[Variations in the leukocyte count & leukocytic formula in relation to adrenal function during bronchopneumonitis].
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Leukocyte counts on synovial fluid are widely used in classification of joint disease as inflammatory or "noninflammatory." We have evaluated estimates of leukocytes (WBC) per high power field (HPF) on wet drop preparations to see if they might be suitable substitutes in some situations. If there was a mean WBC of 0-2/field on 10 HPF, all leukocyte counts were less than 1,300/mm3. Thus, in such fluids expense might be reduced by eliminating the actual leukocyte count. Estimates also roughly correlated with WBC counts at higher counts but were less consistent.
PURPOSE: This study was designed to determine normal values for the peripheral leukocyte count and leukocyte indexes in healthy term neonates at a specific time after birth. METHODS: We prospectively enrolled 193 healthy term-gestation neonates with no identifiable perinatal risk factors for sepsis. At 4 hours of age a blood sample was collected by warmed heel stick. An automated Coulter complete blood cell count and a 100-cell manual differential leukocyte count were performed on each sample. The differential count was performed by a single hematopathologist unaware of the clinical status of each infant. Perinatal factors were identified by review of the mothers' and infants' hospital records. RESULTS: The mean ratio of immature to total neutrophils was 0.16 (SD 0.10), and the 10% to 90% range was 0.05 to 0.27. The mean leukocyte count was 24.06 x 10(9)/L (24,060/mm3), and the 10% to 90% range was 16.2 to 31.5 x 10(9)/L (16,200 to 31,500/mm3). Neutropenia, < 1.5 x 10(9)/L (1500/mm3) segmented plus band form neutrophils, was not observed. Of all the perinatal factors studied, only the duration of stage 1 labor was found to be associated with significant elevations in the leukocyte and absolute neutrophil counts. CONCLUSIONS: Previously published normal ranges for leukocyte indexes in healthy newborn infants during the early neonatal period are too restrictive; reference standards should be broadened.
ADP induces platelet aggregation in human whole blood and platelet-rich plasma (PRP). ATP induces aggregation in whole blood only; this involves leukocytes and is mediated by ADP. Here we studied ATP- and ADP-induced aggregation in patients with raised leukocyte counts (mean 46.2x10(3) leukocytes/microl). Platelet aggregation was measured by platelet counting. ATP, ADP and metabolites were measured by HPLC. Aggregation to ADP (1-10 microM) and ATP (10-100 microM) was markedly reduced, but to ATP (1000 microM) was enhanced (all p<0.001). Aggregation to ADP in PRP was normal. Increasing the leukocyte count in normal blood reproduced the findings in the patients. Adding leukocytes (either MNLs or PMNLs) to normal PRP enabled a response to ATP and caused marked inhibition of ADP-induced aggregation. Breakdown of ATP or ADP to AMP and adenosine in leukocyte-rich plasma was rapid (t1/2=4 min) and far higher than in cell-free plasma or PRP. With ATP there was also formation of ADP, maximal at 4 min. The presence of the ectonucleotidase NTPDase1 (CD39) was demonstrated on MNLs (all of the monocytes and a proportion of the lymphocytes) and all PMNLs by flow cytometry. We conclude that leukocytes provide a means of dephosphorylating ATP which enables ATP-induced aggregation via conversion to ADP, but also convert ADP to AMP and adenosine. Platelet aggregation extent is a balance between these activities, and high white cell counts influence this balance.
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Leukocyte adhesion deficiency type II (LADII) is a rare inherited disorder of fucose metabolism. Patients with LADII lack fucosylated glycoconjugates, including the carbohydrate ligands of the selectins, leading to an immunodeficiency caused by the lack of selectin-mediated leukocyte-endothelial interactions. A simple and effective therapy has recently been described for LADII, based on the administration of oral fucose. Parallel to this treatment the lack of E- and P-selectin ligands on neutrophils was corrected, and high peripheral neutrophil counts were reduced to normal levels. This study reports that discontinuation of this therapy leads to the complete loss of E-selectin ligands within 3 days and of P-selectin ligands within 7 days. Peripheral neutrophil counts increased parallel to the decrease of selectin ligands. Selectin ligands reappeared promptly after resumption of the fucose therapy, demonstrating a causal relationship between fucose treatment and selectin ligand expression and peripheral neutrophil counts.
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It was disclosed in chronic experiments on rats with dextral vagus neuritis that reactive leucocytosis is wave-like in character. Variations in leucocytosis were inversely proportional to adhesiveness of the lung capillary endothelium with respect to leucocytes. The relationship between the number of circulatory leucocytes and adhesiveness of the capillary endothelium is not so pronounced in intact animals as compared to controls.
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We compared the median values of temperature, platelet count, white blood cell count and differential leukocyte count (neutrophils, eosinophils, basophils, lymphocytes and monocytes) just before and after coronary artery bypass grafting of patients transfused with packed red cell units (n = 119), and not transfused with packed red cell units (n = 98). Just before surgery and at 7 h, 13 h, 22 h, 46 h and 142 h after surgery, blood samples were taken. In the patient group undergoing transfusion lower median values at a significance level of alpha = 0.025 were found of their temperature postoperatively at 7 h, platelets at 22 h, 46 h and 142 h, white blood cell count at 13 h and 22 h, neutrophils at 7 h, 13 h and 22 h, lymphocytes at 46 h and 142 h, compared to the patients not transfused.