Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 1998, Taiwan became the first country in Asia to provide free influenza vaccination to high-risk groups, mainly the elderly. The purpose of this study is to determine: (1) the annual mortality rate from influenza and pneumococcal-related illnesses such as pneumonia, chronic bronchitis, pulmonary emphysema and asthma and (2) the effectiveness of and adverse events associated with the influenza vaccination. In the elderly, influenza vaccination caused the annual death rate due chronic bronchitis, pulmonary emphysema, and asthma to decline steadily but had no effect on the annual pneumonia death rate. The only adverse effect of concern was vertigo (in approximately 2-3%).
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PMID:Influenza and pneumococcal vaccination of the elderly in Taiwan. 1524 15

Surfactant protein D (SP-D) is a member of the collectin family of innate defense proteins. Members of this family share four distinct structural domains: an N-terminal cross-linking domain, a collagenous domain, a neck region, and a carbohydrate recognition domain. In this study, the function of the collagenous domain was evaluated by expressing a SP-D collagen deletion mutant protein (rSftpdCDM) in wild type and SP-D null mice (Sftpd(-/-)). rSftpdCDM formed disulfide-linked trimers that further oligomerized into higher order structures. The mutant protein effectively bound carbohydrate and aggregated bacteria in vitro. Whereas rSftpdCDM did not disrupt pulmonary morphology or surfactant phospholipid levels in wild type mice, the mutant protein failed to rescue the emphysema or enlarged foamy macrophages that are characteristic of Sftpd(-/-) mice. Moreover, rSftpdCDM partitioned with small aggregate surfactant in a manner similar to SP-D, but rSftpdCDM did not correct the abnormal surfactant ultrastructure or phospholipid levels observed in Sftpd(-/-) mice. In contrast, rSftpdCDM completely corrected viral clearance and the abnormal inflammatory response that occurs following pulmonary influenza A challenge in Sftpd(-/-) mice. Our findings indicate that the collagen domain of SP-D is not required for assembly of disulfide-stabilized oligomers or the innate immune response to viral pathogens. The collagen domain of SP-D is required for the regulation of pulmonary macrophage activation, airspace remodeling, and surfactant lipid homeostasis.
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PMID:Correction of pulmonary abnormalities in Sftpd-/- mice requires the collagenous domain of surfactant protein D. 1678 26

Pneumomediastinum is a rare condition with an incidence of 1/33,000. It can be a rare complication of diabetic acidoketosis. We present the cases of two diabetic patients and review the literature, focusing our analysis on the interrelationships between these two diseases. Both patients were young subjects, a 21-year-old woman and an 18-year-old man with type 1 diabetes who were admitted for acidoketosis. Clinically, the patients presented the cardinal signs of diabetes and a flu-like syndrome associated with dyspnea and chest pain. Physical examination revealed a poor general health status, tachycardia and polymnea, as well as a painful diffuse tumefaction of the neck with subcutaneous emphysema. Blood tests disclosed elevated glycemia and urine was positive for acetone. The diagnosis of severe metabolic acidosis was retained. The chest x-ray demonstrated the subcutaneous emphysema and air in the anterior mediastinum. On the computed tomography scan obtained in the second patient, the heart was silhouetted with a hyperlucent zone laterally. Treatment consisted in strict bed rest with oxygen therapy, fluid replacement, insulin and heparin. The pneumomediastinum resolved in both patients within three days on average. The causal effect of diabetic acidoketosis in the development of pneumomediastinum in our two patients was retained after ruling out all other potential causes, including chest trauma and asthma.
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PMID:[Rare complication of diabetic acidoketosis: the pneumomediastinum]. 1816 37

Alpha-1-antitrypsin deficiency (AATD) is a genetic disorder that manifests as pulmonary emphysema, liver cirrhosis and, rarely, as the skin disease panniculitis, and is characterized by low serum levels of AAT, the main protease inhibitor (PI) in human serum. The prevalence in Western Europe and in the USA is estimated at approximately 1 in 2,500 and 1 : 5,000 newborns, and is highly dependent on the Scandinavian descent within the population. The most common deficiency alleles in North Europe are PI Z and PI S, and the majority of individuals with severe AATD are PI type ZZ. The clinical manifestations may widely vary between patients, ranging from asymptomatic in some to fatal liver or lung disease in others. Type ZZ and SZ AATD are risk factors for the development of respiratory symptoms (dyspnoea, coughing), early onset emphysema, and airflow obstruction early in adult life. Environmental factors such as cigarette smoking, and dust exposure are additional risk factors and have been linked to an accelerated progression of this condition. Type ZZ AATD may also lead to the development of acute or chronic liver disease in childhood or adulthood: prolonged jaundice after birth with conjugated hyperbilirubinemia and abnormal liver enzymes are characteristic clinical signs. Cirrhotic liver failure may occur around age 50. In very rare cases, necrotizing panniculitis and secondary vasculitis may occur. AATD is caused by mutations in the SERPINA1 gene encoding AAT, and is inherited as an autosomal recessive trait. The diagnosis can be established by detection of low serum levels of AAT and isoelectric focusing. Differential diagnoses should exclude bleeding disorders or jaundice, viral infection, hemochromatosis, Wilson's disease and autoimmune hepatitis. For treatment of lung disease, intravenous alpha-1-antitrypsin augmentation therapy, annual flu vaccination and a pneumococcal vaccine every 5 years are recommended. Relief of breathlessness may be obtained with long-acting bronchodilators and inhaled corticosteroids. The end-stage liver and lung disease can be treated by organ transplantation. In AATD patients with cirrhosis, prognosis is generally grave.
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PMID:Hereditary alpha-1-antitrypsin deficiency and its clinical consequences. 1856 11

A 38-year-old caucasian male, after continuous nose blowing caused by common flu, developed left diplopia, especially in downward gaze, and complained of orbital dull pain during the preceding 48 hours. Clinical signs included left lower eyelid crepitant edema, mild exophthalmos and restriction of the eye movement. The patient had been operated on for orbital fractures 12 days previously. Open reduction had been performed, stabilization had been achieved with osteosynthesis miniplates, and the orbital floor defect was reconstructed with a piece of Liodura. Orbital computerized tomographic scan demonstrated a large air collection, diagnostic of emphysema, without displacement of the fractures. Under local anesthesia, aspiration-decompression was performed using a 25-gauge needle. On the next day, the patient was free of pain, and 2 days after surgery the diplopia and exophthalmos resolved with no sequelae.
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PMID:Delayed appearance of diplopia due to orbital emphysema after repair of orbital fractures. 1858 18

Viral infections have more severe consequences in patients who have been exposed to cigarette smoke (CS) than in those not exposed to CS. For example, in chronic obstructive pulmonary disease (COPD), viruses cause more severe disease exacerbation, heightened inflammation, and accelerated loss of lung function compared with other causes of disease exacerbation. Symptomatology and mortality in influenza-infected smokers is also enhanced. To test the hypothesis that these outcomes are caused by CS-induced alterations in innate immunity, we defined the effects of CS on pathogen-associated molecular pattern-induced (PAMP-induced) pulmonary inflammation and remodeling in mice. CS was found to enhance parenchymal and airway inflammation and apoptosis induced by the viral PAMP poly(I:C). CS and poly(I:C) also induced accelerated emphysema and airway fibrosis. The effects of a combination of CS and poly(I:C) were associated with early induction of type I IFN and IL-18, later induction of IL-12/IL-23 p40 and IFN-gamma, and the activation of double-stranded RNA-dependent protein kinase (PKR) and eukaryotic initiation factor-2alpha (eIF2alpha). Further analysis using mice lacking specific proteins indicated a role for TLR3-dependent and -independent pathways as well as a pathway or pathways that are dependent on mitochondrial antiviral signaling protein (MAVS), IL-18Ralpha, IFN-gamma, and PKR. Importantly, CS enhanced the effects of influenza but not other agonists of innate immunity in a similar fashion. These studies demonstrate that CS selectively augments the airway and alveolar inflammatory and remodeling responses induced in the murine lung by viral PAMPs and viruses.
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PMID:Cigarette smoke selectively enhances viral PAMP- and virus-induced pulmonary innate immune and remodeling responses in mice. 1865 73

We report the use of the Novalung interventional Lung Assist extracorporeal carbon dioxide removal device, (Novalung GmbH, Lotzenacker 3, D-72379 Hechingen, Germany) to treat a 46-year-old female with life-threatening bronchospasm secondary to influenza infection. Despite maximal treatment she developed severe hypercapnia and acidosis. The necessity for high inflation pressures led to the development of gross surgical emphysema. Use of the interventional Lung Assist enabled a rapid correction of hypercapnoea and acidosis, allowing a reduction in airway pressures, reducing further barotrauma. Subsequent resolution of the inflammatory process allowed removal of the interventional Lung Assist after 11 days. She was successfully weaned from mechanical ventilation and made a full recovery.
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PMID:The use of extracorporeal carbon dioxide removal in the management of life-threatening bronchospasm due to influenza infection. 1871 29

1. Virulent influenza bacilli, when injected into the nose and throat of monkeys (Cebus capucinus and Macacus syrichtus), excite an acute inflammation of the upper respiratory tract, characterized by swelling and hyperemia of the mucous membrane, infiltration of the mucosa and subrnucosa with leucocytes, desquamation of epithelial cells, and the production of a mucopurulent exudate. The accessory sinuses are often implicated in the infection. 2. Experimental Bacillus influenzae infections of the upper respiratory tract are frequently accompanied or followed by bronchiolitis, peribronchial infiltration, and bronchopneumonia with hemorrhage and edema in the early stage, emphysema and bronchiectasis in the later stages. In general, the process closely resembles uncomplicated Bacillus influenzae pneumonia in man. 3. The injection of virulent influenza bacilli directly into the trachea of monkeys induces in them an experimental bronchiolitis and hemorrhagic bronchopneumonia, similar in all respects to spontaneous Bacillus influenzae pneumonia. 4. In experimental Bacillus influenzaeinfections of either the upper or lower respiratory tract the influenza bacillus can usually be recovered during .the acute stage by culture, either pure or in association with other bacteria. 5. In experimental Bacillus influenzae infections in monkeys characteristic changes occur in the thymus gland-hyperplasia of the follicles, distention of the lymphatic channels, and infiltration of the parenchyma with leucocytes. This enlargement appears to be merely part of a general hyperplasia of the lymphoid structures in the cervical and thoracic regions.
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PMID:STUDIES ON EXPERIMENTAL PNEUMONIA : X. PATHOLOGY OF EXPERIMENTAL INFLUENZA AND OF BACILLUS INFLUENZAE PNEUMONIA IN MONKEYS. 1986 71

A 49-year-old female presented with diarrhea and a high fever followed by progressive dyspnea. Until this presentation, she had been healthy except for chronic dyspepsia and diarrhea. She had a smoking habit of 15 pack-years. Laboratory tests revealed lymphopenia, hypoalbuminemia and hypogammaglobulinemia. A rapid influenza test in combination with an RT-PCR assay revealed the presence of the novel influenza A (H1N1) virus. Chest computed tomography revealed centrilobular emphysema. This report suggests that regular smoking may become a risk for severe pneumonia in patients presenting with the novel influenza A (H1N1) virus, when accompanying asymptomatic emphysema is combined with other problems such as hypoalbuminemia and hypogammaglobulinemia.
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PMID:Severe pneumonia caused by a novel influenza A (H1N1) virus in an asymptomatic emphysematous smoker. 2068 12

The term COPD which comprises chronic obstructive bronchitis and emphysema, was first defined in 1964. Key milestones to the understanding of the etiopathology of COPD were the discovery of the association between tobacco consumption and the development of chronic bronchitis as well as the discovery of the role of a protease-antiprotease imbalance leading to emphysema. The assessment of functional impairement of patients with COPD was established in the 1960s and the quantification and localisation was predominantly explored in the 1980s. The management of COPD comprises preventative measures (e.g. smoking cessation, vaccination against influenza, reduction of occupation hazards), medical therapies (bronchodilators, corticosteroids), non-pharmacological therapies (exercise training, patient education, physiotherapy) as well as surgical options. The prevention and efficiency management of exacerbations are of particular importance. Optimal management of COPD has to take impact of the disease on other organs into account. The future of COPD-related research lies in the development of international and national networks to facilitate the analysis of genetic factors on the pathology of COPD.
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PMID:[COPD - a historical review, current management and research perspectives]. 2082 37


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