Asthama is a chronic inflammatory disorder of the airway with recurrent airflow obstruction. Chronic airway inflammation is invariably associated with injury and repair of the bronchial epithelium, which results in structural and functional changes known as remodeling Inflammation, remodeling, and altered neural control of the airway are responsible for both recurrent exacerbations of asthma and more permanent airflow obstruction. Asthma exacerbations may be caused by a variety of risk factors including allergens, pollutants, foods and drugs. Prevention of exacerbation aims to reduce the exposure to these risk factors to improve the control of asthma and reduce medication needs. Although no cure for asthma has yet been found, it is resonable to expect that in most patients with asthma, control of the disease can and should be achieved and maintained. Patient education involves a understanding of why and how to manage asthma and how to prevent asthma exacerbation. Medications for asthma can be administered in different ways, including inhaled, oral and parenteral. The major advantage of delivering drugs directly into the airways via inhalation is that high concentrations can be delivered more effectively to the airways, and systemic side effects are avoided or minimized. Therapy should be selected on the basis of the severity of a patient's asthma. According to the GINA guideline 2002, for intermittent asthma, no daily medication is reconmmended for the vast majority of patients. A rapid-acting inhaled β2-agonist may be taken as needed to relieve asthma symptoms. The occasional patient with intermittent asthma, but severe exacerbations, should be treated as having moderate persistent asthma. Patients with mild persistent asthma require controller medication every day to achieve and maintain control of their asthma. Treatment with an inhaled glucocorticosteroid is preferred. Sustained-relase theophyline cromolynes or a leukotriene modifier are other options. The preferred therapy for moderate persistent asthma is regular treatment with a combination of inhaled glucocorticosteroid and a long-acting inhaled glucocorticosteroid and a long-acting inhaled β2-agonist twice daily. Sustained-release theophyline or a leukotriene modifier are alternatives to the β2-agonist in this combination therapy. An alternative to combination therapy is a higher dose of inhaled glucocorticosteriod. The primary therapy for severe persistent asthma includes inhaled steroids at higher doses plus a long acting inhaled β2-agonist twice daily. Any available medications including oral steroid may be added to control asthma symptoms. Once control of asthma is achieved and maintained for at least 3 months, a gradual reduction of the maintenance therapy should be tried.
Allergens ; Asthma* ; Cromolyn Sodium ; Epithelium ; Humans ; Inflammation ; Inhalation ; Patient Education as Topic ; Risk Factors ; Steroids

A controlled study was carried out in 50 patients with perennial bronchial asthma to assess the efficacy and safety of budesonide turbuhaler. Subjects have suffered from cough, wheezing, dyspnea and chest tightness and showed either 15% of reversibility in FEV after bronchodilator inhalation or airway hyperresponsiveness to methacholine(PC20 < or = 25mg/ml.) Patients were randomized to treatment with budesonide turbuhaler or terbutaline turbuhaler for 8 weeks after 2 weeks of run-in period. Budesonide turbuhaler was effective for cough, wheezing, dyspnea and chest tightness. It improved peak expiratory flow rate and FEV1. Budesonide turbuhaler was tolerated well and the laboratory tests showed no abnormality. It is suggested that budesonide turbuhaler is effective and safe in the management of bronchial asthma.
Asthma ; Budesonide* ; Cough ; Dyspnea ; Humans ; Inhalation ; Peak Expiratory Flow Rate ; Respiratory Sounds ; Terbutaline ; Thorax

Meigs' syndrome consists of an ovarian fibroma, or fibroma-like benign tumor, associated with fluid in both abdomen and chest. Characteristically, the ascites and hydrothorax disappeared and do not recurred following removal of the ovarian tumor. The authors presented a case of Meigs' syndrome that was cured by surgical removal of ovarian tumor and resulted in normal pregnancy outcome in 27-year-old pregnant woman with a brief review of literatures.
Abdomen ; Adult ; Ascites ; Female ; Fibroma ; Humans ; Hydrothorax ; Meigs Syndrome* ; Pregnancy Outcome ; Pregnancy* ; Pregnant Women ; Thorax

No abstract available.
Lupus Erythematosus, Systemic*

BACKGROUND: To date, a laparoscopic gastrectomy has been performed by a small number of surgeons around the world, but the laparoscopic approach has been extended to Billroth I and a total gastrectomy. To evaluate the validity of the procedure, we present the results of six patients who underwent a gastrectomy using a laparoscopic technique. METHODS: First, two patients had a totally intra-abdominal laparoscopic B-II gastrectomy, and one of two also had a bilateral truncal vagotomy. The rest had a laparoscopic-assisted gastrectomy. One patient had concurrently an open reduction and an internal fixation with a K-wire for a patellar fracture. Indications were (a) gastric outlet obstruction due to peptic ulcer disease in five patients and (b) duodenal ulcer bleeding in one patient. RESULTS: Except for one patient who had stump leakage, which was solved by conservative therapy, there were no complications or operative mortality. The operating time and the cost were less for the patients who had their operations later in the series and who had laparoscopic-assisted operation. CONCLUSIONS: These forms of laparoscopic gastric surgery for patients with complications of peptic ulcer disease may be useful from the standpoint of minimal access, rapid recovery, less pain, and good cosmesis.
Duodenal Ulcer ; Gastrectomy* ; Gastric Outlet Obstruction ; Gastroenterostomy ; Hemorrhage ; Humans ; Mortality ; Peptic Ulcer ; Stomach Diseases* ; Vagotomy, Truncal

This study was undertaken to clarify the effects of glucocorticosteroids on intraocular pressure and the combined effects of acetazolamide and glucocorticosteroid on ocular pressure. Male and female rabbits, weighing 1.7-2.2kg, were divided into 5 groups: 1) saline-treated group, 2) hydrocortisone (0.5 %)-treated group, 3) prednisolone (0.5 %)-treated group, 4) fludrocortisone (0.1% )-treated group, 5) dexamethasone (0.1% )-treated group. Drugs were instilled 4 times a day for 3 weeks, and ocular pressure was checked in each group on second and third week. Following 3 weeks instillation of glucocorticoids, ocular pressure was checked in each animal at 15, 30, 60, and 120 minutes after intravenous administration of acetazolamide (10mg/kg). Under 0.5% tetracaine anesthesia, facility of outflow and flow rate of the aqueous humor were also measured with a tonometer. The results of the experiments were as follows: 1) The mean ocular pressure rose significantly in all glucocorticoid-treated groups, and the rise was especially marked in the dexamethasone-treated group. 2) The mean facility of outflow of the aqueous humor decreased significantly in the dexamethasonetreated group, but it remained with little change in the other glucocorticoidtreated group. 3) The ocular pressure-lowering action of acetazolamide was suppressed significantly at 30 minutes after the treatment with acetazolamide in the hydrocortisone and prednisolonetreated groups, but it was not suppressed in the fludrocortisone and the dexamethasonetreated groups. 4) The flow rate of the aqueous humor was suppressed significantly (36.2 %) at 30 minutes after the treatment with acetazolamide in the control group, but it was not suppressed significantly in g]ucocorticoid-treated groups.
Acetazolamide* ; Administration, Intravenous ; Adrenal Cortex Hormones* ; Anesthesia ; Animals ; Aqueous Humor ; Dexamethasone ; Female ; Fludrocortisone ; Glucocorticoids ; Humans ; Hydrocortisone ; Intraocular Pressure* ; Male ; Prednisolone ; Rabbits ; Tetracaine

No abstract available.
Asthma*

No abstract available.
Audiometry*

No abstract available.

Major classes of medication in asthma management include bronchodilating beta2-agonists, anti-inflammatory inhaled corticosteroids, leukotriene modifiers and theophyllines. However, all asthmatics do not respond to the same extent to a given medication. Available data suggest that a substantial range of individual variability, as much as 70%, may be due to genetic characteristics of each patient. Pharmacogenomics offers the potential to optimize medications for individual asthmatics by using genetic information to improve efficacy or avoid adverse effects. The best-studied case of the potential contribution of pharmacogenomics to treatment response in asthma comes from studies on human beta2 adrenergic receptors. In addition, genetic variation in beta2-adrenergic receptor (Arg16Gly) may predict response to anticholinergics for the treatment of asthma. In case of inhaled corticosteroids, a recent investigation using a traditional SNP-based approach identified a gene for corticotropin releasing hormone receptor 1 as a potential marker of response. Another major pathway that has been investigated is the pathway underlying response to cysteinyl leukotriene receptor antagonist. It is likely that in the near future, pharmacogenomic approaches based on individual genetic information will be introduced into an asthma treatment guideline and this guideline will allow us to identify those who have the best chance to respond to a specific medication.
Adrenal Cortex Hormones ; Asthma ; Cholinergic Antagonists ; Genes, vif ; Genetic Variation ; Humans ; Pharmacogenetics ; Receptors, Adrenergic ; Receptors, Corticotropin-Releasing Hormone ; Receptors, Leukotriene