RESUMEN
Hypocellular AML being a rare entity with considerable overlapping features and characteristics with various other entities brings a need to have a better and clear understanding of hypocellular AML to differentiate in the decision-making process for therapeutic patient management. With some degree of dysplasia inherently associated with AML it is challenging to differentiate hypocellular AML from Myelodysplastic syndromes. We present a case report where the diagnostic dilemma in an elderly male patient who presented with fever, pallor, weight loss and fatiguability. On clinical examination, the patient had hepatomegaly. The patient was non-affording and was hence given supportive treatment, and he died soon after. Here the diagnostic dilemma is discussed along with the review of literature on hypocellular AML. A better and clear understanding of hypocellular AML is required to differentiate it from other entities due to the considerable overlap in presentation hence improving the decision-making process for therapeutic patient management. The shortcomings are realised, especially when the bone marrow cellularity is less than 10%. Our case report is written to enrich more understanding of the limited published literature on the subject.
RESUMEN
Acute myeloid leukemia (AML), although genetically and morphologically distinct from other B and T cell ALL subtypes, has one of the most rapidly progressing course and worse outcomes. The current diagnostic classification of AML offers best curative intent, the outcomes are not usually those that are expected at the start of therapy. This is partly attributed to the complex mechanism of leukemogenesis and resistance to chemotherapy. The underlying genetic mechanism of resistance is as complex as is the disease etiopathogenesis. Recent advances in therapy of drug resistant AML highlight the role of epigenetic targets. New FDA approved targeted therapy has also provided some evidence at improving outcomes in clinical trials. This review provides a detailed review of FDA approved targets and ongoing clinical trials for targeting CRISPER, CAR-T and other intestinal modalities for approach to epigenetictargets. However, this group of epigenetic targeted therapy needs more validation to prove its clinical efficacy. A systematic review of all published research on these targets, investigational agents and FDA approved targeted therapy summarizes this evidence. It also takes us through a brief review of mechanism of action and targets for therapy.
RESUMEN
INTRODUCTION: The diffuse parenchymal lung diseases (DPLD)/interstitial lung diseases (ILD) are progressive lung disorders with usually unclear etiology, poor long-term survival and no effective treatment. Their pathogenesis is characterized by alveolar epithelial cell injury, inflammation, epithelial-mesenchymal transition, and parenchymal fibrosis. Macrophages play diverse roles in their development, both in the acute phase and in tissue repair. AREAS COVERED: In this review, we summarize the current state of knowledge regarding the role of macrophages and their phenotypes in the immunopathogenesis of DPLDs; CVD-ILD, UIP, NSIP, DIP, RB-ILD, AIP, HP, Sarcoidosis, etc. Our goal is to update the understanding of the immune mechanisms underlying the initiation and progression of fibrosis in DPLDs. This will help in identification of biomarkers and in developing novel therapeutic strategies for DPLDs. A thorough literature search of the published studies in PubMed (from 1975 to 2020) was done. EXPERT OPINION: The macrophage associated inflammatory markers needs to be explored for their potential as biomarkers of disease activity and progression. Pharmacological targeting of macrophage activation may reduce the risk of macrophage activation syndrome (MAS) and help improving the survival and prognosis of these patients.
