Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The predominant pathogen in patients with cystic fibrosis (CF) is Pseudomonas aeruginosa, which results in a chronic lung infection associated with progressive pulmonary insufficiency. In a rat model of chronic P. aeruginosa pneumonia mimicking that in patients with CF, we studied whether the inflammation and antibody responses could be changed by treatment with the Chinese herbal medicine ginseng. An aqueous extract of ginseng was injected subcutaneously, and cortisone and saline were used as controls. Two weeks after challenge with P. aeruginosa, the ginseng-treated group showed a significantly improved bacterial clearance from the lungs (P < 0.04), less severe lung pathology (P = 0.05), lower lung abscess incidence (P < 0.01), and fewer mast cell numbers in the lung foci (P < 0.005). Furthermore, lower total immunoglobulin G (IgG) levels (P < 0.01) and higher IgG2a levels (P < 0.025) in serum against P. aeruginosa sonicate and a shift from an acute type to a chronic type of lung inflammation compared to those in the control and cortisone-treated groups were observed. These findings indicate that ginseng treatment of an experimental P. aeruginosa pneumonia in rats promotes a cellular response resembling a TH1-like response. On the basis of these results it is suggested that ginseng may have the potential to be a promising natural medicine, in conjunction with other forms of treatment, for CF patients with chronic P. aeruginosa lung infection.
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PMID:Ginseng treatment reduces bacterial load and lung pathology in chronic Pseudomonas aeruginosa pneumonia in rats. 914 52

A 45-year-old Japanese woman presented with a high fever, a nonproductive coughing, and severe dyspnea, and was admitted to another hospital. During the week prior to hospitalization, she had been given Shosaikoto for treatment of liver dysfunction of unknown etiology. Mycoplasma pneumonitis was initially suspected, so she was treated with antibiotics (clindamycin and minocycline) and received oxygen therapy. Pulmonary insufficiency worsened rapidly, and she was transferred to our hospital. On admission, a chest roentgenogram revealed bilateral alveolar infiltrates predominantly in the medial lung fields. Furosemide and high-dose methylprednisolone were immediately administered, but hypoxemia increased. When the PaO2 was 55.7 Torr while the patient breathed 100% oxygen, mechanical ventilation with positive end-expiratory pressure (PEEP) was started. Arterial blood-gas values improved dramatically, and the chest roentgenogram became clear. Our diagnosis of noncardiogenic pulmonary edema is based on the chest-roentgenographic findings, infiltration of inflammatory cells as seen in two lung-biopsy specimens and bronchoalveolar lavage fluid, the lack of findings of heart failure on physical examination and electrocardiography, and the good clinical response to PEEP. A positive lymphocyte stimulation test in response to Shosaikoto implicated this non-traditional herbal medicine as an etiologic factor in the non-cardiogenic pulmonary edema. Shosaikoto has been identified as the cause of interstitial pneumonia or eosinophilic pneumonia, but pulmonary edema associated with Shosaikoto has not been previously described. This case suggests that methylprednisolone treatment may be insufficient for Shosaikoto-induced pulmonary edema, and that mechanical ventilation with PEEP is very effective.
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PMID:[Pulmonary edema associated with the Chinese medicine shosaikoto]. 986 80

A 14-year-old boy with X-linked chronic granulomatous disease developed severe invasive pulmonary aspergillosis. He was treated with itraconazole and amphotericin B. However, he deteriorated with progressive pulmonary lesions. Burkholderia cepacia was isolated from his bronchoalveolar lavage. Finally, he was given granulocyte transfusions. Following this procedure, his condition rapidly worsened leading to respiratory failure. His lung biopsy demonstrated organizing pneumonia at his right middle lobe. Then, a methylprednisolone pulse therapy was initiated together with the administration of appropriate antibiotics and adequate amounts of amphotericin B. Dramatically, his condition improved. Therefore, a methylprednisolone pulse therapy with appropriate antimicrobial drugs seems to be beneficial for severe pulmonary insufficiency in this type of patients.
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PMID:Successful treatment with methylprednisolone pulse therapy for a life-threatening pulmonary insufficiency in a patient with chronic granulomatous disease following pulmonary invasive aspergillosis and Burkholderia cepacia infection. 1057 44

We measured KL-6 concentrations in serum samples from measles patients with various forms of pneumonia and abnormally elevated levels of KL-6 were found exclusively in four fatal cases of pulmonary insufficiency.
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PMID:Elevated KL-6 levels in fatal measles pneumonia. 1147 89

With refinements in radiotherapeutic techniques in recent years, the incidence of pulmonary damage attributable to irradiation has decreased. A significant number of patients, however, still show radiographic evidence of irradiation pneumonitis, with or without associated symptoms. Although these appearances are usually transitory, in some patients they may persist and be associated with varying degrees of pulmonary insufficiency.This report presents an evaluation of the radiographic changes, symptoms, and pulmonary function following irradiation of the chest wall (as for cancer of the breast) in one group of patients, and following deep irradiation of the chest (as for cancer of the lung) in a second group. Forty patients were studied, of whom 32 are available for assessment (20 with carcinoma of the breast and 12 with bronchogenic carcinoma). These patients were studied preoperatively, and from three to 15 months following irradiation. The findings with respect to radiographic appearance, pulmonary function, and symptoms of these patients are presented.
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PMID:EFFECTS OF IRRADIATION ON LUNG FUNCTION. 1415 27

Acute respiratory distress syndrome (ARDS) - is a life-threatening acute clinical syndrome of pulmonary insufficiency with high mortality. The causes of the syndrome are of every description - from crustacean poisoning to cardiopulmonary bypass. The rate of ARDS is not clear, because of diagnostical variety of ARDS and acute pulmonary dysfunction. The discussion on ARDS diagnostical criteria lasted for many years. The clinical criteria depend on how the essence of the disease is understood, on the size of lung infiltration, lung compliance and failure as well as degree of hypoxemia. The risk of ARDS increases with the increase of number of predisposing factors. The investigation data depend mainly on used datum-point for diagnostics of ARDS. It is obvious that non-cardiogenic light pulmonary edema is found very often, and serious lung lesions are rare enough. The aim of nowadays treatment is to cure the disease that causes the syndrome and to sustain vital functions. The early diagnostics of ARDS predisposing factors and minimization of their influence, the prevention, early diagnostics and timely treatment of complications are essential. In many cases ARDS caused by collateral factors is the constituent of multiple organ dysfunction syndrome. Anyway the ARDS predisposed by direct factors is often complicated by other organ (cardiovascular, renal, hepatic, hematogenous, central nervous system, gastrointestinal tract, etc.) dysfunction. In this case the treatment becomes more difficult and includes therapy correcting the function of other systems. In spite of intensive treatment, mortality of this syndrome still remains 50-90% according to the literature data. Though some authors state that recently the ARDS mortality decreased, but most of the authors did not notice any improvement during the last 20 years. The prognosis is determinated not only by pulmonary insufficiency itself (the cause of death in 5% of patients), but by the ARDS predisposing factor (the worst is sepsis and septic shock), multiple organ dysfunction syndrome, difficult physical state of the patient, sepsis as a cause or as a complication of ARDS, nosocomial pneumonia, progressive fibroproliferation in the lung. Considering the actuality of ARDS, the diagnostical criteria of ARDS, pathogenesis, clinical course and new treatment methods are reviewed in the publication.
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PMID:[Acute respiratory distress syndrome]. 1464 57

X-linked agammaglobulinemia (XLA) is a primary immunodeficiency caused by mutations in the gene for Bruton tyrosine kinase (BTK) that result in the deficient development of B lymphocytes and hypogammaglobulinemia. Because the disorder is uncommon, no single institution has had sufficient numbers of patients to develop a comprehensive clinical picture of the disorder. Accordingly, a national registry of United States residents with XLA was established in 1999 to provide an updated clinical view of the disorder in a large cohort of patients. A total of 201 patients were registered by 66 physicians. The estimated birth rate for the 10-year period of 1988-1997 was 1/379,000. Infection was the most common initial clinical presentation (85%), followed by a positive family history (41%) and neutropenia (11%). Although the average age of diagnosis was younger in patients with a positive family history (mean, 2.59 yr) than in patients with a negative family history (mean, 5.37 yr) (p < 0.001), only 34.5% of patients with a positive family history at the time of their birth were diagnosed before clinical symptoms developed-that is, based on family history alone. Seventy percent of patients had at least 1 episode of otitis, 62% at least 1 episode of pneumonia, 60% at least 1 episode of sinusitis, 23% at least 1 episode of chronic/recurrent diarrhea, 21% at least 1 episode of conjunctivitis, 18% at least 1 episode of pyoderma and/or cellulitis, 11% at least 1 episode of meningitis/encephalitis, 10% at least 1 episode of sepsis, 8% at least 1 episode of septic arthritis, 6% at least 1 episode of hepatitis, and 3% at least 1 episode of osteomyelitis. Fourteen of 201 (6.9%) patients were dead at the time they were entered in the Registry. However, in a prospective 4 /4-year follow-up of living patients, only 3/80 (3.75%) patients died. Causes of death included disseminated enterovirus infection (n = 6), pulmonary insufficiency (n = 5), adenovirus infection (n = 1), sepsis (n = 1), acquired immunodeficiency disease syndrome (AIDS) (n = 1), myocarditis (n = 1), hepatitis (n = 2), and stem cell transplantation (n = 1).
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PMID:X-linked agammaglobulinemia: report on a United States registry of 201 patients. 1686 44

Eight animals died from 1 to 6 years after the operation, from undetermined diseases, or from pneumonia. Two animals are still alive 7 years after the operation. 1. Condition of the Pleural and Pericardial Cavities.-In the first experiments, extensive pleural and pericardial adhesions were observed 1 year and more after the patching of the pulmonary artery. There was also a great deal of fibrous tissue between the pulmonary artery, the aorta, and the left auricle. In the other experiments, the adhesions of the lungs, pleura, and pericardium were less marked. This was due to some improvements in the technique of handling the viscera. At the time of the operations, it was hoped that no pleural or pericardial adhesions would occur. Great care was taken not to injure the endothelial surfaces by rough handling or by sponging. No blood was allowed to flow into the pleural cavity. The surface of the pericardium was protected by fine silk membranes. The pleural cavity was occluded by thick pads made of cotton and Japanese silk. It seemed that the serous surfaces were almost completely protected against infection and mechanical irritation. The occurrence of primary pleurisy and pericarditis was prevented by this technique. But the development of adhesions in several of the experiments shows that the procedures for the handling of the viscera should be perfected. 2. Condition of the Arterial Wall.-In the experiments in which the orifice was patched, a slight dilatation of the artery was observed. It was not possible to ascertain from the specimen preserved in formaldehyde whether or not there was an insufficiency of the valves. It is probable that there was no leakage, as in none of these cases could any diastolic murmur be heard 6 months after the operation. The only animal which presented clinical evidence of pulmonary insufficiency died during the War. The normal condition of the pulmonary orifice was due to the incision which did not extend far enough on the ventricle, and to the power of redintegration possessed by an organ which is not diseased. The cicatrization of the grafted flap was excellent. Its outline could not be seen on the external side of the wall. Even after opening the artery, the transplant could not be located easily. However, in Experiment 1 the anterior wall of the artery showed a depression about 7 or 8 mm. wide, 18 mm. long, and 2 or 3 mm. deep, behind and above the anterior valve. But the flap was made of human artery, and it is known that a heteroplastic graft always undergoes some dilatation. When transplants of dog tissue were used, no dilatation occurred and the location of the patch could hardly be detected. In Experiment 7, 6 years after the operation, the endothelial surface was smooth, glistening, and no scar could be seen. However, the upper and lower parts of the incision were marked by a slight depression of the wall. The presence of the patch was detected by a distinct thickening of the wall. Although the edges of the incision had not been sutured to the edges of the flap, the endothelial surface was quite smooth. A transverse section of the artery was made through the middle part of the flap in Experiment 4. It showed the width of the arterial opening and the way in which the transplant became adherent to the arterial wall. The examination of these four specimens demonstrated that, in spite of the unfavorable location of the graft, an excellent union had taken place. It showed that homoplastic or heteroplastic tissue can be transplanted onto the pulmonary artery as well as onto the smaller arteries. Where the arterial wall had simply been incised without interposition of a patch, a linear scar was always found. 6 years after the operation, the incision used in the course of an operation for cauterization of the sigmoid and sutured with heavy thread was transformed into a linear scar and the surface of the intima was quite smooth. 3. Condition of the Sigmoid Valves.-In three experiments, the sigmoid valves had been cauterized along their margin and their point of insertion in the artery. One of the animals was still living 7 years after the operation. There was no diastolic murmur. The other animals died 3 and 6 years after the operation. The valves were thin and transparent, and quite normal. However, one of the valves showed two holes, one near the base and the other near the margin. The animal on which the section of the right posterior valve without suture was performed, died 2 or 3 years after the operation. The edges of the incision had not united. They were thickened and the whole valve was rigid. The surface was rough and irregular. No permanent result was obtained by the union of two sigmoid valves by a stitch. There was no stenosis of the orifice, and no union of the valves 4 years after the operation. The stitch had disappeared. There was some scar tissue at the common point of insertion of the posterior valves, which were more rigid and showed thickened edges. 7 years after the section and suture of a sigmoid had been performed, the animal was still living and in good health. No diastolic murmur could be detected.
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PMID:REMOTE RESULTS OF OPERATIONS ON THE PULMONARY ORIFICE OF THE HEART. 1986 69

This review summarizes current understanding of mitochondrial bioenergetic dysfunction applicable to mechanisms of lung diseases and outlines challenges and future directions in this rapidly emerging field. Although the role of mitochondria extends beyond the term of cellular "powerhouse", energy generation remains the most fundamental function of these organelles. It is not counterintuitive to propose that intact energy supply is important for favorable cellular fate following pulmonary insult. In this review, the discussion of mitochondrial dysfunction focuses on those molecular mechanisms that alter cellular bioenergetics in the lungs: (a) inhibition of mitochondrial respiratory chain, (b) mitochondrial leak and uncoupling, (c) alteration of mitochondrial Ca2+ handling, (d) mitochondrial production of reactive oxygen species and self-oxidation. The discussed lung diseases were selected according to their pathological nature and relevance to pediatrics: Acute lung injury (ALI), defined as acute parenchymal lung disease associated with cellular demise and inflammation (Acute Respiratory Distress Syndrome, ARDS, Pneumonia), alveolar developmental failure (Bronchopulmonary Dysplasia, BPD or chronic lung disease in premature infants), obstructive airway diseases (Bronchial asthma) and vascular remodeling affecting pulmonary circulation (Pulmonary Hypertension, PH). The analysis highlights primary mechanisms of mitochondrial bioenergetic dysfunction contributing to the disease-specific pulmonary insufficiency and proposes potential therapeutic targets.
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PMID:Mitochondrial bioenergetics and pulmonary dysfunction: Current progress and future directions. 3106 Sep 47

The etiological agent of COVID-19, which causes severe respiratory diseases such as pneumonia and pulmonary insufficiency, has been confirmed as a new coronavirus, now known as Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). There is currently no authorized medication for the treatment of COVID-19. No vaccines have been authorized. Thus, this study aimed at conducting a review of the use of Remdesivir in patients with COVID-19. The following electronic databases were used MEDLINE, SCIELO, LILACS, and PUBMED. On May 1, Remdesivir received emergency use authorization from the Food and Drug Administration. Remdesivir is currently the most promising molecule in the treatment of COVID-19, taking into account its broad antiviral spectrum (considering the genetic sequences of the virus, it is expected to maintain activity against SARS-CoV-2). There is in vitro and in vivo information available for coronaviruses, as well as an extensive clinical safety database (from a clinical trial of the Ebola virus and in the context of the Monitored Emergency Use of Unregistered and Investigational Interventions - MEURI). Further studies are relevant as available data on the efficacy and safety of Remdesivir against SARS-nCoV-2 are limited.
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PMID:Use of remdesivir for patients with Covid-19: a review article. 3269 62


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