• 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.

• Tuberculosis and Respiratory Diseases
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• v.39 no.5
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• pp.386-391
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• 1992

Background: Recently, bronchial provocation of the airway of atopic asthmatic subjects with inhaled allergen has been shown to produce an initial peripheral blood eosinopenia followed by an eosinophilia occurring approximately 12 to 18 hrs after the challenge. However there are few studies about the change of peripheral eosinophil count (PEC) after bronchial provocation with nonspecific stimuli such as histamine or methacholine. Interestingly our preliminary study demonstrated a notable change of PEC during bronhial provocation with inhaled histamine in some asthmatic subjects. This study was designed to reevaluate our preliminary data and to further investigate the change of PEC during as well as after bronchial provocation with inhaled histamine in bronchial asthma tics. Methods: Sixteen asthmatic subjects participated in this study. Bronchial provocation with inhaled histamine was done between 9 AM and 12 MD. Blood samplings for PEC were done with 5 minutes intervals during the procedure, and repeated at 1 hour, 2 hours, 4 hours, 8 hours, 24 hours, and 48 hours after the procedure. Results: The results were as follows; 1) The patients were divided into two groups characterized by each pattern in the change of PEC during the procedure. A group (11 of sixten, group I) showed an increasing pattern of PEC and another group (5 of sixteen, group II) showed a decreasing pattern of PEC during the procedure. 2) Group I demonstrated a tendency to maintain continuously higher level of PEC than the baseline value until 48 hours after the procedure. 3) Group II demonstrated a tendency to maintain continuously lower level of PEC than the baseline value until 48 hours after the procedure. 4) There were no significant differences in their clinical parameters including baseline eosinophil count, baseline $FEV_1$, $PC_{20}$ of histamine, and serum IgE level between group I and group II. Conclusion: Our results suggest that the change of PEC produced by inhaled histamine in asthmatic subjects is much different from that produced by inhaled allergen, and that each patient may have their individual characteristics in the change of PEC in response to bronchial provocation with inhaled histamine. Alternatively these findings suggest that eosinophils may be partially involved in the early asthmatic reaction.

• 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.

• 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.

• The Journal of the Korean dental association
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• v.8 no.7
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• pp.481-484
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• 1970

• Korean Journal of Veterinary Research
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• v.29 no.4
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• pp.433-436
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• 1989

Hematologic values were determined in blood samples obtained from 203 normal, healthy Jindo dogs of both sexes that ranged in age from 3 months to 10 years. Age-related differences were detected for the total erythrocyte count, hemoglobin content, PCV and the number of eosinophils. The persistent eosinophilia appears to be due to the dirofilariasis and flea-allergy dermatitis.

• 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.49 no.6
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• pp.733-739
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• 2000

Background : Pleural eosinophilia is rare and commonly considered to be an indicator of good prognosis. The diagnostic significance of eosinophilic pleural effusions remains controversial despite a century of observation and discussion. This study was conducted to assess the prevalence of eosinophilia in 446 consecutive samples of pleural fluid, to review the cause of eosinophilic pleural effusion and to determine whether the presence of eosinophils increases the likehood of benign conditions. Method : A retrospective analysis was performed upon patients that underwent first thoracentesis due to pleural effusion between January 1999 and December 1999. Results : Eosinophilic pleural effusions were identified in 24 of the 446 patients (5.4%). Malignancy, parapneumonic effusion and tuberculosis were determined the major causes of pleural effusion (80.6%). Malignancy was diagnosed as frequently in eosinophilic effusions as in non-eosinophilic effusions (54.2% vs 50.5%, p=0.725). No difference was found in the prevalence of eosinophilic and non-eosinophilic effusion according to the etiology. The mean blood eosinophil ratio in patients with eosinophilic pleural effusion was 5.4% and no significant correlation existed between the blood and pleural eosinophilic count. Conclusion : Pleural eosinophilia is not helpful for differentiating benign and malignant etiology and is not related with bood eosinophilia or repeated tapping.

• 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.

• Clinical and Experimental Pediatrics
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• v.45 no.12
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• pp.1577-1584
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• 2002

Purpose : Airway inflammation is considered to be a characteristic feature of asthma, and eosinophils are recognized as the most important inflammatory cells. This study aims to assess the importance of blood eosinophil count and serum eosinophil cationic protein(ECP) levels as a noninvasive marker of bronchial hyperresponsiveness(BHR) in children with suspected asthma. Methods : This study used data from 87 subjects with asthma-like symptoms(6-18 years old). The $FEV_1$ and provocative concentration producing a 20% fall in $FEV_1(PC_{20})$ on methacholin inhalation challenge test were measured. Four groups were classified based on $PC_{20}$[Group I : <2 mg/mL; Group II : 2-8 mg/mL; Group III : 8-18 mg/mL; Group IV : (18 mg/mL], and blood eosinophil count and serum ECP levels were analyzed. In addition, subjects were classified based on the cutoff value of $PC_{20}$(BHR positive group : <18 mg/mL; BHR negative group : (18 mg/mL). Then blood eosinophil count and serum ECP level were compared between these two groups. Results : Likelihood ratio test for trends revealed a significant association between the blood eosinophil count or serum ECP level, and the degree of BHR as measured by methacholine $PC_{20}$. Blood eosinophil count or serum ECP level was significantly higher in the BHR(+) group than in the BHR(-) group. Blood eosinophil count had a positive correlation with serum ECP level. Conclusion : Blood eosinophil count and serum ECP level may be a useful non-invasive clinical marker of BHR in subjects with suspected asthma. This supports the hypothesis that BHR in asthma is a consequence of airway eosinophilic inflammation.