This trial is evaluating whether Hydrocortisone Sodium Succinate will improve 2 primary outcomes, 8 secondary outcomes, and 1 other outcome in patients with Leukemia. Measurement will happen over the course of Up to 90 days.
This trial requires 5956 total participants across 8 different treatment groups
This trial involves 8 different treatments. Hydrocortisone Sodium Succinate is the primary treatment being studied. Participants will be divided into 7 treatment groups. There is no placebo group. The treatments being tested are in Phase 3 and have had some early promising results.
Leukemia is a cancer involving the blood, bone marrow or other leukocytes. Leukemia typically causes a decrease in the production or function of white blood cells, which may cause a drop in blood counts and anemia. Leukemias cause a range of symptoms depending on the type, including fatigue, itching, a dry, sore mouth, weight loss, fever, and hair loss. Symptoms can worsen in the later stages of the disease.
When the course of disease is carefully managed, many patients can live a normal life with minimal symptoms and few relapse episodes. This is possible even when multiple relapses occur during the initial remission phase.
The treatments of acute myeloid leukemia (AML) and chronic myeloid leukemia (CML) are similar. The most common treatment is standard induction chemotherapy, followed by consolidation chemotherapy. The treatment of AML and CML is often a chemo-resistant disease. There is no cure for AML or CML. Treatment of these cancers is targeted to stop tumor cell proliferation or to control damage to other parts of the body. The key to these successful treatments is careful monitoring of the disease and treatment response.
Leukemia and multiple myeloma can be explained by genetic abnormalities and/or exposure to external or internal carcinogens, and these explanations may be applicable to depression as well. Treatment of depression and the causes of acute leukemia are similar.
Around 1 in 6 people have a malignant primary leukemia. About 1 in 3 people die of leukemia, and 1 in 3 people have a lymphoid chronic leukemia.
Cytarabine given for 2 weeks showed similar efficacy in the treatment of acute myeloid leukaemia as a comparator treatment. There was a significant advantage in the number of patients who went into remission.
Cytarabine (ara-C, ara-C) is often used as salvage therapy after more expensive, high-dose chemotherapy. It is effective at treating some acute leukemias, including acute lymphocytic leukaemia and myelodysplastic syndromes, but is less effective than fludarabine in the treatment of acute myeloid leukaemia (and is contraindicated in acute myeloid leukaemia if the patient is an elderly patient with comorbidities). It is sometimes used as induction therapy prior to high-dose chemotherapy.
The research on AML is very diverse. Results from a recent clinical trial summarizes and compares current available information, aiming to highlight some of the most relevant factors. This information will encourage physicians, and most importantly patients, to understand the complexity of this disease and to understand more about the treatment strategies available to them.
Cytosine arabinoside is a medication that is sometimes used to treat Hodgkin's disease and acute myeloid leukemia; however, it is also used recreationally as an illicit drug and the risks and benefits of doing so are not entirely clear. Cytarabine toxicity has been well described in the medical literature, and can be severe and often very severe. The risk factors for cytarabine toxicity are age, disease load, underlying comorbidities, the cumulative dose of Cytarabine, the dose per dose for a given schedule, and the presence of certain genetic causes of cytarabine hypersensitivity.
Despite significant family history, only 1.7% of hematologic MDS patients with a HUS2 mutation had a mutation carrier in their first-degree relatives. Further study is warranted to explore whether there is heterogeneity in the family history or if the penetrance is incomplete.
While the exact etiology of CLL is poorly characterized, several hypotheses are proposed in the present paper, including environmental exposures, genetic predisposition, somatic mutations in the leukemic clone, infectious events, epigenetic factors, or a combination of these. Further studies will be needed to determine the specific pathogenic mechanisms of CLL.