leptin and Lung-Diseases--Interstitial

Scleroderma is a systemic autoimmune disease of unknown etiology whose characteristic features include endothelial cell dysfunction, fibroblast proliferation, and immune dysregulation. Although almost any organ can be pathologically involved in scleroderma, lung complications including interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH) are the leading cause of death in patients with this condition. Currently, the molecular mechanisms leading to development of scleroderma-related lung disease are poorly understood; however, the systemic nature of this condition has led many to implicate circulating factors in the pathogenesis of some of its organ impairment. In this article we focus on a new class of circulating factors derived from adipose-tissue called adipokines, which are known to be altered in scleroderma. Recently, the adipokines adiponectin and leptin have been found to regulate biological activity in endothelial, fibroblast, and immune cell types in lung and in many other tissues. The pleiotropic nature of these circulating factors and their functional activity on many cell types implicated in the pathogenesis of ILD and PAH suggest these hormones may be mechanistically involved in the onset and/or progression of scleroderma-related lung diseases.

Topics: Adipokines; Adiponectin; Humans; Hypertension, Pulmonary; Leptin; Lung Diseases, Interstitial; Scleroderma, Systemic

Adipokines have inflammatory and fibrotic properties that may be critical in interstitial lung disease (ILD). We examined associations of serum adipokine levels with CT imaging-based measures of subclinical ILD and lung function among community-dwelling adults.. A subset of the original Multi-Ethnic Study of Atherosclerosis cohort (n = 1,968) had adiponectin, leptin, and resistin measured during follow-up visits (2002-2005). We used regression models to examine associations of adiponectin, leptin, and resistin levels with (1) high-attenuation areas (HAAs) from CT scans (2004-2005, n = 1,144), (2) interstitial lung abnormalities (ILAs) from CT scans (2010-2012, n = 872), and (3) FVC from spirometry (2004-2006, n = 1,446). We used -(1/HAA. Higher adiponectin was associated with lower HAA on CT imaging among adults with a BMI ≥ 25 kg/m. Higher adiponectin levels were associated with lower HAA on CT imaging among adults with a higher BMI. Higher leptin and resistin levels were associated with lower FVC and greater HAA, respectively.

Topics: Adipokines; Adiponectin; Aged; Asymptomatic Diseases; Body Mass Index; Cohort Studies; Female; Humans; Independent Living; Leptin; Lung; Lung Diseases, Interstitial; Male; Middle Aged; Obesity; Resistin; Smoking; Tomography, X-Ray Computed; Vital Capacity

Obesity has been linked to acute lung injury and is a risk factor for early mortality after lung transplantation.. To examine the associations of obesity and plasma adipokines with the risk of primary graft dysfunction after lung transplantation.. We performed a prospective cohort study of 512 adult lung transplant recipients with chronic obstructive pulmonary disease or interstitial lung disease enrolled in the Lung Transplant Outcomes Group Study. In a nested case-control study, we measured plasma leptin, adiponectin, and resistin before lung transplantation and 6 and 24 hours after lung transplantation in 40 cases of primary graft dysfunction and 80 control subjects. Generalized linear mixed models and logistic regression were used to estimate risk ratios and odds ratios.. Grade 3 primary graft dysfunction developed within 72 hours of transplantation in 29% participants. Obesity was associated with a twofold increased risk of primary graft dysfunction (adjusted risk ratio 2.1; 95% confidence interval, 1.7-2.6). The risk of primary graft dysfunction increased by 40% (confidence interval, 30–50%) for each 5 kg/m(2) increase in body mass index after accounting for center, diagnosis, cardiopulmonary bypass, and transplant procedure. Higher plasma leptin levels were associated with a greater risk of primary graft dysfunction (sex-adjusted P = 0.02). The associations of both obesity and leptin with primary graft dysfunction tended to be stronger among those who did not undergo cardiopulmonary bypass.. Obesity is an independent risk factor for primary graft dysfunction after lung transplantation.

Topics: Adiponectin; Aged; Biomarkers; Body Mass Index; Case-Control Studies; Female; Humans; Leptin; Linear Models; Logistic Models; Lung Diseases, Interstitial; Lung Transplantation; Male; Middle Aged; Obesity; Odds Ratio; Overweight; Primary Graft Dysfunction; Prospective Studies; Pulmonary Disease, Chronic Obstructive; Resistin; Risk Factors; Severity of Illness Index; Survival Analysis; Time Factors; United States