Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A cross-sectional echocardiographic study of 50 black Zimbabwean children with clinical human immunodeficiency virus (HIV) infection was carried out. The median age was 9 months. Seventy per cent had chronic cough, 60% respiratory distress and 40% cyanosis. Sixty per cent had pericardial effusion and 48% right ventricular hypertrophy (RVH) and dilation. However, the clinical diagnosis of heart failure was difficult as most of these children (80%) had hepatomegaly. These findings suggest that respiratory disease plays a role in the causation of RVH in these children. As cardiac causes of RVH were absent, this was presumed to be due to cor pulmonale. HIV-infected children presenting with respiratory distress may have clinically unapparent cor pulmonale. Early and appropriate management may by beneficial.
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PMID:Cor pulmonale in children with human immunodeficiency virus infection. 767 13

Immunodeficiency secondary to cancer chemotherapy (chemotherapy for less than 3 months, or intensive chemotherapy with bone marrow transplant) may be responsible for postoperative infections. To estimate the value of this hypothesis, a prospective study was done over a period of 18 months in patients who had undergone pulmonary surgery. Antibiotic prophylaxis was by pefloxacin, one tablet (400 mg) 1 h before surgery then 11 h after. Clinical examination, a chest X-ray and blood cell count were carried out every day for 10 days and on the 15th day. All the drain-tips were cultured. In a case of infection, samples were obtained and cultured. One group comprised 22 immunodeficient patients (group A), and 33 patients (group B) had received no prior chemotherapy (bone-marrow transplantation = 36.7%). There were differences between the two groups in age (A:33.5 +/- 12.3 years; B:50.8 +/- 18.4 years), and type of tumour (A: metastasis = 95.5%; B: lung cancer = 51.5%). Surgical operation was bilateral for 36.4% of the patients in group A. There was more anatomical resection (pneumonectomy and lobectomy) in group B. Lung function did not differ between the two groups (abnormalities: A = 54.6%; B = 63.6%). In group A, there were 3 pulmonary infections (13.7%), but in group B 10 infections (30.3%) with 9 pulmonary infections (4 with bacteraemia) and 1 wound infection. The bacteriological finding showed two pathogens in 7 cases and no bacteriological isolates in 2 cases. With broad-spectrum antibiotherapy all the patients were cured except 1. There was one postoperative death in group B. This patient died of respiratory distress after pneumonectomy complicated by pneumonia and septicaemia (Streptococcus pneumoniae) in the remaining lung. Surgical procedures are performed with increasing frequency on patients with immunocompromised status. Classically the risk of infection is more important for these patients. In this study prior cancer chemotherapy or bone marrow transplantation did not seem to be an aggravating factor of the risk of infection. But further methodological analysis would not allow us to distinguish between a real impact of chemotherapy and the influence of group heterogeneity.
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PMID:Postoperative infections in immunocompromised patients after oncological surgery. 925 33

A full-length feline immunodeficiency virus NCSU1 (FIV-NCSU1) genome (JSY3) was cloned directly from FIV-NCSU1-infected feline CD4+ lymphocyte (FCD4E) genomic DNA and identified by PCR amplification with 5' long terminal repeat, gag, env, and 3' long terminal repeat primer sets. Supernatant from FCD4E cells cocultured with JSY3-transfected Crandell feline kidney (CrFK) cells was used as an inoculum. Cell-free JSY3 virus was cytopathogenic for FCD4E lymphocytes but did not infect CrFK cells in vitro. To determine in vivo infectivity and pathogenesis, six young adult specific-pathogen-free cats were inoculated with cell-free JSY3 virus. Provirus was detected at 2 weeks postinfection (p.i.) and was still detectable at 25 weeks p.i. as determined by gag region PCR-Southern blot analysis of peripheral blood mononuclear cell lysates. Infectious virus was recovered from peripheral blood mononuclear cells at 6 and 25 weeks p.i., and an antibody response to FIV was detected by 4 weeks. In the acute phase of infection, JSY3 provirus was found only in the CD4+ lymphocyte subset; however, by 14 weeks p.i., the greatest provirus burden was detected in B lymphocytes. All six cats were panlymphopenic at 2 weeks p.i., CD4+/CD8+ ratios were inverted by 6 weeks p.i., and five of the six cats developed lymphadenopathy by 10 weeks p.i. To determine if the JSY3 molecular clone caused immunodeficiency similar to that of the parental wild-type FIV-NCSU1, the cats were challenged with the low-virulence ME49 strain of Toxoplasma gondii at 29 weeks p.i. Five of six cats developed clinical signs consistent with generalized toxoplasmosis, and three of six cats developed acute respiratory distress and required euthanasia. Histopathologic examination of the severely affected cats revealed generalized inflammatory reactions and the presence of T. gondii tachyzoites in multiple tissues. None of the six age- and sex-matched specific-pathogen-free cats inoculated with only T. gondii developed clinical disease. Our results suggest that the pathogenesis of the molecularly cloned NCSU1 JSY3 is similar to that of wild-type FIV-NCSU1.
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PMID:Molecularly cloned feline immunodeficiency virus NCSU1 JSY3 induces immunodeficiency in specific-pathogen-free cats. 862 77

The independent effects of chronic disease, age, severity of illness, lung injury score (LIS) and etiology, and preceding nonpulmonary organ-system dysfunction (OSD) on the outcome of acute lung injury (ALI) have not been examined in an exclusively medical-intensive-care-unit (MICU) population. Therefore, 107 consecutive MICU patients with ALI (76% with acute respiratory distress syndrome [ARDS]) were prospectively investigated. The impact of comorbidities, age > 65 yr, acute physiology score (APS), LIS, etiology of ALI, and OSD on hospital survival were studied. The overall mortality was 62 of 107 patients (58%), including 47 (58%) with ARDS. With univariate analysis, age > 65 yr, organ transplantation, human immunodeficiency virus (HIV) infection, active malignancy, chronic steroid use, and a septic or aspiration-related etiology of ALI were associated with a > or = 1.2-fold greater relative risk (RR) of hospital mortality. With multiple logistic regression, independent predictors of hospital death were age > 65 yr, organ transplantation, HIV infection, cirrhosis, active malignancy, and sepsis. APS, LIS, aspiration-related etiology of ALI, preceding OSD, and other comorbidities were not independently predictive of hospital death. Multivariate analysis of the ARDS cohort showed similar results, although cirrhosis and malignancy did not reach statistical significance. We conclude that comorbid conditions, older age, and sepsis etiology are independent predictors of hospital death in exclusively MICU patients with ALI (76% of whom satisfied criteria for ARDS). These factors should be considered in analyzing studies of new therapies and interpreting trends in mortality for ALI and ARDS.
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PMID:Acute lung injury in the medical ICU: comorbid conditions, age, etiology, and hospital outcome. 956 34

A 33-day-old male infant was admitted to the neonatal intensive care nursery because of respiratory distress, grunting, cyanosis, and radiological findings of bilateral bronchopneumonia. He responded well to intensive therapy, but 11 days later developed hemolytic uremic syndrome, which was treated conservatively with prednisone and plasma transfusions with good response. The hemolytic uremic syndrome resolved, but he subsequently developed severe recurrent infections of unknown etiology and died at the age of 78 days. Necropsy findings revealed necrotizing enterocolitis as well as dysplasia of the thymus and other lymphoid tissues, compatible with the diagnosis of immunodeficiency disorder.
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PMID:Hemolytic uremic syndrome and thymic dysplasia in an infant. 963 44

The aim of our study was to evaluate the success, complications, and morbidity following a modified Thal fundoplication in children with reflux-associated respiratory disease (RARD). We used a procedure consisting of retroesophageal hiatal plasty, wrapping the gastric fundus around the gastroesophageal junction 180 degrees, and fixation of the lesser curvature at the abdominal wall. Follow-up by questionnaire of 128 (77 male, 51 females) out of 196 antireflux procedures between 1992 and 1995 was achieved. Surgical therapy was considered justified whenever there was gastroesophageal reflux resulting in severe recurrent respiratory symptoms. Eleven percent of the children suffered from bronchiectasis. The diagnosis of RARD was based on a high index of suspicion, barium swallow with fluoroscopy, 24-hr two-level pH-monitoring, bronchoscopy, bronchoalveolar lavage and detection of lipid-laden alveolar macrophages, esophago-gastroscopy, and esophageal biopsy. Patients with bronchopulmonary diseases such as allergy, immunodeficiency, cystic fibrosis, primary ciliary dyskinesia, and malformation of the bronchial tree or vessels had been excluded. "Evident improvement" as a result of surgery was reported in 88%, "no change" in 10%, and a "change for the worse" in 2% of patients. Persistent mild difficulties in swallowing were observed in 11%. Paraesophageal hernia, gas-bloat syndrome, and dumping syndrome were not observed. Two children needed a second operation because of relapse. The use of emergency steroidal medication for acute respiratory distress decreased impressively (219 single doses/year before surgery vs. 30 single doses/year after surgery). The need for more than 4 times/year of antibiotic therapy before surgery was reduced from 52. 3% before to 14% after surgery. Most (90.6%) of the parents stated they would agree to have surgery done again if medically indicated. In conclusion, Thal fundoplication is sufficient, safe, and effective in the management of RARD. Complications of the procedure were minor and of little consequence to the patient.
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PMID:Antireflux surgery in children suffering from reflux-associated respiratory diseases. 1128 21

Pulmonary surfactant is a complex and highly surface active material composed of lipids and proteins which is found in the fluid lining the alveolar surface of the lungs. Surfactant prevents alveolar collapse at low lung volume, and preserves bronchiolar patency during normal and forced respiration (biophysical functions). In addition, it is involved in the protection of the lungs from injuries and infections caused by inhaled particles and micro-organisms (immunological, non-biophysical functions). Pulmonary surfactant can only be harvested by lavage procedures, which may disrupt its pre-existing biophysical and biochemical micro-organization. These limitations must always be considered when interpreting ex vivo studies of pulmonary surfactant. A pathophysiological role for surfactant was first appreciated in premature infants with respiratory distress syndrome and hyaline membrane disease, a condition which is nowadays routinely treated with exogenous surfactant replacement. Biochemical surfactant abnormalities of varying degrees have been described in obstructive lung diseases (asthma, bronchiolitis, chronic obstructive pulmonary disease, and following lung transplantation), infectious and suppurative lung diseases (cystic fibrosis, pneumonia, and human immunodeficiency virus), adult respiratory distress syndrome, pulmonary oedema, other diseases specific to infants (chronic lung disease of prematurity, and surfactant protein-B deficiency), interstitial lung diseases (sarcoidosis, idiopathic pulmonary fibrosis, and hypersensitivity pneumonitis), pulmonary alveolar proteinosis, following cardiopulmonary bypass, and in smokers. For some pulmonary conditions surfactant replacement therapy is on the horizon, but for the majority much more needs to be learnt about the pathophysiological role the observed surfactant abnormalities may have.
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PMID:Pulmonary surfactant in health and human lung diseases: state of the art. 1044 27

RSV is the most important respiratory pathogen in infants and young children. About 1% of primary RSV infections result in hospitalization. The virus is spread by large droplets of secretions or contact with contaminated secretions. Infants infected with RSV may demonstrate poor feeding, rhinorrhea, apnea, lethargy, wheezing, and respiratory distress. Diagnosis may be made by clinical signs and symptoms (especially those observed during epidemics), by chest radiographs showing hyperinflation, or by rapid antigen detection with immunofluorescence of nasopharyngeal aspirates. Risk factors for severe disease accompanied by complications include chronic heart disease, chronic lung disease, immunodeficiency, HIV, and prematurity. Immunity is incomplete and of short duration, and reinfection is common. Treatment remains supportive and consists of oxygen administration, hydration, and diligent monitoring. Use of corticosteroids, bronchodilators, antibiotics, and ribavirin is controversial and is dependent largely on physician preference. Use of ribavirin should be reserved for patients who have severe underlying conditions associated with increased mortality rates. Intravenous RSV Ig has been replaced by palivizumab, which is generally recommended for infants at high risk for severe RSV, including those with a history of prematurity and those with chronic lung disease.
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PMID:RSV infection in infants and young children. What's new in diagnosis, treatment, and prevention? 1060 68

The inflammatory response to infection is necessary for host defense but can contribute to the systemic toxicity and lung injury that may result from pneumonia. In some settings, adjunctive treatment of lower respiratory infections with anti-inflammatory agents can reduce morbidity. Corticosteroids have a well-documented role in the management of Pneumocystis carinii pneumonia complicating human immunodeficiency virus (HIV) infection. Corticosteroids also were found to reduce systemic symptoms of tuberculosis in a number of older studies, but their role as adjuncts to contemporary antimicrobial therapy are less clear. Corticosteroids also may be effective under some circumstances in the treatment of inflammatory sequelae of respiratory tract infection, such as tuberculous pleurisy, bronchiolitis obliterans organizing pneumonia, or prolonged acute respiratory distress syndrome. Nonsteroidal anti-inflammatory drugs may have limited applications in the modulation of chronic airway inflammation. Strategies targeting specific cytokines have not been effective to date, but remain active areas of investigation.
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PMID:Anti-inflammatory treatment of acute and chronic pneumonia. 1130 15

We describe a 10-month-old boy diagnosed with X-linked hyper-IgM syndrome (XHIM) after suffering from life-threatening acute respiratory distress syndrome (ARDS) caused by Pneumocystis carinii pneumonia (PCP), although his previous clinical history and first level laboratory tests investigating immunological function did not indicate immunodeficiency. When the patient's overall condition was good, elective bone marrow transplantation from an HLA-matched older brother was performed successfully. We describe how correct diagnosis and successful treatment were made possible thanks to the involvement of a network of specialists.
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PMID:Elective bone marrow transplantation in a child with X-linked hyper-IgM syndrome presenting with acute respiratory distress syndrome. 1210 78


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