Anemia (Macrocytic)
Charles Theisler in Adjuvant Medical Care, 2022
Macrocytic anemia is characterized by large red blood cells, but with reduced hemoglobin levels. This cell malformation is due to inhibition of DNA synthesis during red blood cell production. When DNA synthesis is impaired, the cell cycle cannot progress from the growth stage (G2) to the mitosis (M) stage. This leads to continuing cell growth without cell division, which presents as macrocytosis. Because the cells are abnormally large there are too few of them to carry adequate oxygen.
Peripheral nervous system
Matthew Tate, Johnathan Cooper-Knock, Zoe Hunter, Elizabeth Wood in Neurology and Clinical Neuroanatomy on the Move, 2015
Question 28 A 37-year-old man with a long history of changeable bowel habit and abdominal pain presents with a 5-month history of worsening tingling and burning pain in his hands and feet. On examination, he has no weakness or wasting of the distal limb muscles, and Romberg’s sign is negative, although he has impairment of vibration sense and proprioception in a glove-and-stocking distribution. Investigations reveal a macrocytic anaemia (mean corpuscular volume [MCV] 102).
Case 36: Supporting haematopoiesis
Sunil R. Lakhani, Caroline J. Finlayson, Susan A. Dilly, Mitesh Gandhi in Basic Pathology, 2016
Additional details in this case are the neutropenia and a macrocytic anaemia. Answer 2 In the bone marrow. The bone marrow synthesizes these three cellular elements of the peripheral blood. This is referred to as trilineage haematopoiesis and comprises erythropoiesis (red cells), myelopoiesis (granulocytes) and megakaryopoiesis (platelets via megakaryocytes).
Acquired platelet dysfunction and overproduction of platelet cyclic AMP in two patients with myeloid malignancies
Published in Platelets, 2019
Anna Lecchi, Eti A. Femia, Silvia La Marca, Francesco Onida, Andrea Artoni
The pathophysiology of impaired platelet function in acquired disorders is often poorly understood. We report two unrelated patients with hematologic malignancies associated with acquired severe bleeding diathesis, and complex platelet function abnormalities, including overproduction of the physiological inhibitor cyclic-AMP (cAMP). Patient 1, with mild macrocytic anemia and thrombocytopenia (100 x 109/L), was diagnosed with chronic myelomonocytic leukemia a few months after the onset of her bleeding diathesis and our analysis of platelet function. Patient 2, with bleeding diathesis of recent onset, was studied when his myelodysplastic syndrome with excess blasts had already progressed to acute myeloid leukemia. In both patients, platelet aggregation/ATP secretion, serum thromboxane B2, intraplatelet content of ADP, ATP, serotonin, and fibrinogen were severely impaired. Baseline platelet cAMP levels were mildly elevated and markedly increased after stimulation by prostaglandin E1. In conclusion, these are the first patients with myeloid malignancies associated with acquired severe platelet dysfunction and overproduction of cAMP.
Closing in on the pathogenesis of the 5q- syndrome
Published in Expert Review of Anticancer Therapy, 2010
Sean M Post, Alfonso Quintás-Cardama
Evaluation of: Barlow JL, Drynan LF, Hewett DR et al. A p53-dependent mechanism underlies macrocytic anemia in a mouse model of human 5q- syndrome. Nat. Med. 16(1), 59–66 (2010); and Starczynowski DT, Kuchenbauer F, Argiropoulos B et al. Identification of miR-145 and miR-146a as mediators of the 5q- syndrome phenotype. Nat. Med. 16(1), 49–58 (2009). Patients with 5q- syndrome are characterized by macrocytic anemia, normal to elevated platelet counts, and a propensity to develop acute myeloid leukemia. The 5q- syndrome is believed to be a clonal disorder of the hematopoietic precursors. Until recently, little was known regarding the molecular pathogenesis of this malignancy. Two recently published studies using genetic approaches have unraveled a small array of genes whose alteration recapitulates critical features of the 5q- syndrome including dysplasia, clonal dominance, and progression to acute myeloid leukemia.
Starvation marrow – gelatinous transformation of bone marrow
Published in Journal of Community Hospital Internal Medicine Perspectives, 2014
Eric Osgood, Salman Muddassir, Minal Jaju, Robert Moser, Farwa Farid, Nishith Mewada
Gelatinous bone marrow transformation (GMT), also known as starvation marrow, represents a rare pathological entity of unclear etiology, in which bone marrow histopathology demonstrates hypoplasia, fat atrophy, and gelatinous infiltration. The finding of gelatinous marrow transformation lacks disease specificity; rather, it is an indicator of severe illness and a marker of poor nutritional status, found in patients with eating disorders, acute febrile illnesses, acquired immunodeficiency syndrome, alcoholism, malignancies, and congestive heart failure. We present a middle-aged woman with a history of alcoholism, depression, and anorexia nervosa who presented with failure to thrive and macrocytic anemia, with bone marrow examination demonstrative of gelatinous transformation, all of which resolved with appropriate treatment. To our knowledge, there are very few cases of GMT which have been successfully treated; thus, our case highlights the importance of proper supportive management.
Related Knowledge Centers
- Anemia
- Erythrocytes
- Hemoglobin
- Red Blood Cell
- McV
- Megaloblasts
- McH