• Tuberculosis and Respiratory Diseases
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• v.64 no.3
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• pp.177-186
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• 2008

호산구성 폐렴은 혈중 호산구가 $1,000/mm^3$ 이상이거나 폐포 내 호산구 분획이 25% 이상으로 나타나는 다양한 폐 질환을 총괄하여 부르는 용어이다. 혈중 호산구증가증은 특발성 급성 호산구 폐렴의 초기나 이미 부신피질호르몬 제제를 투여받은 환자에서는 나타나지 않을 수 있다. 호산구성 폐렴은 무증상의 폐 침윤에서 기계 환기가 필요한 급성 호흡 부전 증후군까지 증상의 중증도도 다양하다. 호산구성 폐렴의 원인으로 약제나 기생충이 있지만 많은 경우 원인을 찾을 수 없다. 폐 외 증상이 동반될 경우 Churg-Strauss 증후군이나 과다호산구증가 증후군의 가능성을 생가해야 되며 이런 경우 심장을 침범하였는지 여부에 따라 예후가 결정된다. 가능한 원인에 대한 노출을 피하는 것 외에는, 부신피질호르몬 제제 투여가 가장 중요하며 대부분 극적인 호전을 보인다. 하지만 약제의 감량 중이나 치료 종결 후 재발하는 경우가 자주 있다. HES의 골수 증식성 변이형 치료에 imatinib의 효과가 최근 입증 되었다.

• Journal of the Korean Society for Aviation and Aeronautics
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• v.20 no.1
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• pp.34-38
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• 2012

호산구는 염증 반응에 의해 활성화되며, 주로 기생충 감염이나 알러지 질환 등에 대한 면역 작용을 담당한다고 알려져 있다. 호산구 증가증은 약물 반응, 알러지, 국소적인 기생충 감염 등에 의한 경우가 많지만, 자가면역성 질환이나 종양에 의한 경우도 있다. 최근 연구를 통해 위염의 대표적인 원인균 중 하나인 유문나선균 역시 위점막에서 나타나는 조직 호산구 증가증의 원인이 될 수 있다고 밝혀지고 있으나, 유문나선균에 의한 호산구 증가증 발생 기전이나 빈도는 아직까지 확립되지 않고 있다. 위점막 내 호산구 침윤과 동반되는 위염은 복통, 오심, 구토, 설사, 장폐색 등을 일으킬 뿐만 아니라, 아토피성 피부염, 천식, 위식도 역류, 염증성 장질환 등의 발생과 관련이 있다고 보고되고 있다. 위염 및 다양한 관련 질환에 의한 증상은 공중 근무자들의 임무 수행 능력을 저하시켜 항공기 사고를 발생시킬 수 있는 가능성을 가지고 있다는 점에서 항공의학적으로 매우 중요하며, 실제로 호산구성 위염이나 유문나선균 감염의 치료 여부가 공중 근무자에게 일시적 또는 영구적 비행임무정지를 부과할 수 있는 기준이 되기도 한다. 본 연구에서는 대한민국 공군 장병 환자를 대상으로 내시경을 통해 얻은 위점막 조직 내 호산구수를 측정하고, 이를 위점막 표면의 유문나선균 존재 유무와 관련지어 보았다. 111명 중 20명의 환자에서 한 고배율 시야 당 30개 이상의 호산구가 관찰되었고, 63명의 환자의 위점막 표면에서 유문나선균을 확인하였다. 또한 위점막 내 호산구의 밀도와 유문나선균의 존재 간의 관계는 통계학적으로 유의하였다. 본 연구의 결과는 대한민국 공군 장병을 대상으로 하여 조직 호산구 증가증과 유문나선균의 빈도 및 상호 관계를 최초로 분석했다는 점에서 의의가 있으며, 추후 유문나선균이 어떤 기전으로 위점막 조직 내 호산구의 증가에 관여하는지에 대한 연구를 진행하기 위한 기초 자료로서 활용될 수 있을 것이다.

• Clinical and Experimental Pediatrics
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• v.53 no.1
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• pp.28-32
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• 2010

Purpose : Although eosinophilia is a common laboratory finding in many neonatal intensive care units (ICUs), its causative mechanisms remain obscure. We aimed to determine the causes of eosinophilia in the neonatal ICU environment. Methods : Serial eosinophil counts were determined weekly for 288 hospitalized, appropriately grown neonates. Infants were divided into four groups according to gestational age, and the incidence and etiologic factors of eosinophilia were retrospectively studied. Results : Absolute eosinophilia (>$700/mm^3$) was documented in 18% (52/288) of neonates. Twenty-two infants (42.3%) exhibited mild eosinophilia ($700-999cells/mm^3$), 27 (51.9%) exhibited moderate eosinophilia ($1,000-2,999cells/mm^3$), and 3 (5.8%) exhibited severe eosinophilia (>$3,000cells/mm^3$). Of the 288 infants studied, 54 suffered sepsis. Thirty of these 54 infants (55.6%) showed eosinophilia, and 22 out of the remaining 234 infants (9%) without sepsis showed eosinophilia, indicating that eosinophilia was more prevalent in the sepsis group (P <0.05). All 5 infants suffering from bronchopulmonary dysplasia showed eosinophilia, and 47 out of the remaining 283 infants (16.7%) without bronchopulmonary dysplasia showed eosinophilia. Thus, eosinophilia was more prevalent in the bronchopulmonary dysplasia group (P<0.05). Furthermore, increased prevalence of eosinophilia was associated with respiratory distress syndrome, ventilator use, blood transfusion, and total parenteral nutrition (P<0.05). Conclusion : Our results suggest that eosinophilia is influenced by sepsis and bronchopulmonary dysplasia, although it can also occur idiopathically at birth. Moreover, the potential role of eosinophils in conditions such as wound healing and fibrosis in sepsis or chronic lung disease may be a cause of eosinophilia.

• Tuberculosis and Respiratory Diseases
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• v.43 no.3
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• pp.359-366
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• 1996

Background : Eosinophilic leukocytes are prominent cellular participants in the pathogenesis of allergic disease and asthma. Chemotaxis is still a very useful method in evaluating the response of human eosinophil to novel modulators. Degranulated mast cells and activated T lymphocytes are responsible for the pathophysiology of asthma and tryptase is one of most important proteases released after activation of mast cells. The purpose of this study was to investigate the actions of trypsin and chymotrypsin on eosinophils in terms of chemotaxis and activation. Method : Eosinophils were isolated by negative immunoselection from the peripheral blood of atopic donors. Chemotaxis was studied by using micro-Boyden chambers and ECP release was assayed by fluoroimmunoassay. Results : Eosinophil showed a chemotactic response to trypsin. Maximal chemotactic response was with $1000{\mu}g/ml$ trypsin ($56.52{\pm}14.50$/HPF) which was comparable to PAP. But chymotrypsin showed no significant chemotactic response to eosinophils. Trypsin at the concentration of 10, 100, $1000{\mu}g/ml$ induced secretion of ECP, which at the concentration of $10{\mu}g/ml$ represented about 2.7 times of the spontaneous rate of release. Soybean protease inhibitor reduced trypsin induced ECP release. Conclusion : Trypsin can induce chemotactic response to eosinophils and activation of eosinophils that can induce secretion of ECP. On the contrary, chymotrypsin showed no direct effect on eosinophils. We propose a role of trypsin on the chemotaxis and activation of eosinophils.

• Journal of Gastric Cancer
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• v.5 no.1
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• pp.47-51
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• 2005

Eosinophilic gastroenteritis is a rare clinicopathologic entity of unknown etiology with a variety of digestive symptoms. The pathogenesis is poorly understood. Diagnostic criteria include demonstration of eosinophilic infiltration of the affected bowel wall, lack of evidence of extraintestinal disease, and exclusion of various disorders that could mimic similar conditions. The disease might involve any area of the gastrointestinal tract from the esophagus to the rectum, but the stomach and the proximal small bowel are most commonly affected. The clinical features depend on which layer and site are involved. We report the case of a 59-year-old male patient with a 3-week history of post-prandial vomiting with malnutrition and weight loss. An abdominopelvic CT showed a gastric outlet obstruction with diffuse wall thickening, as with linitis plastica. Three gastrofiberscopic biopsies showed chronic gastritis. We carried out a radical total gastrectomy with D2 lymph node dissection. The pathologic report revealed a mural type eosinophilic gastritis with a marked hypertrophic scar formation at the proper muscle layer. We report this case with a brief review of the literature. (J Korean Gastric Cancer Assoc 2005;5:47-51)

• Tuberculosis and Respiratory Diseases
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• v.42 no.1
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• pp.99-104
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• 1995

Most cases of eosinophilic pneumonia reported previously have followed a chronic course. The case presented here was acute in onset, suggesting a acute eosinophilic pneumonia. A model of criteria for acute and chronic eosinophilic pneumonia was made by Umeki in 1992. A previously healthy young man presented with cough, sputum, fever, and multiple small nodules on the chest radiograph. We confirmed eosinophilic pneumonia with bronchoalveolar lavage analysis and transbronchial lung biopsy. This case examplifies the recently descrived acute eosinophilic pneumonia.

• Tuberculosis and Respiratory Diseases
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• v.43 no.3
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• pp.348-358
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• 1996

Background : Interleukin-5 (IL-5) is responsible for eosinophilia in allergic diseases. In allergic bronchial asthma, there is a correlation between the extent of eosinophil infiltration in bronchial mucosa and IL-5 concentrations. In addition, IL-2 concentration is elevated in the airways and associated with eosinophilia in symptomatic patients with bronchial asthma. In animal studies, IL-2 can induce eosinophilia by increasing the synthesis of IL-5, however, it is still unknown how IL-2 can induce eosinophila in human being. The aim of this study is to evaluation the effect and mechanism of IL-2 on prolongation of eosinophil survival. Methods : After purifiing the eosinophils from the venous blood of allergic patients with eosinophilia, we measured the survival rates of eosinophils using trypan blue dye exclusion test, and the number of eosinophils with Randolp's solution. We compared the survival rates of eosinophils in the presence of IL-2 or IL-5. Neutralizing antibody for IL-5 was added in IL-2 treated eosinophils to reveal whether IL-2 induced prolongation of eosinophil survival was mediated by IL-5. We checked IL-5 m-RNA expression of lymphocytes in the presence of IL-2 by using Reverse transcription-Polymerase chain reaction (RT-PCR) method to revealed the effect of IL-2 on IL-5 m-RNA expression on lymphocyte. $\alpha$ and $\beta$ IL-2 receptors were measured on eosinophils and lymphocytes with flow-cytometer after stimulated with IL-2. Results : 1) Eosinophil survival rates increased dose dependently on IL-5 and IL-2. 2) The eosinophil survival rates increased by IL-2 were not inhibited by the pretreatment with neutralizing antibody for IL-5. 3) IL-5 m-RNA was not expressed on lymphocytes by the treatment with IL-2 up to 96 hours. 4) IL-2 upregulate the expression of IL-$2R{\alpha}$ on eosinophils, instead of no effect on the expression of IL-$2R{\beta}$. Conclusion: Interleukin-2 had the enhancing effect on the survival rates of eosinophils. The mechanism behind IL-2 induced eosinophilia might be the increment of IL-2 receptors on eosinophils rather than IL-5 synthesis by lymphocytes.

• Pediatric Infection and Vaccine
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• v.13 no.2
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• pp.186-190
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• 2006

Eosinophilic fasciitis(EF) is a very rare clinical syndrome, especially during childhood. It is characterized by diffuse fasciitis and peripheral eosinophilia. Little is known about the pathogenesis of EF, and it is suggested that immunologic alteration may play a role. Epstein-Barr virus(EBV) is known to cause a variety of diseases via immune mechanism. We report a 22 month old boy with EF following EBV infection, which may be associated with pathogenesis of EF.

• Tuberculosis and Respiratory Diseases
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• v.55 no.2
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• pp.206-210
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• 2003

Eosinophilic lung diseases are heterogenous disorder which are characterized by the presence of pulmonary symptoms or an abnormal chest radiograph accompanied by inflammatory cellular infiltrates in the airways and lung parenchyma which contain large numbers of eosinophils. The incidence of drug-induced pulmonary disorder is increasing, with at least 40 drug entities having been reported to cause this pulmonary disease. However, nonsteroidal anti-inflammatory drugs (NSAIDs) are rarely mentioned in the lists of drugs in published articles describing drug induced eosinophilic pneumonia. The following is a case of eosinophilic pneumonia that we believe was related to ibuprofen therapy.

• Pediatric Infection and Vaccine
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• v.22 no.1
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• pp.23-28
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• 2015

Purpose: The aim of this study was to investigate the clinical manifestations and laboratory characteristics of eosinophilic meningitis in Severance Children's Hospital. Methods: We examined 6,335 children under the age of 18 years old who had visited the tertiary hospital in Seoul, Korea, and had received cerebrospinal study results between January 2007 and July 2012. The medical records of the patients identified as eosinophilic meningitis were retrospectively reviewed. Results: Eosinophilic meningitis was diagnosed in 39 patients (0.6%). The mean age was 6 years (range 0-18 years) and the sex ratio was 1.3:1 (22 males and 17 females). The underlying diseases and past history were neurologic disease (n=36, 92%). Eosinophilic meningitis was diagnosed in thirty-five patients who had undergone postoperation neurosurgery (90%). The most common symptoms were fever (50%), headache (20%), vomiting (15%), seizure (10%), and dizziness (5%). The average duration for recovery was five days, and intravenous antibiotics or steroids were used. Conclusions: Manifestations of eosinophilic meningitis are similar to other types of meningitis. The most common cause of eosinophilic meningitis in children was neurosurgery. Eosinophilic meningitis should be considered for patients showing fever and headache after neurosurgery. Through careful investigation, use of improper antibiotics could be avoided.