Utility of the peripheral blood white blood cell count for identifying sick young infants who need lumbar puncture

2003 ◽  
Vol 41 (2) ◽  
pp. 206-214 ◽  
Author(s):  
Bema K. Bonsu ◽  
Marvin B. Harper
Keyword(s):  
Blood Cell ◽  
Cell Count ◽  
Lumbar Puncture ◽  
White Blood Cell Count ◽  
White Blood Cell ◽  
Peripheral Blood ◽  
Blood Cell Count ◽  
Young Infants

Cerebral abscesses in early infancy

1970 ◽  
Vol 33 (2) ◽  
pp. 172-177 ◽  
Author(s):  
Harold J. Hoffman ◽  
E. Bruce Hendrick ◽  
James L. Hiscox
Keyword(s):  
Blood Cell ◽  
Cell Count ◽  
White Blood Cell Count ◽  
White Blood Cell ◽  
Early Infancy ◽  
Blood Cell Count ◽  
Content Type ◽  
Source Of Infection ◽  
Young Infants ◽  
Fine Print

✓ Experience with large cerebral abscesses in six newborn or very young infants is the basis for this report and discussion. Hydrocephalus, an afebrile state, and an elevated white blood cell count were characteristic. Diagnosis by aspiration was usually fortuitous in the process of subdural tap or ventriculography. Treatment by multiple aspirations was reasonably successful, but ultimate excision of the shrunken abscess may be wise. In only one case was the source of infection obvious.

scholarly journals Physiological changes of white blood cell count in peripheral blood of radiation workers.

Sangyo Igaku ◽  
1989 ◽  
Vol 31 (1) ◽  
pp. 18-19
Author(s):  
Seiichi AKIYAMA ◽  
Yoshihumi EDAGAWA ◽  
Atsumi KAWANAMI ◽  
Chiyosaburo NAKAGAWA ◽  
Hisashi URAI ◽  
...  
Keyword(s):  
Blood Cell ◽  
Cell Count ◽  
White Blood Cell Count ◽  
White Blood Cell ◽  
Peripheral Blood ◽  
Physiological Changes ◽  
Blood Cell Count ◽  
Radiation Workers

scholarly journals Telomere shortening in peripheral blood cells was related with aging but not with white blood cell count

1996 ◽  
Vol 41 (4) ◽  
pp. 413-417 ◽  
Author(s):  
Hiroe Satoh ◽  
Keiko Hiyama ◽  
Masahiro Takeda ◽  
Yukikazu Awaya ◽  
Kenichiro Watanabe ◽  
...  
Keyword(s):  
Blood Cell ◽  
Cell Count ◽  
White Blood Cell Count ◽  
White Blood Cell ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Peripheral Blood Cells ◽  
Blood Cell Count ◽  
Telomere Shortening

scholarly journals Defining Cerebrospinal Fluid White Blood Cell Count Reference Values in Neonates and Young Infants

PEDIATRICS ◽  
2010 ◽  
Vol 125 (2) ◽  
pp. 257-264 ◽  
Author(s):  
L. A. Kestenbaum ◽  
J. Ebberson ◽  
J. J. Zorc ◽  
R. L. Hodinka ◽  
S. S. Shah
Keyword(s):  
Cerebrospinal Fluid ◽  
Blood Cell ◽  
Cell Count ◽  
White Blood Cell Count ◽  
White Blood Cell ◽  
Reference Values ◽  
Blood Cell Count ◽  
Young Infants ◽  
Count Reference

scholarly journals Cell-Intrinsic Depletion of AML1-ETO-Positive Pre-Leukemic HSCs By Kras Activating Mutation

Blood ◽  
2017 ◽  
Vol 130 (Suppl_1) ◽  
pp. 787-787
Author(s):  
Cristina Di Genua ◽  
Ruggiero Norfo ◽  
Alba Rodriguez-Meira ◽  
Roy Drissen ◽  
Christopher Booth ◽  
...  
Keyword(s):  
Blood Cell ◽  
Cell Count ◽  
Signaling Pathway ◽  
White Blood Cell Count ◽  
White Blood Cell ◽  
Peripheral Blood ◽  
Detrimental Effect ◽  
Myeloid Cells ◽  
Blood Cell Count ◽  
Normal White Blood Cell

Abstract Mutations in acute myeloid leukemia (AML) are acquired hierarchically. Pre-leukemic mutations, such as AML1-ETO, are acquired within the hematopoietic stem cell (HSC) compartment as an early event, whereas signaling mutations, such as KRAS, are late events acquired within transformed leukemic progenitors and rarely detectable within the HSC compartment (PMID 24550281). This raises the possibility that signaling pathway mutations are detrimental to clonally expanded pre-leukemic HSC. To explore this hypothesis, we generated mice carrying A ml1ETO/+ or KrasG12D/+ conditional knock-in alleles, either individually or combined (AEK), crossed to an Mx1- Cremouse line. Due to previously described spontaneous recombination in primary KrasG12D/+ mice with Mx1- Cre, competitive transplantation was performed using 250,000 fetal liver (FL) cells and 1x106wild-type (WT) bone marrow (BM) competitor cells into lethally irradiated recipients. Mutations were induced with polyI:C 4 weeks post-transplantation, and mice were culled 8 weeks post-polyI:C to assess the hematopoietic phenotype. Transplantation of Aml1ETO/+ FL was insufficient to induce a hematological malignancy in primary recipient mice. In contrast, recipients of KrasG12D/+ FL developed a fatal myeloproliferative neoplasm (MPN) including leukocytosis (white blood cell count 50±22 x109/L), anemia (11.5±0.7 g/dL), splenomegaly (564±71mg) and an increase in the Mac1+Gr1lo myeloid cells in the peripheral blood (fc = 10.04, p < 0.0001) and spleen (fc = 48.56, p < 0.0001) compared to WT. Strikingly, transplantation of AEK FL cells did not result in a more aggressive disease but led to the amelioration of key features of the MPN phenotype associated with KrasG12D/+, including restoration of normal white blood cell count and hemoglobin levels, reduction in spleen size (fc = 0.69, p < 0.05) and a decrease in the number of Mac1+Gr1lo myeloid cells in the peripheral blood (fc = 0.54, p < 0.05) and spleen (fc = 0.51, p < 0.05) compared to KrasG12D/+ . We reasoned that the amelioration of the MPN phenotype in AEK FL recipients might be due to disease propagating HSCs being functionally compromised by both mutations in combination. Numbers of phenotypic donor HSCs (CD45.2 Lin-Sca1+cKit+Flt3-CD150+) were increased in Aml1ETO/+ FL recipients compared to WT (fc = 5.17, p < 0.0001) and were normal in recipients of KrasG12D/+ FL. In comparison with Aml1ETO/+ FL recipients, numbers of HSCs were markedly reduced in AEK FL recipients (fc = 0.30, p < 0.0001) supporting the idea that KrasG12D/+ has a specific detrimental effect on Aml1ETO/+ HSCs. Secondary transplantation revealed an increase in myeloid reconstitution (fc = 3.37, p < 0.01) and HSC number (fc = 9.64, p < 0.05) in Aml1ETO/+ mice compared to WT. In contrast, BM from primary recipients of KrasG12D/+ or AEK FL showeda lack of engraftment in secondary recipients and markedly reduced HSC number. These results indicate that in the absence of a signaling pathway mutation, Aml1ETO/+ confers a clonal advantage to HSCs. However, KrasG12D/+ has a marked detrimental effect on Aml1ETO/+ expressing pre-leukemic HSCs leading to a clonal disadvantage due to loss of phenotypic and functional HSCs. RNA-sequencing of WT, Aml1ETO/+, KrasG12D/+ and AEK HSCs revealed an enrichment for E2f (p < 0.01) and Myc (p < 0.01) targets in AEK HSCs compared to Aml1ETO/+ HSCs, indicating an increase in cell cycle activation. This was confirmed by flow cytometry as we found a marked decrease in AEK HSCs in G0 compared to Aml1ETO/+ (fc = 0.16, p < 0.001). Several candidate genes have been identified, including Gzmb (log2FC = -2.21, p < 0.0001) and Gja1 (log2FC = -3.65, p < 0.0001) which were both down-regulated in Aml1ETO/+, but up-regulated in AEK HSCs (Gzmb log2FC = 0.96, p < 0.0001; Gja1 log2FC = 2.76, p < 0.0001). Knock-outs of Gzmb and Gja1 have been shown to increase HSC reconstitution (PMID 24752302) and cause an expansion of the Lin-Sca1+cKit+ compartment (PMID 16531325) respectively, indicating a potential role of the down-regulation of these genes for pre-leukemic HSC expansion. Our data provides evidence that KrasG12D/+ has a marked detrimental impact on Aml1ETO/+ pre-leukemic HSCs, associated with distinct transcriptional signatures, helping to explain why signaling mutations such as KRAS mutations are not observed within pre-leukemic HSCs in AML patients. Disclosures Mead: BMS: Honoraria; Pfizer: Honoraria; Novartis: Honoraria, Research Funding, Speakers Bureau.

Reactive increase of cerebrospinal fluid white blood cell count after lumbar puncture: Fact or fiction?

2020 ◽  
Vol 414 ◽  
pp. 116876
Author(s):  
Bernhard Neumann ◽  
Tim Steinberg ◽  
De-Hyung Lee ◽  
Johanna Kress ◽  
Marco Kufner ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Blood Cell ◽  
Cell Count ◽  
Lumbar Puncture ◽  
White Blood Cell Count ◽  
White Blood Cell ◽  
Blood Cell Count

Clinical and Cost-Effectiveness of Outpatient Strategies for Management of Febrile Infants

PEDIATRICS ◽  
1992 ◽  
Vol 89 (6) ◽  
pp. 1135-1144
Author(s):  
Tracy A. Lieu ◽  
Marc N. Baskin ◽  
J. Sanford Schwartz ◽  
Gary R. Fleisher
Keyword(s):  
High Risk ◽  
Blood Cell ◽  
Cell Count ◽  
Lumbar Puncture ◽  
Antibiotic Treatment ◽  
White Blood Cell Count ◽  
White Blood Cell ◽  
Clinical Judgment ◽  
Outpatient Management ◽  
Blood Cell Count

Young infants with fever are at risk for serious bacterial infection, but no consensus exists on the optimal approach to diagnosis and treatment. Although the traditional recommendation is always to perform all sepsis tests, including lumbar puncture, and administer intravenous (IV) antibiotics until culture results are negative, recent studies suggest administering intramuscular (IM) ceftriaxone with outpatient follow-up or using laboratory and clinical data to exclude low-risk patients from hospitalization, further testing, and antibiotic treatment. A decision analysis model was used to evaluate six strategies for the diagnosis and treatment of infants aged 28 to 90 days with temperature ≥38.0°C. Data from the literature, data from a 1991 study of 503 febrile infants, and direct, short-term costs from the Children's Hospital of Philadelphia were used as model inputs. The model was run for a hypothetical cohort of 100 000 febrile infants who did not require admission for focal infection or for other reasons that clearly necessitated admission. The model included six strategies: (1) no intervention; (2) all sepsis tests (lumbar puncture, blood culture, urine culture, white blood cell count, and urinalysis) followed by hospitalization and IV antibiotics for all infants; (3) all sepsis tests followed by IM ceftriaxone and outpatient management for most infants; (4) blood and urine cultures with white blood cell count and urinalysis followed by either lumbar puncture and IV antibiotics for high-risk infants or outpatient management without antibiotics for low-risk infants; (5) white blood cell count and urinalysis followed by either lumbar puncture, blood and urine cultures, and IV antibiotics for high-risk infants or outpatient management without antibiotics for low risk infants; and (6) clinical judgment followed by either all sepsis tests and IV antibiotics for high-risk infants or outpatient management without antibiotics for low-risk infants. The two "all sepsis tests" strategies prevented the most cases of death or neurologic impairment, 78% (when IV antibiotics were used) and 76% (when IM ceftriaxone was used) of all potential cases. The most cost-effective strategy was to use all sepsis tests followed by IM ceftriaxone for all patients without meningitis, at an incremental cost of only $3900 per sequela prevented relative to no intervention. Strategies under which only those patients selected as high-risk by laboratory criteria received antibiotic treatment were less effective but incurred lower rates of antibiotic complications. Clinical judgment alone was the least clinically effective and the second least cost-effective strategy. The model's results depended most on assumptions about the effectiveness of IM ceftriaxone, the sensitivity of the white blood cell count, and the sensitivity of clinical judgment in identifying young infants with serious bacterial infection. Combining all sepsis tests with IM ceftriaxone has superior clinical and cost-effectiveness compared with other strategies for managing febrile infants in this model. Strategies that use selective antibiotic treatment based on laboratory tests or clinical judgment are acceptable when the sensitivity of the criterion used is high, but they do not surpass strategies that combine all sepsis tests and antibiotic treatment until the criterion's sensitivity is greater than 96%.

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