BACKGROUNDs: A retrospective study was performed to define objective radiologic parameters in diagnosing epiglottitis on soft-tissue lateral neck radiographic study. METHODS: Parameters of soft-tissue structures(epiglottis width, third vertebral body width, ratio of epiglottic width to third vertebral body width) in 30 adult patients compared with those of age and sex-matched controls with foreign body in throat whose radiographic reading was normal. RESULTS: Epiglottis width of more than 11mm, ratio of epiglottis width(EW) to the third vertebral body width(C3W) of more than 0.5 were, respectively, found to be 100% sensitive and specific in differentiating between patients with and without epiglottitis. CONCLUSION: These preliminary results suggest that EW/C3W ratio of more than 0.5, EW of more than 11mm, respectively, may be useful in the diagnosis of epiglottitis in adult patients.
Adult* ; Diagnosis* ; Epiglottis ; Epiglottitis* ; Foreign Bodies ; Humans ; Neck ; Pharynx ; Retrospective Studies

No abstract available.
Urticaria*

Several observation suggest that the antimelanocyte autoantibodies could play a role in melanocyte destruction. Some experiments indicate that melanocyte antibodies from patients with vitiligo can kill melanocyte in vitro. In these experiments, we demonstrated that vitiligo patient's sera containing antimelanocyte antibodies can lyse cultured human melanocytes by complement activation. Melanocyte cytotoxicity was measured using the ethidium bromide/ acridine orange viability assay. Significant melanocyte cytotoxicity was seen in sera from patients with both active and inactive vitiligo(p<0.01). Melanocyte cytotoxicity measured with complement-mediated cytotoxicity decreased after systemic steroid treatment(p<0.05) ; however melanocyte cytotoxicity showed no significant change with systemic PUVA therapy.
Acridine Orange ; Antibodies ; Autoantibodies* ; Complement Activation ; Ethidium ; Humans ; Melanocytes ; PUVA Therapy ; Vitiligo*

No abstract available.
Antibodies, Neutralizing* ; Feces* ; Rotavirus*

Acute myocardial infarction after a bee sting is a very rare process. Among proposed mechanisms, vasospasm of the coronary artery is the most probable mechanism. Many mediators are included in the venom of wasps, and those mediators have vasoconstrictive properties and may constrict the coronary artery. Furthemore, those mediators have thrombogenic properties that lead to thrombogenesis in the coronary artery and aggravate myocardial ischemia. Epinephrine, commonly used in the management of anaphylactic shock, may further aggravate myocardial ischemia. We experienced two cases of acute myocardial infarction after a bee sting. In the first case, we could find no underlying abnormalities of the coronary vessel because the patient died during coronary angiography. In the second case, the electrocardiogram showed inferior wall myocardial infarction, but only mild stenosis of the right coronary artery was seen in coronary angiography.
Anaphylaxis ; Bees* ; Bites and Stings* ; Constriction, Pathologic ; Coronary Angiography ; Coronary Vessels ; Electrocardiography ; Epinephrine ; Humans ; Inferior Wall Myocardial Infarction ; Myocardial Infarction* ; Myocardial Ischemia ; Venoms ; Wasps

BACKGROUND: PUVA has been used effectively in the treat,ment of vitiligo, but the mechanism by which PUVA stimulat.es melanocyte proliferation in vitiligo is not known. Several mechanisms have been suggested to be involved in the process of repigmentation of vitiligo. First, UV light, with or without psoralen, directly stimulates the proliferation of melanocytes. Secondly, PUVA may act. on epidermal keratinocytes or dermal components to stimulate t,hem to release certain melanocyte growth st,inulation factors that enhance the proliferation of melanocytes in depigmented lesions. Thirdly, PUVA irnmunologically leads to the impairment of epidermal Langerhans cell function and alteration of circulating T and B cell function, which results in the suppression of the stimuli is for rnelanocyte destruction during the therapy. OBJECTIVE: To test, th hypothesis that PUVA induced repigmentation in vitiligo results from the stimulation of growth factors that induce melanocyte proliferation, and that PUVA may suppress the immune reacticin to melanocytes, especially in autoantibody synt,hesis, we examined the effects of sera on the growth of epidermal melanocytes and control cells, and t,he incidence of antibodies to melanocyte and melanoma cells(SK-Mel 2~3) in the sera of patients with vitiligo. We also had normal control individuals and studied the changes of the antibody titer in the sera of patients with vitiligo. METHODS: The rate of H thymidine uptake was estimat,ed in cultured melanocytes and fibroblasts t,reated by patients sera before and after PUVA treatment. SDS-PAGE and immunoblotting analysis were used to idcntify anti pigment cell autoantibodies and were compared to the titers of autoantibodies after PUVA. RESULTS: 1. Melanocyte and fibrablast proliferation was increased by PUVA treated sera. Their proliferation was in proportion to the duration of the PUVA treatment. Melanocytes proliferated more than fibroblasts. 2. Significant differences between vitiligo patients and normal controls were found in the inci dence of anti-pigment cell antibodies. The antibodies were predominantly directed to melanocyte antigens of 110 kD, 65 kD, 45 kD and melanoma cell antigens of 110 kD, 103 kD, 88kD, 70 kD, 56 kD, 41 kD. 3. The titer of anti piment cell antibodies showed a tendency to decrease after PUVA treat- ment in most patients regardless of clinical improvement. Conclusion ; PUVA treated sera induced proliferation of melanocytes and fibroblasts and the production of aut,oantibodies was suppressed against pigment cell antigens through irnmunosuppression, which might help in the repigmentation of vitiligo.
Antibodies ; Autoantibodies* ; Electrophoresis, Polyacrylamide Gel ; Fibroblasts ; Ficusin ; Humans ; Immunoblotting ; Incidence ; Intercellular Signaling Peptides and Proteins ; Keratinocytes ; Melanocytes* ; Melanoma ; Thymidine ; Ultraviolet Rays ; Vitiligo*

BACKGROUND: PUVA has been used effectively in the treat,ment of vitiligo, but the mechanism by which PUVA stimulat.es melanocyte proliferation in vitiligo is not known. Several mechanisms have been suggested to be involved in the process of repigmentation of vitiligo. First, UV light, with or without psoralen, directly stimulates the proliferation of melanocytes. Secondly, PUVA may act. on epidermal keratinocytes or dermal components to stimulate t,hem to release certain melanocyte growth st,inulation factors that enhance the proliferation of melanocytes in depigmented lesions. Thirdly, PUVA irnmunologically leads to the impairment of epidermal Langerhans cell function and alteration of circulating T and B cell function, which results in the suppression of the stimuli is for rnelanocyte destruction during the therapy. OBJECTIVE: To test, th hypothesis that PUVA induced repigmentation in vitiligo results from the stimulation of growth factors that induce melanocyte proliferation, and that PUVA may suppress the immune reacticin to melanocytes, especially in autoantibody synt,hesis, we examined the effects of sera on the growth of epidermal melanocytes and control cells, and t,he incidence of antibodies to melanocyte and melanoma cells(SK-Mel 2~3) in the sera of patients with vitiligo. We also had normal control individuals and studied the changes of the antibody titer in the sera of patients with vitiligo. METHODS: The rate of H thymidine uptake was estimat,ed in cultured melanocytes and fibroblasts t,reated by patients sera before and after PUVA treatment. SDS-PAGE and immunoblotting analysis were used to idcntify anti pigment cell autoantibodies and were compared to the titers of autoantibodies after PUVA. RESULTS: 1. Melanocyte and fibrablast proliferation was increased by PUVA treated sera. Their proliferation was in proportion to the duration of the PUVA treatment. Melanocytes proliferated more than fibroblasts. 2. Significant differences between vitiligo patients and normal controls were found in the inci dence of anti-pigment cell antibodies. The antibodies were predominantly directed to melanocyte antigens of 110 kD, 65 kD, 45 kD and melanoma cell antigens of 110 kD, 103 kD, 88kD, 70 kD, 56 kD, 41 kD. 3. The titer of anti piment cell antibodies showed a tendency to decrease after PUVA treat- ment in most patients regardless of clinical improvement. Conclusion ; PUVA treated sera induced proliferation of melanocytes and fibroblasts and the production of aut,oantibodies was suppressed against pigment cell antigens through irnmunosuppression, which might help in the repigmentation of vitiligo.
Antibodies ; Autoantibodies* ; Electrophoresis, Polyacrylamide Gel ; Fibroblasts ; Ficusin ; Humans ; Immunoblotting ; Incidence ; Intercellular Signaling Peptides and Proteins ; Keratinocytes ; Melanocytes* ; Melanoma ; Thymidine ; Ultraviolet Rays ; Vitiligo*

BACKGROUND: Epinephrine used in surgery to provide hemostasis may elicit ventricular arrhythmias. A desirable anesthetic would not sensitize the myocardium to exogenously administered epinephrine. So the effect of sevoflurane, which was introduced to clinical anesthesia recently, on cardiac arrhythmias induced by the infusion of epinephrine was compared with those of halothane which was already known to epinephrine-induced arrhythmia in the 14 mongrel dogs. METHODS: The authors compared the arrhythmogenicity (three or more premature ventricular contractions, PVCs)of intravenously administered epinephrine in 14 mongrel dogs who were randomly assigned to receive sevoflurane (1.7 vol%) or halothane (0.75 vol%) anesthesia equipotently. The arrhythmogenic doses of epinephrine determined in this comparative study were expressed by both infusion rates of epinephrine during sevoflurane and halothane anesthesia. RESULTS: The mean values of the arrythmogenic infusion rates of epinephrine were 27.1 7.6 g/kg for sevoflurane and 2.7 0.8 g/kg for halothane. CONCLUSIONS: We concluded that the arrythmogenic doses of epinephrine during sevoflurane were significantly higher than those during halothane anesthesia.
Anesthesia* ; Animals ; Arrhythmias, Cardiac ; Dogs* ; Epinephrine* ; Halothane* ; Hemostasis ; Myocardium ; Ventricular Premature Complexes

No abstract available.
Amniotic Fluid* ; Animals ; Embryonic Structures* ; Female ; Humans* ; Mice*

BACKGROUND: The clinical behavior of vitiligo has not been clearly understood and hypothesis concerning the pathogenesis of the disease has been confusing and contradictory though autoimmune mechanisms have been considered important by many authors. OBJECTIVE: The purpose of this study was to develop a better understanding of the clinical features and pathogenesis of vitiligo. METHODS: We investigated clinical features of vitiligo in 1315 patients, and also compared the clinical course and features of non-segmental type(type A) and segmental type(type B) vitiligo patients to see whether the two types of vitiligo have a different pathogenic mechanism. RESULTS: Previously reported clinical patterns of the disease were reviewed and compared with our data, and the different clinical findings between the two types which supported the hypothesis of Koga et al. that type A and type B vitiligo had a different pathogenesis and autoimmune mechanisms played a role only in type A were shown. CONCLUSION: We investigated the clinical characteristics of vitiligo in Korea and showed that the type A vitiligo might have a different pathogenic mechanism with type B.
Clinical Study* ; Humans ; Korea ; Vitiligo*