Leukaemias - Lab Results Page for Hoslink and Australian Pathlink

Lab Results for Haematological Disorders

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Iron Deficiency Anaemia	Megaloblastic Anaemias and Vitamin B12 Deficiency	Folic Acid	Anaemia of Chronic Disease
Anaemia of Chronic Renal Insufficiency	Anaemia of Hypometabolism	Hereditary Spherocytosis	Glucose-6-Phosphate
Pyruvate Kinase deficiency	The Thallasemias	Sickle Cell Disease	Haemoglobin C Disease
Autoimmune Haemolytic Anaemia	Drug Induced Immune Haemolysis	Haemolytic-Uraemic Syndrome	Paroxysmal Nocturnal Haematuria
Haemolytic Disease of the Newborn	Aplastic Anaemia	Sideroblastic Anaemia	Anaemia of Marrow Infiltration
Haemophilia A	Von Willebrands Disease	Haemophilia B	Disseminated Intravascular Coagulation
Ideopathetic Thrombocytopenic Purpura	Chronic Granulomatous Disease	Myelofibrosis With Myeloid Metaplasia	Polycythaemia Vera
Essential Thrombocytopenia	Acute Leukaemia	Chronic Myelocytic Leukaemia	Chronic Lymphocytic Leukaemia
Malignant/Non-Hodgkin's Lymphomas	Hodgkins Disease	Immunoproliferative Disorders	Leukaemic Reticuloendotheliosis
Multiple Myelomas	Macroglobulinaemia	Heavy Chain Disease	.

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LEUKAEMIAS

ACUTE LEUKAEMIAS
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LABORATORY FINDINGS

Peripheral Blood

Normocytic anaemia, occasionally macrocytic - progressive, severe
Thrombocytopenia - progressive, severe
Leukocyte count - normal or decreased (aleukaemic leukaemia) or increased (50,000/ul - 100,000/ul). Therapy usually produces granulocytopenia.
Differential count - occasional blast to 100%; lymphoblasts or myeloblasts; immature leukocytes
Auer bodies may be seen in the cytoplasm of myeloblasts; they do not occur in lymphoblasts.
In acute myelocytic leukaemia, granulocytes may have failure of normal nuclear lobe development, resembling Pelger Huët anomaly.
Nucleated RBC, polychromatophilia
Decreased leukocyte alkaline phosphatase
Cytochemical staining may help differentiate the various blast cells:
nonlymphoblasts stain for myeloperoxidase, chloroacetate esterae, nonspecific esterase, Sudan Black B. Lymphoblasts do not show these staining reactions.

Bone Marrow

Hypercellular marrow with increased blasts, even when none are found in the peripheral blood; increased immature leukocytes; increased M-E ratio.
Rarely, the marrow is hypocellular with only clusters of blasts.
Occasionally, megaloblastic changes are seen in RBC precursors.
Decreased RBC and megakaryocytic elements

Other Laboratory Findings

Positive cultures of blood, urine, sputum - various indigenous and opportunistic organisms occur as infectious complications of leukaemia
Cerebrospinal fluid (CSF) may contain leukaemic cells (25% - 50% of children).
Increased serum uric acid - this is the end product of nucleic acid catabolism and is seen with high WBC and during chemotherapy.

Terminal deoxynucleotidyl transferase (TdT)

This is a biochemical marker of some leukaemic cells, it is found in 95% of patients with acute lymphocytic leukaemia and 5-10% of patients with acute myelocytic leukaemia.

Immunologic Characteristics

The identification of cell surface markers helps to categorise normal and leukaemic lymphocytes as thymus-derived (T cells) or bursal type (B cells). Lymphocytes without surface markers have been termed null cells.

Cytogenetic Studies

No consistent findings occur in the acute leukaemias. The presence of the Philadelphia chromosome (Ph1 chromosome) in adult acute leukaemia indicates that the acute leukaemia arose as an acute transformation or blast crisis from chronic myelocytic leukaemia.

CHRONIC MYELOCYTIC LEUKAEMIA

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LABORATORY FINDINGS

Peripheral Blood

Leukocytosis (50,000/ul - 500,000/ul). All granulocytic precursors are present, with mature granulocytes and metamyelocytes predominating. <10% blasts are present. Increased eosinophils, basophils, and monocytes.
Normocytic anaemia (Hb 9 g/dl - 12 g/dl) due to marrow displacement and impaired erythropoiesis. Severity of the anaemia is proportional to the degree of leukocyte proliferation.
Normal or slightly increased reticulocyte count
Few nucleated RBC, slight polychromatophilia
Normal platelet count (50%) or increased platelet count (40%) in early stages; this is not related to the WBC count; thrombocytopenia occurs in later stages

Bone Marrow

Hypercellular bone marrow with predominance of all granulocytic elements showing orderly maturation; M - E ratio is 10:1 - 30:1; increased basophils and eosinophils
Increased megakaryocytes, some of which are atypical
Increased reticulin fibres and fibrosis may appear in a biopsy taken late in the course of the disease (30% - 40% of patients).
Decreased stainable iron

Other Laboratory Findings

Decreased or absent leukocyte alkaline phosphatase in approximately 90% of patients
Presence of Ph1 chromosome in 70% - 90% of patients
Increased serum and urine uric acid, especially when chemotherapy is given, reflects WBC breakdown.
Increased serum vitamin B12 and unsaturated B12 binding capacity reflect elevated vitamin B12 binding protein derived from breakdown of leukaemic granulocytes
Increased serum LDH reflects RBC and WBC breakdown.
Presence of terminal deoxynucleotidyl transferase (TdT) in 20% - 30% of patients with chronic myelocytic leukaemia in blast crisis. This enzyme is usually found in lymphoblasts.

CHRONIC LYMPHOCYTIC LEUKAEMIA

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CLL is the most common form of leukemia in the Western Hemisphere. It accounts for approximately 25 to 30 percent of all leukemias. CLL occurs more frequently in older individuals but is increasingly seen in younger patients as well. Although the etiology of CLL is unknown, recent laboratory investigations have improved our knowledge of this disorder. CLL is a growth of malignant B lymphocytes that grow slowly but have an extended life span. The result is an ever increasing number of leukemia cells. Because of this accumulation of leukemia cells, production of normal bone marrow and blood cells is diminished. Patients can experience severe anemia as well as low platelet counts which can put patients at risk of life-threatening bleeding. Patients with CLL may develop serious infections because of reduced numbers of infection-fighting cells known as neutrophils.

LABORATORY FINDINGS

Peripheral Blood

Leukocytosis (20,000/ul - 250,000/ul) - over 90% of cells are small lymphocytes; many smudge cells, which are fragile leukaemic cells. The total lymphocyte count does not correlate with the degree of organ involvement.
Mild normocytic anaemia, early; severe anaemia in later stages due to decreased RBC production and shortened RBC survival
Normal or decreased reticulocytes
Normal platelets in the early stage; thrombocytopenia in the later stage

Bone Marrow

Early, slight lymphocytosis
Later, lymphocytes gradually replace the entire marrow and all other cellular elements are decreased.

Other Laboratory Findings

Immunologically, the lymphocytes in 98% of patients are B-lymphocytes.
Decrease in serum proteins, especially immunoglobulin,s contributes to increased susceptibility to bacterial, fungal, and viral infections
Monoclonal y-globulin (5% of cases), usually IgM
AIHA, IgG type (5% - 10% of cases) - increased LDH, spherocytes, and reticulocytes reflect the haemolytic process.

Peripheral Blood

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LEUKAEMIC RETICULOENDOTHELIOSIS

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LABORATORY FINDINGS

Peripheral Blood

Decreased WBC, RBC, and platelets
Small to medium-sized mononuclear cells with moderate to abundant cytoplasm showing hairlike projections
Tumour cells contain acid phosphatase, which is not removed by incubation with tartrate - this is a common but not consistent finding.

Bone Marrow

Aspirate often yields no cells.
Biopsy shows focal or diffuse infiltrate of the characteristic leukaemic cells.
Bone-marrow biopsy usually is diagnostic.

MALIGNANT LYMPHOMAS

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NON-HODGKIN'S LYMPHOMAS

LABORATORY FINDINGS

Biopsy of lymph node or other tissue that shows morphologic cell type in a nodular or diffuse pattern - required for definitive diagnosis
Anaemia, normocytic (50% of patients) - due to one or more of the following:
lymphoma involvement of bone marrow, bone marrow suppression resulting from therapy, hypersplenism, autoimmune haemolytic anaemia, bleeding from GI lymphoma, or secondary to a low platelet count
Peripheral blood rarely shows circulating lymphoma cells; 5% - 10% of cases may evolve into leukaemia
Bone-marrow biopsy may show involvement by lymphoma.
Serum protein electrophoresis shows decreased albumin as the disease progresses; there may be a monoclonal gammopathy, usually IgM type, or occasionally hypogammaglobulinemia.
Cytological examination of pleural or peritoneal fluid may show lymphoma tumour cells.
Classification of tumours into B cell, T cell, or null cell types uses immunofluorescent, immunoperoxidase, or cell suspension techniques.
Cytochemical studies of tumour cells help differentiate lymphocytes from histiocytes

HODGKIN'S DISEASE

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Hodgkin's Disease is a cancer of the lymph nodes. It develops when normal lymph cells mutate and grow uncontrollably. The lymphatic system comprises of many vessels that are networked throughout the body. The primary function of the lymphatic system is to help fight infection and the lymph nodes, which are located throughout the body, act as a kind of filter, removing debris that has been destroyed by the immune system.

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LABORATORY FINDINGS

Lymph Node Biopsy

Required for definitive diagnosis.

Peripheral Blood

Normocytic or microcytic anaemia, moderate; worsens as disease progresses
Haemolytic anaemia occasionally occurs in advanced disease; the Coombs' test is usually negative.
Leukocytosis, which is characterised by increased granulocytes and decreased lymphocytes
Pancytopenia reflects extensive bone marrow involvement, the effect of therapy, or hypersplenism.

Bone Marrow

Requires biopsy to demonstrate involvement, which occurs in approximately 11% of cases

Other Laboratory Findings

Increased sedimentation rate reflects disease activity.
Increased leukocyte alkaline phosphatase during the active phase of disease; not increased during remission
Protein electrophoresis - decreased albumin, increased globulins; reflects active disease
Decreased serum iron and increased ferritin reflect chronic disease anaemia.

Hodgkin's Disease differs from Non-Hodgkins Lymphomas in 2 primary ways

Hodgkin's progression is contigious, that is, the disease spreads from one lymph node to the next. It never skips one part of the lymphatic system. Non-Hodgkin's cancers can skip from a lymph node directly to a distant organ.
Hodgkin's has the presence of the characteristic Reed-Sternberg cells when examined histologically. These are absent in other lymphomas.

The cause of HD is unknown. Some researchers are examining the relationship with the Epstein-Barr virus which is found in approx 50% of all HD patients. This remains contentious. Whatever the cause, the NCI reports about 7000 new cases in the US each year. There is a slight bias of 1.5:1 men to women.

IMMUNOPROLIFERATIVE DISORDERS

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MULTIPLE MYELOMA

LABORATORY FINDINGS

Peripheral Blood

Normochromic, normocytic anaemia, mild to moderate (Hb 7 g/dl - 10 g/dl), reflects the number of plasma cells in the marrow; anaemia is also due to shortened RBC survival, increased blood loss, increased plasma volume, renal insufficiency, and the effects of radiation therapy or chemotherapy.
Rouleaux formation due to increase in serum protein
Blue-gray background of blood smear when observed macroscopically is due to increase in serum protein.
Mild degree of leukopenia and thrombocytopenia
Relative lymphocytosis; rare plasma cells
Nucleated RBC and immature granulocytes - this leukoerythroblastic reaction, or pancytopenia, might occur late in the disease as a result of myeloma replacement of the bone marrow.

Bone Marrow

Increased plasma cells, > 20% (average 36%); immature atypical plasma cells are termed myeloma cells. The percentage of plasma cells is not a reliable indicator of the extent of disease. Marrow biopsy may be necessary to show plasma-cell aggregates.
Increased lymphocytes (> 20%)

Protein Abnormalities

Increased serum total protein due to increased globulins (8 g/dl - 15 g/dl); decreased albumin
Serum protein electrophoresis - Monclonal protein in the Beta or y zone, usually IgG or IgA. There might be decreased y-globulin, which suggests IgD myeloma or light-chain myeloma. In light-chain myeloma, no heavy chains are formed.
Serum protein immunoelectrophoresis - identifies the heavy and light chains of the monoclonal protein. Approximately 11% of plasma-cell tumours form only light-chain proteins. Presence of free light chains in the serum reflects impaired renal excretion.
Marked increase in the monoclonal protein (5 - 10 times > normal) - produced by a single clone of malignant plasma cells. The most frequently produced monoclonal protein is IgG.
Moderate to marked decrease in the nonmonoclonal immunoglobulins. Impaired synthesis of normal immunoglobulins is a characteristic finding.
Proteinuria
Urine protein electrophoresis - May show one or more of the following: a monoclonal protein similar to that in the serum; multiple proteins similar to normal serum proteins, indicating nephrosis; and albumin, reflecting a glomerular filtration defect.
Urine protein immunoelectrophoresis - identifies the specific monoclonal protein present, which is usually similar to that in the serum. Monoclonal light chains of either the xx or xx type are termed Bence Jones Proteins. These proteins occur in 60% of IgG myelomas, 70% of IgA myelomas, 100% of IgD myelomas, and 100% of light-chain myelomas.

Other Laboratory Findings

Increased serum viscosity, evidenced as cryoglobulins or cryofibrinogens; most frequently seen in IgA myeloma, which tends to polymerize readily.
Increased sedimentation rate - result of increased immunoglobulin or fibrinogen
Increased BUN and serum creatinine; decreased creatinine clearance - indicate impaired renal function, chiefly due to Bence Jones protein damage to renal tubules
Urine casts and renal epithelial cells reflect progressive renal failure.
Increased serum calcium reflects bone resorption by myeloma infiltrates and tumour-cell secretion of an "osteoclast-stimulating factor." Hypercalcaemia is usually associated with extensive bone disease, azotemia, and hyperuricaemia.
Positive cultures of sputum, blood, and urine usually yield gram-negative bacteria - reflect increased susceptibility to infection

Multiple Myeloma

Myeloma in pneumonia	This slide shows a bone marrow smear from a patient presenting with hypercalcaemia and bone pain. The large cells are plasma cells and the diagnosis is multiple myeloma. Myeloma is a monoclonal proliferation of bone marrow plasma cells. Its associated with a plasma paraproteinaemia and Bence Jones (BJ) proteinuria. About 15% of patients have BJ protein in their urine without a paraproteinaemia. BJ proteinuria results from free IgG light chains. The median survival for patients with myeloma is two years.

Multiple Myeloma

Myeloma in pneumonia

This slide shows a bone marrow smear from a patient presenting with hypercalcaemia and bone pain. The large cells are plasma cells and the diagnosis is multiple myeloma. Myeloma is a monoclonal proliferation of bone marrow plasma cells. Its associated with a plasma paraproteinaemia and Bence Jones (BJ) proteinuria. About 15% of patients have BJ protein in their urine without a paraproteinaemia. BJ proteinuria results from free IgG light chains. The median survival for patients with myeloma is two years.

MACROGLOBULINEMIA

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LABORATORY FINDINGS

Peripheral Blood

Normochromic, normocytic anaemia, marked (Hb 6 g/dl - 9 g/dl) - this is primarily due to decreased RBC formation; other factors contributing to the anaemia include increased plasma volume, RBC destruction, and blood loss
Rouleaux formation, marked - this is due to adhesion of RBC to each other in the viscous serum
Immature lymphocytes, late in disease

Bone Marrow

Hypercellular; marrow is diffuseley replaced by lymphocytes with features resembling plasma cells

Other Laboratory Findings

Increased sedimentation rate, marked - due to RBC aggregation
Increased total serum protein and globulins
Serum protein electrophoresis - monoclonal protein present in Beta or y region
Serum protein immunoelectrophoresis - the abnormal protein is IgM xx or IgM xx.
Immunoglobulins, quantitative - increased IgM, decreased IgG and IgA
Proteinuria
Urine protein electrophoresis and immunoelectrophoresis - 25% - 40% of cases show free xx or xx light chains (Bence Jones proteins) in the urine
Presence of serum cryoglobulins, cryofibrinogens, or pyroglobulins
Increased serum viscosity - this may cause false-positive results in tests using latex particles, such as tests for rheumatoid arthritis, pregnancy, fibrin split products
Increased cold agglutinins
Impaired platelet adhesion, aggregation, platelet-factor-3 release; prolonged bleeding time - these are the result of IgM coating of platelets
Impaired function of coagulation factors II, V, VII, or VIII prolonging prothrombin time of partial thromboplastin time - this may be the result of immune-complex formation with IgM
Prolonged thrombin time - this frequent finding is thought to be due to immunoglobulin binding to fibrin during clot formation and polymerization

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Waldenstrom's Macroglobulinaemia

HEAVY-CHAIN DISEASE

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LABORATORY FINDINGS

All Heavy-Chain Diseases

Serum protein electrophoresis - decreased albumin and y-globulin; abnormal broad heterogenous protein in xx, Beta, or y region
Urine protein electrophoresis - identical pattern to that of serum.

Gamma Heavy-Chain Disease

Normocytic anaemia, leukopenia, thrombocytopenia - due to hypersplenism
Eosinophilia and atypical lymphocytes or plasma cells in peripheral blood
Increased sedimentation rate
Proteinuria - up to 1 g/day
Increased lymphocytes and plasma cells in the bone marrow
Immunoelectrophoresis of serum and urine shows increased y chains but no light chains - this is the diagnostic finding.
Decreased serum IgA and IgM

Alpha Heavy-Chain Disease

Normal peripheral blood and bone marrow
Immunoelectrophoresis of serum and urine shows increased xx chains but no light chains - this is the diagnostic finding.
Laboratory findings of intestinal malabsorption

Mu Heavy-Chain Disease

Peripheral blood resembles that of chronic lymphocytic leukaemia.
Bone marrow shows 70% - 80% of lymphocytes and vacuolated plasma cells.
Immunoelectrophoresis shows u chains but no light chains in serum - this is the diagnostic finding.
xx light chains present in the urine

Immunodeficiency Disorders

SYNDROME	CLINICAL FEATURES	LABORATORY FINDINGS
.Predominant Humoral Abnormality	.	.
X-linked agamaglobulinemia	Increased bacterial sinus and pulmonary infections; rheumatoid arthritis: affects males	All Ig decreased or absent; absence of plasma cells in all sites
IgA deficiency	Steatorrhea and nontropical sprue	Absence of serum and secretory IgA, may have IgA antibodies
Ig deficiencies with hyper-IgM	Increased bacterial respiratory infections; increased autoimmune diseases	Increased IgM and decreased IgA and IgG
.	.	.
Predominant Cell-Mediated Abnormality	.	.
Thymic dysplasia Nezelof's syndrome)	Increased fungal and viral infections	Decreased granulocytes; 50% of patients have decreased IgA or IgG
.	.	.
Congenital thymic aplasia (DiGeorge's syndrome)	Increased fungal and viral infections: absent parathyroids, thymus; cardiovascular, tracheal, and esophageal malformations	Normal serum Ig levels; decreased calcium; diminished cell-mediated immunity
Combined Immunologic Abnormalities	.	.
Wiskott-Aldrich syndrome	Thrombocytopenia and eczema; increased bacterial and viral infections; bleeding	Decreased IgM, increased IgA: decreased lymphocytes and cellular immunity
Ataxia-telangiectasia	Cerebellar ataxia; telangiectasia in skin and eyes; ovarian dysgenesis; sinus and pulmonary infections	Decreased serum and secretory IgA and IgE; impaired cellular immunity
Severe combined immunodeficiency	Overwhelming widespread bacterial and viral infections; failure to thrive; malabsorption	Marked decrease in all Ig; decreased to absent lymphocytes and plasma cells; impaired cellular immunity
Common variable hypo-gammaglobulinemia	Recurrent bacterial respiratory infections and GI disorders including malabsorption; frequent occurrence of autoimmune diseases	Absence of plasma cells; variable decrease in immunoglobulins, especially IgG

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