Acute eosinophilic pneumonia(AEP) is one of uncommon causes of fatal respiratory failure. Since first reported in 1979, AEP is considered as different disease entity from chronic eosinophilic pneumonia. Recently, consensus is evolving in regard to diagnostic criteria. We experienced a 21-year old male patient presenting typical clinical and radiological characteristics of AEP. Bronchoalveolar lavage showed eosinophilia and transbronchial lung biopsy revealed infiltration of eosinophils and lymphocytes in interstitium and alveoli. This patient completely recovered within three weeks without corticosteroid. We report this case with brief review of literature.
Biopsy ; Bronchoalveolar Lavage ; Consensus ; Eosinophilia ; Eosinophils* ; Humans ; Lung ; Lymphocytes ; Male ; Pulmonary Eosinophilia* ; Respiratory Insufficiency ; Young Adult

We experienced two cases of occupational asthma induced by Elk dander in Elk-feeders and confirmed these cases by the bronchial provocation test with Elk dander. Both of them showed dual asthmatic response. They also showed positive reaction to the skin prick test with EIK dander. Now one of them has no asthmatic symptoms at all after complete avoidnce of EIK dander.
Asthma, Occupational* ; Bronchial Provocation Tests ; Dander ; Skin

BACKGROUND: Eosinophils are suggested to play a deleterious role in the inflammatory disease of the respiratory mucosa by releasing granule substances such as major basic prorein and eosinophil cationic protein. To investigate the contribution of eosinophils in the pathogenesis of nasal polyps and the mechanism of their accumulation and activation, we observed the eosinophil inhllration and expression of endotjelial and epithelial cell adhesion molecules in the nasal polyp tissues. MATERIALS AND METHODS: Polyp and inferior turbinate mueosal specimens (polyp group) taken out of 20 patients and 10 inferior turbinate mucosa specimens of non-allergic and non-infectious controls (control group) were immunohistochemically stained using EG1, EG2, and mAb for the ICAM-1, VCAM-1 and E-seleetin. The number of EG1 (+) and EG2 (+) cells within lmm2 of tissue and the expression of ICAM-1, VCAM-1 and E-seleetin on the vessels (% of total vessel) and epithelial eelis (area x intensity) were compared among three groups. RESULTS:The inferior turbinate mucosae of nasal polyp patients .were infiltrated by signifieantly higher number of eosinophils (EG1:17, EG2:16/mm2) compared with those of controls (EGi:0, EG2:0/mm2) (p<0.05), and the polyp tissue revealed much more eosinophils (EG1: 213, EG2:154/mm2) than inferior turbinates of same patients and those of controls (p<0.001). ICAM-1 expression in the vessels was frequenly observed both in polyps and in the turbinate mucosae with significant difference (median:85% vs. 67%, p<0.05), and ICAM-1 expression in the epithelial ceils was significantly different between the polyp and turbinate groups (median:9 vs. 2.5, p<0. 01). VCAM-1 was moderately expressed on the vessels of both polyps and turbinate mucosac (median:37%, 14%, respectively) and their expressions were significantly different (p<0.01). E-selectin expression was moderate to low both in the polyps and in the turbinate mucosae (median:18%, 10% respectively) and their expressions were not significantly different (p>0.05). CONCLUSION: Most of the eosinophils infiltrated into nasal tissue as well as nasal polyps were activated forms and they were significantly increased in the nasal polyps compared to the inferior turbinate mueosae of the same patients and control subjects. Significantly increased expression of ICAM-1 and VCAM-1 on the vessels and increased epithelial ICAM-1 expression in the nasal polyps indicate that interactions of eosinophils with ICAM-1 and VCAM-1 participate in the pathogenesis of nasal polyps.
E-Selectin ; Eosinophil Cationic Protein ; Eosinophils* ; Epithelial Cells ; Humans ; Intercellular Adhesion Molecule-1 ; Mucous Membrane ; Nasal Polyps* ; Polyps ; Respiratory Mucosa ; Turbinates ; Vascular Cell Adhesion Molecule-1

Idiopathic anaphylaxis is a life-threatening systemic reaction of unknown cause. The pathophysiology has not been established, although it has been postulated that the clinical manifestations of idiopathic anaphylaxis may result from the chemical mediators released by mast cells or basophils. The diagnosis of idiopathic anaphylaxis is made after an appropriate allergic evaluation and exclusion of provocative triggers. We report an unusual case of idiopathic anaphylaxis manifesting with periodically repeated urticaria, angioedema, dyspnea, and hypotension. His symptoms were not related to known causes of anaphylaxis such as foods, drugs, insect stings, or exercise. Other diseases simulating anaphylaxis were excluded by careful history, physical examination, and relevant diagnostic tests. High dose prednisolone, hydroxyzine, salbutamol, ketotifen, and methotrexate were prescribed to prevent recurrent episodes, but the symptoms relapsed 5 months after cessation of the treatment.
Albuterol ; Anaphylaxis* ; Angioedema ; Basophils ; Diagnosis ; Diagnostic Tests, Routine ; Dyspnea ; Hydroxyzine ; Hypotension ; Insect Bites and Stings ; Ketotifen ; Mast Cells ; Methotrexate ; Physical Examination ; Prednisolone ; Urticaria

Hypersensitivity myocarditis is an inflammatory disease of the myocardium usually related to drug allergy. The clinical manifestation may be nonspecific, and the diagnosis is seldom suspected or established during the life. So in most of the reported patients, the diagnosis was made at autopsy. Although, retrospectively, more than 90% of the patients described have had clinically recognizable cardiac involvement before death, tole clinical suspicion of hypersensitivity myocarditis is rare. The presence of nonspecific cardiac finding in a patient receiving any drug associated with hypersensitivity should alert the clinician to the possibility of drug related myocarditis. We experienced a case of hypersensitivity myocarditis accompanying allergic skin lesion in a 58 years old man with a history of taking cefadroxil. Fortunately, the outcome was favorable, therefore we do not have histologic confirmation of the diagnosis.
Autopsy ; Cefadroxil ; Diagnosis ; Drug Hypersensitivity ; Humans ; Hypersensitivity* ; Middle Aged ; Myocarditis ; Myocardium ; Retrospective Studies ; Skin

We studied sputum eosinophil count of patients with chronic cough. Differential count of sputum cells(simple direct smear with Wright stain) were successfully examined in 44(73%) among 60 patients with chronic cough. The patients were divided according to PC2O value; 20(45%) patients had increased airway hyper responsiveness(AHR) (PC2O < 24mg/ml), remained 24 Patients did not have any evidence of airway AHR. Age, sex, duration and severity of symptoms, serum total IgE and positive skin test reaction were not different between two groups. In patients with increased AHR, increased sputum eosinophil ratio(10%) was found in 11 patients (55%) and increased peripheral blood eosinophil ratio(>5%) was found in 66% of patients with increased AHR. In patients without increased AHR, increased sputum eosinophil ratio was found in three patients(12%) and increased peripheral blood eosinophil ratio was found in 24%. This discrepancy between two groups was statisticalla significant(p<0.01). In regarding to sputum eosinophilia, increased sputum eosinophil ratio was in 14(32%) of 44 patients with chronic cough. Eleven patients(78%) of them had increased AHR. Only nine(30%) among 30 patients without sputum eosinophilia had increased AHR. These discrepancies between two groups were statistically significant(p<0.01). To predict AHR, sputum eosinophilia has 55% of sensitivity and 88% of specificity. Significant positive correlation between peripheral blood eosinophil ratio and sputum eosinophil ratio was found in patients with cough-variant asthma (r=0.76, p<0.01), We suggest that simple direct smear for sputum eosinophil count could be an useful test to diagnose the patients with chronic cough.
Asthma ; Cough* ; Eosinophilia ; Eosinophils* ; Humans ; Immunoglobulin E ; Sensitivity and Specificity ; Skin Tests ; Sputum*

Aspirin(ASA) and NSAIDs can induce bronchoconstriction in 10~20% of adult asthmatics patients. Inhalation of lysine-ASA(L-ASA) has been described as an alternative method for diagnosis of ASA-sensitive asthma. To further understand the characterlstics of ASA-sensitive asthmas. we studied 38 asthmatic patients with ASA -sensitivity (36 intrinsic and 2 extrinsic asthma) proven by L-ASA bronchoprovocation test (BPT). Most were female (male to female ratio was 27:73). Twenty (53%) of them had no previous history of adverse reactions when exposed to ASA. Twenty nine (79%) had rhino-sinusitis symptoms. Early asthmatic response was observed in 16 (42%) patients, late only response in 16(42%), and dual response in 6(16%) patients. The threshold of L-ASA to provoke a positive response ranged from 11.2 to 180 mg/ml and most (68.3%) had a positive response after the inhalation of 180 mg/ml. Concurrent sensitivity to sulfite was noted in 14 (36%) patients, followed by sensitivity to tartrazine in one (3%) patient. None showed a positive response to sodium benzoate. After the avoidance from ASA/ NSAIDs with administration of anti-asthmatic medications, symptom and medication scores reduced in 26(87%) patients among 30 followed patients. They were classified into the improved group: four (13%) patients belonged to the not-improved group. There were no significant differences in clinical characteristics between the improved and not- improved group (p>0.05). In conclusion, L-ASA BPT could be considered as a useful method to diagnose ASA -sensitive asthma and be used to screen the causative agent for asthmatic patients with intrinsic type, especially in female patients with rhino-sinusitis and/or nasal polyp, even though they do not have arty history of adverse reactions. Cessation of exposure and proper treatment may allow to reduce symptom and medication scores.
Adult ; Anti-Inflammatory Agents, Non-Steroidal ; Asthma* ; Bronchoconstriction ; Diagnosis ; Female ; Humans ; Inhalation ; Nasal Polyps ; Sodium Benzoate ; Tartrazine

Although basic mechanisms of atopic dermatitis remain largely speculative, many studies on pathogenesis suggest the importance of food and inhalent allergens. To evaluate the frequency of food and house dust mite hypersensitivity and differences in this frequency according to ages, we measured the levels of specific IgE antibodies to egg white, egg yolk, milk, soy, and house dust mites in 119 children with atopic dermatitis. The results showed that 53% of patients had positive RAST to any one kind of allergens. The frequency of food and house dust mite hypersensitivity were 34.5%, 30.3 %, respectively. Among allergens, house dust mites and egg white are the most prevalent allergens in all atopic dermatitis patients. The Prevalence of egg white is most common under the age of 2 years, but those of house dust mites are the dust mites are the highest in the ages of 5-12 years. In conclusion, we recommend an egg restriction diet in atopic dermatitis patients who are less than 2 years old when their symptoms do not improve with general skin care.
Allergens ; Antibodies ; Antigens, Dermatophagoides ; Child* ; Child, Preschool ; Dermatitis, Atopic* ; Diet ; Dust* ; Egg White ; Egg Yolk ; Humans ; Hypersensitivity ; Immunoglobulin E ; Mites ; Ovum ; Prevalence ; Pyroglyphidae* ; Skin Care ; Soy Milk

As molecular size of the most major allergens of house dust mite(HDM) are known to be less than 30 kD, allergic immune reactions may be different according to the molecular fractions of HDM allergens. In this study, we fractionated D. pteronyssinus (D. pt) antigen according to its molecular weights, fraction I(FI), II(FII, more than 30 kD), III( FIII, less than 30 kD), and evaluated the differences of allergic immune responses in 40 atopic patients. FIII(A/H ratio-2.44+/-0.61) elicited stronger response on intradermal skin test than FI (0.76 +/-0.10, p<0.001) and FII(0.88+/-0.12, p<0.001). The immunoblot analysis revealed that the nine out of 10 atopics had IgE binding bands with 15 kD protein of FIII which were not found in FI and FII. The geometric mean of absorben value of specific IgE to FIII was 0.067, which was higher than that of FII(0.013, p<0.001), with no difference from that of FI(0.042). The skin reactivity to whole D. pt antigen correlated with FIII- specific IgE(r=0.3862, p<0.01), not with FI-(r=0.2605, p=0.07) and FII-specific IgE(r=0. 1103, p=0.45). FI-specific IgG levels in atopic sera(n=40) were significantly higher than that of FII and FIII in all IgG subclasses (p<0.001). Both atopic(n=4) and nonatopic (n=4) groups showed multiple IgG, IgG1, and IgG2 binding bands at high molecular proteins in immunoblot analysis. The prevalence and density of the IgG and IgG1 binding bands to 15 kD were higher and more intense in atopics than those of nonatopics. In conclusion, we suggest that fractionated antigens of D. pteronyssinus had different antigenicities and that the allergic immune responses to HDMs in atopics and nonatopic are different according to molecular fractions of HDM.
Allergens ; Dermatophagoides pteronyssinus* ; Dust ; Humans ; Immunoglobulin E ; Immunoglobulin G ; Molecular Weight ; Prevalence ; Pyroglyphidae* ; Skin ; Skin Tests

In asthma, eosinophil roles as main end inflammatory effector cell, but neither the activation process nor the stimuli of that is known clearly, yet. Even though allergic asthma is IgE-mediated type I hypersensitivity disease, it is not clear whether there is FcepsilonRI on the surface of eosinophil like mast cell or basophil which is activated through the FcepsilonRl bridging with sensitized allergens. In this study, we speculate if there's FcepsilonRI on the eosinophil, sensitized allergen activates it like mast cell in allergic asthmatics, and with this result we can find out one of the stimuli of eosinophil in asthma and can suggest the possibility of the existence of FcepsilonRI on the eosinophil. We did direct stimulation of the house dust mite -sensitized astknatics'purified peripheral blood normodense eoisnophils with Dermatophagoides pteronyssiuns. Then we measured the LTC4 and ECP from the supernatant by RIA kit and observed the morphological changes with electron microscopy. There was neither increase in LTC4 and ECP level nor the morphological changes in asthmatics. And there were no significant differences in both LTC4, and ECP level, and morphologic changes between asthmatics and controls. We would summerize that house dust mite dose not dirctly activate eosinophil from house dust mite-sensitized asthmatics and couldn't find out the possibility that there's FcepsilonRI on the surface of eoslnophils. But no exitstence of FcepsilonRI on the eosinophil is the indirect evidence, so from now on we try to find more direct evidence of that by blotting.
Allergens ; Asthma ; Basophils ; Dust* ; Eosinophils* ; Humans* ; Hypersensitivity, Immediate ; Leukotriene C4 ; Mast Cells ; Microscopy, Electron ; Pyroglyphidae*