Leukemia, Hairy Cell
Leukemia, Lymphocytic, Chronic, B-Cell
Drug Administration Schedule
Antibodies, Monoclonal, Murine-Derived
Antineoplastic Combined Chemotherapy Protocols
Drug Screening Assays, Antitumor
Inhibitory Concentration 50
Leukemia, Myeloid, Acute
Drug Resistance, Neoplasm
Neoplasms, Second Primary
Neoplasm Recurrence, Local
Dose-Response Relationship, Drug
Treatment of mantle-cell lymphomas with intermittent two-hour infusion of cladribine as first-line therapy or in first relapse. (1/220)PURPOSE: Cladribine (2-chlorodeoxyadenosine, 2-CdA) has been reported to be effective in the treatment of low-grade lymphomas. The objective of this multicenter study was to evaluate the activity of cladribine in mantle-cell lymphomas as first-line therapy or in first relapse using an intermittent two-hour infusion of cladribine. PATIENTS AND METHODS: A total of 47 courses, or an average of four courses per patient, were administered to 12 patients (seven untreated, five relapsed) with 5 mg/m2 cladribine given as an intermittent two-hour infusion over five consecutive days for a maximum of six cycles every four weeks. RESULTS: Cladribine showed activity in patients with mantle-cell lymphomas, achieving a response rate of 58% (95% confidence interval (95% CI): 28%-85%). Myelosuppression was the major toxicity with 17% of grade 3 and 4 neutropenia. Thrombocytopenia was rare with only 2% of grade 3 and 4. CONCLUSION: These results demonstrate single-agent activity of cladribine in mantle-cell lymphomas using the intermittent two-hour infusion dosage regimen. To further improve treatment results, cladribine should be combined with other agents active in mantle-cell lymphomas. (+info)
Weekly administration of 2-chlorodeoxyadenosine in patients with hairy-cell leukemia is effective and reduces infectious complications. (2/220)BACKGROUND AND OBJECTIVE: It has been widely demonstrated that one single 7-day course continuous infusion (c.i.) 2-chlorodeoxyadenosine (2-CdA) at a dose of 0.1 mg/kg daily is dramatically effective in inducing high and prolonged complete remission (CR) rates in patients with hairy-cell leukemia (HCL). However, 2-CdA administration often results in severe neutropenia and lymphocytopenia both responsible for the infectious complications observed in these patients. We previously reported preliminary data regarding the effectiveness and toxicity of a modified protocol of 2-CdA administration (0.15 mg/kg 2 hours infusion once a week for 6 courses) in 25 HCL patients. This treatment schedule produced a similar overall response rate compared to standard 2-CdA regimen and appeared to be followed by a lower incidence of infectious episodes. In the present study we report response rate and toxicity of weekly 2CdA administration in a larger cohort of patients and with a longer follow-up. DESIGN AND METHODS: In a group of HCL patients with a pronounced decrease in neutrophils count (< 1 x 10(9)/L), we modified the standard protocol (0.1 mg/kg daily x 7 days c.i.) by administering 2-CdA at a dose of 0.15 mg/kg 2 hours infusion once a week for 6 courses. Thirty HCL patients, 24 males and 6 females with a median age of 56 years (range 37-76), entered into this protocol. Seventeen out of 30 patients were at diagnosis while the remaining 13 had been previously treated with alpha-interferon (alpha-IFN) (7), or 2-CdA (4) or deoxycoformycin (DCF) (2). RESULTS: Overall, 22/30 (73%) patients achieved CR and 8 (27%) partial remission (PR) with a median duration of response at the time of writing of 35 months, ranging from 6 to 58 months. Five patients (1 CR and 4 PR) have so far progressed. The treatment was very well tolerated. Five out of 30 patients (16%) developed severe neutropenia (neutrophils < 0.5 x 10(9)/L) and only in two of them we did register an infectious complication which required treatment with systemic antibiotics and granulocyte colony-stimulating factor (G-CSF). INTERPRETATION AND CONCLUSIONS: In conclusion, we confirm that weekly administration of 2-CdA at a dose of 0.15 mg/kg for 6 courses appears to be very effective in HCL inducing a high CR rate, similar to that observed with daily c.i. administration. CR durability and relapse/progression rates are also comparable to standard 2-CdA schedule. Moreover this new regimen seems to be safer in pancytopenic patients, markedly reducing life-threatening infectious complications. (+info)
Cladribine with cyclophosphamide and prednisone in the management of low-grade lymphoproliferative malignancies. (3/220)The feasibility of combining cladribine with cyclophosphamide and prednisone in the management of indolent lymphoid malignancies was determined. Nineteen patients [nine chronic lymphocytic leukaemia (CLL), seven non-Hodgkin's lymphoma (NHL) and three macroglobulinaemia (M))] received cladribine 0.1 mg kg(-1) per day as a subcutaneous bolus injection on days 1-3 (up to 5 injections) with intravenous cyclophosphamide 500 mg m(-2) on day 1 and oral prednisone 40 mg (m-2) on days 1-5 at 4-weekly intervals up to a maximum of six courses. A total of 80 courses were given. Overall response rate was 88%, with four patients achieving a complete clinical and haematological response and 12 achieving a partial response. Neutropenia WHO grade 4 in two patients and WHO grade 3 infection in one patient were the limiting toxicities on treatment. During the follow-up, WHO grade >3 haematological complications occurred in five patients and WHO grade >3 non-haematological complications in five patients. There were no treatment-related deaths. This study demonstrates the feasibility of the cladribine/cyclophosphamide/prednisone (CCP) combination that appears highly active and safe in the management of indolent lymphoid malignancies. (+info)
Filgrastim for cladribine-induced neutropenic fever in patients with hairy cell leukemia. (4/220)Cladribine treatment of hairy cell leukemia (HCL) is complicated by neutropenic fever in 42% of patients despite documented infections being relatively uncommon. We performed a study of priming filgrastim followed by cladribine and then filgrastim again to determine if filgrastim would lead to a reduction of neutropenia and febrile episodes. Thirty-five patients received filgrastim and cladribine and were compared with 105 historic controls treated with cladribine alone. Cladribine was administered at 0.1 mg/kg/d by continuous infusion for 7 days. Filgrastim was administered at 5 micrograms/kg/d subcutaneously on days -3, -2, and -1 and then again after the completion of cladribine until the absolute neutrophil count (ANC) was >/=2 x 10(9)/L on 2 consecutive days (days +8, +9, etc). After filgrastim priming, the median ANC increased from 0.9 x 10(9)/L to 2.26 x 10(9)/L (2.5-fold increase), and after cladribine, the median nadir ANC in the filgrastim-treated group was 0.53 x 10(9)/L compared with 0.29 x 10(9)/L among historic controls (P =. 04). The median number of days to an ANC greater than 1.0 x 10(9)/L was 9 days in the filgrastim-treated group versus 22 days among historic controls (P < 10(-5)). The percentage of febrile patients, number of febrile days, and frequency of admissions for antibiotics were not statistically different in the two groups. Filgrastim regularly increases the ANC in patients with HCL and shortens the duration of severe neutropenia after cladribine. This phase II study, with comparison to historical controls, failed to detect any clinical advantage from the use of filgrastim and cladribine in the treatment of HCL. Accordingly, the routine adjunctive use of filgrastim with cladribine in the treatment of HCL cannot be recommended. (+info)
Cladribine activity in adult langerhans-cell histiocytosis. (5/220)Langerhans-cell histiocytosis (LCH) results from the accumulation of tissue histiocytes derived from the same progenitor cells as monocytes. Because cladribine is potently toxic to monocytes, we conducted a phase II trial of cladribine. Cladribine was administered to 13 LCH patients at 0.14 mg/kg per day by 2-hour intravenous infusion for 5 consecutive days, every 4 weeks for a maximum of six courses. Median age was 42 years (range, 19 to 72) and median pretreatment disease duration was 99 months (range, 6 to 252). One patient was untreated, one had received prior prednisone only, one prior radiation only, six prior radiation and chemotherapy, and four prior surgery, radiation, and chemotherapy. Seven patients had cutaneous involvement, six multifocal osseous, six pulmonary, two each with soft tissue and nodal involvement, and four had diabetes insipidus. Of 13 patients, 12 were evaluable for response and all for toxicity. After a median of three courses (range, 1 to 6), seven (58%) patients achieved complete responses (two pathologic and five clinical) and two (17%) patients achieved partial responses; overall response rate, 75%. Median response follow-up duration was 33 months (range, 1 to 65). Seven patients experienced grade 3 to 4 neutropenia. Only one patient had a documented infection, dermatomal herpes zoster. At a median follow-up of 42 months (range, 5 to 76), 12 patients remain alive and one patient has died. Thus, cladribine has major activity in adult LCH and warrants further investigation in both pediatric and adult LCH as a single agent and in combination with other drugs. (+info)
Basic fibroblast growth factor is expressed by CD19/CD11c-positive cells in hairy cell leukemia. (6/220)Several features are characteristic for hairy cell leukemia (HCL). Among those are pancytopenia, bone marrow fibrosis, and the appearance of a defined tumor cell phenotype in peripheral blood (PB), bone marrow (BM), and spleen. Hairy cells (HC) coexpress antigens specific for B lymphocytes and monocytes/macrophages and thus the malignant cell does not seem to be restricted to a defined lineage. When serum or bone marrow aspirate was screened by enzyme-linked immunosorbent assay (ELISA) for basic fibroblast growth factor (bFGF), specimen derived from HCL (serum: mean value, 29 pg/mL; BM aspirate: mean value, 641 pg/mL) contained significantly higher levels than those from healthy subjects. To study whether peripheral blood mononuclear cells (PBMC) derived from patients suffering from HCL and healthy donors (HD) were capable of producing bFGF, culture supernatant (conditioned medium, [CM]) was tested for the presence of this cytokine. While bFGF was not detectable in cell cultures from HD, HCL-derived CM contained relatively high levels of bFGF. CM was successfully used for stimulation of mesenchymal cell proliferation, which could be inhibited by a neutralizing anti-bFGF antibody. Cellular activation by pokeweed mitogen (PWM) or the combination of 12-o-tetradecanoyl-phorbol-13-acetate (TPA) plus calcium ionophore (Ca-Ip) led to an enhanced mRNA expression. Results of Western blot experiments showed that HC synthesize at least three isoforms (approximately 18, 23, and 25 kD), but only the 23-kD isoform is exported. To assess the nature of the producer cell, double immunofluorescence analysis using a bFGF-specific and an anti-CD11c monoclonal antibody (MoAb) was undertaken. The majority of cells scoring positive for CD11c were also reactive with the anti-bFGF MoAb. Furthermore, enrichment of CD19/CD11c-positive cells correlated with enhanced bFGF levels, thereby supporting the argument for HC being the producer cells of bFGF. A biological function of bFGF in HCL might be mediation of chemoresistance, as 2-chlorodeoxyadenosine (2-CdA)-induced inhibition of cell proliferation can be reversed by bFGF. Endogenous bFGF production by HC is not affected by this purine analogue and 2-CdA-induced apoptosis is diminished in bFGF-producing HC as compared with normal PBMC. Therefore, bFGF expression by HC might be important for resistance to chemotherapy and survival of the malignant cells. (+info)
Minimal residual disease in patients with hairy cell leukemia in complete remission treated with 2-chlorodeoxyadenosine or 2-deoxycoformycin and prediction of early relapse. (7/220)The purine nucleoside analogues 2-chlorodeoxyadenosine (2-CdA) and 2'-deoxycoformycin (2'-DCF) induce complete remission (CR) in the majority of patients with hairy cell leukemia. However, minimal residual disease (MRD) has been detected in bone marrow core biopsies using immunohistochemical techniques in patients achieving CR by conventional criteria. This study was designed to compare the prevalence of MRD with each agent in patients in CR by using conventional criteria and the relapse-free survival for patients with and without MRD. Bone marrow biopsies from 39 patients treated with a single cycle of 2-CdA and 27 patients treated with multiple cycles of 2'-DCF were studied. The monoclonal antibodies anti-CD20, DBA.44, and anti-CD45RO were used to evaluate the paraffin-embedded bone marrow core biopsies for MRD. Five of 39 patients (13%) treated with 2-CdA had MRD, as compared to 7 of 27 patients (26%) treated with 2'-DCF (two-tailed P = 0.21). Relapse has occurred in two of the five patients with MRD after 2-CdA treatment and in four of the seven patients with MRD after 2'-DCF treatment. In total, 6 of the 12 patients (50%) with MRD have relapsed, whereas 3 of 54 patients (6%) without MRD have relapsed, and 2 patients have died without evidence of relapse. The estimated 4-year relapse-free survival among patients with MRD is 55% (+/- 15%, SE), compared to 88% (+/- 5%, SE) among patients without MRD (two-tailed P = 0.0023). The prevalence of MRD detected in a subset of patients in CR after either 2-CdA or 2'-DCF treatment did not differ significantly. However, the presence of MRD is associated with an increased risk of relapse. (+info)
Biochemical pharmacology and resistance to 2-chloro-2'-arabino-fluoro-2'-deoxyadenosine, a novel analogue of cladribine in human leukemic cells. (8/220)The objective of the present study was to investigate the biochemical pharmacology of 2-chloro-2'-arabino-fluoro-2'-deoxyadenosine (CAFdA)--a fluorinated analogue of cladribine [2-chloro-2'-deoxyadenosine, Leustatin (CdA)] with improved acid and metabolic stability--in human leukemic cell lines and in mononuclear cells isolated from patients with chronic lymphocytic leukemia (CLL) and acute myelocytic leukemia (AML). We have also made and characterized two cell lines that are not sensitive to the growth inhibitory and cytotoxic effects of CAFdA. Incubation of cells isolated from the blood of CLL and AML patients with various concentrations of CdA or of CAFdA accumulated CdA and CAFdA nucleotides in a dose-dependent manner. A significantly higher rate of phosphorylation to monophosphates was observed for CAFdA than for CdA in cells from CLL patients (n = 14; P = 0.04). The differences in the phosphorylation were even more pronounced for the respective triphosphates in both CLL (n = 14; P = 0.001) and AML (n = 4; P = 0.04) cells. Retention of CAFdA 5'-triphosphate (CAFdATP) was also longer than that for CdA 5'-triphosphate (CdATP) in cells from leukemic patients. The relative efficacy of CAFdA as a substrate for purified recombinant deoxycytidine kinase (dCK), the key enzyme in the activation of nucleoside analogues, was very high and exceeded that of CdA as well as the natural substrate, deoxycytidine, by a factor of 2 and 8, respectively. The Km for CAFdA with dCK was also lower than that for CdA, as measured in crude extracts from the human acute lymphoblastic leukemia cell line CCRF-CEM and the promyelocytic leukemia cell line HL60. Acquired resistance to CAFdA in HL60 and in CCRF-CEM cell lines was directly correlated to the decreased activity of the nucleoside phosphorylating enzyme, dCK. Resistant cells also showed a considerable degree of cross-resistance to analogues that were activated by dCK. These observations demonstrated that dCK phosphorylates CAFdA more efficiently than CdA. Furthermore, CAFdATP is apparently more stable than CdATP and the mechanisms of resistance to CAFdA are similar to those leading to CdA resistance. These results encourage studies on the clinical effect of CAFdA in lymphoproliferative diseases. (+info)
Hairy cell leukemia typically affects older adults, and it is usually slow-growing and progresses gradually over many years. Symptoms of hairy cell leukemia can include fatigue, weakness, weight loss, fever, night sweats, and swollen lymph nodes.
Hairy cell leukemia is diagnosed through a combination of physical examination, medical history, blood tests, and bone marrow biopsy. Treatment for hairy cell leukemia typically involves chemotherapy, radiation therapy, or a combination of both. In some cases, the disease may go into remission with treatment, but it can also be a chronic condition that requires ongoing management.
Prevention: There is no known prevention for hairy cell leukemia, as the cause of the disease is not fully understood. However, early detection and treatment can improve outcomes.
Prognosis: The prognosis for hairy cell leukemia varies depending on the individual patient and the aggressiveness of the disease. In general, the condition tends to be slow-growing and progresses gradually over many years. With appropriate treatment, some patients can achieve long-term remission or even be cured. However, in more advanced cases, the disease can be more difficult to treat and may have a poorer prognosis.
Symptoms: Symptoms of hairy cell leukemia can include fatigue, weakness, weight loss, fever, night sweats, and swollen lymph nodes. These symptoms can develop gradually over time, and they may be mild at first but become more severe as the disease progresses.
Treatment: Treatment for hairy cell leukemia typically involves chemotherapy, radiation therapy, or a combination of both. The specific treatment plan will depend on the individual patient and the severity of their condition. In some cases, watchful waiting may be appropriate, especially if the disease is not causing significant symptoms.
Lifestyle Changes: There are no lifestyle changes that can cure hairy cell leukemia, but they can help improve overall health and well-being. These changes may include eating a healthy diet, getting regular exercise, getting enough rest, and managing stress. In addition, avoiding exposure to certain chemicals and toxins may be beneficial for some patients.
Medications: There are several medications that can be used to treat hairy cell leukemia. These include chemotherapy drugs such as pentostatin and cladribine, which can help kill cancer cells and slow the progression of the disease. In addition, some patients may receive radiation therapy to help shrink swollen lymph nodes or other affected tissues.
Supportive Care: Supportive care is an important part of treatment for hairy cell leukemia. This type of care focuses on managing symptoms and improving quality of life, rather than directly targeting the cancer cells. Supportive care may include medications to manage pain, fatigue, or infection, as well as blood transfusions to help improve anemia.
Bone Marrow Transplant: In some cases, bone marrow transplant may be an option for patients with hairy cell leukemia. This involves replacing the patient's bone marrow with healthy cells from a donor, which can help cure the disease. However, this is typically reserved for patients who have not responded to other treatments or who have experienced significant complications from the disease.
Overall, the prognosis for hairy cell leukemia is generally good, with many patients experiencing a good response to treatment and a low risk of complications. However, it is important for patients to work closely with their healthcare team to develop a personalized treatment plan that meets their individual needs and helps them achieve the best possible outcome.
In LLCB, the B cells undergo a mutation that causes them to become cancerous and multiply rapidly. This can lead to an overproduction of these cells in the bone marrow, causing the bone marrow to become crowded and unable to produce healthy red blood cells, platelets, and white blood cells.
LLCB is typically a slow-growing cancer, and it can take years for symptoms to develop. However, as the cancer progresses, it can lead to a range of symptoms including fatigue, weakness, weight loss, fever, night sweats, and swollen lymph nodes.
LLCB is typically diagnosed through a combination of physical examination, blood tests, bone marrow biopsy, and imaging studies such as X-rays or CT scans. Treatment options for LLCB include chemotherapy, radiation therapy, and in some cases, stem cell transplantation.
Overall, while LLCB is a serious condition, it is typically slow-growing and can be managed with appropriate treatment. With current treatments, many people with LLCB can achieve long-term remission and a good quality of life.
Note: This definition is a summary of key points and may not include all information or nuances relevant to medical professionals.
The disease is named after the Swedish physician Jan G. Waldenström, who first described it in 1944. It is also known as lymphoplasmacytic lymphoma or IgM multoculullarity.
The exact cause of Waldenström macroglobulinemia is not known, but it is believed to be linked to genetic mutations that occur in the plasma cells. The condition usually affects older adults and is more common in males than females.
Symptoms of Waldenström macroglobulinemia can include:
* Weight loss
* Enlargement of the liver and spleen
* Swelling in the legs, ankles, and hands
* Pain in the bones or joints
* Increased risk of infections
* Numbness or tingling in the hands and feet
The diagnosis of Waldenström macroglobulinemia is based on a combination of physical examination, blood tests, and imaging studies. Treatment options include chemotherapy, immunomodulatory drugs, and stem cell transplantation. The prognosis for the disease varies depending on the severity of the symptoms and the response to treatment.
Overall, Waldenström macroglobulinemia is a rare and complex condition that requires careful management by a team of healthcare professionals. With appropriate treatment, many patients with this condition can experience long-term remission and improved quality of life.
There are several subtypes of NHL, including:
1. B-cell lymphomas (such as diffuse large B-cell lymphoma and follicular lymphoma)
2. T-cell lymphomas (such as peripheral T-cell lymphoma and mycosis fungoides)
3. Natural killer cell lymphomas (such as nasal NK/T-cell lymphoma)
4. Histiocyte-rich B-cell lymphoma
5. Primary mediastinal B-cell lymphoma
6. Mantle cell lymphoma
7. Waldenström macroglobulinemia
8. Lymphoplasmacytoid lymphoma
9. Myelodysplastic syndrome/myeloproliferative neoplasms (MDS/MPN) related lymphoma
These subtypes can be further divided into other categories based on the specific characteristics of the cancer cells.
Symptoms of NHL can vary depending on the location and size of the tumor, but may include:
* Swollen lymph nodes in the neck, underarm, or groin
* Weight loss
* Night sweats
* Abdominal pain
* Swollen spleen
Treatment for NHL typically involves a combination of chemotherapy, radiation therapy, and in some cases, targeted therapy or immunotherapy. The specific treatment plan will depend on the subtype of NHL, the stage of the cancer, and other individual factors.
Overall, NHL is a complex and diverse group of cancers that require specialized care from a team of medical professionals, including hematologists, oncologists, radiation therapists, and other support staff. With advances in technology and treatment options, many people with NHL can achieve long-term remission or a cure.
Recurrence can also refer to the re-emergence of symptoms in a previously treated condition, such as a chronic pain condition that returns after a period of remission.
In medical research, recurrence is often studied to understand the underlying causes of disease progression and to develop new treatments and interventions to prevent or delay its return.
A residual neoplasm is a remaining portion of a tumor that may persist after primary treatment. This can occur when the treatment does not completely remove all of the cancer cells or if some cancer cells are resistant to the treatment. Residual neoplasms can be benign (non-cancerous) or malignant (cancerous).
It is important to note that a residual neoplasm does not necessarily mean that the cancer has come back. In some cases, a residual neoplasm may be present from the start and may not grow or change over time.
Residual neoplasms can be managed with additional treatment, such as surgery, chemotherapy, or radiation therapy. The choice of treatment depends on the type of cancer, the size and location of the residual neoplasm, and other factors.
It is important to follow up with your healthcare provider regularly to monitor the residual neoplasm and ensure that it is not growing or causing any symptoms.
Symptoms of neutropenia may include recurring infections, fever, fatigue, weight loss, and swollen lymph nodes. The diagnosis is typically made through a blood test that measures the number of neutrophils in the blood.
Treatment options for neutropenia depend on the underlying cause but may include antibiotics, supportive care to manage symptoms, and in severe cases, bone marrow transplantation or granulocyte-colony stimulating factor (G-CSF) therapy to increase neutrophil production.
There are several subtypes of lymphoma, B-cell, including:
1. Diffuse large B-cell lymphoma (DLBCL): This is the most common type of B-cell lymphoma and typically affects older adults.
2. Follicular lymphoma: This type of lymphoma grows slowly and often does not require treatment for several years.
3. Marginal zone lymphoma: This type of lymphoma develops in the marginal zone of the spleen or other lymphoid tissues.
4. Hodgkin lymphoma: This is a type of B-cell lymphoma that is characterized by the presence of Reed-Sternberg cells, which are abnormal cells that can be identified under a microscope.
The symptoms of lymphoma, B-cell can vary depending on the subtype and the location of the tumor. Common symptoms include swollen lymph nodes, fatigue, fever, night sweats, and weight loss.
Treatment for lymphoma, B-cell usually involves chemotherapy, which is a type of cancer treatment that uses drugs to kill cancer cells. Radiation therapy may also be used in some cases. In some cases, bone marrow or stem cell transplantation may be recommended.
Prognosis for lymphoma, B-cell depends on the subtype and the stage of the disease at the time of diagnosis. In general, the prognosis is good for patients with early-stage disease, but the cancer can be more difficult to treat if it has spread to other parts of the body.
Prevention of lymphoma, B-cell is not possible, as the exact cause of the disease is not known. However, avoiding exposure to certain risk factors, such as viral infections and pesticides, may help reduce the risk of developing the disease. Early detection and treatment can also improve outcomes for patients with lymphoma, B-cell.
Lymphoma, B-cell is a type of cancer that affects the immune system and can be treated with chemotherapy and other therapies. The prognosis varies depending on the subtype and stage of the disease at diagnosis. Prevention is not possible, but early detection and treatment can improve outcomes for patients with this condition.
AML is a fast-growing and aggressive form of leukemia that can spread to other parts of the body through the bloodstream. It is most commonly seen in adults over the age of 60, but it can also occur in children.
There are several subtypes of AML, including:
1. Acute promyelocytic leukemia (APL): This is a subtype of AML that is characterized by the presence of a specific genetic abnormality called the PML-RARA fusion gene. It is usually responsive to treatment with chemotherapy and has a good prognosis.
2. Acute myeloid leukemia, not otherwise specified (NOS): This is the most common subtype of AML and does not have any specific genetic abnormalities. It can be more difficult to treat and has a poorer prognosis than other subtypes.
3. Chronic myelomonocytic leukemia (CMML): This is a subtype of AML that is characterized by the presence of too many immature white blood cells called monocytes in the blood and bone marrow. It can progress slowly over time and may require ongoing treatment.
4. Juvenile myeloid leukemia (JMML): This is a rare subtype of AML that occurs in children under the age of 18. It is characterized by the presence of too many immature white blood cells called blasts in the blood and bone marrow.
The symptoms of AML can vary depending on the subtype and the severity of the disease, but they may include:
* Shortness of breath
* Pale skin
* Easy bruising or bleeding
* Swollen lymph nodes, liver, or spleen
* Bone pain
* Confusion or seizures
AML is diagnosed through a combination of physical examination, medical history, and diagnostic tests such as:
1. Complete blood count (CBC): This test measures the number and types of cells in the blood, including red blood cells, white blood cells, and platelets.
2. Bone marrow biopsy: This test involves removing a small sample of bone marrow tissue from the hipbone or breastbone to examine under a microscope for signs of leukemia cells.
3. Genetic testing: This test can help identify specific genetic abnormalities that are associated with AML.
4. Immunophenotyping: This test uses antibodies to identify the surface proteins on leukemia cells, which can help diagnose the subtype of AML.
5. Cytogenetics: This test involves staining the bone marrow cells with dyes to look for specific changes in the chromosomes that are associated with AML.
Treatment for AML typically involves a combination of chemotherapy, targeted therapy, and in some cases, bone marrow transplantation. The specific treatment plan will depend on the subtype of AML, the patient's age and overall health, and other factors. Some common treatments for AML include:
1. Chemotherapy: This involves using drugs to kill cancer cells. The most commonly used chemotherapy drugs for AML are cytarabine (Ara-C) and anthracyclines such as daunorubicin (DaunoXome) and idarubicin (Idamycin).
2. Targeted therapy: This involves using drugs that specifically target the genetic abnormalities that are causing the cancer. Examples of targeted therapies used for AML include midostaurin (Rydapt) and gilteritinib (Xospata).
3. Bone marrow transplantation: This involves replacing the diseased bone marrow with healthy bone marrow from a donor. This is typically done after high-dose chemotherapy to destroy the cancer cells.
4. Supportive care: This includes treatments to manage symptoms and side effects of the disease and its treatment, such as anemia, infection, and bleeding. Examples of supportive care for AML include blood transfusions, antibiotics, and platelet transfusions.
5. Clinical trials: These are research studies that involve testing new treatments for AML. Participating in a clinical trial may give patients access to innovative therapies that are not yet widely available.
It's important to note that the treatment plan for AML is highly individualized, and the specific treatments used will depend on the patient's age, overall health, and other factors. Patients should work closely with their healthcare team to determine the best course of treatment for their specific needs.
There are several possible causes of thrombocytopenia, including:
1. Immune-mediated disorders such as idiopathic thrombocytopenic purpura (ITP) or systemic lupus erythematosus (SLE).
2. Bone marrow disorders such as aplastic anemia or leukemia.
3. Viral infections such as HIV or hepatitis C.
4. Medications such as chemotherapy or non-steroidal anti-inflammatory drugs (NSAIDs).
5. Vitamin deficiencies, especially vitamin B12 and folate.
6. Genetic disorders such as Bernard-Soulier syndrome.
7. Sepsis or other severe infections.
8. Disseminated intravascular coagulation (DIC), a condition where blood clots form throughout the body.
9. Postpartum thrombocytopenia, which can occur in some women after childbirth.
Symptoms of thrombocytopenia may include easy bruising, petechiae (small red or purple spots on the skin), and prolonged bleeding from injuries or surgical sites. Treatment options depend on the underlying cause but may include platelet transfusions, steroids, immunosuppressive drugs, and in severe cases, surgery.
In summary, thrombocytopenia is a condition characterized by low platelet counts that can increase the risk of bleeding and bruising. It can be caused by various factors, and treatment options vary depending on the underlying cause.
Previous articleNeoplastic Cells
Disease progression can be classified into several types based on the pattern of worsening:
1. Chronic progressive disease: In this type, the disease worsens steadily over time, with a gradual increase in symptoms and decline in function. Examples include rheumatoid arthritis, osteoarthritis, and Parkinson's disease.
2. Acute progressive disease: This type of disease worsens rapidly over a short period, often followed by periods of stability. Examples include sepsis, acute myocardial infarction (heart attack), and stroke.
3. Cyclical disease: In this type, the disease follows a cycle of worsening and improvement, with periodic exacerbations and remissions. Examples include multiple sclerosis, lupus, and rheumatoid arthritis.
4. Recurrent disease: This type is characterized by episodes of worsening followed by periods of recovery. Examples include migraine headaches, asthma, and appendicitis.
5. Catastrophic disease: In this type, the disease progresses rapidly and unpredictably, with a poor prognosis. Examples include cancer, AIDS, and organ failure.
Disease progression can be influenced by various factors, including:
1. Genetics: Some diseases are inherited and may have a predetermined course of progression.
2. Lifestyle: Factors such as smoking, lack of exercise, and poor diet can contribute to disease progression.
3. Environmental factors: Exposure to toxins, allergens, and other environmental stressors can influence disease progression.
4. Medical treatment: The effectiveness of medical treatment can impact disease progression, either by slowing or halting the disease process or by causing unintended side effects.
5. Co-morbidities: The presence of multiple diseases or conditions can interact and affect each other's progression.
Understanding the type and factors influencing disease progression is essential for developing effective treatment plans and improving patient outcomes.
This definition of 'Neoplasm Recurrence, Local' is from the Healthcare Professionals edition of the Merriam-Webster Medical Dictionary, copyright © 2007 by Merriam-Webster, Inc.
List of antineoplastic agents
Management of multiple sclerosis
Hairy cell leukemia
Multiple sclerosis drug pipeline
Mosquito bite allergy
Mantle cell lymphoma
Cotton wool spots
Gluten-sensitive enteropathy-associated conditions
New Drug Application
Malignant multiple sclerosis
List of drugs: Cj-Cl
Ribonucleotide reductase inhibitor
ATC code L04
ATC code L01
Individualized Dosing of Cladribine Cuts Lymphopenia Risk
Cladribine: MedlinePlus Drug Information
MedlinePlus - Search Results for: CLADRIBINE
Cladribine - PubMed
Cladribine - PubChem Substance - NCBI
Cladribine - Drugs and Lactation Database (LactMed®) - NCBI Bookshelf
Cladribine and Rituximab in Treating Patients With Hairy Cell Leukemia - Full Text View - ClinicalTrials.gov
Erdheim Chester Disease treated successfully with cladribine - Fingerprint - Mayo Clinic
Specific Patterns of Immune Cell Dynamics May Explain the Early Onset and Prolonged Efficacy of Cladribine Tablets | Neurology...
Common and Rare Side Effects for Mavenclad
Cladribine (Leustatin, Mavenclad) | Davis's Drug Guide
Mavenclad® (cladribine) Tablets for RRMS & SPMS | Risk Info
Cladribine plus rituximab is an effective therapy for newly diagnosed mantle cell lymphoma. | Leuk Lymphoma;52(8): 1488-94,...
EMD Serono Receives Refuse to File Letter from FDA on Cladribine Tablets NewDrug Application - Pharmaceutical Processing World
Comments on Cladribine Oral Tablets (10mg) for Multiple Sclerosis
MS Treatments - MS Australia
Research Projects & Publications at the Global Neurology Research Group
Table 2 - Analysis of MarketScan Data for Immunosuppressive Conditions and Hospitalizations for Acute Respiratory Illness,...
Effectiveness of cladribine therapy in patients with pulmonary Langerhans cell histiocytosis. | Read by QxMD
Pharmaceutical Benefits Scheme (PBS) | PBS Medicine Search
Mavenclad side effects: What they are and how to manage them
Prochlorperazine Monograph for Professionals - Drugs.com
Is the COVID-19 Vaccine Safe If You Have MS?
Mavenclad - Side Effects, Uses, Dosage, Overdose, Pregnancy, Alcohol | RxWiki
Cladribine Market will reach at a CAGR of 5.1% from to 2033
Hairy cell leu21
- Serious neurological toxicity (including irreversible paraparesis and quadraparesis) has been reported in patients who received cladribine injection by continuous infusion at high doses (4 to 9 times the recommended dose for Hairy Cell Leukemia). (nih.gov)
- Acute nephrotoxicity has been observed with high doses of cladribine (4 to 9 times the recommended dose for Hairy Cell Leukemia), especially when given concomitantly with other nephrotoxic agents/therapies. (nih.gov)
- In a clinical investigation, 17 patients with Hairy Cell Leukemia and normal renal function were treated for 7 days with the recommended treatment regimen of cladribine (0.09 mg/kg/day) by continuous intravenous infusion. (nih.gov)
- Cladribine is used to treat hairy cell leukemia (cancer of a certain type of white blood cell). (nih.gov)
- Cladribine is a purine analogue and antineoplastic agent used primarily in the therapy of hairy cell leukemia. (nih.gov)
- Cladribine (klad' ri been) is a purine analogue (2-chlorodeoxyadeosine) that is used predominantly in the treatment of hairy cell leukemia. (nih.gov)
- Cladribine has been used off-label to treat low grade lymphomas and other hematologic malignancies, but its current formal indications are limited to therapy of active hairy cell leukemia. (nih.gov)
- In high doses, above what is recommended for hairy cell leukemia, cladribine has been reported to have acute neurologic toxicity. (nih.gov)
- Since its approval and wide scale use in hairy cell leukemia there have been no reports of clinically apparent liver injury attributable to cladribine administration. (nih.gov)
- Hairy cell leukemia (HCL) is highly responsive to but not curable by cladribine (CdA). (nih.gov)
- 1. High prevalence of antibiotic allergies in cladribine-treated patients with hairy cell leukemia - lessons for immunopathogenesis and prescribing. (nih.gov)
- 3. High incidence of skin rash in patients with hairy cell leukemia treated with cladribine. (nih.gov)
- 4. Primary peg-filgrastim prophylaxis versus filgrastim given "on demand" for neutropenia during therapy with cladribine for hairy cell leukemia. (nih.gov)
- 7. Cladribine in a weekly versus daily schedule for untreated active hairy cell leukemia: final report from the Polish Adult Leukemia Group (PALG) of a prospective, randomized, multicenter trial. (nih.gov)
- 8. 2-chlorodeoxyadenosine (cladribine) in the treatment of hairy cell leukemia and hairy cell leukemia variant: 7-year experience in Poland. (nih.gov)
- 9. Treatment of hairy cell leukemia-variant with cladribine. (nih.gov)
- 12. Multicenter retrospective analysis regarding the clinical manifestations and treatment results in patients with hairy cell leukemia: twenty-four year Turkish experience in cladribine therapy. (nih.gov)
- 14. Very long-term eradication of minimal residual disease in patients with hairy cell leukemia after a single course of cladribine. (nih.gov)
- 15. Cladribine in hairy cell leukemia. (nih.gov)
- 16. Cladribine in the treatment of hairy cell leukemia: initial and subsequent results. (nih.gov)
- Treatment for hairy cell leukemia with cladribine was initiated after 10 weeks of antimicrobial drug treatment. (cdc.gov)
- tell your doctor and pharmacist if you are allergic to cladribine, any other medications, or any of the ingredients in cladribine tablets. (medlineplus.gov)
- Background: The COVID-19 pandemic has become a significant concern for patients with multiple sclerosis (MS) and their healthcare providers, prompting various guidelines on the appropriate use of disease-modifying therapies (DMT) such as cladribine tablets (CladT). (cmscscholar.org)
- Merck, a leading science and technology company, today announced that the European Commission (EC) has granted marketing authorization for MAVENCLAD® 10mg (Cladribine Tablets) for the treatment of highly active relapsing multiple sclerosis* (RMS)  in the 28 countries of the European Union (EU) in addition to Norway, Liechtenstein and Iceland. (reachmd.com)
Courses of cladribine3
- We retrospectively studied 5 patients (aged 37-55 years, 3 females) with PLCH who received 3 to 4 courses of cladribine therapy as a single agent (0.1 mg/kg per day for 5 consecutive days at monthly intervals). (qxmd.com)
- To compare response and MRD after the 1st and 2nd courses of cladribine. (nih.gov)
- HCL with 0-1 prior courses of cladribine and treatment indicated. (nih.gov)
Allergic to cladribine1
- are allergic to cladribine. (mavenclad.com)
Eliminated by rituximab1
- In studies with limited follow-up, MRD detected by tests other than RQ-PCR can be eliminated by rituximab after cladribine in greater than 90 percent of patients, but MRD rates after cladribine alone are unknown. (nih.gov)
- Cladribine is available as a solution for injection generically and under the trade name Leustatin. (nih.gov)
- Cladribine Injection, USP is available in single-use vials containing 10 mg (1 mg/mL) of cladribine, a chlorinated purine nucleoside analog. (nih.gov)
- Cladribine is generally used in patients who have already tried another treatment for MS. Cladribine in a class of medications called purine antimetabolites. (medlineplus.gov)
- Expert review of hepatotoxicity of cancer chemotherapeutic agents published in 1999 mentions that fludarabine and cladribine were new purine analogues that had yet to be implicated in causing hepatic injury). (nih.gov)
- Cladribine Injection should be administered under the supervision of a qualified physician experienced in the use of antineoplastic therapy. (nih.gov)
- Cladribine Injection, USP (also commonly known as 2-chloro-2´-deoxy-ß-D-adenosine) is a synthetic antineoplastic agent for continuous intravenous infusion. (nih.gov)
- Each mL of cladribine injection, USP contains 1 mg of the active ingredient and 9 mg (0.15 mEq) of sodium chloride as an inactive ingredient. (nih.gov)
- According to the Market Statsville Group (MSG), the global cladribine market size is expected to grow at a CAGR of 5.1% from 2023 to 2033. (a2zbookmarks.com)
- Patients in complete remission (CR) to cladribine have minimal residual disease (MRD) by immunohistochemistry of the bone marrow biopsy (BMBx IHC), a risk for early relapse. (nih.gov)
- 11. Long-term durable remission by cladribine followed by rituximab in patients with hairy cell leukaemia: update of a phase II trial. (nih.gov)
- Deoxycytidine kinase phosphorylates cladribine to CdATP, which incorporates into DNA, leading to DNA strand breaks and inhibition of DNA synthesis. (nih.gov)
- The lack of hepatotoxicity of cladribine may relate to the short duration of therapy, low doses used and its minimal hepatic metabolism. (nih.gov)
- Only 4 HCL-specific trials are listed on Cancer.gov: a phase II trial of cladribine followed 4 weeks later by 8 weekly doses of rituximab, and phase I-II trials of recombinant immunotoxins targeting CD22 (BL22, HA22) and CD25 (LMB-2). (nih.gov)
- if you are taking any other medications by mouth, take them 3 hours before or 3 hours after cladribine. (medlineplus.gov)
- however, severe neurological toxicity has been reported rarely following treatment with standard cladribine dosing regimens. (nih.gov)
- You should use birth control to prevent pregnancy during each course of treatment with cladribine and for at least six months after your last dose of each treatment course. (medlineplus.gov)
- If you are using hormonal (estrogen) contraceptives (birth control pills, patches, rings, implants, or injections) you should also use another method of birth control during each course of treatment with cladribine and for at least 4 weeks after your last dose of each treatment course. (medlineplus.gov)
- If you are a male with a female partner who could become pregnant, be sure to use birth control during each course of treatment with cladribine and for at least six months after your last dose of each treatment course. (medlineplus.gov)
- Your doctor or pharmacist will give you the manufacturer's patient information sheet (Medication Guide) when you begin treatment with cladribine and each time you refill your prescription. (medlineplus.gov)
- They gave written consent to receive off-label cladribine in the absence of validated treatment. (qxmd.com)
- Functional class dyspnea improved with cladribine therapy in 4 out of 5 cases, and forced expiratory volume in 1 second (FEV1) increased in all cases by a mean of 387 ml (100-920 ml), contrasting with a steady decline prior to treatment. (qxmd.com)
- Cladribine is typically given intravenously daily for 7 days, usually as a single course, and has not been associated with serum enzyme elevations during therapy or with instances of clinically apparent acute liver injury with jaundice. (nih.gov)
- In clinical trials, cladribine was not associated with elevations in serum enzymes or bilirubin levels either during or after therapy. (nih.gov)
- To determine if MRD levels and tumor markers (soluble CD25 and CD22) after cladribine and/or rituximab correlate with response and clinical endpoints. (nih.gov)
- Chest high-resolution computed tomography (HRCT) features improved with cladribine therapy in 4 patients. (qxmd.com)
- Cladribine as a single agent may be effective therapy in patients with progressive PLCH. (qxmd.com)
- Patients with the CD25-negative variant (HCLv) respond poorly to initial cladribine but do respond to rituximab in anecdotal reports. (nih.gov)
- Rituximab 375 mg/m2/week times 8 weeks, randomized half to begin day 1, then repeat for all patients with blood-MRD relapse at least 6 months after cladribine. (nih.gov)
- Stratification: 68 patients with 0 and 62 with 1 prior course of cladribine. (nih.gov)
- Results Booster dose increased anti-RBD-IgG titers in fingolimod-treated, cladribine-treated and IFN-β-treated patients, but not in ocrelizumab-treated patients, although antibody titres were lower than HCWs. (bmj.com)
- In addition, opportunistic viral infections are common during the month after cladribine therapy and appropriate vaccination is recommended before its use. (nih.gov)
- The MASTER-2 trial is an observational study to evaluate the effectiveness and patient-reported outcomes in people with relapsing forms of multiple sclerosis who are transitioning from ocrelizumab to cladribine. (massgeneral.org)
- Cladribine was found to have marked activity against hairy leukemia and was approved for this use in the United States in 1993. (nih.gov)
- Emergency Central , emergency.unboundmedicine.com/emergency/view/Davis-Drug-Guide/51158/11.0/cladribine. (unboundmedicine.com)
- Non-randomized arm: 20 with HCLv will begin rituximab with cladribine. (nih.gov)
- To determine if HCL MRD differs at 6 months after cladribine with or without rituximab administered concurrently with cladribine. (nih.gov)
- Review of hepatotoxicity of hepatotoxicity of anticancer agents does not discuss cladribine). (nih.gov)
- To evaluate the effects of cladribine and rituximab on normal T- and B-cells. (nih.gov)