Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Objective This study determines trends in demographics and hospitalization outcomes among patients admitted for systemic sclerosis (SScl) and evaluates the differences between comorbidities. Methods The study used data from the Nationwide Inpatient Sample (NIS) for the years 2010-2014. We identified SScl as the primary diagnosis and the associated medical and psychiatric comorbidities using validated International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) codes. The differences in comorbidities and in-hospital mortality were quantified using multinomial logistic regression (odds ratio (OR)). Results Inpatient admissions for SScl decreased over the period 2010-2014 by 15.9% (p < 0.001). There was an increasing trend in the 61-80 years age group as they had a 29% increase in admissions and a higher risk of in-hospital mortality (OR = 2.113; p = 0.020). The differences between races showed weaker linear trends, with Caucasians (57.5%) showing an increasing trend, and African Americans (24.3%) and Hispanics (11.8%) having a decreasing trend (p < 0.001). However, Hispanics had the highest risk of mortality (OR = 1.295; p = 0.001) during hospitalization. In-hospital mortality had a linear decreasing trend, with a 10.3% decrease in deaths in 2010, and a 9.1% decrease in 2014 (p < 0.001). Hypertension (47.3%), pulmonary circulation disorders (40.1%), pulmonary fibrosis (29.7%), and congestive heart failure (24.4%) constituted the majority of comorbidities. Comorbid diabetes increased the risk of in-hospital mortality in SScl patients by four times (OR = 3.914; p = 0.003). Esophageal reflux disorder was present in only 6.7% of SScl patients, but it increased the risk of in-hospital mortality (OR = 2.643: p < 0.001). Among psychiatric comorbidities, depression (OR = 1.526; p = 0.001) and psychosis (OR = 1.743; p = 0.039) both increased the risk of in-hospital mortality. Conclusion We observed the various comorbidities that were associated with substantial and significant differences in the risk of in-hospital mortality. We assert that these findings indicate that comorbid conditions are influential factors that must be considered in models of health-related quality of life (HRQOL) in SScl. More attention needs to be paid to the elderly population at risk of having a higher risk of inpatient death. Further research to guide the development of clinical care models for targeting early diagnosis and treatment of comorbidities in SScl is necessary to reduce both mortality and morbidity, as well as improve the quality of care for these patients.
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PMID:Trends in Demographics, Hospitalization Outcomes, Comorbidities, and Mortality Risk among Systemic Sclerosis Patients. 3002 20

BACKGROUND The clinical association between gastroesophageal reflux disease (GERD) and idiopathic pulmonary fibrosis (IPF) has been known for many years, but it is still unclear. The present study investigated the association between experimentally simulated aspiration and pulmonary fibrosis. MATERIAL AND METHODS A total of 120 male Sprague-Dawley rats were randomly divided into a negative control group, a bleomycin group, and 3 simulated aspiration groups. The bleomycin group was administered a one-time intratracheal injection of bleomycin, whereas the 3 simulated aspiration groups were treated either with an intratracheal instillation of gastric fluid combined with pepsin, with pepsin alone, or with hydrochloric acid, all twice a week, and the negative control group was administered normal saline twice a week. Lung tissues were collected to evaluate pathological changes and the mRNA expression levels of connective tissue growth factor (CTGF), type I collagen, and transforming growth factor. RESULTS The results demonstrated that the degree of fibrosis in the early stage was low in each of the 3 simulated aspiration groups, but gradually increased over time. The expression levels of the downstream factor of fibrosis, CTGF, and type I collagen also reflected this trend. CONCLUSIONS The study demonstrates that aspiration of gastric contents can cause pulmonary fibrosis, and mixed aspiration of pepsin and gastric fluid can accelerate this process. This study provides strong evidence in support of a potential association between human GERD and IPF.
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PMID:Gastric Acid and Pepsin Work Together in Simulated Gastric Acid Inhalation Leading to Pulmonary Fibrosis in Rats. 3141 18


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