High Protein, Low Carbohydrate, High Non-Trans Fat, and Decitabine for Survival-ITP and LGC Leukemia
Abstract
Introduction: Therapy of TP53, mutation of MSD/AML with Niclosamide plus Azacitidine, is the end-stage phase of ITP/LGC Leukemia. The Constant therapy is unbroken with CHOP or R-CHOP as the second line therapy, plus nutrition HPLCHF, and decitabine ever since the early phase which should be given. Aims: No transfusion should beheld since this early phase. Cytokine storm is the inducer of this advancement. Hypothesis: High Protein Low Carbohydrate High Fat (HPLCHF) and decitabine without transfusion should be the winner for survival ITP/LGC. Liquid therapy and aspirin are the first line symptomatic during the cytokine storm phase. Two dead cases of Large Granular Chronic Leukemia support this study. Method: Hybrid My library and ChatGPT based, with academic search engine using Science Direct and EBSCOHost MEDLINE full text using
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Introduction
Anemia Immune Thrombocytopenia (ITP) a.k.a. Previously Idiopathic Thrombocytopenia Purpura progressed to MDS/AML or is a Life-threatening situation “bridge therapy” to surgery or invasive procedure,1 splenectomy and or chemotherapy. ITP due to Defective Peripheral Immune Response often has high prevalence causes of this disease in our everyday practice.1 ITP turns to MDS which increases bone marrow increasing of CD 34-blast, and CD16-granulocytes,2 then progresses to AML. Germline genetic (and epigenetic) have been recorded in MDS and AML traditional outpatients.3 AML is an aggressive hematological malignancy with a higher incidence in older people.4 Clonal hematopoiesis (Ch) is a common premalignant state in the blood and confers an increased risk of blood cancers and all-cause mortality.5 Variables drugs are recorded such as pro- apoptotic agent Venetoclax a Bcl2-inhibitor,4,6,7 Fistumatinib a spleen tyrosine Kinase inhibitor,8 decitabine/azacitidine hypomethylation agent,7,9,10 due to R-loop dysregulation and resultant genomic instability in the disease progression of MDS & AML,10 a therapy strategy for Myeloid cancers.10 Erythropoietin agents 11 and/or with RBC transfusion,12 which reported as a cause of first hospitalization due the decreasing hemoglobin which drops common everyday Quality of Life (QL).11 Daratumumab in refractory autoimmune cytopenia.13 Plasmapheresis (plasma exchange) for inflammation cytokine as the pathogenesis of MDS is yet to be fully established.12,14 Novel Anti-CD38 monoclonal antibody for treating ITP,15 Notable treatment advances have been made for patients with MDS/ neoplasm to live longer and better for what will likely remain a largely incurable disease,16describe the failure to complete recovery. This study brings to parsimony and calm reaction therapy like in fluidic only therapy on DHF in 16.000 platelet count is usually successful.(Case Report)
Conclusion
HPLCHF nutrition and decitabine ever since the early phase should be given to support the body to cure themselves.
