Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032290 (aspiration pneumonia)
 2,291 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A prematurely born 5-year-old boy with chronic lung disease, hypoxic-ischemic encephalopathy, cerebral palsy, repeated aspiration pneumonia, and stroke underwent percutaneous endoscopic jejunostomy (PEJ) to alleviate repeated aspiration pneumonia. Studies, including 24-hour esophageal pH monitoring, 99mTc gastric emptying time, upper gastroesophageal barium radiography, and endoscopic examinations showed severe gastroesophageal reflux and prolonged gastric emptying. Percutaneous endoscopic gastrostomy (PEG) was performed first, followed by placement of a polyurethane J-tube (9 French) through the preexisting gastrostomy site. We passed the style-guided J-tube through the pyloric ring endoscopically and advanced it to the jejunum. The position of the J-tube was confirmed by radiologic study. Feeding with an elemental formula, 20 mL/hour, commenced immediately after the procedure, and the rate was gradually increased to 50 mL/hour. No further episodes of aspiration pneumonia have occurred since J-tube placement. Our initial experience with jejunal feeding through a PEJ is encouraging.
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PMID:Pediatric percutaneous endoscopic jejunostomy by J-tube extension through a preexisting gastrostomy site: a preliminary report. 988 93

We report three personal cases of hydrocarbide aspiration pneumonia. High-viscosity non-volatile hydrocarbides (paraffin oil, for instance) cause often pseudotumoral exogenous fat-aspiration lung disease. Low-viscosity volatile hydrocarbides (petroleum, gasoline, white spirit, for instance) cause acute pseudo-infectious lung disease with dyspnea and fever which usually resolves within a few weeks but which may also be life-threatening. Purely symptomatic treatment has greatly progressed with advances in intensive ventilatory assistance. Gastric emptying with emetic agents or lavage procedures is dangerous and must be avoided except for exceptional cases. When required, the airways must be protected with tracheal intubation. Volatile hydrocarbides should be stored in protected areas in containers with safety stoppers which children cannot open.
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PMID:[Pneumopathies caused by inhalation of hydrocarbons: apropos of 3 cases]. 1110 22

Pulmonary manifestations contribute significantly to the morbidity and mortality of the idiopathic inflammatory myopathies, ranging from intrinsic lung disease to secondary complications that include aspiration pneumonia, opportunistic infection, congestive heart failure, and hypoventilation. Newer classification schemes for interstitial lung disease have permitted closer correlation between histologic subtype and clinical outcome, while diagnostic techniques such as bronchoalveolar lavage have begun to define the cellular elements responsible for immune-mediated pulmonary dysfunction. Investigators have identified several serum markers correlating with inflammatory disease activity in the lung that should enhance noninvasive monitoring of therapeutic responses to newer regimens involving agents such as cyclosporine and tacrolimus. Taken together, these advances have contributed to better understanding of the immunopathogenesis of myositis-associated interstitial lung disease that should ultimately translate into more effective treatment.
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PMID:Pulmonary complications of inflammatory myopathy. 1221 46

We report a case of neurogenic pulmonary edema associated with epileptic seizure. A 36-year-old woman had had several episodes of fainting and postictal respiratory failure, and since July 1998 had been admitted to a nearby hospital three times. On October 12, 1999, she was again admitted to a nearby hospital with the same symptom, and was transferred from that hospital to ours for evaluation of the recurrent respiratory disorder. Low-grade fever, mild leukocytosis, hypoxemia and bilateral diffuse opacities were observed as previously on chest radiography, and improved within several days without any specific therapy. The negative C reactive protein level, normal cardiac function and faintly bloody bronchoalveolar lavage fluid were also observed. There was no evidence of aspiration pneumonia, infectious disease, or underlying heart or lung disease. Electroencephalography showed spikes in accord with the left temporal lobe, and the cause of the patient's fainting was thought to be temporal lobe epilepsy. After all other causes had been excluded, this case was diagnosed as neurogenic pulmonary edema associated with epileptic seizure. Only about 40 cases of the postictal pulmonary edema have been reported since 1908, and the pathophysiologic mechanism of this condition is still unknown. Neurogenic pulmonary edema associated with epileptic seizure is rare, but the importance of awareness of this condition needs to be emphasized because it is suspected to be the cause of unexpected sudden death in epileptics. We should consider the disease as important in the differential diagnosis of acute respiratory failure associated with epilepsy.
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PMID:[A case of neurogenic pulmonary edema associated with epileptic seizure]. 1264 14

The inflammatory diseases of muscle are a group of disorders characterized by proximal muscle weakness. Most cases fall into three major diagnostic categories, polymyositis (PM), dermatomyositis and inclusion body myositis. Respiratory complications are a common feature and are an important cause of morbidity and mortality. The three main types of pulmonary involvement are interstitial lung disease, aspiration pneumonia and ventilatory incapacity (VI) due to muscle weakness. There are few reported cases in which mechanical ventilation has been used in patients with PM and VI in absence of lung disease. We present a patient with PM and VI due to muscle weakness who underwent therapy maintenance with mechanical ventilator and was weaned 4 months later.
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PMID:[Polymyositis with ventilatory incapacity and respiratory insufficiency]. 1462 52

Chronic graft-vs.-host disease (cGVHD) occurs in 20-50% of patients who survive for at least 100 d after allogeneic stem cell transplantation (SCT). cGVHD includes scleroderma-like skin changes, chronic cholangitis, obstructive lung disease and general wasting syndrome. Polymyositis or myopathy are rare manifestations of cGVHD with approximately 40 reported cases. Polymyositis accompanied by hemosiderin deposits in cGVHD has been reported only once, and there are no reports on lipofuscin deposits in skeletal muscle cells in cGVHD. We report here on a 56-yr-old male who underwent allogeneic SCT in 1999 for osteomyelofibrosis and progressive hematopoietic insufficiency. In February 2004, the patient was hospitalized for progressive muscular weakness with loss of the ability to walk. Laboratory tests demonstrated normal values for serum creatine kinase, aldolase and lactic dehydrogenase; the ferritin level was highly elevated. The femoral muscle biopsy showed mostly perifascicular atrophy as well as numerous subsarcolemmal hemosiderin and lipofuscin deposits. Intravenous administration of the chelating agent deferoxamine was ineffective. Three weeks later the patient died of aspiration pneumonia. Interestingly, autopsy disclosed moderate hemosiderin deposits in the liver, the organ usually involved in hemosiderosis.
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PMID:Hemosiderin deposits in chronic graft-vs.-host disease related myopathy. 1631 67

The authors report the first case of levetiracetam-induced diffuse interstitial lung disease. The patient is a 9-year-old girl who was admitted to the pediatric intensive care unit for aspiration pneumonia. She has a history of epilepsy, cerebral palsy, mental retardation, asthma, and repeated hospitalizations for presumed aspiration pneumonia, which resolved with conventional medical treatment. She has been on low-dose levetiracetam for her epilepsy over the past 2 years, and the dosage was increased just prior to this admission. However, this time, with conventional treatment, the patient's aspiration pneumonia did not improve, which led to a lung biopsy. The biopsy demonstrated a diffuse interstitial process of relatively recent onset, with features consistent with diffuse lung disease. Levetiracetam was implicated in the pathogenesis of the interstitial pneumonitis. The patient improved clinically after the discontinuation of levetiracetam and with the treatment of steroids.
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PMID:Levetiracetam-induced diffuse interstitial lung disease. 1769 72

Idiopathic pulmonary fibrosis (IPF) is a relentlessly progressive lung disease that commonly results in respiratory failure and death. However, the cause of death in these patients has not previously been fully defined. The current study reviews the clinical records and pathological findings of 42 consecutive patients with IPF who underwent a post mortem at the Mayo Clinic (Rochester, MN, USA) over a 9-yr period, from January 1996 to December 2004. The median (range) age at post mortem for the patients was 74 (46-98 yrs) yrs, which included 25 (60%) males. A total of 31 (74%) patients died in the hospital. The immediate causes of death were reported as: respiratory (64%), cardiovascular (21%), or noncardiopulmonary (14%). Acute exacerbation of IPF was the most common immediate cause of death (29%). Pneumonia, aspiration and drug-induced lung disease were identified as other causes of respiratory death. Evidence of pulmonary hypertension was present in the post mortem of 19 (45%) patients and was the immediate cause of death in two of these patients. The immediate cause of death was clinically unsuspected in five (12%) patients and IPF was diagnosed post mortem in nine (21%) patients. The majority of patients with idiopathic pulmonary fibrosis who had undergone a post mortem were found to have died from respiratory causes. Acute exacerbation of idiopathic pulmonary fibrosis was found to be the most common cause of death whilst death from the gradual progression of idiopathic pulmonary fibrosis was found to be less common.
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PMID:Autopsy findings in 42 consecutive patients with idiopathic pulmonary fibrosis. 1825 70

Obesity is the most common metabolic disease in the world and its prevalence has been increasing over several decades. The World Health Organization (WHO) predicts that, by 2015, around 700 million adults will be obese (at least 10% of the projected global population). This will be a huge health and economic burden with associated increases in diabetes, cardiovascular and musculoskeletal disease, and malignancy. While there has been little focus on the impact of obesity on respiratory disease, there are clear effects on pulmonary function and inflammation which will increase the prevalence and morbidity of lung disease. There is an inverse relationship between body mass index and forced expiratory volume in 1 s. Increases in body weight lead to worsening of pulmonary function. The reasons for this include the mechanical effects of truncal obesity and the metabolic effects of adipose tissue. Obesity is linked to a wide range of respiratory conditions including chronic obstructive pulmonary disease, asthma, obstructive sleep apnoea, pulmonary embolic disease and aspiration pneumonia. It is important for those providing care for people with respiratory disease to appreciate the impact of obesity and to provide appropriate advice for weight reduction. Healthcare planners should consider the impact of obesity for future resources in respiratory care.
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PMID:Obesity and the lung: 1. Epidemiology. 1858 31

The first report of acute respiratory distress syndrome (ARDS) was published in 1967, and even now acute lung injury (ALI) and ARDS are severe forms of diffuse lung disease that impose a substantial health burden all over the world. Recent estimates indicate approximately 190,000 cases per year of ALI in the United States each year, with an associated 74,500 deaths per year. Common causes of ALI/ARDS are sepsis, pneumonia, trauma, aspiration pneumonia, pancreatitis, and so on. Several pathologic stages of ALI/ARDS have been described: acute inflammation with neutrophil infiltration, fibroproliferative phase with hyaline membranes, with varying degrees of interstitial fibrosis, and resolution phase. There has been intense investigation into the pathophysiologic events relevant to each stage of ALI/ARDS, and much has been learned in the alveolar epithelial, endobronchial homeostasis, and alveolar cell immune responses, especially neutrophils and alveolar macrophages in an animal model. However, these effective results in the animal models are not equally adoptive to those in randomized, controlled trials. The clinical course of ALI/ARDS is variable with the likely pathophysiologic complexity of human ALI/ARDS. In 1994, the definition was recommended by the American-European Consensus Conference Committee, which facilitated easy nomination of patients with ALI/ARDS for a randomized, clinical trial. Here, we review the recent randomized, clinical trials of ALI/ARDS.
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PMID:Acute lung injury review. 1942 Aug 6


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