• Tuberculosis and Respiratory Diseases
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• v.57 no.2
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• pp.193-196
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• 2004

Acute respiratory distress syndrome after silicone fluid injection is uncommon. Reasons that organic silicone is inactive in the human body and has low surface tension and is not affected by physical factors such as time or temperature make this material to be widely used as a medical product. However, lately some of its side effects have been noted and also cause respiratory problems in rare occasions. The mechanism is not clear but silicone injection cause one to cough, produce hemoptysis, fever, pleuritic chest pain, and dyspnea, and may even lead to acute respiratory failure. In other countries, these side effects were reported from 1970s and several cases started to appear in Korea from 1990s. We report a 58 years-old female who recovered from acute respiratory distress syndrome after injection of silicone fluid into vaginal wall by a conservative therapy.

• Tuberculosis and Respiratory Diseases
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• v.51 no.2
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• pp.166-172
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• 2001

Silicone fluid is a biomaterial widely used in modern cosmetic procedures because there are few side effects, considerable chemical stability and predictable physical properties. However, many local and systemic adverse reactions have reported. In particular some serious pulmonary complications have been reported such as pulmonary thromboembolism, acute respiratory distress syndrome with some cases leading to mortality. Most of the serious complicated cases were induced by an illegal silicone fluid injection. We experienced two cases of acute respiratory distress syndrome with pulmonary hemorrhage induced by an illegal silicone fluid injection. The patients were 41 & 51 year old women, who complained of dyspnea. The chest X-ray and HRCT scan findings showed a bilateral ground glass attenuation on the bilateral dependent portion of the upper and middle lung zone. The patients clinical symptoms and the radiologic and other laboratory findings were compatible with acute respiratory distress syndrome induced by the silicon fluid injection. Here we report two cases of acute respiratory distress syndrome with pulmonary hemorrhage induced by an illegal silicone injection with a review of the relevant literature.

• Clinical and Experimental Pediatrics
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• v.57 no.4
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• pp.157-163
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• 2014

Respiratory distress syndrome (RDS) among preterm infants is typically due to a quantitative deficiency of pulmonary surfactant. Aside from the degree of prematurity, diverse environmental and genetic factors can affect the development of RDS. The variance of the risk of RDS in various races/ethnicities or monozygotic/dizygotic twins has suggested genetic influences on this disorder. So far, several specific mutations in genes encoding surfactant-associated molecules have confirmed this. Specific genetic variants contributing to the regulation of pulmonary development, its structure and function, or the inflammatory response could be candidate risk factors for the development of RDS. This review summarizes the background that suggests the genetic predisposition of RDS, the identified mutations, and candidate genetic polymorphisms of pulmonary surfactant proteins associated with RDS.

• Tuberculosis and Respiratory Diseases
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• v.80 no.1
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• pp.95-95
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• 2017

• Tuberculosis and Respiratory Diseases
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• v.48 no.4
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• pp.513-521
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• 2000

Background : TNF may play an important role(central mediator) in the development of an acute respiratory distress syndrome. Since TNF induced lung injury in the acute respiratory distress syndrome and abnormalities in surfactant function have been described in acute respiratory distress syndrome, the authors investigated the effects of TNF on the regulation of surfactant protein A, B and C mRNA accumulation. Methods : The effects of TNF on gene expression of surfactant protein A, B, and C were analyzed using filter hybridization, 12 and 24 hours after intravenous injection of TNF in rats. Results : 1. The accumulation of SP-A mRNA in the TNF treated group (12 and 24 hours after TNF injection) was significantly decreased by 22.9% and 27.4%, respectively, compared to the control group (P<.025, P<.025). 2. The accumulation of SP-B mRNA in 24 hours after TNF treated group was significantly decreased by 20.5% compared to that of the control group(P<.01). 3. The accumulation of SP-C mRNA in 12 hours after TNF treated group was significantly decreased by 31% the compared to that of the control group(P<.01). Conclusions : These findings indicate the marked inhibitory effects of tumor necrosis factor on surfactant proteins expression in vivo. This finding. in turn, supports the idea of inhibitory effects of tumor necrosis factor on surfactant proteins expression as it relates to pathogenesis of acute respiratory distress syndrome.

• Journal of Yeungnam Medical Science
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• v.35 no.2
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• pp.187-191
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• 2018

Background: Respiratory distress syndrome (RDS) is a one of the most common cause of respiratory morbidity and mortality in neonates. This study was conducted to investigate the risk factors for RDS in full-term neonates. Methods: We conducted this retrospective study using medical records. The study group included 80 full-term neonates diagnosed with RDS and hospitalized in the neonatal intensive care unit between January 2012 and December 2016, at Yeungnam University Hospital. We analyzed sex, gestational age, birth weight, delivery method, maternal age, number of pregnancy, history of abortion, and complication of pregnancy. The control group included 116 full-time neonates who were hospitalized with jaundice during the same period. Results: The incidence of full-term RDS was more common in males (odds ratio [OR], 3.288; 95% confidence interval [CI], 1.446-7.479), cesarean section (OR, 15.03; 95% CI, 6.381-35.423), multiparity (OR, 4.216; 95% CI, 1.568-11.335). The other factors rendered no significant results. Conclusion: The risk factors for RDS in full-tern neonates were identified as male sex, cesarean section, and multiparity. Further studies involving more institutions are needed to clarify the risk factors for RDS in full-term infants.

• 아동간호학회:학술대회논문집
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• 1996.12a
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• pp.31-35
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• 1996

• Tuberculosis and Respiratory Diseases
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• v.80 no.3
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• pp.311-312
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• 2017

• Tuberculosis and Respiratory Diseases
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• v.51 no.1
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• pp.5-16
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• 2001

• Tuberculosis and Respiratory Diseases
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• v.50 no.5
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• pp.525-539
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• 2001