Israel Medical Association Journal

Background: The pathogenesis of anemia associated with acute infection in children has not been well delineated.

Objectives: To characterize this type of anemia in children with acute infection, mainly in relation to iron status.

Methods: These two cross-sectional studies compared the prevalence and severity of anemia between outpatient febrile children and age-matched non-febrile controls.

Results: In part 1 of the study, children with acute infection (n=58) had a significant decrease in hemoglobin levels compared with 54 non-febrile controls. Mean corpuscular volume (MCV) did not change this association. Moreover, there was no significant difference in MCV, mean cell hemoglobin or red cell distribution width values between the two groups. Regarding part 2, of the 6534 blood counts obtained in community clinics, 229 were defined as “bacterial infection.” Chart survey confirmed this diagnosis. White blood cell level was significantly inversely associated with hemoglobin level (r = -0.36, P < 0.0001). Anemia was significantly more prevalent among children with bacterial infection compared to those without: 21.4% vs. 14.1% (P = 0.002). Mean values of iron status parameters were all within normal limits.

Conclusions: Acute illness is associated with anemia. The pathogenesis of this anemia does not appear to be associated with disruption of iron metabolism.

Objectives: To compare leukocyte counts and blood levels of various inflammatory cytokines in children and adults diagnosed with community-acquired bronchopneumonia.

Methods: We prospectively evaluated all pediatric and adult patients admitted for bronchopneumonia based on clinical and chest X-ray findings.. Blood was drawn for complete blood count and serum concentration of the following cytokines: granulocyte colony-stimulating factor, interleukins-6, 8 and 10, interferon-gamma, tumor necrosis factor, as well as matrix metalloproteinase-9 and intercellular adhesion molecule-1.

Results: There were 31 children and 32 adults. The patients in both groups had similar parameters of infection severity. None of them required admission to the Intensive Care Unit. Mean (± SD) leukocyte counts in the pediatric and adult groups were 21,018/mm (± 10,420) and 12,628/mm (± 6735) respectively (P = 0.02). Age was inversely correlated with leukocytes in the pediatric group (P = 0.0001). A significant inverse correslation was also found between age and platelet counts. Although cuytokine levels in both groups were not significantly different, age was

Conclusions: The immune response in community-aquired bronchopneumonia is, at least partly, age-dependent.

Background: Cigarette smoking is a well-known risk factor for the development of endothelial dysfunction and the progression of atherosclerosis. Oxidative stress and inflammation have recently been implicated in endothelial dysfunction.

Objectives: To assess the concomitant contribution of polymorphonuclear leukocytes to systemic oxidative stress and inflammation in cigarette smokers.

Methods: The study group comprised 41 chronic cigarette-smoking, otherwise healthy males aged 45.0 ± 11.5 (range 31–67 years) and 41 male non-smokers aged 42.6 ± 11.3 (range 31–65) who served as the control group. The potential generation of oxidative stress was assessed by measuring the rate of superoxide release from separated, phorbol 12-myristate 13-acetate-stimulated PMNL[1] and by plasma levels of reduced (GSH) and oxidized (GSSG) glutathione. Inflammation was estimated indirectly by: a) determining the in vitro survival of PMNL, reflecting cell necrosis; b) in vivo peripheral PMNL counts, reflecting cell recruitment; and c) plasma alkaline phosphatase levels, indicating PMNL activation and degranulation.

Results: PMA[2]-stimulated PMNL from cigarette smokers released superoxide at a faster rate than PMNL from the controls. Smokers had decreased plasma GSH[3] and elevated GSSG[4] levels. In vitro incubation of control and smokers' PMNL in sera of smokers caused necrosis, while control sera improved smoker PMNL survival. Smokers' PMNL counts, although in the normal range, were significantly higher than those of controls. Plasma ALP[5] levels in smokers were significantly higher than in controls and correlated positively with superoxide release and PMNL counts.

Conclusions: Our study shows that PMNL in smokers are primed in vivo, contributing concomitantly to systemic oxidative stress and inflammation that predispose smokers to endothelial dysfunction, and explains in part the accelerated atherosclerosis found in smokers.

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[1] PMNL = polymorphonuclear leukocytes

[2] PMA = phorbol 12-myristate 13-acetate

[3] GSH = reduced glutathione

[4] GSSG = oxidized glutathione

[5] ALP = alkaline phosphatase