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Published in Andrew Schofield, Paul Schofield, The Complete SAQ Study Guide, 2019
Andrew Schofield, Paul Schofield
Macrocytic anaemia is diagnosed with finding a high MCV with low haemoglobin on full blood count. It has many causes, such as the ones mentioned above, and can be divided into megaloblastic and nonmegaloblastic. A megaloblast is a large nuclear red blood cell. A simple blood film will reveal if any megaloblasts are present. Pernicious anaemia is the commonest cause for megaloblastic macrocytic anaemia. It is an autoimmune disease, causing a lack of intrinsic factor due to autoimmune destruction of gastric parietal cells. Parietal cell antibodies are found in 90% of pernicious anaemia cases. Folate deficiency is another common cause for megaloblastic anaemia. There are four causes of deficiency: poor diet, e.g in vegans; increased demand occurring, e.g. in pregnancy; malabsorption, notably in coeliac disease; anti-folate drugs, e.g. methotrexate.
Barbiturates, Alcohol, And Tranquilizers
Published in S.J. Mulé, Henry Brill, Chemical and Biological Aspects of Drug Dependence, 2019
Prolonged ingestion of alcohol is commonly associated with megaloblastic anemia, and morphological changes in bone marrow smears. Vacuolation of erythroblasts and myelocytes occurs in proportion to the amount of ethanol taken. Such bone marrow changes may be related to a recently reported transient hemolysis associated with stomatocytosis (red cells in which the central area of pallor is replaced by a mouth-like unstained area) in acute alcoholics.31 When alcohol replaces a significant proportion of the diet and folate deficiency occurs, ring sideroblasts (indicative of abnormal iron incorporation into haem) appear in bone marrow. Normoblastic erythropoiesis is converted to megaloblastic in about ten days. Suppression of bone marrow hemopoiesis appears to be a direct toxic effect of ethanol since alcohol can suppress the normal erthropoietic response to minimum dietary doses of folic acid.32 Pyridoxine (vitamin B6) utilization also appears to be affected by alcohol, inasmuch as parenteral pyridoxal phosphate, but not pyridoxine, has caused the disappearance of ring sideroblasts from the marrow of alcoholics while alcohol was being continued. Megaloblasts, however, persisted in marrow smears.33
Case 15
Published in Atul B. Mehta, Keith Gomez, Clinical Haematology, 2017
Pernicious anaemia (PA). The blood film shows macrocytosis, anisocytosis and hypersegmented polymorphonuclear leukocytes. There is also a circulating megaloblast. Deficiency of vitamin B12 is caused by failure of gastric absorption of the vitamin. Antibodies to gastric parietal cells are present in 95% of patients with pernicious anaemia but only 10% of normal individuals. Antibodies to intrinsic factor are found in 60% of people with pernicious anaemia.
Diabetes mellitus and pernicious anemia: interrelated therapeutic triumphs discovered shortly after William Osler’s death
Published in Baylor University Medical Center Proceedings, 2020
In 1877, William Gardner and Osler described a patient who was almost certainly the first with the clinical, hematologic, and pathologic features to leave no doubt it was Addisonian pernicious anemia.12,13 The case was that of a 52-year-old Englishman who complained of weakness and dyspnea on exertion, numbness of the fingers and the hands (difficulty buttoning his clothes), and a throbbing sensation in his temples. He died of progressive symptoms 3 months later. In the peripheral blood, Osler described macro-ovalocytes that measured up to 14 × 9 µ and large nucleated red cells with abnormal chromatin. At autopsy, pallor of the skin and organs was described, as well as a peculiar lemon tint to the skin and a thin gastric membrane. The bone marrow disclosed intense hyperplasia and was filled with large nucleated red cells having homogeneous stroma and finely granulated nuclei. This was the first clear description of the megaloblast so named by Paul Ehrlich 3 years later. Osler rejected William Pepper’s idea that PA was a form of pseudo-leukemia but hypothesized instead that it was a reversion of the bone marrow to an embryonic state, though why he did not know. Osler remarked it was “a disease … concerning the pathology of which we still have a good deal to learn, and concerning the successful treatment of which we as yet know nothing.”
Autopsy of a case of rheumatoid arthritis with severe bicytopoenia due to gelatinous transformation of the bone marrow
Published in Modern Rheumatology Case Reports, 2021
Hiroshi Kataoka, Tomoko Tomita, Makoto Kondo, Keishi Makita, Takahiro Tsuji, Masaya Mukai
Autopsy of this case showed severe bicytopoenia with massive pleural effusion. The possible causes of cytopoenia on admission were chronic inflammation due to RA, toxicity of MTX that was overused or accumulated in pleural fluid and ascites, oral mucosal haemorrhage, and mild renal insufficiency. According to her primary care physician’s information, the disease activity of RA was stationary and controlled by MTX treatment. However, deformity was observed in her hands and toes possibly due to high disease activity at its onset. Oral pain associated with oozing oral ulcers suggested that MTX toxicity could be an underlying cause of anaemia, but it was unlikely to be a major cause because there was no evidence of overuse and serum folate levels were elevated. In addition, there were no megaloblasts indicating inhibited DNA biosynthesis due to folate deficiency caused by MTX toxicity [10]. On physical examination and autopsy, there was no site of active intestinal bleeding that could cause haematemesis or melena resulting in massive blood loss. Her kidneys were not atrophic, there was no decrease in serum erythropoietin, and no glomerular change or interstitial damage despite a history of proteinuria; these findings helped us exclude renal anaemia. As serum ferritin levels were normal, iron deficiency was unlikely. Hypozincemia is associated with rheumatoid arthritis caused by imbalanced helper T cells and the malfunction of B cells and NK cells [11]. In addition, zinc deficiency induces the loss of zinc-finger transcription factor GATA-1, resulting in disordered erythropoiesis and anaemia [12]. Hypocupremia induces cytopoenia, but the patient’s serum copper level was within the normal range. Thus, the decreased level of serum zinc due to malnutrition and RA was possibly one of the causes of anaemia but not of leukopenia in this patient. She had no history of taking drugs that induced neutropoenia. Therefore, we looked for other causes of bicytopoenia. The autopsy suggested that gelatinous transformation of the bone marrow (due to malnutrition and possibly RA) in addition to a possible history of repetitive haemorrhage of the penetrating gastric ulcer were the causes for severe anaemia with leukopenia. To the best of our knowledge, there is no other report of gelatinous transformation of the bone marrow with RA.