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Boletin Medico Del Hospital Infantil de... 2017Evans syndrome is characterized by the reduction of at least two blood cell lineages in the absence of other diagnoses; it was previously described as the simultaneous...
BACKGROUND
Evans syndrome is characterized by the reduction of at least two blood cell lineages in the absence of other diagnoses; it was previously described as the simultaneous or sequential development of autoimmune hemolytic anemia and immune thrombocytopenia with unknown etiology. An incidence of 37% and mortality rate of 10% were reported for Evans syndrome.
CLINICAL CASES
We report the clinical presentation and evolution of Evans syndrome in two infants who were initially diagnosed with immune thrombocytopenia. The clinical diagnosis was supported on complementary studies, where hematological disorders were corroborated. Both cases received treatment with steroids and intravenous immunoglobulin.
CONCLUSIONS
For the management of children with thrombocytopenia, the pediatrician must analyze for other cell lineage disorders. In the cases that we report here, we found the presence of autoimmune hemolytic anemia and monocytosis. Therefore, infectious and immunological studies must be included. The first-line treatment of choice are steroids, and intravenous immunoglobulin can be considered if severe immune thrombocytopenia is associated, as observed in these cases.
Topics: Anemia, Hemolytic, Autoimmune; Glucocorticoids; Humans; Immunoglobulins, Intravenous; Infant; Male; Purpura, Thrombocytopenic, Idiopathic; Thrombocytopenia
PubMed: 29382497
DOI: 10.1016/j.bmhimx.2017.01.004 -
Veterinary World Nov 2020Tick-borne pathogens such as , , and can cause serious disease in canines. Each blood parasite can be associated with different hematological characteristics in...
BACKGROUND AND AIM
Tick-borne pathogens such as , , and can cause serious disease in canines. Each blood parasite can be associated with different hematological characteristics in infected dogs. Identification of hematological alterations during routine laboratory screening of blood samples from dogs displaying clinical signs is essential for diagnosing blood parasitic infections. This study aimed to evaluate parasitic infections and hematological alterations in blood samples of infected dogs in Southern Thailand.
MATERIALS AND METHODS
A total of 474 blood samples were collected from dogs presented at the Veterinary Teaching Hospital of the Prince of Songkla University between 2016 and 2019. An automatic hematology analyzer was used to establish hematological values; peripheral blood films were screened for blood parasites and their detection was associated with hematological alterations to determine the odds ratio (OR).
RESULTS
This study found that (n=127) was the most common blood parasite infecting dogs in southern Thailand, followed by (n=100) and (n=24). Hematological alterations caused by infections included anemia, thrombocytopenia, monocytosis, and eosinophilia (OR=14.64, 17.63, 20.34, and 13.43, respectively; p<0.01). The blood samples of -infected dogs were characterized by anemia, thrombocytopenia, leukocytosis, neutrophilia, and monocytosis (OR=6.35, 3.16, 12.80, 11.11, and 17.37, respectively; p<0.01). Anemia, thrombocytopenia, eosinopenia, and lymphopenia (OR=10.09, 33.00, 20.02, and 66.47 respectively; p<0.01) were associated with -infected dogs.
CONCLUSION
These data support the fact that hematological abnormalities are a hallmark for the identification of tick-borne infections. The hematological values, hereby reported, can be used as a guideline for the clinical diagnosis of canine blood parasitic infections in Southern Thailand.
PubMed: 33363331
DOI: 10.14202/vetworld.2020.2388-2394 -
Journal of Clinical Laboratory Analysis Jan 2021Chronic myelomonocytic leukemia (CMML) is characterized by persistent monocytosis and dysplastic features of blood cells. No specific genetic abnormalities are present...
BACKGROUND
Chronic myelomonocytic leukemia (CMML) is characterized by persistent monocytosis and dysplastic features of blood cells. No specific genetic abnormalities are present in CMML, and reactive monocytosis should be excluded. An increase in classical monocytes (MO1) has been suggested as a screening tool for CMML.
METHODS
We evaluated monocyte subsets in the peripheral blood of patients with CMML (n = 16), patients with reactive monocytosis (n = 19), and normal controls (n = 15) with flow cytometry using antibodies against CD14, CD16, CD56, CD24, CD45, and CD2. The cutoff of MO1 ≥94% was validated, and the optimal cutoff was analyzed with receiver operating curve analysis.
RESULTS
The sensitivity of monocyte subset testing for screening for CMML was 0.938 (0.717-0.997), and the specificity was 0.882 (0.734 - 0.953) using the cutoff of MO1 ≥94%. Serial samples from patients who responded to hypomethylating therapy showed an MO1 < 94%. However, few patients with reactive monocytosis, including patients with nonhematologic malignancies and acute myeloid leukemia, showed an increase in the MO1 ≥ 94%. Monocyte subset results were correlated with the response to hypomethylating therapy in follow-up samples.
CONCLUSION
Monocyte subset analysis is useful in screening for and monitoring CMML. Harmonization of the protocols for monocyte subset analysis is required.
Topics: Adult; Aged; Aged, 80 and over; Female; Flow Cytometry; Humans; Leukemia, Myelomonocytic, Chronic; Male; Middle Aged; Monocytes; Sensitivity and Specificity
PubMed: 32931067
DOI: 10.1002/jcla.23576 -
Frontiers in Neurology 2021Systemic inflammation after subarachnoid hemorrhage (SAH) is implicated in delayed cerebral ischemia (DCI) and adverse clinical outcomes. We hypothesize that early...
Systemic inflammation after subarachnoid hemorrhage (SAH) is implicated in delayed cerebral ischemia (DCI) and adverse clinical outcomes. We hypothesize that early changes in peripheral leukocytes will be associated with outcomes after SAH. SAH patients admitted between January 2009 and December 2016 were enrolled into a prospective observational study and were assessed for Hunt Hess Scale (HHS) at admission, DCI, and modified Ranked Scale (mRS) at discharge. Total white blood cell (WBC) counts and each component of the differential cell count were determined on the day of admission (day 0) to 8 days after bleed (day 8). Global cerebral edema (GCE) was assessed on admission CT, and presence of any infection was determined. Statistical tests included student's -test, Chi-square test, and multivariate logistic regression (MLR) models. A total of 451 subjects were analyzed. Total WBCs and neutrophils decreased initially reaching a minimum at day 4-5 after SAH. Monocyte count increased gradually after SAH and peaked between day 6-8, while basophils and lymphocytes decreased initially from day 0 to 1 and steadily increased thereafter. Neutrophil to lymphocyte ratio (NLR) reached a peak on day 1 and decreased thereafter. WBCs, neutrophils, monocytes, and NLR were higher in patients with DCI and poor functional outcomes. WBCs, neutrophils, and NLR were higher in subjects who developed infections. In MLR models, neutrophils and monocytes were associated with DCI and worse functional outcomes, while NLR was only associated with worse functional outcomes. Occurrence of infection was associated with poor outcome. Neutrophils and NLR were associated with infection, while monocytes were not. Monocytes were higher in males, and ROC curve analysis revealed improved ability of monocytes to predict DCI and poor functional outcomes in male subjects. Monocytosis was associated with DCI and poor functional outcomes after SAH. The association between neutrophils and NLR and infection may impact outcomes. Early elevation in monocytes had an improved ability to predict DCI and poor functional outcomes in males, which was independent of the occurrence of infection.
PubMed: 34381415
DOI: 10.3389/fneur.2021.694996 -
Annals of Laboratory Medicine Sep 2018The 2016 WHO diagnostic criteria for chronic myelomonocytic leukemia (CMML) require both absolute and relative monocytosis (≥1×10⁹/L and ≥10% of white blood cell...
The 2016 WHO diagnostic criteria for chronic myelomonocytic leukemia (CMML) require both absolute and relative monocytosis (≥1×10⁹/L and ≥10% of white blood cell counts) in peripheral blood. Moreover, myeloproliferative neoplasm (MPN) features in bone marrow and/or MPN-associated mutations tend to support MPN with monocytosis rather than CMML. We assessed the impact of the 2016 WHO criteria on CMML diagnosis, compared with the 2008 WHO criteria, through a retrospective review of the medical records of 38 CMML patients diagnosed according to the 2008 WHO classification. Application of the 2016 WHO criteria resulted in the exclusion of three (8%) patients who did not fulfill the relative monocytosis criterion and eight (21%) patients with an MPN-associated mutation. These 11 patients formed the 2016 WHO others group; the remaining 27 formed the 2016 WHO CMML group. The significant difference in the platelet count and monocyte percentage between the two groups indicated that the 2016 WHO criteria lead to a more homogenous and improved definition of CMML compared with the 2008 WHO criteria, which may have led to over-diagnosis of CMML. More widespread use of molecular tests and more sophisticated clinical and morphological evaluations are necessary to diagnose CMML accurately.
Topics: Aged; Female; Humans; Janus Kinase 2; Leukemia, Myelomonocytic, Chronic; Male; Middle Aged; Monocytes; Mutation; Myeloproliferative Disorders; Platelet Count; Retrospective Studies; Trisomy; World Health Organization
PubMed: 29797820
DOI: 10.3343/alm.2018.38.5.481 -
Frontiers in Oncology 2022Poor outcomes in glioma patients indicate a need to determine prognostic indicators of survival to better guide patient specific treatment options. While preoperative...
INTRODUCTION
Poor outcomes in glioma patients indicate a need to determine prognostic indicators of survival to better guide patient specific treatment options. While preoperative neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and monocyte-to-lymphocyte ratio (MLR) have been suggested as prognostic systemic inflammation markers, the impact of post-radiation changes in these cell types is unclear. We sought to identify which hematologic cell measurements before, during, or after radiation predicted for patient survival.
METHODS
A cohort of 182 patients with pathologically confirmed gliomas treated at our institution was retrospectively reviewed. Patient blood samples were collected within one month before, during, or within 3 months after radiation for quantification of hematologic cell counts, for which failure patterns were evaluated. Multivariable cox proportional hazards analysis for overall survival (OS) and progression-free survival (PFS) was performed to control for patient variables.
RESULTS
Multivariable analysis identified pre-radiation NLR > 4.0 (Hazard ratio = 1.847, p = 0.0039) and neutrophilia prior to (Hazard ratio = 1.706, p = 0.0185), during (Hazard ratio = 1.641, p = 0.0277), or after (Hazard ratio = 1.517, p = 0.0879) radiation as significant predictors of worse OS, with similar results for PFS. Post-radiation PLR > 200 (Hazard ratio = 0.587, p = 0.0062) and a percent increase in platelets after radiation (Hazard ratio = 0.387, p = 0.0077) were also associated with improved OS. Patients receiving more than 15 fractions of radiation exhibited greater post-radiation decreases in neutrophil and platelet counts than those receiving fewer. Patients receiving dexamethasone during radiation exhibited greater increases in neutrophil counts than those not receiving steroids. Lymphopenia, changes in lymphocyte counts, monocytosis, MLR, and changes in monocyte counts did not impact patient survival.
CONCLUSION
Neutrophilia at any time interval surrounding radiotherapy, pre-radiation NLR, and post-radiation thrombocytopenia, but not lymphocytes or monocytes, are predictors of poor patient survival in glioma patients.
PubMed: 36158642
DOI: 10.3389/fonc.2022.1000280 -
Journal of the American College of... Jan 2002
Topics: Angioplasty, Balloon, Coronary; Biomarkers; Humans; Inflammation; Leukocytes, Mononuclear; Myocardial Infarction; Prognosis; Ventricular Remodeling
PubMed: 11788215
DOI: 10.1016/s0735-1097(01)01733-8 -
Modern Pathology : An Official Journal... Mar 2018Monocytosis can develop during disease course in primary myelofibrosis simulating that seen in chronic myelomonocytic leukemia, and should not lead to disease...
Monocytosis can develop during disease course in primary myelofibrosis simulating that seen in chronic myelomonocytic leukemia, and should not lead to disease reclassification. In contrast, at presentation, rare cases have clinical, morphologic, and molecular genetic features truly intermediate between primary myelofibrosis and chronic myelomonocytic leukemia. The taxonomy and natural history of these diseases are unclear. We identified cases which either: (1) fulfilled the 2008 World Health Organization criteria for primary myelofibrosis but had absolute monocytosis and, when available, chronic myelomonocytic leukemia-related mutations (ASXL1, SRSF2, TET2) or (2) fulfilled criteria of chronic myelomonocytic leukemia but had megakaryocytic proliferation and atypia, marrow fibrosis, and myeloproliferative-type driver mutations (JAK2, MPL, CALR). Patients with established primary myelofibrosis who developed monocytosis and those with chronic myelomonocytic leukemia with marrow fibrosis were excluded. By combining the pathology databases of two large institutions, six eligible cases were identified. Patients were predominantly male and elderly with monocytosis at diagnosis (average 17.5%/2.3 × 10/μl), organomegaly, primary myelofibrosis-like atypical megakaryocytes admixed with a variable number of chronic myelomonocytic leukemia-like hypolobated forms, variable myelodysplasia, marrow fibrosis and osteosclerosis. All had a normal karyotype and no myelodysplasia-associated cytogenetic abnormalities. Five of the patients in whom a more extensive molecular characterization was performed showed co-mutations involving JAK2 or MPL and ASXL1, SRSF2, TET2, NRAS, and/or KRAS. Disease progression has occurred in all and two have died. Rare patients present with features that overlap between primary myelofibrosis and chronic myelomonocytic leukemia and are thus difficult to classify based on current World Health Organization criteria. Biologically, these cases likely represent primary myelofibrosis with monocytosis, dysplasia, and secondary (non-driver) mutations at presentation. Alternatively, they may represent a true gray zone of neoplasms. Their clinical behavior appears aggressive and innovative therapeutic approaches may be beneficial in this particular subset.
Topics: Aged; DNA-Binding Proteins; Diagnosis, Differential; Dioxygenases; Disease Progression; Female; GTP Phosphohydrolases; Humans; Janus Kinase 2; Leukemia, Myelomonocytic, Chronic; Male; Membrane Proteins; Middle Aged; Mutation; Primary Myelofibrosis; Proto-Oncogene Proteins; Proto-Oncogene Proteins p21(ras); Receptors, Thrombopoietin; Repressor Proteins; Serine-Arginine Splicing Factors
PubMed: 29192651
DOI: 10.1038/modpathol.2017.148 -
Atherosclerosis Apr 2018Leukocytosis, particularly monocytosis, has been shown to promote atherosclerosis in both diabetic and non-diabetic mouse models. We previously showed that hyperglycemia...
BACKGROUND AND AIMS
Leukocytosis, particularly monocytosis, has been shown to promote atherosclerosis in both diabetic and non-diabetic mouse models. We previously showed that hyperglycemia independently promotes monocytosis and impairs the resolution of atherosclerosis. Since patients with chronic diabetes often develop dyslipidemia and also have increased risk for atherosclerosis, we sought to examine how controlling blood glucose affects atherosclerosis development in the presence of severe hyperlipidemia.
METHODS
Diabetes was induced using streptozotocin (STZ) in low density lipoprotein receptor (Ldlr) knockout (Ldlr) mice after which they were fed a high-cholesterol diet for 4 weeks. Control and diabetic mice were treated with vehicle or sodium glucose cotransporter inhibitor (SGLT2i, Phlorizin or Dapagliflozin) for the duration of the diet.
RESULTS
Induction of diabetes resulted in a dramatic increase in plasma cholesterol (TC) and triglyceride (TG) levels. These mice also exhibited an increased number of circulating monocytes and neutrophils. Monocytosis was driven by increased proliferation of progenitor cells in the bone marrow. Tighter glycemic control by SGLT2i treatment not only reduced monocytosis and atherosclerosis but also improved plasma lipoprotein profile. Interestingly, improved lipoprotein profile was not due to decreased TG synthesis or clearance via low density lipoprotein receptor-related protein (Lrp) 1 or scavenger receptor class B member (Scarb1) pathways, but likely mediated by heparin sulfate proteoglycans (HSPG)-dependent clearance mechanisms in the liver. Further examination of the liver revealed an important role for bile acid transporters (Abcg5, Abcg8) and cytochrome P450 enzymes in the clearance of hepatic cholesterol.
CONCLUSIONS
These data suggest that tighter glycemic control in diabetes can improve lipoprotein clearance exclusive of Ldlr, likely via HSPG and bile acid pathways, and has an overall net positive effect on atherosclerosis.
Topics: ATP Binding Cassette Transporter, Subfamily G, Member 5; ATP Binding Cassette Transporter, Subfamily G, Member 8; Animals; Atherosclerosis; Benzhydryl Compounds; Biomarkers; Blood Glucose; Cholesterol, Dietary; Cytochrome P-450 Enzyme System; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 1; Glucosides; Heparin; Hyperlipidemias; Lipoproteins; Liver; Male; Mice, Inbred C57BL; Mice, Knockout; Monocytes; Phlorhizin; Proteoglycans; Receptors, LDL; Sodium-Glucose Transporter 2 Inhibitors; Streptozocin
PubMed: 29518749
DOI: 10.1016/j.atherosclerosis.2018.02.028 -
Scientific Reports Nov 2020Maternal stress during pregnancy is widespread and is associated with poor offspring outcomes, including long-term mental health issues. Prenatal stress-induced fetal...
Maternal stress during pregnancy is widespread and is associated with poor offspring outcomes, including long-term mental health issues. Prenatal stress-induced fetal neuroinflammation is thought to underlie aberrant neurodevelopment and to derive from a disruption in intrauterine immune homeostasis, though the exact origins are incompletely defined. We aimed to identify divergent immune and microbial metagenome profiles of stressed gestating mice that may trigger detrimental inflammatory signaling at the maternal-fetal interface. In response to stress, maternal glucocorticoid circuit activation corresponded with indicators of systemic immunosuppression. At the maternal-fetal interface, density of placental mononuclear leukocytes decreased with stress, yet maternal whole blood leukocyte analysis indicated monocytosis and classical M1 phenotypic shifts. Genome-resolved microbial metagenomic analyses revealed reductions in genes, microbial strains, and metabolic pathways in stressed dams that are primarily associated with pro-inflammatory function. In particular, disrupted Parasutterella excrementihominis appears to be integral to inflammatory and metabolic dysregulation during prenatal stress. Overall, these perturbations in maternal immunological and microbial regulation during pregnancy may displace immune equilibrium at the maternal-fetal interface. Notably, the absence of and reduction in overt maternal inflammation during stress indicates that the signaling patterns driving fetal outcomes in this context are more nuanced and complex than originally anticipated.
Topics: Animals; Brain; Burkholderiales; Disease Models, Animal; Female; Fetal Development; Gastrointestinal Microbiome; Glucocorticoids; Humans; Leukocytes, Mononuclear; Maternal-Fetal Exchange; Mental Health; Metagenomics; Mice; Neuroimmunomodulation; Placenta; Pregnancy; Pregnancy Complications; Prenatal Exposure Delayed Effects; Stress, Psychological
PubMed: 33219314
DOI: 10.1038/s41598-020-77265-x