• Journal of the Korea Academia-Industrial cooperation Society
• /
• v.10 no.2
• /
• pp.438-446
• /
• 2009

This study aims to investigate chemotherapy-induced neutropenia, nutritional status and both relation of patients with acute myeloid leukemia during 1st consolidation chemotherapy and the therapy-related cytopenic phase in order to determine more effective nutritional support. We review medical records of total 54 cases received first consolidation chemotherapy on P hospital in Busan. The duration of neutropenia(Absolute Neutrophil Count<$1000/{\mu}{\ell}$) is mean 14.78 days, neutropenia occur on mean 10th(9.54) day of chemotherapy(D10). The nutritional parameters of total protein, body weight, BMI showed no significant interval change during chemotherapeutic cycle except albumin, cholesterol. The neutropenia wasn't dependent on general factor of gender, age, comorbidities, Body Surface Area(BSA). The correlation wasn't revealed between neutropenia and nutritional status. In conclusion, although nutritional status didn't affect neutropenia, this study provides detailed information on the neutropenic response of acute myeloid leukemia patients during induction chemotherapy.

• Korean Journal of Clinical Laboratory Science
• /
• v.48 no.2
• /
• pp.102-108
• /
• 2016

Der p 2 is the major allergen of the house dust mite (HDM) associated with the development of allergic diseases. The pathogenic mechanism of the allergy is related to cytokine release of lymphocytes and constitutive apoptosis of neutrophils. In the present study, we examined whether Der p 2 induces cytokine release of lymphocytes, which is involved in regulation of neutrophil apoptosis. In normal and allergic subjects, Der p 2 enhanced the secretion of IL-6, IL-8, MCP-1, and GM-CSF in a time-dependent manner. Although Der p 2 was weakly effective against neutrophil apoptosis, conditioned media collected from normal and allergic lymphocytes after Der p 2 treatment inhibited the apoptosis of normal and allergic neutrophils. Der p 2 showed stronger inhibition of apoptosis of allergic neutrophils cocultured with allergic lymphocytes than normal neutrophils cocultured with normal lymphocytes. These findings improve our understanding of the role of Der p 2 in regulation of lymphocytes and neutrophils and will enable elucidation of allergy pathogenesis.

• Clinical and Experimental Pediatrics
• /
• v.51 no.2
• /
• pp.204-208
• /
• 2008

Purpose : The aim of this study was to investigate the incidence and course of neutropenia following intravenous immunoglobulin (IVIG) therapy in children with idiopathic thrombocytopenic purpura (ITP). Methods : From January 2001 to June 2006, fifty-four patients with ITP were enrolled in this study. Forty-two of 54 patients were treated with IVIG, while the other 12 were treated with anti-D immunoglobulin (Anti-D Ig). Post-treatment absolute neutrophil counts (ANC) were compared between patients who received IVIG and those who received Anti-D Ig. Comparison of post-treatment ANC between patients who treated with two different IVIG regimens (400 mg/kg/day for 5 days and 1 g/kg/day for 2 days) was also performed. Results : Pretreatment ANC were not significantly different between the two treatment groups. After treatment with IVIG, 32 out of 42 patients (76.2%) showed more than 50% decrease of ANC from the baseline. On the other hand, only 2 out of 12 patients (16.7%) showed more than 50% decrease of ANC from the baseline after treatment Anti-D Ig. No significant difference was observed in the decline of ANC between the first IVIG treatment (42 patients) and repeated IVIG treatment groups (7 patients). There was no statistical difference in post-treatment ANC between patients who treated with two different IVIG regimens. The neutropenia induced by IVIG had resolved spontaneously in 38 out of 39 patients (97%) after several days. Conclusion : Neutropenia following IVIG administration may not be an uncommon finding in children with ITP. It seems to be transient and self limited.

• Applied Microscopy
• /
• v.33 no.1
• /
• pp.1-16
• /
• 2003

As is well known that N-nitroso-N-methylurethane (NNNMU) causes acute lung injury (ALI) in experimental animals. And ALI caused by NNNMU is very similar to ARDS in human being in its pathology and progress. In its context, we investigated the pathogenetic mechanism of ARDS associated with oxidative stress by neutrophils in Sprague-Dawley rat model of NNNMU-induced ALI. NNNMU had increased lung weight/body weight ratio (L/B ratio), lung myeloperoxidase (MPO) activity, protein content and number of neutrophils in bronchoalveolar fluid (BALF) compared with those of control rat (p<0.001, respectively). In contrast, the amount of pulmonary surfactant in BALF was decreased by NNNMU (p<0.001). Morphologically, light microscopic examination denoted pathological findings such as formation of hyaline membrane, infiltration of neutrophils and perivascular cuffing in the lungs of NNNMU-treated rats. In addition, ultrastructural changes such as the necrosis of endothelial cells, swelling and vacuolization of lamellar bodies of alveolar type II cells, and the degeneration of pulmonary surfactant were identified after treatment of NNNMU. Very interestingly, cerium chloride electron microscopic cytochemistry showed that NNNMU had increased the production of cerrous-peroxide granules in the lung, which signified the increased production of hydrogen peroxide in the lung. Collectively, we conclude that NNNMU causes acute lung leak by the mechanism of neutrophilic oxidative stress of the lung.

• Journal of Gastric Cancer
• /
• v.2 no.2
• /
• pp.63-68
• /
• 2002

위의 parietal cell 혹은 대식세포와 유사한 세포 내부에서 H. pylori가 발견된다는 보고가 있기는 하나 일반적으로 H. pylori는 Shigella와 같은 침습성 세균은 아닌 것으로 알려져 있다. 그럼에도 불구하고 H. pylori에 감염된 위점막에는 많은 수의 호중구를 위시한 염증세포의 침윤이 관찰되는데 H. pylori가 위상피세포에 부착할 경우 위상피세포를 자극하여 interleukin-8을 위시한 cytokine을 발현케하고 이에 의하여 호중구 등의 염증세포가 몰려들게 된다. 한편 고유층에 몰려든 호중구에서는 다시 interleukin-8을 위시한 일련의 호중구 활성화 chemokine을 분비하여 염증반응을 증폭해 나갈 것이다. 호중구에서 발현되는 myeloperxidase나 활성산소 등도 위점막의 조직 손상에 기여할 것이다. 위상피세포를 덮고 있는 점액층은 위상피세포를 보호한다고 알려져 있으나 H. pylori 감염의 경우 점액층에 의하여 H. pylori의 운동성이 증가하고 이것이 위상피세포로부터의 cytokine 발현을 자극하여 염증반응을 증폭하는 데 관여할 가능성도 있다. H. pylori는 위상피세포에 대하여 apoptosis를 유도함과 동시에 고유층에 몰려든 호중구에 대하여는 apoptosis를 억제케하여 궁극적으로 염증반응을 증폭 및 지속시켜 나가는 쪽으로 작용한다. 한편 H. pylori는 위상피세로로부터 COX-2의 발현을 증가시키는데 이는 위상피세포의 APOPTOSIS를 억제하는 방향으로 작용한다. 이외에 H. pylori의 urease에 의하여 발생한 암모니아나 H. pylori 자신이 분비하는 세포독소가 세포 손상을 유발할 가능성도 있다. 상술한 여러 독성 인자들 중 어느 하나가 단독으로 작용하기보다는 여러 인자가 같이 동시에 또는 시차를 두고 작용할 가능성이 많다고 생각된다.

• Korean Journal of Clinical Pharmacy
• /
• v.23 no.1
• /
• pp.77-80
• /
• 2013

메치실린 저항성 황색 포도상구균(MRSA)에 감염된 환자에게 단기간 연속적으로 반코마이신을 투여했을 때 비정상적으로 호중구의 수치가 감소한 약인성 부작용 사례를 보고하고자 한다. 해당 여성 환자는 61세로서 MRSA 감염증을 판정받고 반코마이신 투여와 더불어 점차 백혈구(WBC)와 절대호중구수치(ANC)가 감소하였고, 제10일째에 이르러 호중구 감소증이 발생하여 ANC가 최저 430 $cells/mm^3$까지 낮아졌으나, 반코마이신의 투여를 중단하자 곧 정상수준으로 회복되었다. 본 사례는 Naranjo Probability Scale과 Korean Algorithm Score(Ver. 2.0)로 각각 평가하였을 때 반코마이신의 투여와 호중구감소증의 발현 사이에 모두 '가능한(probable)' 정도의 인과관계를 가진 것으로 평가되었다. 이는 통상적으로 20일 이상 연속투여를 할 때 임상적으로 관측되던 반코마이신-유래 호중구감소증이 단지 10일 정도의 단기간 투여만으로도 발생할 수 있다는 임상적 약물부작용의 사례로서, 향후 MRSA환자에게 반코마이신을 선택할 때에는 이와 같은 부작용을 고려하여 환자의 WBC와 ANC를 면밀히 관찰하면서 투여할 필요성이 있음을 시사한다.

• Tuberculosis and Respiratory Diseases
• /
• v.43 no.4
• /
• pp.547-557
• /
• 1996

Background : An excessive accumulation of neutrophils in lung tissue has been known to play an important role in mediating the tissue injury among the adult respiratory distress syndrome, idiopathic pulmonary fibrosis and cystic fibrosis by releasing toxic oxygen radicals and proteolytic enzymes. Therefore, it is important to understand a possible mechanism of neutrophil accumulation in lung tissue. In many species, exposure to hyperoxic stimuli can cause changes of lung tissues very similar to human adult respiratory distress syndrome and neutrophils are also functioning as the main effector cells in hyperoxic lung injury. The purpose of the present study was to examine whether neutrophils function as a key effector cell and to study the nature of possible neutrophil chemotactic factors found in bronchoalveolar lavage fluid from the hyperoxia exposed rats. Methods : We exposed the rats to the more than 95% oxygen for 24, 48, 60 arid 72 hours and bronchoalveolar lavage(BAL) was performed. Neutrophil chemotactic activity was measured from the BAT- fluid of each experimental groups. We also evaluated the molecular weight of neutrophil chemotactic tractors using fast performance liquid chromatography and characterized the substances by dialyzer membrane and heat treatment. Results : 1) The neutrophil proportions in bronchoalveolar lavage fluid began to rise from 48 hours after oxygen exposure, and continued to be significantly increased with exposure times. 2) chemotactic index for neutrophils in lung lavages from rats exposed to hyperoxia was significantly higher in 48 hours group than in control group, and was significantly increased with exposure time. 3) No deaths occured until after 48 hours of exposure. However, mortality rates were increased to 33.3 % in 60 hours group and 81.3 % in 72 fours group. 4) Gel filtration using fast performance liquid chromatography disclosed two peaks of neutrophil chemotactic activity in molecular weight of 104,000 and 12,000 daltons. 5) Chemotactic indices of bronchoalveolar lavage fluid were significantly deceased when bronchoalveolar lavage fluid was treated with heat ($56^{\circ}C$ for 30 min or $100^{\circ}C$ for 10 min) or dialyzed (dialyzer membrane molecular weight cut off : 12,000 daltons). Conclusion : These results suggested that the generation of neutrophil chemotactic factor and subsequent neutrophil influx into the lungs are playing an important roles in hyperoxia-induced acute lung injury. Neutrophil chemotactic factor in the lung lavage fluids consisted of several distinct components having different molecular weight and different physical characteristics.

• Tuberculosis and Respiratory Diseases
• /
• v.40 no.1
• /
• pp.16-22
• /
• 1993

Background: The Microbicidal and cytotoxic activities of neutrophils are to a large extent dependent on a burst of oxidative metabolism which generates superoxide anion, hydrogen peroxide, and other reactive products of oxygen. The respiratory burst of PMN is initiated by intracellular calcium mobilization that follows immune or particular stimulation and is very sensitive to modulation by c-AMP or adenosine. Despite its antagonism against adenosine, earlier study has demonstrated potent theophylline inhibition of the PMN respiratory burst at variable ranges of blood concentrations of theophylline in the healthy normal volunteers and in the septic animals pretreated or early post-treated with aminophylline (AMPH) or pentoxifylline. However it is unclear whether theophylline inhibits the superoxide generation or not in the established human sepsis caused by acute pneumonia, as taking into consideration of the fact that full activation of neutrophils have occurred within minutes after the septic insult in the animal experiments. Methods: We measured the $O_2$ generation of peripheral arterial neutrophils obtained from 11 human septic subjects caused by acute pneumonia before and 1 hour after completion of continuous AMPH infusion. Patients were identified and studied within 48 hour of admission. All subjects were administered an intravenous loading and maintenance dose of AMPH. The generation of $O_2$ was measured at a discrete time point (60 min) by the reduction of ferricytochrome c.PMA (10 ${\mu}g/ml$) was used as a stimulating agent. PMNs were isolated at a concentration of $2{\times}10^6$ cells/ml. The arterial oxygen tension, blood pressure and heart rates were also checked to evaluate the systemic effects of AMPH in the acute pneumonia. Results: The mean serum concentration of AMPH at 60 minutes was $8.8{\pm}0.6{\mu}g/ml$. Sixty minutes after AMPH infusion the generatition of $O_2$ was decreased from $0.076{\pm}0.034$ to $0.013{\pm}0.004$(OD) (p<0.05) and from $0.177{\pm}0.044$ to $0.095{\pm}0.042$(OD) (p<0.01) in the resting and stimulated PMNs respectively. $PaO_2$ was not changed after AMPH infusion. Conclusion: AMPH may compromise host defense by significant inhibition of neutrophil release of superoxide anion and it had no effect on improving $PaO_2$ in the acute pneumonia.

• Tuberculosis and Respiratory Diseases
• /
• v.48 no.6
• /
• pp.887-897
• /
• 2000

Background : Since the exact pathogenesis of sepsis-induced ARDS has not been elucidated, the mechanisms of enhanced neutrophilic respiratory burst were probed in endotoxin primed neutrophils associated with the roles of phospholipase A2(PLA2), platelet activating factor(PAF) and apoptosis. Methods : In isolated fresh human neutrophils, effects of the inhibition of PLA2 and PAF on the apoptosis were examined by the method of Annexin-FITC/dual PIflow cytometry. The roles of PLA2 and PAF on the neutrophilic respiratory burst were also examined by measuring oxidant generation in cytochrome-c reduction assay. Activities of the PLA2 and lysoPAF acetyltransferase (lysoPAF AT) of the neutrophils were determined to understand the effect of endotoxin on these enzymatic activities which may be related to the neutrophilic respiratory burst and apoptosis. In addition, the role roles of PLA2 and PAF in neutrophilic adhesion to bovine endothelial cells were examined in vitro by neutrophil adhesion assay. To investigate the effect of oxidants on pulmonary surfactant, cytochemical ultrastructural microscopy was performed. To inhibit PLA2 and PAF, non-specific PLA2 inhibitor mepacrine (100 nM) and WEB 2086 (100 nM) or ketotifen fumarate (10 ${\mu}g$/ml) were used respectively in all in vitro experimental sets. WEB 2086 is PAF receptor antagonist, and ketotifen fumarate is a lyso PAF AT inhibitor. Results: The mapacrine treatment, provided and the endotoxin (ETX) treatment, resulted in increased apoptosis of neutrophils (p<0.001) while treatments of WEB 2086 and ketotifen did not. The inhibition of PLA2 and PAF decreased (p<0.001) production of oxidants from PMA-stimulated neutrophils. While endotoxin increased the PLA2 activity of neutrophils (p<0.01), mepacrine supressed (p<0.001) the activity, provided after treatment of ETX. The lyso PAF actyltransferase activity (lyso PAF AT) increased (p<0.01) after treatment of ETX. In contrast, mepacrine, WEB 2086 and ketotifen showed a tendency of decreasing the activity after treatment of ETX. The treatment of ETX incresed (p<0.001) neutrophil adhesion to endothelial cells, which was reversed by inhibition of PLA2 and PAF (p<0.01). The binding of oxidants to pu1monary surfactant was identified histologically. Conclusions : The enhanced neutrophilic respiratory burst by ETX plays a pivotal role in the pathogenesis of ARDS in terms of oxidayive oxidative stress. Increased production of oxidants from neutrophils is mediated by the activations of PLA2 and lyso PAF AT.

• Journal of fish pathology
• /
• v.9 no.1
• /
• pp.87-93
• /
• 1996

To examine the effectiveness of $\beta$-glucan in non-specific defence mecanisms of Korean catfish(Silurus asotus), the activities of peripheral neutrophils and serum lysozyme were evaluated after once or twice $\beta$-glucan injections. The number of peripheral neutrophils increased after the injection. The increased number in neutrophils in twice $\beta$-glucan injections maintained longer than in single glucan injecton. But the neutrophils did not showed any remarkable changes in PAS-positive reaction. Peripheral neutrophils from fish injected glucan had enhanced phagocytic activities but there was no significant difference in phagocytic index for the glucan and control groups. An elevation of lysozome activity was also observed in the fish received twice glucan but neither single glucan or physiological saline injection could not evoked an increase of lysozyme activity. These results suggest that $\beta$-glucan can enhance the resistance of Korean catfish against to bacteria infection through the activation of peripheral neutrophils and lysozyme.