ABSTRACT
BACKGROUND: As there had been no reduction in the TB burden in South Korea since 2000, a public-private mix (PPM) strategy was launched in 2011. The purpose of this study was to investigate the reasons for lost to follow-up (LTFU) among TB patients and their clinical characteristics.METHOD: A multicentre, cross-sectional study based on in-depth interviews with patients and their families by TB specialist nurses was conducted. Patients who were reported with a final outcome of LTFU in 2015-2017 at all PPM hospitals across the country were enrolled. Enrolled patients were classified into six subgroups by age and three major reasons for LTFU (adverse effects, refusal of treatment, marginalisation) and their clinical features were compared.RESULTS: Among 780 patients, those who were lost to follow-up due to adverse effects accounted for the largest proportion (n = 387). LTFU in those aged <65 years who refused treatment (n = 189) and those aged <65 years who were marginalised (n = 108) were related to having smear-positive TB and a previous history of unfavourable outcomes.CONCLUSION: To reduce LTFU in South Korea, comprehensive strategies, including management of adverse effects, systematic counselling and education, should be implemented.
Subject(s)
Tuberculosis , Aged , Cross-Sectional Studies , Hospitals, Public , Humans , Republic of Korea , Tuberculosis/drug therapy , Tuberculosis/epidemiologyABSTRACT
The airway epithelium regulates responses to aeroallergens, acting as a physical and immunological barrier. In asthma, epithelial barrier function and the expression of adherens junction protein E-cadherin is compromised, but it is unknown whether this is cause or consequence of the disease. We hypothesized that airway epithelial loss of E-cadherin is a critical step in the development of manifestations of asthma. We generated a transgenic mouse model with conditional loss of E-cadherin in lung epithelial cells at birth and onwards. We observed normal lung development at the time of birth in mice lacking E-cadherin in the lung epithelium. However, E-cadherin deficiency led to progressive epithelial damage in mice growing into adulthood, as evidenced by airway epithelial denudation, decreased zonula occludens (ZO)-1 expression, loss of ciliated cells, and enlarged alveolar spaces. In addition, spontaneous goblet cell metaplasia with mucus production was observed. These epithelial changes were accompanied by elevated levels of the epithelial-derived chemokine CCL17, infiltration of eosinophils and dendritic cells, and mucus production. In conclusion, loss of E-cadherin induces features in the lung reminiscent of those observed in asthma, indicating that the disruption of E-cadherin-mediated cell-cell contacts may play a key role in the development of asthma manifestations.
Subject(s)
Cadherins/metabolism , Respiratory Mucosa/metabolism , Respiratory Mucosa/pathology , Adherens Junctions/metabolism , Animals , Asthma/metabolism , Cadherins/genetics , Cadherins/physiology , Chemokine CCL17/metabolism , Dendritic Cells/immunology , Disease Models, Animal , Eosinophils/metabolism , Epithelial Cells/metabolism , Epithelium/metabolism , Goblet Cells/metabolism , Lung/pathology , Metaplasia/metabolism , Mice , Mice, Inbred C57BL , Mice, Transgenic , Tight Junctions/metabolism , Zonula Occludens-1 Protein/metabolismABSTRACT
SETTING: Factors that influence the annual rate of decline of lung function need to be verified. OBJECTIVE: To determine the effects of metabolic syndrome, especially hypertension, on the annual rate of decline in lung function. DESIGN: A total of 635 healthy participants without known respiratory disease completed baseline and follow-up routine check-ups, including a pulmonary function test, for at least 3 years. Age, sex, height, weight, waist circumference, smoking status, other underlying diseases, and pulmonary function and blood test results were carefully reviewed. RESULTS: In a multivariable analysis of baseline data, diabetes was associated with lower forced vital capacity (FVC). In longitudinal analysis using mixed linear regression, hypertension was an independent predictor for acceleration of FVC decline rate compared to subjects without hypertension (-37.2 vs. -18.5 ml/year), while anti-hypertensive medication decelerated FVC decline in hypertensive subjects (-58.9 vs. -32.3 ml/year). The annual rate of decline in forced expiratory volume in 1 second (FEV1) in groups with and without hypertension did not differ significantly. No significant difference was found in FEV1 or FVC annual rates of decline with regard to the presence of diabetes, dyslipidaemia, obesity or abdominal obesity. CONCLUSION: Hypertension is associated with an accelerated decline in FVC, but anti-hypertensive medication might abate the rate of decline in asymptomatic healthy subjects.
Subject(s)
Hypertension/physiopathology , Lung/physiopathology , Metabolic Syndrome/physiopathology , Adult , Antihypertensive Agents/therapeutic use , Chi-Square Distribution , Female , Forced Expiratory Volume , Humans , Hypertension/diagnosis , Hypertension/drug therapy , Linear Models , Longitudinal Studies , Male , Metabolic Syndrome/diagnosis , Metabolic Syndrome/drug therapy , Middle Aged , Multivariate Analysis , Predictive Value of Tests , Retrospective Studies , Risk Factors , Spirometry , Time Factors , Vital CapacityABSTRACT
Polyarteritis nodosa (PAN) is a systemic necrotizing vasculitis involving predominantly medium-sized muscular arteries. It commonly involves skin, kidney, cardiovascular system, gastrointestinal system, and neurological system. But bronchial artery involvement of PAN is rarely identified. We report a case of PAN with initial presentation of hemoptysis. On admission, chest radiograph and chest CT angiography revealed no focus of bleeding. Angiography showed a bronchial artery aneurysm and multiple arterial aneurysms in both renal, hepatic, mesenteric and branches of small bowel arteries. These findings were compatible with the diagnosis of PAN. The patient was started on steroid and cyclophosphamide.
