occasional patients, principally male, present with thrombocytosis (>400 x 109/liter).74 Pancytopenia followed by a period of spontaneous hematopoietic recovery may precede the diagnosis of ALL in rare cases.75 Coagulopathy, usually mild, can be seen in 3 to 5 percent of patients, most of whom have T cell ALL, and is only rarely associated with clinical bleeding.63,76 The level of serum lactate dehydrogenase is increased in most patients with ALL and is well correlated with the size of the leukemic infiltrate.77 Increased levels of serum uric acid are common in patients with a large leukemic cell burden, a finding that reflects an increased rate of purine catabolism. Patients with massive renal involvement can have increased levels of creatinine, urea nitrogen, uric acid, and phosphorus. Occasionally, patients with T cell ALL present with acute renal failure, despite a relatively small leukemic infiltrate.78 Rarely, patients present with hypercalcemia resulting from release of parathyroid hormone-like protein from lymphoblasts and leukemic infiltration of bone.79 Liver dysfunction as a result of leukemic infiltration occurs in 10 to 20 percent of patients, usually is mild, and has no important clinical or prognostic consequences.59 Serum immunoglobulin levels (mostly IgA and IgM classes) are modestly decreased in approximately one third of children with ALL. The reduction reflects the decreased number and impaired function of normal lymphocytes.80 Urinalysis may show microscopic hematuria and the presence of uric acid crystals.

Chest radiography is needed to detect enlargement of the thymus or mediastinal nodes, with or without pleural effusion (see Fig. 91-3). Although bony abnormalities, such as metaphyseal banding, periosteal reactions, osteolysis, osteosclerosis, and osteopenia, can be found in 50 percent of patients, especially children with low leukocyte counts at presentation,81 skeletal roentgenography is not necessary for case management. Spinal roentgenography is useful in patients with suspected vertebral collapse.

Examination of the cerebrospinal fluid (CSF) is an essential diagnostic procedure. Leukemic blasts can be identified in as many as one third of pediatric patients at diagnosis of ALL; most of these patients lack neurologic symptoms.82 Traditionally, CNS leukemia is defined by the presence of at least five leukocytes per microliter of CSF (with leukemic blast cells apparent in a cytocentrifuged sample) or by the presence of cranial nerve palsies. However, with the omission of prophylactic cranial irradiation in contemporary clinical trials, the presence of any leukemic blast cells in the CSF is associated with increased risk of CNS relapse and is an indication to intensify intrathecal therapy.83 Different opinions exist regarding when the first lumbar puncture should be performed. Many leukemia therapists perform the procedure at diagnosis but do not instill chemotherapeutic agents intrathecally in the event a second diagnostic test is needed to verify the presence of leukemic cells. Others delay the examination because of concern that circulating leukemic cells from the peripheral blood will "seed" the CNS. Two studies have shown that contamination of the CSF by leukemic cells as a result of traumatic lumbar puncture at diagnosis is associated with an inferior treatment outcome in children with ALL.84,85 In view of this finding, intrathecal therapy is administered immediately after the diagnostic lumbar puncture in all patients with confirmed leukemia (e.g., the presence of circulating leukemic cells) at St. Jude Children's Research Hospital. The risk of traumatic lumbar puncture can be decreased by administering platelet transfusions to thrombocytopenic patients and by having the most experienced clinician perform the procedure after the patient is under deep sedation or general anesthesia.83,86"


[I cannot copy the table into this answer for some reason,
but if you email me, I will be happy to attempt to email you the
table]

Hoping this helps some,
Janice
[e-mail]