Find information on thousands of medical conditions and prescription drugs.

Acute lymphocytic leukemia

Acute lymphoblastic leukemia (ALL), also known as acute lymphocytic leukemia, is a cancer of the white blood cells, characterised by the overproduction and continuous multiplication of malignant and immature white blood cells (referred to as lymphoblasts) in the bone marrow. It is a hematological malignancy. It is fatal if left untreated as ALL spreads into the bloodstream and other vital organs quickly (hence "acute"). It mainly affects young children and adults over 50. more...

Home
Diseases
A
Aagenaes syndrome
Aarskog Ose Pande syndrome
Aarskog syndrome
Aase Smith syndrome
Aase syndrome
ABCD syndrome
Abdallat Davis Farrage...
Abdominal aortic aneurysm
Abdominal cystic...
Abdominal defects
Ablutophobia
Absence of Gluteal muscle
Acalvaria
Acanthocheilonemiasis
Acanthocytosis
Acarophobia
Acatalasemia
Accessory pancreas
Achalasia
Achard syndrome
Achard-Thiers syndrome
Acheiropodia
Achondrogenesis
Achondrogenesis type 1A
Achondrogenesis type 1B
Achondroplasia
Achondroplastic dwarfism
Achromatopsia
Acid maltase deficiency
Ackerman syndrome
Acne
Acne rosacea
Acoustic neuroma
Acquired ichthyosis
Acquired syphilis
Acrofacial dysostosis,...
Acromegaly
Acrophobia
Acrospiroma
Actinomycosis
Activated protein C...
Acute febrile...
Acute intermittent porphyria
Acute lymphoblastic leukemia
Acute lymphocytic leukemia
Acute mountain sickness
Acute myelocytic leukemia
Acute myelogenous leukemia
Acute necrotizing...
Acute promyelocytic leukemia
Acute renal failure
Acute respiratory...
Acute tubular necrosis
Adams Nance syndrome
Adams-Oliver syndrome
Addison's disease
Adducted thumb syndrome...
Adenoid cystic carcinoma
Adenoma
Adenomyosis
Adenosine deaminase...
Adenosine monophosphate...
Adie syndrome
Adrenal incidentaloma
Adrenal insufficiency
Adrenocortical carcinoma
Adrenogenital syndrome
Adrenoleukodystrophy
Aerophobia
Agoraphobia
Agrizoophobia
Agyrophobia
Aicardi syndrome
Aichmophobia
AIDS
AIDS Dementia Complex
Ainhum
Albinism
Albright's hereditary...
Albuminurophobia
Alcaptonuria
Alcohol fetopathy
Alcoholic hepatitis
Alcoholic liver cirrhosis
Alektorophobia
Alexander disease
Alien hand syndrome
Alkaptonuria
Alliumphobia
Alopecia
Alopecia areata
Alopecia totalis
Alopecia universalis
Alpers disease
Alpha 1-antitrypsin...
Alpha-mannosidosis
Alport syndrome
Alternating hemiplegia
Alzheimer's disease
Amaurosis
Amblyopia
Ambras syndrome
Amelogenesis imperfecta
Amenorrhea
American trypanosomiasis
Amoebiasis
Amyloidosis
Amyotrophic lateral...
Anaphylaxis
Androgen insensitivity...
Anemia
Anemia, Diamond-Blackfan
Anemia, Pernicious
Anemia, Sideroblastic
Anemophobia
Anencephaly
Aneurysm
Aneurysm
Aneurysm of sinus of...
Angelman syndrome
Anguillulosis
Aniridia
Anisakiasis
Ankylosing spondylitis
Ankylostomiasis
Annular pancreas
Anorchidism
Anorexia nervosa
Anosmia
Anotia
Anthophobia
Anthrax disease
Antiphospholipid syndrome
Antisocial personality...
Antithrombin deficiency,...
Anton's syndrome
Aortic aneurysm
Aortic coarctation
Aortic dissection
Aortic valve stenosis
Apert syndrome
Aphthous stomatitis
Apiphobia
Aplastic anemia
Appendicitis
Apraxia
Arachnoiditis
Argininosuccinate...
Argininosuccinic aciduria
Argyria
Arnold-Chiari malformation
Arrhythmogenic right...
Arteriovenous malformation
Arteritis
Arthritis
Arthritis, Juvenile
Arthrogryposis
Arthrogryposis multiplex...
Asbestosis
Ascariasis
Aseptic meningitis
Asherman's syndrome
Aspartylglycosaminuria
Aspergillosis
Asphyxia neonatorum
Asthenia
Asthenia
Asthenophobia
Asthma
Astrocytoma
Ataxia telangiectasia
Atelectasis
Atelosteogenesis, type II
Atherosclerosis
Athetosis
Atopic Dermatitis
Atrial septal defect
Atrioventricular septal...
Atrophy
Attention Deficit...
Autoimmune hepatitis
Autoimmune...
Automysophobia
Autonomic dysfunction
Familial Alzheimer disease
Senescence
B
C
D
E
F
G
H
I
J
K
L
M
N
O
P
Q
R
S
T
U
V
W
X
Y
Z
Medicines

Symptoms

Initial symptoms of ALL are quite aspecific, but worsen to the point that medical help is sought:

  • Generalised weakness and fatigue
  • Anemia
  • Frequent or unexplained fever and infections
  • Weight loss and/or loss of appetite
  • Excessive bruising or bleeding from wounds, nosebleeds, petechiae (red pinpoints on the skin)
  • Bone pain, joint pains (caused by the spread of "blast" cells to the surface of the bone or into the joint from the marrow cavity)
  • Breathlessness
  • Enlarged lymph nodes, liver and/or spleen

The signs and symptoms of ALL result from the lack of normal and healthy blood cells because they are crowded out by malignant and immature white blood cells. Therefore, people with ALL experience symptoms from their red blood cells, white blood cells, and platelets not functioning properly. Laboratory tests which might show abnormalities include blood counts, renal functions, electrolytes and liver enzymes.

Diagnosis

Diagnosing leukemia usually begins with a medical history and physical examination. If there is a suspicion of leukemia, the patient will then proceed to undergo a number of tests to establish the presence of leukemia and its type. Patients with this constellation of symptoms will generally have had blood tests, such as a full blood count.

These tests may include complete blood count (blasts on the blood film generally lead to the suspicion of ALL being raised). Nevertheless, 10% have a normal blood film, and clinical suspicion alone may be the only reason to perform a bone marrow biopsy, which is the next step in the diagnostic process.

Bone marrow is examined for blasts, cell counts and other signs of disease. Pathological examination, cytogenetics (e.g. presence of the Philadelphia chromosome) and immunophenotyping establish whether the "blast" cells began from the B lymphocytes or T lymphocytes.

If ALL has been established as a diagnosis, a lumbar puncture is generally required to determine whether the malignant cells have invaded the central nervous system (CNS).

Lab tests (mentioned above) and clinical information will also determined if any other medical imaging (such as ultrasound or CT scanning) may be required to find invasion of other organs such as the lungs or liver.

Pathophysiology

The etiology of ALL remains uncertain although some doctors believe that ALL develops from a combination of genetic and environmental factors. However, there is no definite way of determining the cause of leukemia.

Scientific research has shown that all malignancies are due to subtle or less subtle changes in DNA that lead to unimpaired cell division and breakdown of inhibitory processes. In leukemias, including ALL, chromosomal translocations occur regularly. It is thought that most translocations occur before birth during fetal development. These translocations may trigger oncogenes to "turn on", causing unregulated mitosis where cells divide too quickly and abnormally, resulting in leukemia. There is little indication that propensity for ALL is passed on from parents to children.

Read more at Wikipedia.org


[List your site here Free!]


A 74-year-old Man With Chronic Lymphocytic Leukemia, Cough, and a Lung Mass - )
From CHEST, 12/1/99 by Douglas Michaelsen

(CHEST 1999; 116:1798-1801)

The patient was a 74-year-old white man with a history of stage IV chronic lymphocytic leukemia (CLL) diagnosed 6 years previously. The last cycle of chemotherapy that he received was fludarabine 14 months prior to admission. Additional history was significant for bouts of recurrent bronchitis over the previous 6 months. One month prior to admission, the patient presented with a persistent cough, and he was noted to have a decreased hematocrit and platelet count. Chest CT done at that time demonstrated increased subcarinal, mediastinal, and hilar adenopathy. Therefore, a decision was made to restart fiudarabine treatment. The patient presented to the clinic 1 day after initiation of fiudarabine with complaints of severe cough that was productive of greenish-yellow, blood-tinged sputum. He also complained of increased shortness of breath, shaking chills, and fever to 38.8 [degrees] C.

Physical Examination

The patient was an ill-appearing white man in no acute distress. His temperature was 37.2 [degrees] C and pulse was 94 beats/min. His BP was 153/64 mm Hg and respirations were 20 breaths/min. There was pronounced cervical and axillary adenopathy. A chest examination demonstrated diffuse rhonchi and expiratory wheezes. A cardiovascular examination was significant for an unchanged II/VI systolic murmur. The abdomen was soft without tenderness or hepatosplenomegaly.

Laboratory Findings

Laboratory values were as follows: WBC count, 26.3 x [10.sup.3]/[micro]L; 3% neutrophils; 95% lymphocytes, 1% eosinophils; hematocrit, 26%; platelets, 34 x [10.sup.3]/[micro]L; and lactate dehydrogenase, 541 IU/L (range, 313 to 618 IU/L).

Chest radiograph (Fig 1) showed left mid-lung zone peripheral mass, hilar and mediastinal adenopathy, cardiomegaly, and bilateral pleura] thickening.

[Figure 1 ILLUSTRATION OMITTED]

Chest CT (Fig 2) showed bilateral pleura] effusions, mediastinal adenopathy, and a dense parenchymal mass. Other CT images (not shown) revealed cervical, axillary, and hilar adenopathy. Other discrete pulmonary nodules were noted in the right lung.

[Figure 2 ILLUSTRATION OMITTED]

What procedure would you recommend next?

What is your diagnosis?

Diagnosis: Pulmonary involvement with CLL/ small lymphocytic lymphoma (SLL).

CLL can have varying pulmonary manifestations that are often difficult to distinguish from other pulmonary disorders on clinical grounds. Pulmonary infiltrates, pleural effusion, and hilar and mediastinal adenopathy are common radiographic findings. Infectious causes account for the majority of pulmonary infiltrates seen in patients with CLL. Streptococcus pneumoniae, Haemophilus influenzae, and Staphyloccus aureus, as well as Legionella and Nocardia spp are frequent bacterial pathogens that cause pneumonia in CLL. Opportunistic infections such as Pneumocystis carinii, fungi, viruses, and mycobacteria are also seen in CLL patients, most commonly in those being treated with corticosteroids and/or fludarabine.

Pulmonary infiltrates may also represent pulmonary toxicity from therapeutic agents used in the treatment of CLL. Respiratory complications in patients treated with fludarabine are almost always due to infection. This is presumably the result of the effect that the drug has on the CD4 count, which can be suppressed for extended periods of time following therapy. A less common respiratory complication is a hypersensitivity reaction to fludarabine, with resultant interstitial pneumonitis.

The alkylating agent chlorambucil is frequently used in the treatment of CLL. Although reports of chlorambucil-induced pulmonary fibrosis are rare in comparison to other alkylating agents such as busulfan and cyclophosphamide, it does occur. The symptoms are nonspecific (cough, dyspnea, fever, anorexia), and the chest radiograph usually shows a diffuse reticulonodular pattern with relative sparing of the apices. Pulmonary function tests show a restrictive defect with a decreased diffusion capacity. Chlorambucil-induced pulmonary fibrosis cannot be distinguished pathologically from other causes of drug-induced pulmonary fibrosis.

Pulmonary infiltrates in CLL may be the result of alveolar hemorrhage, especially in thrombocytopenic patients. Infiltrates can also be seen as a result of pulmonary leukostasis, although less commonly in CLL than in other leukemias.

Patients with CLL are at higher risk for the development of secondary neoplasms, the most common of which is lung cancer. Approximately 5% of CLL patients develop a diffuse large cell lymphoma at some point during their disease course. The histologic progression of CLL to diffuse large cell lymphoma, termed Richter's syndrome, is associated with an aggressive disease course and an average survival of only 5 months.

Direct pulmonary infiltration by leukemic cells occurs more frequently in CLL than in other types of leukemia. Approximately 17% of pulmonary infiltrates seen in CLL are secondary to direct pulmonary extension, whereas only 10% of infiltrates seen in other types of leukemia represent direct tumor involvement. Pathologically, pulmonary infiltration of CLL reveals small mature-appearing lymphocytes (somewhat larger than normal lymphocytes) with condensed chromatin and rounded nuclei. Histologically, these findings are identical in both CLL and SLL, a low-grade malignant lymphoma. Therefore, SLL is considered to be the tissue counterpart of CLL. Clinically, these two entities are similar as well. Common presenting symptoms of pulmonary CLL/ SLL include dry cough, low-grade fever, and progressive dyspnea. Either diffuse or localized infiltrates may be seen on chest radiograph, as well as intrathoracic adenopathy. Pleural effusions are less common. Most cases of pulmonary CLL/SLL have been diagnosed with open lung biopsy; however, at least one report has shown that both transbronchial biopsy and BAL may also be used effectively to make the diagnosis. Both CLL and SLL are treated using the same chemotherapeutic agents, usually 5-day cycles of fludarabine given at 4-week intervals.

The patient was admitted to the hospital, antibiotic therapy was begun for suspected community-acquired pneumonia, and further fludarabine therapy was withheld. Despite treatment, his clinical status did not improve. He subsequently underwent CT-guided biopsy of the pleural mass seen in Figure 2, and the results were consistent with SLL. The patient had demonstrated prior intolerance to full-dose fludarabine therapy, and the new biopsy results confirmed disease progression despite dose-reduced therapy. Therefore, the decision was made to initiate therapy with rituximab, a monoclonal antibody used in patients with CLL refractory to more established therapeutic agents. He tolerated the therapy without difficulty, his symptoms resolved, and subsequent CT scans have demonstrated a marked reduction in disease.

PEARLS

1. The majority of infiltrates seen in patients with CLL are secondary to infectious causes. Opportunistic infections are uncommon, except in patients being treated with fludarabine and/or corticosteroids.

2. Other less common causes of pulmonary infiltrates in CLL include alveolar hemorrhage and pulmonary leukostasis, as well as therapy-related pulmonary drug toxicity effects causing pulmonary fibrosis or interstitial pneumonitis.

3. SLL is the tissue counterpart of CLL and should be considered in the differential diagnosis of a patient with CLL and pulmonary infiltrates on chest radiograph

4. Most cases of pulmonary SLL have been diagnosed by open lung biopsy, although recent literature suggests that the diagnosis can be made using transbronchial biopsy, BAL, or transthoracic needle biopsy.

SUGGESTED READING

Berkman N, Polliak A, Breuer R, et al. Pulmonary involvement as the major manifestation of chronic lymphocytic leukemia. Leuk Lymphoma 1992; 8:495-499

Dear A, Goldstein D, Salem HH. Pulmonary chronic lymphocytic leukemia: difficulty in establishing a tissue diagnosis [letter]. Eur J Haematol 1995; 54:130-133

Khong HT, McCarthy J. Chlorambucil-induced pulmonary disease: a case report and review of the literature. Ann Hematol 1998; 7:85-87

Morrison WH, Hoppe RT, Weiss LM, et al. Small lymphocytic lymphoma. J Clin Oncol 1989; 7:598-606

(*) From the Department of Medicine (Dr. Michaelsen) and the Division of Pulmonary and Critical Care, Allergy and Clinical Immunology (Dr. Judson), Medical University of South Carolina, Charleston, SC.

Manuscript received January 28, 1999; revision accepted April 6, 1999.

Correspondence to: Marc A. Judson, MD, FCCP, Division of Pulmonary and Critical Care, Allergy and Clinical Immunology, Medical University of South Carolina, 96 Jonathan Lucas St, 812 CSB, Box 250623, Charleston, SC 29425

COPYRIGHT 1999 American College of Chest Physicians
COPYRIGHT 2000 Gale Group

Return to Acute lymphocytic leukemia
Home Contact Resources Exchange Links ebay