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We report the pathological and virological findings of the first autopsy case of the 2009 pandemic influenza (A/H1N1pdm) virus infection in Japan. A man aged 33 years with chronic heart failure due to dilated cardiomyopathy, mild diabetes mellitus, atopic dermatitis, bronchial asthma, and obesity died of respiratory failure and multiple organ dysfunction syndrome. Macroscopic examination showed severe pulmonary edema and microscopically the lung sections showed very early exudative-stage diffuse alveolar damage (DAD). Immunohistochemistry revealed proliferation of the influenza (A/H1N1pdm) virus in alveolar epithelial cells, some of which expressed SAalpha2-3Gal on the cell surface. Influenza (A/H1N1pdm) virus genomic RNA and mRNA were also detected in alveolar epithelial cells. Real-time PCR revealed 723 copies/cell in the left lower lung section from which the influenza (A/H1N1pdm) virus was isolated. Electron microscopic analysis revealed filamentous viral particles in the lung tissue. The concentrations of various cytokines/chemokines in the serum and the autopsied lung tissue were measured. IL-2R, IL-6, IL-8, IL-10, IFN-alpha, MCP-1, and MIG levels were elevated in both. These findings indicated a case of viral pneumonia caused by influenza (A/H1N1pdm) virus infection, showing characteristic pathological findings of the early stage of DAD.
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PMID:The first autopsy case of pandemic influenza (A/H1N1pdm) virus infection in Japan: detection of a high copy number of the virus in type II alveolar epithelial cells by pathological and virological examination. 2009 68

Novel influenza A (H1N1) at the origin of the 2009 pandemic flu developed mainly in subjects of less than 65 years contrary to the seasonal influenza, which usually developed in elderly patients of more than 65 years. Elderly subjects are partly protected by old meetings with close stocks. Influenza A(H1N1) can arise in serious forms within 60 to 80% of cases a fulminant acute respiratory distress syndrome (ARDS) "malignant and fulminant influenza" in subjects without any comorbidity, which makes the gravity and the fear of this influenza. The fact that this influenza A (H1N1) can develop in healthy young patients and evolve in few hours to a severe ARDS with a refractory hypoxemia gave to the foreground the possible interest of the recourse to extracorporeal oxygenation (ECMO) in some selected severe ARDS (5-10%). The first publications of patients admitted in intensive care unit (ICU) for severe influenza A (H1N1) often associated to an ARDS reported a mortality rate from 15 to 40%. This mortality variability may be explained in part by different studied populations, ARDS characteristics and human and material resources in the ICUs between the countries. Indeed, the highest mortality rates (30-40%) have been reported by in Mexico which were affected the first by pandemic flu and which were not prepared. A bacterial pneumonia was associated to H1N1 influenza in approximately 30% of the cases as at admission in ICU or following the days of the admission justifying an early antibiotherapy associated to the antiviral treatment by oseltamivir (Tamiflu). Obesity, pregnancy and respiratory diseases (asthma, COPD) seem to be associated to the development of a severe viral pneumonia due to influenza A (H1N1) often with ARDS. Older age, high APACHE II and SOFA scores and a delay of initiation of the antiviral treatment by oseltamivir are associated to higher morbidity and mortality. Other analyses of the results obtained from the first published papers included more patients and future studies would permitted to better define the role of therapeutics such as steroids and ECMO.
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PMID:[ARDS and influenza A (H1N1): patients' characteristics and management in intensive care unit. A literature review]. 2011 70

The characteristics of pandemic influenza 2009 differ from those of seasonal influenza. In Australia-New Zealand the number of admissions to the intensive care unit (ICU) increased by 15-fold in the southern winter. We compared the characteristics of the Spanish series of the first ICU admissions in July with those of series published in Canada and Australia-New Zealand up to October 2009. Unlike the situation in Spain, only half the admissions in Canada and Australia-New Zealand were due to primary viral pneumonia but bacterial pneumonia was much more frequent. In all series, young people, many of whom had no comorbidities, were the most frequently affected population. The most common comorbidities were obesity, chronic pulmonary disease, pregnancy and heart disease. Diagnosis through reverse-transcriptase polymerase chain reaction can have a false-negative rate of 10%. Shock and acute renal insufficiency were more frequent in the Spanish series. A total of 10-30% of patients required ICU admission and 6 of 10 patients required mechanical ventilation with a high frequency of failure of non-invasive ventilation (75%). Mortality was similar among the series (14-25%) but was higher in patients requiring mechanical ventilation (30%). Early oseltamivir administration (< 48h after symptom onset) has been associated with better outcome. Therefore, early administration of this drug in patients with risk factors or those who, although free from risk factors, show clinical progression, could reduce ICU admissions and mortality.
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PMID:[Pandemic influenza A (H1N1)v in the intensive care unit: what have we learned?]. 2035 56

We describe the epidemiology, clinical features, radiological findings, therapy and course for 15 patients hospitalized at the Infectious Diseases UOC of Gravina Hospital Caltagirone for a serious respiratory condition with verified infection A (H1N1) from 9 November to 22 December 2009. We retrospectively reviewed medical records, laboratory and instrumental tests performed on hospitalized patients. All patients had significant respiratory impairment: nine had co-morbidities and risk factors such as obesity, pregnancy, immunosuppressant conditions and muscular dystrophy. Symptoms were similar to those of seasonal influenza; radiological investigation of the chest (RX and CT) presents lung involvement in 80% of patients and changes in the bio-humoral indices. Development into acute respiratory distress syndrome (ARDS) was observed in six patients: three were ventilated with a Venturi mask, three were treated in intensive care and two patients used extracorporeal membrane oxygenation (ECMO). Two died. All patients received antiviral and symptomatic therapy for 5-21 days. A(H1N1) virus infection led to a mild to moderate flu syndrome, which was often cured by symptomatic treatment; some patients required hospitalization for viral pneumonia, mixed pneumonia or ARDS. In previous flu epidemics there was no development into ARDS (40% in our series).
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PMID:[Pulmonary complications from pandemic AH1N1 influenza: clinical-radiological features]. 2147 43

Three years after the pandemic, major advances have been made in our understanding of the innate and adaptive immune responses to the influenza A(H1N1)pdm09 virus and those responses' contribution to the immunopathology associated with this infection. Severe disease is characterized by early secretion of proinflammatory and immunomodulatory cytokines. This cytokine secretion persisted in patients with severe viral pneumonia and was directly associated with the degree of viral replication in the respiratory tract. Cytokines play important roles in the antiviral defense, but persistent hypercytokinemia may cause inflammatory tissue damage and participate in the genesis of the respiratory failure observed in these patients. An absence of pre-existing protective antibodies was the rule for both mild and severe cases. A role for pathogenic immunocomplexes has been proposed for this disease. Defective T cell responses characterize severe cases of infection caused by the influenza A(H1N1)pdm09 virus. Immune alterations associated with accompanying conditions such as obesity, pregnancy or chronic obstructive pulmonary disease may interfere with the normal development of the specific response to the virus. The role of host immunogenetic factors associated with disease severity is also discussed in this review. In conclusion, currently available information suggests a complex immunological dysfunction/alteration that characterizes the severe cases of 2009 pandemic influenza. The potential benefits of prophylactic/therapeutic interventions aimed at preventing/correcting such dysfunction warrant investigation.
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PMID:Immunopathogenesis of 2009 pandemic influenza. 2311 88

Acute respiratory infections are a leading cause of death worldwide. Clinical data is conflicted regarding whether statins improve outcomes for pneumonia. Potential confounding factors including specific etiology of pneumonia as well as obesity could potentially mask protective benefit. Obesity is a risk factor for high cholesterol, the main target for statin therapy. We demonstrate that statin intervention conferred no protective benefit in the context of wild-type mice regardless of infectious agent. Statin intervention conferred either a protective benefit, during influenza infection, or detrimental effect, in the case of pneumococcal infection, in obese animals. These data suggest etiology of pneumonia in the context of obesity could be dramatically altered by the protective effects of statin therapy during bacterial and viral pneumonia.
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PMID:Protective Capacity of Statins during Pneumonia Is Dependent on Etiological Agent and Obesity. 2949 2

Objective: This study examined the full spectrum of comorbid disorders in all statutory-health-insured children aged 5 to 14 years with ADHD in 2017 by using nationwide claims data in Germany. Method: Children with ADHD (n = 258,662) were compared for the presence of 864 comorbid diseases with a control group matched by gender, age, and region of residence (n = 2,327,958). Results: Among others, metabolic disorders (odds ratio [OR] = 9.18; 95% confidence interval [CI] = [8.43, 9.99]), viral pneumonia (OR = 4.95; 95% CI = [2.37, 10.33]), disorders of white blood cells (OR = 4.55; 95% CI = [3.83, 5.40]), kidney failure (OR = 3.33; 95% CI = [2.65, 4.18]), hypertension (OR = 3.26; 95% CI = [3.00, 3.55]), obesity (OR = 2.85; 95% CI = [2.80, 2.91]), type 2 diabetes (OR = 2.61; 95% CI = [2.11, 3.23]), migraine (OR = 2.49; 95% CI = [2.37, 2.61]), asthma (OR = 2.19; 95% CI = [2.16, 2.22]), atopic dermatitis (OR = 2.10; 95% CI = [2.16, 2.23]), juvenile arthritis (OR = 1.56; 95% CI = [1.39, 1.76]), glaucoma (OR = 1.51; 95% CI = [1.30, 1.75]), and type 1 diabetes (OR = 1.30; 95% CI = [1.20, 1.40]) were more likely to be diagnosed in ADHD children. Conclusion: Along with psychiatric diseases, various somatic diseases were more common in ADHD children. The results have direct implications for patient care, including fine-grained diagnostics and personalized therapy.
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PMID:Psychiatric and Nonpsychiatric Comorbidities Among Children With ADHD: An Exploratory Analysis of Nationwide Claims Data in Germany. 3136 81

COVID-19 is an outbreak of viral pneumonia which became a global health crisis, and the risk of morbidity and mortality of people with obesity are higher. SARS-CoV-2, the pathogen of COVID-19, enters into cells through binding to the Angiotensin Converting Enzyme (ACE) homolog-2 (ACE2). ACE2 is a regulator of two contrary pathways in renin angiotensin system (RAS): ACE-Ang-II-AT1R axis and ACE2-Ang 1-7-Mas axis. Viral entry process eventuates in downregulation of ACE2 and subsequent activation of ACE-Ang-II-AT1R axis. ACE-Ang II-AT1R axis increases lipid storage, reduces white-to-beige fat conversion and plays role in obesity. Conversely, adipose tissue is an important source of angiotensin, and obesity results in increased systemic RAS. ACE-Ang-II-AT1R axis, which has proinflammatory, profibrotic, prothrombotic, and vasoconstrictive effects, is potential mechanism of more severe SARS-CoV-2 infection. The link between obesity and severe COVID-19 may be attributed to ACE2 consumption and subsequent ACE-Ang-II-AT1R axis activation. Therefore, patients with SARS-CoV-2 infection may benefit from therapeutic strategies that activate ACE2-Ang 1-7-Mas axis, such as Ang II receptor blockers (ARBs), ACE inhibitors (ACEIs), Mas receptor agonists and ACE2.
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PMID:Angiotensin II receptors: Impact for COVID-19 severity. 3264 28

Background Community-acquired pneumonia due to viral pathogens is an under-recognized cause of healthcare-associated mortality and morbidity worldwide. We aimed to compare mortality rates and outcome measures of disease severity in obese vs non-obese patients admitted with viral pneumonia. Methods Adult patients admitted with viral pneumonia were selected from the Nationwide Inpatient Sample of 2016 and 2017. The arms were stratified based on the presence of a secondary discharge diagnosis of obesity. The primary outcome was inpatient mortality. Secondary outcomes included sepsis, acute respiratory failure, acute respiratory distress syndrome, acute kidney injury, and pulmonary embolism. Results and interpretation In total, 89,650 patients admitted with viral pneumonia were analyzed, and 17% had obesity. There was no significant difference in mortality between obese and non-obese patients (aOR: 0.98, 95% CI: 0.705 - 1.362, p < 0.001). Compared to non-obese patients, obese patients had higher adjusted odds of developing acute hypoxic respiratory failure (aOR: 1.37, 95% CI: 1.255 - 1.513, p < 0.001), acute respiratory distress syndrome (aOR: 2.29, 95% CI: 1.554 - 3.381, p < 0.001), need for mechanical ventilation (aOR: 1.50, 95% CI: 1.236 - 1.819, p < 0.001), and pulmonary embolism (aOR: 1.69, 95% CI: 1.024 - 2.788, p = 0.040). Conclusions Obesity was not found to be an independent predictor of inpatient mortality in patients admitted with viral pneumonia. However, obesity is associated with worse clinical outcomes and disease severity as defined by the presence of complications, greater incidence of acute respiratory failure (ARF), acute respiratory distress syndrome (ARDS), need for mechanical ventilation, acute kidney injury (AKI), pulmonary embolism (PE), stroke, and sepsis.
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PMID:Predicting COVID-19 Using Retrospective Data: Impact of Obesity on Outcomes of Adult Patients With Viral Pneumonia. 3304 81