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Toxic Facts for Benzene (Benceno) How
likely is benzene to cause cancer?
General
Information Chronic lymphocytic leukemia (CLL) is a disorder of morphologically mature but immunologically less mature lymphocytes and is manifested by progressive accumulation of these cells in the blood, bone marrow, and lymphatic tissues. In this disorder, lymphocyte counts in the blood are usually equal to or higher than 5,000 per cubic millimeter with a characteristic immunophenotype (CD5 and CD23 positive B cells).[1] As assays have become more sensitive for detecting monoclonal B-CLL-like cells in peripheral blood, researchers have detected a monoclonal lymphocytosis of undetermined significance (MLUS, in analogy to the monoclonal gammopathy of undetermined significance, MGUS) in 3% of individuals over 40 years of age and 6% in those over 60 years of age.[2] Such earlier diagnosis and recognition of cases that would never have crossed the threshold of diagnosis previously may falsely suggest improved survival for the group and may unnecessarily worry or result in therapy for some patients who would have remained undiagnosed in their lifetime, a circumstance known in the literature as overdiagnosis or pseudodisease. At the present time, the natural history or clinical significance of these findings is unknown. For patients with progressing CLL, treatment with conventional doses of chemotherapy is not curative; selected patients treated with allogeneic stem cell transplantation have achieved prolonged disease-free survival.[3-6] The overall 5-year survival is approximately 60%, but depends on stage of disease. Antileukemic therapy is frequently unnecessary in uncomplicated early disease.[7] CLL occurs primarily in middle-aged and elderly individuals, with increasing frequency in successive decades of life.[8] The clinical course of this disease progresses from an indolent lymphocytosis without other evident disease to one of generalized lymphatic enlargement with concomitant pancytopenia. Complications of pancytopenia, including hemorrhage and infection, represent a major cause of death in these patients.[9] Immunological aberrations, including Coombs-positive hemolytic anemia, immune thrombocytopenia, and depressed immunoglobulin levels may all complicate the management of CLL.[10] Prognostic factors that may help predict clinical outcome include cytogenetic subgroup [11] and immunoglobulin mutational status.[12-15] Confusion with other diseases may be avoided by determination of cell surface markers. CLL lymphocytes coexpress the B-cell antigens CD19 and CD20 along with the T-cell antigen CD5.[16] This coexpression only occurs in one other disease entity, mantle cell lymphoma. CLL B cells express relatively low levels of surface-membrane immunoglobulin (compared with normal peripheral blood B cells) and a single light chain (kappa or lambda).[7] CLL is diagnosed by an absolute increase in lymphocytosis and/or bone marrow infiltration coupled with the characteristic features of morphology and immunophenotype. The differential diagnosis must exclude hairy cell leukemia (refer to the PDQ summary on Hairy Cell Leukemia Treatment for more information), and Waldenström’s macroglobulinemia (refer to the PDQ summary on Adult Non-Hodgkin’s Lymphoma Treatment for more information). Waldenström’s macroglobulinemia has a natural history and therapeutic options similar to CLL, with the exception of hyperviscosity syndrome associated with macroglobulinemia as a result of elevated immunoglobulin M. Prolymphocytic leukemia (PLL) is a rare entity characterized by excessive prolymphocytes in the blood with a typical phenotype that is positive for CD19, CD20, and surface-membrane immunoglobulin and negative for CD5. These patients demonstrate splenomegaly and poor response to low-dose or high-dose chemotherapy.[7,17] Cladribine (2-chlorodeoxyadenosine) appears to be an active agent (60% complete remission rate) for patients with de novo B-cell prolymphocytic leukemia.[18] [Level of evidence: 3iiiDiii] Alemtuzumab (campath-1H), an anti-CD52 humanized monoclonal antibody, has been used for 76 patients with T-cell prolymphocytic leukemia after failure of prior chemotherapy (usually pentostatin or cladribine) with a 51% response rate (95% confidence interval, 40%-63%) and median time to progression of 4.5 months (range 0.1 to 45.4 months).[19] [Level of evidence: 3iiiDiii] These response rates have been confirmed by other investigators.[20] Patients with CLL who show prolymphocytoid transformation maintain the classic CLL phenotype and have a worse prognosis than PLL patients. Large granular lymphocytic leukemia is characterized by lymphocytosis with a natural killer cell immunophenotype (CD2, CD16, and CD56) or a T-cell immunophenotype (CD2, CD3, and CD8).[21,22] These patients often have neutropenia and a history of rheumatoid arthritis. The natural history is indolent, often marked by anemia and splenomegaly. This condition appears to fit into the clinical spectrum of Felty’s syndrome.[23] Therapy includes steroids, low doses of oral cyclophosphamide or methotrexate, and treatment of the bacterial infections acquired during severe neutropenia.[21,24,25]
Alternative names Return to top Acute
myeloid leukemia (AML); Acute granulocytic leukemia; Acute nonlymphocytic leukemia
(ANLL) Acute
myelogenous leukemia involves a malignancy (cancer) of blood-forming tissues of
the bone marrow characterized by the proliferation of immature white blood cells.
There are 8 categories of AML, categorized as M0 to M7, based on which blood cells
are abnormal. Acute myelogenous leukemia (AML) may occur at any age, but it primarily affects adults and children younger than one year old. This discussion focuses on AML in adults. In this condition, certain blood cells of the immune system, which are grown in the bone marrow, lose their ability to mature and specialize (differentiate). These cells multiply rapidly and replace normal blood cells. Bone marrow failure occurs as malignant cells replace normal bone marrow elements. The person becomes susceptible to bleeding and infection as the normal blood cells lose their ability to fight microorganisms and decrease in number. Most cases have no apparent cause. However, radiation, some toxins such as benzene, and some chemotherapy agents (including etoposide and drugs known as alkylating agents) are thought to cause some kinds of leukemia, including AML. Genetic abnormalities may also play a role in the development of this condition. Risk factors include the following: exposure
to radiation and chemicals Symptoms Return to top Prolonged
bleeding, bruising easily A physical examination may show evidence of anemia, pallor and bleeding. Less commonly an enlarged spleen and liver or enlarged lymph nodes may be found.. A
WBC count can be high, low or normal. The objective of treatment is to eliminate the cancer cells with chemotherapy. Unfortunately, this process also eliminates normal cells that may be present in the bone marrow, so during treatment the patient is at risk from excessive bleeding caused by low numbers of platelets and infection caused by a low white blood count. It takes several weeks for the bone marrow to recover and start producing normal cells. During this time supportive care is intensive. It consists of patient isolation to prevent infection, antibiotics to treat infection, transfusions of platelets to control bleeding and red blood cell transfusions to combat anemia. After remission is achieved, further treatment is known as consolidation and is necessary in order to achieve a permanent cure. Consolidation may consist of either further chemotherapy, a bone marrow transplant or a stem cell transplant. These transplants may also be used in patients with relapsed disease. Most of the different subtypes of AML have similar treatment. However, there are some differences in the treatment of one type of leukemia known as acute promyelocytic leukemia (APL). In this type of leukemia (and only this type), a medicine called all-trans retinoic acid (ATRA) is used to cause the leukemia cells to mature into normal white blood cellss. ATRA is used during remission and consolidation treatments and has increased the cure rate for this type of AML. Additionally, the drug arsenic trioxide is approved for use in patients with APL who have failed treatment with ATRA or the usual chemotherapy. It can be used to achieve first remission or for later relapse. Support Groups Return to top The
stress of illness can often be helped by joining a support group where members
share common experiences and problems. See cancer - support group and leukemia
- support group. Complete
remission occurs in 70% to 80% of patients. Overall, about 20% to 30% of people
survive free of disease at 5 years from diagnosis. Patients who have not experienced
a relapse during this time are considered permanently cured, since most relapses
occur within 2 years of diagnosis. Patients who are less than 60 years of age
have a better chance of survival than their older counterparts. This is related
to many factors including the ability to tolerate the strong chemotherapy medicines.
Without treatment, life expectancy is about 3 to 4 months. Relapse
of the disease Call for an appointment with your health care provider if symptoms suggestive of AML develop. Call
your health care provider if persistent fever or other signs of infection occur
in a person with AML. Get protection from occupational exposure to agents associated with the development of acute leukemia and minimize radiation exposure. Update Date: 8/4/2002
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Lipitor | Ziagen | Topamax | Cypher | Nortrel | Genotropin | Viga |Intergel | Vinerol | Lindane | Procrit | Avonex | Rapamune | Serevent
* HOT CASES: ARAVA AVANDIA BAYCOL BEXTRA DISABILITY ENBREL EPHEDRA EPHEDRINE FEN-PHEN LARIAM LOTRONEX MERIDIA MEDICAL INSURANCE FRAUD LAWSUITS NORPLANT NURSNG HOME NEGLIGENCE OXYCONTIN PPA PERMAX PREMPRO PROPULSID REMICADE REZULIN RISPERDAL SERZONE SILICOSIS STADOL SULZER STROKE THIMEROSAL MERCURY AUTISM VIOXX WELDING FUMES WRONGFUL DEATH CLASS ACTION Acute myelogenous leukemia Acute myelogenous leukemia