Zidovudine
M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson in Kucers’ The Use of Antibiotics, 2017
Macrocytosis, which is reversible on cessation of therapy, develops within weeks of commencing zidovudine, with megaloblastic changes observed in the bone marrow of most patients (Richman et al., 1987a; Gelmon et al., 1989; Weber et al., 1991). Macrocytosis occurs both in patients who become anemic and in those who maintain a normal hemoglobin (Walker et al., 1988). It is a useful clinical tool as a check that the patient is taking zidovudine (Mugisha et al., 2012) and may be a useful surrogate marker of clinical effectiveness (Kim et al., 2013). The mean corpuscular volume increases gradually to a mean value of 110/μm3 over the first 5–12 months of therapy before stabilizing (Graham et al., 1991a) and a gradual fall in hemoglobin also occurs, particularly in the first 3 months of therapy (Richman et al., 1987b; Cooper et al., 1991; Cooper et al., 1993a).
Hematopoietic System
Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard in Toxicologic Pathology, 2018
Dysplastic changes in erythroid, myeloid, or megakaryocytic lineages are the result of maturation defects resulting in abnormal nuclear and/or cytoplasmic morphology. If significant, the alteration in maturation may be associated with ineffective hematopoiesis with concomitant peripheral cytopenias in affected cell line(s). Red blood cell indices may be indicative of erythrocyte macrocytosis or microcytosis. Marrow cellularity may be decreased, normal, or increased depending on the causative agent or inciting event, with increased numbers of precursors related to ineffective hematopoiesis often observed. Hematopoietic cell dysplasia is best identified on cytologic preparations, although changes in megakaryocytes can be seen in histologic sections. Dysplasia, while a characteristic feature of myelodysplastic syndrome (MDS) and other myeloproliferative disorders, has also been associated with drug or chemical exposure, nutritional deficiencies, chronic blood loss, and recovery from previous hypoplasia with increased cell production.
Nutritional Deficiencies
Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw in Hankey's Clinical Neurology, 2020
Hematologic workup: May be normal.Anemia or pancytopenia.Macrocytosis.Neutrophil hypersegmentation (may be present even in the absence other hematologic abnormalities).
Vitamin B12 deficiency in Indian infants and children
Published in Paediatrics and International Child Health, 2020
Jatinder Singh Goraya
Nutritional vitamin B12 deficiency (NVBD) in Indian infants has been described for more than 60 years. In 1957, a case series of 25 infants was reported with a constellation of symptoms and signs characterised by pallor, skin hyperpigmentation and regression of neurodevelopment [1]. These infants were exclusively breastfed by strictly vegetarian mothers from a poor socio-economic background. Although they looked plump, the infants had other signs of malnutrition. Moderate-to-severe anaemia with a tendency to macrocytosis was detected in all of them. Bone marrow examination in one case demonstrated megaloblastic change. The infants were treated with liver extract alone or in combination with B complex factor or B12. The response was uniformly good in all cases and was seen as early as the third or fourth day. The author called this condition ‘nutritional dystrophy with anaemia’ and it was speculated that vitamin B12 deficiency was the underlying cause. Jadhav and co-authors in 1962 [2] and Srikantia and Reddy in 1967 [3] confirmed a causal relationship between the clinical presentation and vitamin B12 deficiency by means of appropriate laboratory evidence of vitamin B12 deficiency (macrocytosis, megaloblastic bone marrow) and observing a good therapeutic response to vitamin B12 supplementation. These authors found that the mothers of affected infants were also vitamin B12-deficient as they had low levels of vitamin B12 in their serum and breast-milk [2,3].
How I approach new onset thrombocytopenia
Published in Platelets, 2020
Fiona Swain, Robert Bird
Alcohol can cause myelotoxicity in the absence of apparent toxicity to other organs. Thrombocytopenia can be seen in 3–43% of alcoholics in the community and 14–81% of hospitalized alcoholics. The platelet count can be expected to rise after 2–5 days of abstinence and generally returns to the normal range within one week. Often rebound to higher than normal levels is seen, unless other contributors such as splenomegaly (sequestration) or cirrhosis (decreased thrombopoietin production) are present [23]. Macrocytosis is usually seen, and this persists for 2–4 months after abstinence and is the most reliable pointer to potential alcoholic etiology [24].
ZRSR2 mutation in a child with refractory macrocytic anemia and Down Syndrome
Published in Pediatric Hematology and Oncology, 2019
Meghna Srinath, Emily Coberly, Kimberly Ebersol, Kirstin Binz, Katsiaryna Laziuk, William T. Gunning, Barbara Gruner, Richard Hammer, Bindu Kanathezhath Sathi
Individuals with Down syndrome (DS) are frequently found to have neutropenia and macrocytosis without anemia1,2 and the etiology remains unclear. Macrocytosis appears to be independent of serum vitamin B12 and folate status, fetal hemoglobin (Hb) concentration and hypothyroidism in most cases.2,3