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1.
Journal of the Korean Ophthalmological Society ; : 1126-1133, 2016.
Article in Korean | WPRIM | ID: wpr-174274

ABSTRACT

PURPOSE: To evaluate long-term change in intraocular pressure (IOP) in eyes undergoing laser iridotomy (LI) and early phacoemulsification after LI in patients with acute angle-closure glaucoma (AACG). METHODS: The retrospective, comparative chart review included patients with AACG, Group A who underwent only LI and Group B who underwent early phacoemulsification within 1 month after LI. Patients were followed up on day 1; week 1; and months 1, 3, 6, and 12 after LI. IOP changes were studied. RESULTS: This study included a total 99 eyes from 99 patients, 37 in group A and 62 in group B. The mean IOP were not significantly different between the two groups at the initial visit or 1 month later. However, group B showed a consistently lower mean IOP that that of group A at 3, 6, and 12 months (p= 0.003, <0.001, <0.001, respectively). The prevalence of IOP increase to greater than 21 mmHg was 3 (8.11%), 5 (13.51%), and 5 patients (13.51%) in group A and 0, 2 (5.41%), and 1 patients (1.61%) in group B at 3, 6, and 12 months, respectively. Group B showed a significantly lower prevalence of IOP increase (p = 0.050, 0.038, 0.026). CONCLUSIONS: We found that patients treated with early phacoemulsification after LI had better outcomes of well-maintained IOP compared to those undergoing LI alone. For AACG patients with coexisting cataract, early phacoemulsification after LI can be considered as a reasonable treatment to maintain IOP.


Subject(s)
Humans , Cataract , Glaucoma, Angle-Closure , Intraocular Pressure , Phacoemulsification , Prevalence , Retrospective Studies
2.
Journal of Korean Medical Science ; : 677-679, 2005.
Article in English | WPRIM | ID: wpr-25776

ABSTRACT

We report here a case with hypereosinophilia and peripheral artery occlusion. A 32-yr-old Korean woman presented to us with lower extremity swelling and pain. Angiography revealed that multiple lower extremity arteries were occlusive. The biopsy specimen showed perivascular and periadnexal dense eosinophilic infiltration in dermis and subcutaneous adipose tissue. Laboratory investigations revealed a persistent hypereosinophilia. She was prescribed prednisolone 60 mg daily. Her skin lesion and pain were improved and the eosinophil count was dramatically decreased. After discharge, eosinophil count gradually increased again. Cyanosis and pain of her fingers recurred. She had been treated with cyclophosphamide pulse therapy. Her eosinophilia was decreased, but the cyanosis and tingling sense were progressive. The extremity arterial stenoses were slightly progressed. Skin biopsy showed perivascular eosinophilic infiltration in the dermis and CD40 ligand (CD40L) positive eosinophilic infiltration. The serum TNF-alpha was markedly increased. These results suggest that CD40L (a member of TNF-alpha superfamily) could play a role in the inflammatory processes when eosinophil infiltration and activation are observed. We prescribed prednisolone, cyclophosphamide, clopidogrel, cilostazol, beraprost and nifedipine, and she was discharged.


Subject(s)
Adult , Female , Humans , Arterial Occlusive Diseases/diagnosis , CD40 Ligand/analysis , Cyanosis/etiology , Diagnosis, Differential , Eosinophilia/diagnosis , Gangrene/etiology , Hypereosinophilic Syndrome/blood , Immunohistochemistry , Peripheral Vascular Diseases/diagnosis , Skin/chemistry , Tumor Necrosis Factor-alpha/metabolism , Vasculitis/diagnosis
3.
Journal of Asthma, Allergy and Clinical Immunology ; : 826-832, 2003.
Article in Korean | WPRIM | ID: wpr-218669

ABSTRACT

Eosinophilic cellulitis was first described by Wells, which is characterized by cellulitis like skin lesion, eosinophilic infiltration of dermis and subcutaneous fat with characteristic flame figure appearance of chollagen bundles. Peripheral eosinophilia is not necessary for the diagnosis of eosinophilic cellulitis, but association with hypereosinophilic syndrome was reported. Episodic angioedema associated with eosinophilia was first described by Gleich et al. as recurrent attack of angioedema; peripheral eosinophilia; and body weight gain; they described this as separate disease entity rather than variant of the hypereosinophilic syndrome. Both angioedema associated with eosinophilia and eosinophilic cellulitis were reportedly associated with hypereosinophilic syndrome, and we believe both diseases are variants of idiopathic hypereosinophilic syndrome. We experienced a patient with eosinophilic cellulitis who has expressed skin lesion resembling angioedema associated with eosinophilia, and who also has involvement of pleura and gastrointestinal tract. We speculate that this patient represents an overlap syndrome of idiopathic hypereosinophilic syndrome, eosinophilic cellulitis and angioedema associated with eosinophilia.


Subject(s)
Humans , Angioedema , Body Weight , Cellulitis , Dermis , Diagnosis , Eosinophilia , Eosinophils , Gastrointestinal Tract , Hypereosinophilic Syndrome , Pleura , Skin , Subcutaneous Fat
4.
Korean Journal of Medicine ; : 431-435, 2002.
Article in Korean | WPRIM | ID: wpr-11150

ABSTRACT

The hemolytic uremic syndrome (HUS) is a clinical syndrome defined by the presence of thrombocytopenia, microangiopathic hemolytic anemia and acute renal failure with or without a clinically apparent etiology. The conventional treatment of choice is plasmapheresis as a first-line therapy. Most patients respond to plasmapheresis whereas some patients are refractory to the therapy. The second-line therapy is not well established although various therapies such as steroid, vincristine, intravenous immunoglobulin have been suggested. The intravenous immunoglobulin therapy in refractory hemolytic-uremic syndrome have rarely been successful in complete remission. We report a case of refractory HUS in a 48 year-old man who developed hemolytic anemia, thrombocytopenia, acute renal failure and ischemic retinopathy. The patient was refractory to plasmapheresis as a first-line therapy. The patient received intravenous immunoglobulin therapy as a second-line therapy after 8 days of plasmapheresis, which subsequently resulted in a complete remission of refractory HUS. The complete remission using immunoglobulin in HUS has not been previously reported in Korea.


Subject(s)
Humans , Middle Aged , Acute Kidney Injury , Anemia, Hemolytic , Hemolytic-Uremic Syndrome , Immunization, Passive , Immunoglobulins , Korea , Plasmapheresis , Thrombocytopenia , Vincristine
5.
Journal of Asthma, Allergy and Clinical Immunology ; : 977-985, 2001.
Article in Korean | WPRIM | ID: wpr-94702

ABSTRACT

Churg-Strauss syndrome is a rare subset of the group of systemic necrotizing vasculitis. Acute respiratory failure is an extremely rare presentation of Churg-Strauss syndrome. The authors report a case of Churg-Strauss syndrome presenting with acute respiratory failure due to diffuse pulmonary hemorrhage. A 28-year-old male suffering from not-well responding bronchial asthma developed erythematous maculopapulous skin lesion and progressive infiltrative pulmonary consolidation on chest X-ray but initially there was no eosinophilia in the peripheral blood. One week later, acute respiratory failure developed with peripheral eosinophilia. Chest X-ray showed bilateral multiple consolidations and patchy densities. The patient was supported on mechanical ventilator and we performed skin biopsy and bronchoscopic examination immediately. The lung biopsy specimens demonstrated capillaritis and prominent interstitial and alveolar eosinophil infiltrates. Grossly bloody bronchoalveolar lavage fluid showed predominant increase in eosinophilic increase and many hemosiderin laden macrophages. Therefore the patients was diagnosed with Churg-Strauss syndrome presenting with pulmonary hemorrhage. Treatment with intravenous methylprednisolone produced symptomatic improvement and normalized peripheral eosinophilia. This case emphasizes that Churg-Strauss syndrome should be considered in the differential diagnosis of acute respiratory failure, and early intervention or diagnostic approach is needed.


Subject(s)
Adult , Humans , Male , Asthma , Biopsy , Bronchoalveolar Lavage Fluid , Churg-Strauss Syndrome , Diagnosis, Differential , Early Intervention, Educational , Eosinophilia , Eosinophils , Hemorrhage , Hemosiderin , Lung , Macrophages , Methylprednisolone , Respiratory Insufficiency , Skin , Thorax , Vasculitis , Ventilators, Mechanical
6.
Journal of Korean Medical Science ; : 407-410, 2001.
Article in English | WPRIM | ID: wpr-79895

ABSTRACT

The pathogenetic mechanism of nonatopic asthma has not yet been defined. The idea of a possible involvement of autoimmunity in the pathogenesis of nonatopic asthma has been proposed by earlier studies. To evaluate the possible involvement of autoimmune response against bronchial epithelial cell in the pathogenesis of nonatopic asthma, we measured circulating autoantibodies to cultured human bronchial epithelial cell (BEAS-2B cell line) using enzyme-linked immunosorbent assay. We used stored serum samples form 38 age-matched healthy controls, 26 adult patients with atopic asthma, 16 adult patients with nonatopic asthma, and 12 adult patients with systemic lupus erythematosus. Levels of IgG autoantibodies to bronchial epithelial cell were significantly higher in patients with nonatopic asthma (mean+/-SD of absorbance values; 0.135+/-0.030) and systemic lupus erythematosus (0.293+/-0.181) than in healthy controls (0.112+/-0.016) and patients with atopic asthma (0.116+/-0.031) (p<0.05). This study showed that levels of circulating IgG autoantibodies to bronchial epithelial cell were increased in adult patients with nonatopic asthma. Further studies are needed to evaluate the possible involvement of autoimmune mechanism in the pathogenesis of nonatopic asthma.


Subject(s)
Adult , Humans , Asthma/immunology , Autoantibodies/blood , Bronchi/immunology , Cells, Cultured , Epithelial Cells/immunology , Hypersensitivity/immunology , Immunoglobulin G/blood
7.
Korean Journal of Medicine ; : 829-835, 1999.
Article in Korean | WPRIM | ID: wpr-48433

ABSTRACT

No abstract available.


Subject(s)
Asthma
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