Psychopharmacology EMIs
Michael Reilly, Bangaru Raju in Extended Matching Items for the MRCPsych Part 1, 2018
Carbamazepine.Gabapentin.Lamotrigine.Leucopenia.Lithium.Neutrophilia.Thrombocytopenia.Valproate.Verapamil.
Benign Disorders of Leukocytes
Harold R. Schumacher, William A. Rock, Sanford A. Stass in Handbook of Hematologic Pathology, 2019
Neutrophilic leukocytosis or neutrophilia may be defined as an increase in circulating neutrophils to over the upper limit of normal, usually over 7.5 × 109/L in adults. An increase in only the percentage of neutrophils (including bands) to over 80 is referred to as relative neutrophilia and carries little, if any, clinical significance. Additional features that generally accompany a nonleukemic neutrophilic leukocytosis or reactive neutrophilia include (a) “shift to the left,” toward more immature neutrophilic cells, primarily bands, but a few metamyelocytes and myelocytes may be present—blasts and promyelocytes are generally absent; and (b) toxic changes including toxic granulation (primary azurophilic granules), vacuolization, and Döhle bodies (remnants of RNA) in the cytoplasm of neutrophils and bands (Fig. 1). Neutrophilia may result from (a) a shift of neutrophils from the marginal pool to the circulating pool, (b) reduced exit rate of cells from the circulation, (c) increased release of cells from the bone marrow stores, (d) increased production in the bone marrow, or (e) any combination of these. The conditions associated with neutrophilia are summarized in Table 1.
Other Myeloproliferative Neoplasms
Wojciech Gorczyca in Atlas of Differential Diagnosis in Neoplastic Hematopathology, 2014
Blood smear shows marked neutrophilia with predominance of segmented forms and bands (≥80%) and prominent toxic granules (Figure 31.14). There is no thrombocytosis, prominent basophilia and eosinophilia, circulating myeloblasts, or dyspoietic (Pelgeroid) features of neutrophils. Monocytes may be present but are <1 × 109/L. The BM is hypercellular with an increased M:E ratio due to expansion of neutrophilic granulopoiesis with a granulocytic maturation pattern and without excess of myeloblasts or promyelocytes (<5% blasts in the BM and <1% in the blood). There is no evidence of dysplasia or striking reticulin fibrosis. Megakaryocytes appear normal without overt atypia or clustering. No hypolobated micromegakaryocytes are present.
Dexamethasone differentially depletes tumour and peripheral blood lymphocytes and can impact the efficacy of chemotherapy/checkpoint blockade combination treatment
Published in OncoImmunology, 2019
Wayne J. Aston, Danika E. Hope, Alistair M. Cook, Louis Boon, Ian Dick, Anna K. Nowak, Richard A. Lake, W. Joost Lesterhuis
We optimized dexamethasone treatments in mice to mimic the depletion of lymphocyte populations including CD4+ and CD8+ T cells in the peripheral blood of patients.4 The dose required to induce significant lymphodepletion in mice is analogous to that in humans when calculated relative to body surface area.24 However, at these dosages, there was no change in any of the immune subtypes in tumours, indicating that while dexamethasone may have a systemic lymphodepleting effect, this is not necessarily reflected in the tumour microenvironment. Neutrophilia, characterised by an average increase of circulating neutrophils by 32%, was observed in peripheral blood, presumably due to inhibition of spontaneous neutrophil apoptosis which also mimics patient data.25 Again, this was not observed within the tumour. Checkpoint molecule expression within tumours did not change markedly after dexamethasone treatment in vivo. However, it has been shown that dexamethasone enhances the level of PD-1 expression in vitro when cultured with mouse or human T cells, which did correlate with our findings.26
A summary of the diagnostic and prognostic value of hemocytometry markers in COVID-19 patients
Published in Critical Reviews in Clinical Laboratory Sciences, 2020
T. A. Khartabil, H. Russcher, Ajam van der Ven, Y. B. de Rijke
Neutrophil results were present in seven out of the 11 largest studies. The data summarized in Table 2 indicates that neutrophil numbers were mostly normal in non-severe cases but were increased in severe infections. Most smaller studies not included in Table 1 drew the same conclusion but with a few exceptions. For example, several studies reported neutrophilia present in COVID-19 patients even from the early stages of hospitalization [11,22], especially in severe cases [5,18,19,25]. Hu et al. found that even within the severe group there was variability, with 87.5% of critical patients having neutrophilia [6]. Lin et al. also reported neutrophilia in some elderly patients upon admission [17]. The possibility of neutrophilia being a predictor of disease severity has been further supported by Zhang et al., who investigated 82 deaths of COVID-19 patients and showed that neutrophilia was present in 74.3% of the cases upon admission, and that it further increased to 100% in the last 24 h before death [26]. Neutrophil counts were higher in non-survivors compared to survivors [20]. This was also supported by Wang et al., who suggested that neutrophilia might be related to the cytokine storm induced by the invasion of COVID-19 [27].
Haematological profile of COVID-19 patients from a centre in Singapore
Published in Hematology, 2021
Valencia Shihuan Long, Jinghao Nicholas Ngiam, Nicholas Chew, Sai Meng Tham, Zhen Yu Lim, Tony Li, Shuyun Cen, Jayagowtham K. Annadurai, Sandi Myo Thant, Paul Anantharajah Tambyah, Amelia Santosa, Winnie Z.Y. Teo, Eng Soo Yap, Gail Brenda Cross, Ching-Hui Sia
Haematological abnormalities have been described in COVID-19 patients [1]. These patients demonstrate various degrees of leukopenia and lymphopenia. Haematological variations have also been shown to correlate with disease severity and prognosis. The existing literature suggests that neutrophilia and lymphopenia are typically seen in severe cases, and both are early prognosticators of severity. T cell counts (CD4, CD8) were also seen to be decreased in patients with severe disease [2]. The mechanisms behind lymphopenia are not presently fully elucidated, but Tavakolpour et al have postulated that the inflammatory cytokine storm (including elevated interleukin-6 levels) may be closely associated with lymphopenia [3].