Background: Acinetobacter infections are difficult to treat as they often exhibit multiple resistance to the antibiotics that are currently available for the treatment of pneumonia. Colistin is active against gram-negative bacteria, including the multiple drug resistant (MDR) Acinetobacter species. However, intravenous administration of colistin was abandoned because of its nephrotoxicity and neurotoxicity. The aims of this study were to examine the efficacy and safety of colistin administered by aerosol in the treatment of pneumonia caused by MDR Acinetobacter baumannii. Methods: We retrospectively reviewed the medical records of patients admitted to the intensive care unit (ICU) from Dec. 2006 to Aug. 2007 who had been diagnosed as suffering from pneumonia due to MDR Acinetobacter baumannii and had been treated with nebulized colistin. Results: 31 patients received aerosolized colistin. The average duration of the treatment was 14±7 days and the daily dose of ranged from 225 mg to 300 mg. All patients received concomitant intravenous antimicrobial agents. The average length of the stay in the ICU was 34±21 days and in the hospital 58±52 days. The overall microbiological eradication was observed in 25 patients (80.6%). 14 of these (56%) were cured, and 11 (44%) were infected with other microorganisms. The overall crude mortality of the ICU was 48%. Nephrotoxicity and significant bronchial constriction did not occur in any patient during neublized colistin treatment. Conclusion: Nebulized colistin may be a safe and effective option in the treatment of pneumonia due to MDR Acinetobacter baumannii. Its role in therapy warrants further investigation in comparative studies.
Background: The melanoma antigen-encoding (MAGE) genes are known to be expressed in various cancer cells, including non-small cell lung cancer (NSCLC), and are silent in all normal tissues except for the testis. In patients with peripheral NSCLC, bronchial washing fluid can be used to detect the MAGE genes, suggesting a diagnosis of lung cancer. In order to evaluate the diagnostic utility of the MAGE test in patients with peripheral NSCLC, bronchial washing fluid was investigated in patients with peripheral pulmonary nodules, which were invisible as detected by bronchoscopy.Methods: Bronchial washing fluid from 37 patients was used for cytological examinations and MAGE gene detection, using RT-nested-PCR of common A1-A6 mRNA. Results were compared to a final diagnosis of patients as confirmed by pathology.Results: Among the 37 subjects, NSCLC was diagnosed in 21 patients, and benign pulmonary diseases were diagnosed in 16 patients. MAGE mRNA was detected in 10 of 21 (47.6%) NSCLC patients, while conventional cytology examinations were positive for MAGE expression in 2 of 21 (9.5%) cases. MAGE expression was observed in 4 of 16 (25%) benign pulmonary disease patients.Conclusion: The MAGE test of bronchial washing fluid can be used as a sensitive predictor of peripheral NSCLC patients.
Background: Staphylococcus aureus frequently colonizes and infects hospitalized patients. Respiratory infections with Staphylococcus aureus are common in patients with compromised airway defenses. However the mechanisms of S. aureus invasion from colonization to the epithelium are unclear. Cell invasion by S. aureus would require destruction of the extracellular matrix, which is believed to be the result of increased matrix metalloproteinases (MMP) activity. Methods: In this study, respiratory epithelial cells were infected with S. aureus. After removing the extracellular bacteria by washing, the internalized bacteria in the cells were assessed by counting the colonized forming units (CFUs). The cell adhesion proteins, dysadherin and E-cadherin, were evaluated by Western blotting. The MMPs in the bacterial invasion were evaluated by pretreating the cells with GM6001, a MMP inhibitor.Results: The internalization of S. aureus was found to be both time and dose dependent, and the increase in MMP 2 and 9 activity was also dependent on the incubation time and the initial amount of bacterial inoculation. The invasion of S. aureus was attenuated by GM6001 after 12 hours incubation with a multiply of infection (MOI)=50. The expression of dysadherin, a membrane protein, was increased in a time and dose dependent manner, while the expression of E-cadherin was decreased. Conclusion: MMPs may mediate the invasion of S. aureus into epithelial cells.
Pulmonary arterial thrombosis develops during hypercoagulable states, intra-arterial tumorous conditions, and congenital heart disease accompanied by pulmonary hypertension. Thrombosis in the main pulmonary arterial stump after pneumonectomy can also occur. Herein, we report a very rare case of pulmonary arterial thrombosis in a patient with pulmonary hypertension and a lung destroyed by tuberculosis. He presented with aggravated dyspnea without fever or purulent sputum. His chest computerized tomography scan showed left main pulmonary arterial thrombosis as a convex shape, with the ipsilateral distal arteries and arterioles showing parenchymal destruction. After excluding pulmonary thromboembolism and hypercoagulable disorders, we diagnosed pulmonary arterial thrombosis and treated him with an anticoagulant.
Alcaligenes xylosoxidans is a catalase and oxidase positive, motile, nonfermentative and gram-negative rod bacterium. A. xylosoxidans infection is a rare cause of pulmonary infection and little information concerning treatment is available. The majority of patients that develop A. xylosoxidans infection belong to a high-risk group due to an immunocompromised condition or due to pulmonary cystic fibrosis. We report two rare cases of immunocompentent patients that developed a pulmonary infection due to A. xylosoxidans. A 77-year-old man was admitted with a lung abscess. The patient denied having any prior medical illness. A culture of bronchial washing fluid showed the presence of A. xylosoxidans. Despite appropriate antibiotic treatment, the patient died from acute respiratory distress syndrome (ARDS). Another patient, a 61-year-old man without an underlying disease, was admitted with empyema. Under the condition of a closed thoracostomy, a high fever persisted and the empyema was also aggravated. A. xylosoxidans was detected from a culture of pleural fluid. Susceptible antibiotic treatment was provided and surgical intervention was performed. We report these cases with a review of the literature.
A hiccup is caused by involuntary, intermittent, and spasmodic contractions of the diaphragm and intercostal muscles. It starts with a sudden inspiration and ends with an abrupt closure of the glottis. Even though a hiccup is thought to develop through the hiccup reflex arc, its exact pathophysiology is still unclear. The etiologies include gastrointestinal disorders, respiratory abnormalities, psychogenic factors, toxic-metabolic disorders, central nervous system dysfunctions and irritation of the vagus and phrenic nerves. Most benign hiccups can be controlled by traditional empirical therapy such as breath holding and swallowing water. However, though rare, a persistent hiccup longer than 48 hours can lead to significant adverse effects including malnutrition, dehydration, insomnia, electrolyte imbalance, and cardiac arrhythmia. An intractable hiccup can sometimes even cause death. We herein describe a patient with non-small cell lung cancer who was severely distressed by a persistent hiccup.
Chronic expanding hematoma of the thorax is a specific subtype of the chronic empyema. It presents as a slowly expanding intrathoracic mass which result in dyspnea or recurrent hemoptysis. The symptoms develop months or years after tuberculous pleurisy, trauma or surgery. Usually, it shows three common findings: a giant mass lesion in the thorax, some surrounding calcifications, the absence of signs or symptoms of infection. We report a case of chronic expanding hematoma of the thorax, initially presenting as massive hemoptysis through bronchopleural fistula which resulted in radiologic findings of new air-fluid level within the previous pleural lesion filled with unknown materials.
A pheochromocytoma is a neuroectodermal tumor that originates from the chromaffin cells of the sympathetic system. Typical symptoms or signs are periodic attacks of paroxysmal hypertension, spell, palpitation, headache and sweating. However, the clinical presentation is quite variable. Therefore, an atypical clinical presentation sometimes makes a diagnosis difficult. Hemoptysis as a presenting symptom is very rare in pheochromocytoma. We recently experienced a patient with diffuse alveolar hemorrhage due to pheochromocytoma. A chest PA showed diffuse consolidation and ground glass opacities in both lungs. A chest CT showed diffuse consolidation and ground glass opacities in the central, middle and lower portion predominance of the lungs, sparing the costophrenic angles and apices of the lungs. In Korea, a case of pheochromocytoma that presented initially as massive hemoptysis due to diffuse alveolar hemorrhage has not been previously reported. We report the case with a review of the literature.