Scleroderma Study Links Sleep Apnea With High Blood Pressure in Lungs - Scleroderma News
Scleroderma Study Links Sleep Apnea With High Blood Pressure in Lungs - Scleroderma News |
| Scleroderma Study Links Sleep Apnea With High Blood Pressure in Lungs - Scleroderma News Posted: 20 Jul 2020 12:00 AM PDT Obstructive sleep apnea (OSA) is associated with an increased risk of pulmonary hypertension in people with scleroderma, a study suggests. The study, "Impact of concomitant obstructive sleep apnea on pulmonary involvement and main pulmonary artery diameter in adults with scleroderma," was published in the journal Sleep and Breathing. Up to 90% of people with scleroderma experience some form of lung involvement. For instance, up to 40% of people with scleroderma will develop pulmonary arterial hypertension (PAH), which refers to high blood pressure within the lungs. OSA occurs when the muscles of the throat relax abnormally during sleep, causing the airways to become blocked. Although the association of OSA with inflammatory disease has been suggested, the link between OSA and scleroderma, with or without pulmonary involvement, is less clear. "It is also unclear to which extent a concomitant OSA is associated with pulmonary hypertension in scleroderma patients," the researchers wrote. To address this, they conducted a clinical trial (NCT02740569) reporting data for 62 people with scleroderma (58 women, mean age 48 years) who underwent sleep assessments as well as tests of lung function. Forty-three participants had limited scleroderma, and 19 had diffuse scleroderma. The gold standard for detecting PAH is right heart catheterization, where a thin tube is inserted into the blood vessels near the heart. However, since this method is invasive, the researchers used high-resolution computed tomography (HRCT) imaging to measure main pulmonary artery diameter (mPAD) — the width of the primary artery connecting the heart with the lungs. An enlarged mPAD, defined as a minimum of 27 millimeter (mm) in women and at least 29 mm in men, is thought to be predictive of PAH. Lung involvement, more generally, was also derived from HRCT data by calculating the Warrick score, which rates the severity of abnormalities. A Warrik score of 7 or greater was defined as pulmonary involvement. Individuals with diffuse scleroderma were more likely than those with limited scleroderma to have lung involvement, as indicated by both a higher mean Warrick score (17.1 vs. 10) and a greater percentage of individuals with a Warrick score of 7 or above (84.2% vs. 55.8%). In the overall group, 20 participants (32.3%) had OSA, 17 of whom had limited scleroderma and three had diffuse disease. Patients with OSA were significantly older (mean age 55.14 vs. 45.3) and had a higher rate of obesity (55% vs. 23.8%) and hypertension (35% vs. 9.5%). The rate of lung involvement did not significantly differ based on OSA status: about two-thirds of participants with OSA had lung involvement, and a similar rate was found for patients who did not have OSA. Also, no significant differences were seen in average scores of lung function tests, such as forced vital capacity. A significantly higher rate of enlarged mPAD was found among individuals with OSA (50%) than without (14.3%). In addition, participants with OSA had a higher mean mPAD (27.8 mm) than those without OSA (24.2 mm). Additional analyses showed that having OSA correlated with a 4.7 times greater risk for enlarged mPAD, after accounting for factors such as age and body mass index. "We conclude that OSA was associated with risk for pulmonary hypertension independent of pulmonary involvement in this cohort," the researchers wrote. However, the limited number of participants and the fact this was a single-center study warrant further research to validate the results, they added. Also, the data do not suggest that OSA causes high lung blood pressure, but rather that the two are associated. As such, it is impossible to predict if treating OSA would have benefits for pulmonary hypertension based on the current results. "Whether or not the treatment of concomitant OSA in patients with scleroderma reduces this risk [of pulmonary hypertension] needs to be further evaluated," the scientists wrote.  Marisa holds an MS in Cellular and Molecular Pathology from the University of Pittsburgh, where she studied novel genetic drivers of ovarian cancer. She specializes in cancer biology, immunology, and genetics. Marisa began working with BioNews in 2018, and has written about science and health for SelfHacked and the Genetics Society of America. She also writes/composes musicals and coaches the University of Pittsburgh fencing club. × Marisa holds an MS in Cellular and Molecular Pathology from the University of Pittsburgh, where she studied novel genetic drivers of ovarian cancer. She specializes in cancer biology, immunology, and genetics. Marisa began working with BioNews in 2018, and has written about science and health for SelfHacked and the Genetics Society of America. She also writes/composes musicals and coaches the University of Pittsburgh fencing club. Latest Posts  |
| Interleukin-32 Shows Potential as Early Biomarker for PAH in... - Pulmonary Hypertension News Posted: 17 Jul 2020 12:00 AM PDT A protein called interleukin-32 may serve as a biomarker for pulmonary arterial hypertension (PAH) in scleroderma patients, for whom PAH is a severe complication. The study reporting the findings, "Interleukin-32 in systemic sclerosis, a potential new biomarker for pulmonary arterial hypertension," was published in the journal Arthritis Research and Therapy. Systemic sclerosis, also called systemic scleroderma (SSc), is an autoimmune disease characterized by the buildup of scar tissue in the skin and several internal organs, including the arteries. Cardiopulmonary involvement in the disease is the most common cause of mortality among SSc patients. Survival rates for SSc patients who develop PAH (SSc-PAH) range from 50–81% within the first year of diagnosis, making early detection vital. No specific biomarker for PAH has yet been identified, although many have been explored. Interleukin-32 (IL-32) — a pro-inflammatory cytokine (small proteins important in cell signaling) — surfaced as a candidate biomarker, because it is thought to regulate many of the activities of endothelial cells that line the pulmonary artery. Moreover, IL-32 is known to be activated in damaged vascular cells. Researchers at the University of L'Aquila, in Italy, analyzed whether IL-32 could be a new biomarker of PAH in SSc patients. The team tested the serum (blood) levels of 18 SSc-PAH patients, 21 SSc patients without PAH, 15 patients with idiopathic PAH (iPAH, meaning that the cause of PAH is unknown) and 14 healthy controls. Serum levels of IL-32 were significantly higher in SSc-PAH patients than in any of the other groups — 99.9 picograms per milliliter (pg/ml). In fact, IL-32 was nearly undetectable in SSc patients without PAH, as well as in healthy controls. In the iPAH group, the mean levels of IL-32 were of 62.1 pg/ml. IL-32 levels also correlated strongly with other measures of PAH, such as mean and systolic pulmonary arterial pressure (mPAP and sPAP, respectively), as measured by both right heart catheterization (RHC) and Doppler echocardiography, an ultrasound technique. RHC is a standard and reliable means of diagnosing PAH, but also is highly invasive, consisting of inserting a long tube (catheter) into the pulmonary artery. Researchers also found increased IL-32 levels in various skin cells of SSc patients with PAH, compared with those without PAH. In the case of one particular subset of SSc, called diffuse cutaneous SSc, the presence of these cells correlated with the modified Rodnan skin score (mRSS), a key measure of skin thickness used in evaluating SSc. Further analysis suggested that a cut-off value of 11.12 pg/ml for IL-32 could predict patients with PAH. Researchers concluded the results "suggested that sera determination of IL-32 may be a promising approach to evaluate the presence of PAH in SSc patients and together with longitudinal future studies could help to increase the understanding how these biomarkers mirror the vascular changes and the inflammatory process during SSc."  Forest Ray received his PhD in systems biology from Columbia University, where he developed tools to match drug side effects to other diseases. He has since worked as a journalist and science writer, covering topics from rare diseases to the intersection between environmental science and social justice. He currently lives in Long Beach, California. × Forest Ray received his PhD in systems biology from Columbia University, where he developed tools to match drug side effects to other diseases. He has since worked as a journalist and science writer, covering topics from rare diseases to the intersection between environmental science and social justice. He currently lives in Long Beach, California. Latest Posts  |
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