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skin rashes and eruptions.

Slide show: Common skin rashes - MayoClinic.com Slide show: Common skin rashes PREVIOUS| NEXT 1 | 2 | 3 | 4 | 5 | 6 | 7 | 8 | 9 | 10 | 11 | 12 | 13 Not usually serious, but sometimes painful Your skin is surprisingly resistant to a wide variety of assaults, but it's still susceptible to various invaders. Viruses, parasites, fungi, heat and medications can all cause skin rashes and eruptions. Though not life-threatening, rashes are often bothersome, uncomfortable or even painful. Some, such as heat rash and swimmer's itch, clear up on their own. Others, including rosacea and drug rashes, require medical treatment. Here's a look at common skin rashes, their causes and when you might need to see your doctor. return to Latex allergy Dec 23, 2004 © 1998-2006 Mayo Foundation for Medical Education and Research (MFMER). All rights reserved.  A single copy of these materials may be reprinted for noncommercial personal use only. "Mayo," "Mayo Clinic," "MayoClinic.com," "Mayo Clinic Health Information," "Reliable information for a healthier life" and the triple-shield Mayo logo are trademarks of Mayo Foundation for Medical Education and Research.  SN00016 slideshow About this site · Site help · Contact us · e-Newsletter · Site map Privacy policy updated Oct 7, 2005 Terms and conditions of use updated Jun 3, 2004 LEGAL CONDITIONS AND TERMS OF USE APPLICABLE TO ALL USERS OF THIS SITE. ANY USE OF THIS SITE CONSTITUTES YOUR AGREEMENT TO THESE TERMS AND CONDITIONS OF USE. © 1998-2006 Mayo Foundation for Medical Education and Research. All rights reserved. Mayo Clinic Medical Services | MayoClinic.com Bookstore Diseases & Conditions Drugs & Supplements Treatment Decisions Healthy Living Ask a Specialist Health Tools Home Log in Register now SKIN Educational grant provided by: Eucerin Advertising and sponsorship policy Jan 26, 2006

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Pulmonary arterial hypertension in patients with sleep apnoea syndrome -- Bady et al. 55 (11): 934 -- Thorax HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS Author Keyword(s) Vol Page [Advanced] This Article Abstract Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this link to a friend Similar articles in this journal Similar articles in PubMed Add article to my folders Download to citation manager Cited by other online articles Google Scholar Articles by Bady, E Articles by Laaban, J-P Articles citing this Article PubMed PubMed Citation Articles by Bady, E Articles by Laaban, J-P Related Collections Sleep Apnea Thorax 2000; 55 : 934-939( November ) Pulmonary arterial hypertension in patients with sleep apnoeasyndrome E Bady, A Achkar, S Pascal, E Orvoen-Frija, J-P Laaban Department ofPneumology, Hotel-Dieu, 75181 Paris Cedex 04, France Correspondence to: Professor J-PLaaban j-pierre.laaban{at}htd.ap-hop-paris.fr Received 19 April 1999 ; Returned to authors 9 July 1999 ; Revised version received 24 March 2000 ; Accepted for publication 25July 2000 Abstract Top Abstract Introduction Methods Results Discussion References BACKGROUND Pulmonaryarterial hypertension (PAH) in patients with sleep apnoea syndrome(SAS) is classically ascribed to associated chronic obstructivepulmonary disease (COPD). The aim of this retrospective study was toevaluate the possible occurrence of PAH as a complication of SAS inpatients without COPD. METHODS Right heartcatheterisation was performed in 44 patients with SAS and without COPDconfirmed by polysomnography (apnoea index >5/h) admitted for theadministration of nasal continuous positive airway pressure (CPAP). RESULTS PrecapillaryPAH, defined as mean pulmonary arterial pressure of >20 mm Hg withpulmonary capillary wedge pressure <15 mm Hg, was observed in 12/44(27%) patients with SAS. There were no significant differences inapnoea index between patients with (PAH+) and those without PAH (PAH-)(42.6 (26.3) versus 35.8 (21.7) apnoeas/h). The PAH+ group differedsignificantly from the PAH- group in the following respects: lowerdaytime arterial oxygen tension (Pa O 2 ) (9.6 (1.1) versus 11.3 (1.5) kPa, p=0.0006); higher daytime arterial carbondioxide tension (Pa CO 2 ) (5.8 (0.5) versus 5.3 (0.5) kPa, p=0.002); more severe nocturnal hypoxaemia with a higherpercentage of total sleep time spent at Sa O 2 <80% (32.2 (28.5)% versus 10.7 (18.8)%, p=0.005); and higher bodymass index (BMI) (37.4 (6) versus 30.3 (6.7) kg/m 2 ,p=0.002). The PAH+ patients had significantly lower values of vitalcapacity (VC) (87 (14)% predicted versus 105 (20)% predicted, p=0.005), forced expiratory volume in one second (FEV 1 ) (82 (14)% predicted versus 101 (17)% predicted, p=0.001), expiratoryreserve volume (40 (16)% predicted versus 77 (41)% predicted,p=0.003), and total lung capacity (87 (13)% predicted versus 98 (18)%predicted, p=0.04). Stepwise multiple regression analysis showed thatmean pulmonary artery pressure (PAPm) was positively correlated with BMI and negatively with Pa O 2 . CONCLUSION Pulmonaryarterial hypertension is frequently observed in patients with SAS, evenwhen COPD is absent, and appears to be related to the severity ofobesity and its respiratory mechanical consequences. ( Thorax 2000; 55: 934-939) Keywords: sleep apnoea syndrome; pulmonary arterialhypertension; obesity Introduction Top Abstract Introduction Methods Results Discussion References It has been shown that sleep apnoeas may induce acute pulmonaryhypertension, the main mechanism being hypoxia related pulmonary vasoconstriction. 1 2 Other contributing factors arehypercapnia induced pulmonary vasoconstriction and exaggerated negativeintrathoracic pressure during obstructive apnoeas. 3 However, the prevalence of sustained precapillary pulmonary arterialhypertension (PAH) in patients presenting with sleep apnoea syndrome(SAS) varies from 10% to 79%. 4-7 Most authors claimthat nocturnal apnoea cannot induce permanent PAH and that PAH inpatients with SAS is related to an associated obstructive ventilatorydefect. However, a few recent studies have produced different resultswhich suggest a direct link between nocturnal apnoea and daytime PAH. These discrepancies can be interpreted in many ways. Firstly, themethods for assessing PAH vary between studies, ranging from rightheart catheterisation to echocardiography or simple clinicalevaluation. 5-8 In some studies pulmonary capillary wedge pressure was not measured when right heart catheterisation was performed, and this could lead to an overestimation of the prevalence of precapillary PAH. 9 The other causes of precapillary PAH such as thromboembolic disease and the use of appetite suppressants have not necessarily been excluded. Most of the published studies didnot exclude patients with chronic obstructive pulmonary disease (COPD),a major cause of PAH. Only three studies assessing the prevalence ofPAH in SAS have excluded patients with associated COPD. 6 10 11 Weber etal 10 reported a 10% prevalence of PAH in 89 patients with SAS without COPD using right heart catheterisation fordiagnosis of PAH. Sanner etal 11 reported a prevalence of 20% using rightheart catheterisation, but almost half of the patients with PAH hadsimultaneously increased pulmonary capillary wedge pressure. Sajkov et al 6 observed a PAHprevalence of 41% in patients with SAS without obstructive ventilatorydefect, but the patient numbers were very small (n=27) and thediagnosis of PAH was based on echocardiography Döppler measurementswhich are known to be limited in the diagnosis of moderate PAH. This study was undertaken to evaluate the prevalence of precapillarypulmonary hypertension using haemodynamic measurements in patients withSAS without COPD, and to clarify the mechanisms of PAH in such patients. Methods Top Abstract Introduction Methods Results Discussion References STUDY GROUP Sixty nine patients with SAS consecutively admitted for theadministration of nasal continuous positive airway pressure (nCPAP) were considered for inclusion in the study. Inclusion criteria The study patients were recruited from a patient population withSAS confirmed by prior polysomnographic evaluation with an apnoea index(AI) of >5 apnoeas/h. The indications for nCPAP were as follows: AI>20/h and/or apnoea-hypopnoea index (AHI) of >30/h and/or profoundnocturnal desaturation and/or severe daytime sleepiness. In thesepatients arterial blood gas analysis, lung function tests, and rightheart catheterisation were performed to assess cardiorespiratory complications of SAS. Exclusion criteria The following exclusion criteria were applied: obstructiveventilatory defect defined as forced expiratory volume in one second (FEV 1 ) of <70% predicted and an FEV 1 /vitalcapacity (VC) ratio of <60%; any restrictive ventilatory defect otherthan those related to obesity (pulmonary fibrosis, sequelae ofpulmonary tuberculosis, or chest wall defect disease); associateddisease potentially responsible for PAH such as the use of appetitesuppressants or a clinical history of venous thromboembolic disease;bronchopulmonary infection or cardiac or respiratory failure in theprevious two months; and mixed or postcapillary PAH identified byhaemodynamic measurements (pulmonary capillary wedge pressure 15 mm Hg). A total of 25 patients were excluded from the study (eight with COPD,three with prior use of anorexigens, four with prior venousthromboembolism, three who refused catheterisation, one in whomcatheterisation was unsuccessful, and six with postcapillary PAH),leaving 44 patients for inclusion in the study. POLYSOMNOGRAPHY An overnight polygraphic sleep study was carried out in the sleeplaboratory using standard recording techniques with the Alvarpolygraphic recorder (Medical Equipment International, Lyon, France)and Nightingale software (Deltamed, Paris, France). Sleep was monitoredby electroencephalography, electro-oculography, and chin electromyography. Air flow was recorded with an oronasal thermistor. Apnoeas were definedas cessation of air flow for at least 10 seconds. AI was calculated asthe number of apnoeas per hour of sleep. The type of apnoea(obstructive, central or mixed) was defined by analysis ofthoracoabdominal movements which were recorded by respiratory inductiveplethysmography using a mercury strain gauge (Volucapt). Thetransducers were placed around the chest and abdomen. Arterialoxyhaemoglobin saturation (Sa O 2 ) was recorded with a pulse oximeter (Oxyshuttle, Sensor Medics). The following oxyhaemoglobin desaturation parameters were measured: (1)minimal Sa O 2 ; (2) percentage of total sleeptime (TST) spent at Sa O 2 <90%(TST-Sa O 2 <90%); (3) percentage of TST spent at Sa O 2 <80%(TST-Sa O 2 <80%). RIGHT HEART CATHETERISATION Right heart catheterisation was carried out in all patientsthrough the basilic vein under fluoroscopic control. The venous puncture was made by means of an 18 gauge needle according to theSeldinger's technique, followed by local anaesthesia and skin incisionin order to facilitate insertion of the introducer. An introducer withan 8 French gauge was used for a 7 French gauge Swan-Ganz catheter(Baxter model 131 F7). The catheter was pushed forward under control ofthe pressure curve until it reached the right ventricle. The balloonwas then inflated and the catheter pushed into the pulmonary arteryunder fluoroscopy. The patients rested for 30 minutes after placement of the catheter inthe pulmonary artery before the measurements were taken. After checkingthe baseline values the pressure curves were recorded using a Sirecust1281 Siemens monitor under constant electrocardiographic monitoring.End expiratory pressures were recorded and occlusion pulmonary arterypressure was obtained after fully inflating the distal balloon. Cardiac output was measured using the thermodilution technique with theballoon deflated and the tip of the catheter positioned in thepulmonary artery. The measurements were taken at room temperature bymanually injecting 10 ml of 5% dextrose in water for less than fourseconds using a Baxter American Edwards type COM-1 cardiac outputmonitor. The average of three recorded values with a variability ofless than 10% was recorded. The following parameters were measured: mean right atrial pressure(RAP), systolic pulmonary artery pressure (PAPs), diastolic pulmonaryartery pressure (PAPd), mean pulmonary artery pressure (PAPm), meanpulmonary capillary wedge pressure (PCP), and cardiac output (CO). PAPmwas measured by electronic averaging. Cardiac index (CI) and pulmonaryvascular resistances (PVR) were calculated using standard equations: CI (l/mn/m 2 ) = CO/total body surface PVR (IU/m 2 ) = PAPm PCP/CI Pulmonary arterial hypertension was defined as PAPm of >20 mm Hg.This cut off value was chosen because it has been used in previousstudies to evaluate the presence of chronic PAH in patients withSAS. 7 9 11 12 Precapillary pulmonary hypertension wasdefined as PAPm >20 mm Hg associated with a PCP of <15 mm Hg. ARTERIAL BLOOD GAS ANALYSIS An arterial blood sample was taken during daytime wakefulness withthe patient in a semi-recumbent position. The sample was analysed bymeans of IL 1306 or BG (Instrumentation Laboratory, Milano, Italy). LUNG FUNCTION TESTS Pulmonary volumes and flows were measured using a wet spirometer(Pulmonet III; Sensormedics Inc, Anheim, CA, USA) and the results wereexpressed as percentages of reference values. 13 ANTHROPOMETRIC MEASUREMENTS Body weight (kg) and height (m) were measured and body mass index(BMI) was calculated as body weight/height 2 (kg/m 2 ). STATISTICAL ANALYSIS The results are presented as mean (SD) values and as percentages.Mean values were compared in patients with PAH (PAH+) and those withoutPAH (PAH-) using the Student's t test andpercentages were compared in the two groups using the 2 test. Univariate analyses were performed to observe correlations between PAPm and all the anthropometric parameters, lung function data,arterial blood gas tensions, and polysomnographic parameters. Finally, multivariate stepwise analysis was made using Statview 4.2 software. Results Top Abstract Introduction Methods Results Discussion References Pulmonary arterial hypertension was present in 12 of the 44 patients (27%) with SAS. The overall PAPm was 20 (6.6) mm Hg; in thePAH+ group it was 28.5 (6.2) mm Hg. The results of the haemodynamicstudy are given in table 1 . View this table: [in this window] [in a new window] Table 1 Haemodynamic data There was no significant difference between the PAH+ and PAH- groupswith regard to age, sex ratio, height and smoking history (table 2 ).However, patients in the PAH+ group were significantly heavier thanthose in the PAH- group (113.6 (20.4) kg versus 87.6 (18.3) kg).Body mass index was also significantly higher in the PAH+ than in thePAH- group (37.4 (6.0) kg/m 2 versus 30.3 (6.7) kg/m 2 ). View this table: [in this window] [in a new window] Table 2 General characteristics of the studypatients Arterial blood gas tensions are shown in table 3 .Pa O 2 was significantly lower in patients in thePAH+ group than in those in the PAH- group (9.6 (1.1) kPa versus 11.3 (1.5) kPa). The PAH+ group also had a significantly higherPa CO 2 than the PAH- group (5.8 (0.5) kPaversus 5.3 (0.5) kPa). The percentage of patients with hypoxaemia(Pa O 2 <9.3 kPa) was significantly higher inthe PAH+ group (33.3% versus 3.1%). It is noteworthy that none of thepatients in this series had severe hypoxaemia(Pa O 2 <8 kPa). No significant difference wasseen in the percentage of patients with hypercapnia(Pa CO 2 6 kPa) between the two groups and no patient had Pa CO 2 of >6.6 kPa. In the PAH+group all the patients with hypoxaemia and/or hypercapnia had a bodymass index exceeding 30 kg/m 2 and an FEV 1 /VCratio of over 70%. View this table: [in this window] [in a new window] Table 3 Arterial blood gas data Table 4 shows the results of the lung function tests. Significantlylower values of VC, FEV 1 , expiratory reserve volume (ERV), and total lung capacity (TLC) were observed in the PAH+ group than inthe PAH- group. The two groups showed no significant difference inFEV 1 /VC ratio (73 (7)% versus 75 (7)%). A mild decreasein FEV 1 /VC (ranging from 60% to 75%) was observed inthree patients in the PAH+ group and in five patients in the PAH-group, without any significant difference. The lowestFEV 1 /VC ratio was 68% in the PAH+ group and 66% in thePAH- group. The residual volume (RV) did not differ significantlybetween the two groups. View this table: [in this window] [in a new window] Table 4 Lung function data Polysomnographic data are presented in table 5 . No significantdifference was seen between the two groups in the apnoea index (42.6 (26.3) in the PAH+ group and 35.8 (21.7) in the PAH- group) or in theapnoea-hypopnoea index (53.4 (25) in the PAH+ group and 43.3 (22.9) inthe PAH- group). Minimal oxyhaemoglobin saturation was significantlylower in the PAH+ group and the percentages of TST spent atSa O 2 <90% and <80% were significantlyhigher in the PAH+ group than in the PAH- group. The maximalSa O 2 at the beginning of the night wassignificantly lower in the PAH+ group than in the PAH-group. View this table: [in this window] [in a new window] Table 5 Polysomnographic data Table 6 shows the results of the significant correlations found inunivariate analysis between PAPm and each of the anthropometric, lungfunction, and polysomnographic parameters. Significant positive correlations were observed between PAPm and body weight, BMI, % TST-Sa O 2 <90%, % TST-Sa O 2 <80%, andPa CO 2 (fig 1 ). Significant negativecorrelations were observed between PAPm and minimal nocturnal Sa O 2 , maximal nocturnalSa O 2 , VC, FEV 1 , ERV, andPa O 2 (fig 2 ). No correlation was found betweenPAPm and apnoea index or apnoea-hypopnoea index (fig 3 ). View this table: [in this window] [in a new window] Table 6 Significant linear correlationsbetween mean pulmonary artery pressure and anthropometric, sleep, andrespiratory parameters View larger version (14K): [in this window] [in a new window] Figure 1 Correlation between mean pulmonary artery pressure(PAPm) and body mass index (BMI); r = 0.50, p = 0.0006. View larger version (16K): [in this window] [in a new window] Figure 2 Correlation between mean pulmonary artery pressure(PAPm) and expiratory reserve volume (ERV); r = -0.40, p = 0.007. View larger version (14K): [in this window] [in a new window] Figure 3 Absence of significant correlation between meanpulmonary artery pressure (PAPm) and apnoea-hypopnoea index (AHI). Multivariate analysis showed that PAPm correlated positively with BMIand negatively with Pa O 2 with the followingcorrelation equations: PAPm = 0.46 × BMI + 5.06 ( r = 0.50, p = 0.0006, 95% CI of slope 0.21 to 0.71) PAPm = -0.3 × Pa O 2 + 44.81 ( r = -0.55, p = 0.0002, 95% CI of slope-0.45 to -0.16) Discussion Top Abstract Introduction Methods Results Discussion References The results of this study show that precapillary PAH was presentin 27% of a group of 44 patients without COPD presenting with severeSAS requiring nCPAP. The FEV 1 /VC ratio was in the normalrange and did not differ between patients with or without PAH, whichsuggests that an obstructive ventilatory defect involving the largeairways is probably not a major contributing factor in the pathogenesisof PAH. Pulmonary arterial hypertension in our patients is notexplained by a moderate obstructive ventilatory defect, unlike thepatients studied by Weitzenblum etal 5 and Chaouat etal 7 in whom a moderate obstructive ventilatorydefect was present which may have contributed to the development of PAH. Our patients had moderate pulmonary hypertension with PAPm of 28.5 (6.2) mm Hg which is commonly reported by other authors. According tothe literature, the PAPm of patients presenting with SAS and PAH rangesbetween 25 and 30 mm Hg. 7 9 10 The prevalence of PAH in our series was 27%, which is markedly lowerthan that of about 60% reported in earlier publications. 4 This difference is probably explained by the large number of patients with overlap syndrome in those series. Weitzenblum et al 5 found a prevalence ofPAH of 20% measured by right heart catheterisation in a study of 46 patients presenting with SAS and a moderate obstructive ventilatorydefect (FEV 1 = 2510 (780) ml). Only Sajkov et al , 6 Weber et al , 10 and Sanner et al 11 excluded patients withCOPD and the prevalence of PAH in their SAS patients was 41%, 10%, and 20%, respectively. The study by Weber etal 10 is only published as an abstract so details ofthe methodology are not available. Sajkov etal 6 measured PAP by Döppler echocardiographywhich is not a very reliable method for diagnosing moderate pulmonary hypertension, and Sanner etal 11 did not differentiate between precapillary andpostcapillary pulmonary arterial hypertension. Our results are more valid as PAP was measured by right heartcatheterisation, precapillary PAH was confirmed by excluding increasedPCP and because, unlike the other studies, subjects with other causesof precapillary PAH such as thromboembolic disease, the use of appetitesuppressants, and coexisting COPD were also excluded. However, ourstudy population is not representative of all patients with sleepapnoea as it included patients with severe SAS requiring nCPAP. Ourresults cannot be extended to patients with less severe SAS. As in most studies, we did not find any link between the severity ofSAS, expressed as the AI or AHI, and the presence of pulmonary hypertension. Similar to other studies, we found the daytimePa O 2 to be significantly lower in the PAH+ thanin the PAH- group. Such hypoxaemia was mostly related to associatedmoderate COPD in the other studies. Daytime hypoxaemia in our study wasobserved in the absence of even moderate COPD. Daytime hypoxaemia inour PAH+ group was moderate (9.6 (1.1) kPa) and none of our patientshad a Pa O 2 of <8 kPa. Daytime hypoxaemia wasnot sufficiently severe in our patients solely to explain thedevelopment of PAH. Thus, in patients with COPD, PAH usually developsonly in those with a severe obstructive ventilatory defect(FEV 1 <1000 ml) and marked daytime hypoxaemia (Pa O 2 <8 kPa). The cause of daytimehypoxaemia in our patients was obviously obesity which was more severein the PAH+ group. Moreover, all the patients with PAH and hypoxaemiawere obese. Nocturnal hypoxaemia was more severe in the PAH+ group than in thePAH- group, although the AI and AHI did not differ between the twogroups. Obesity and its ventilatory consequences (decreased ERV, VC,and TLC) were significantly more severe in the PAH+ group than in thePAH- group and this presumably accounts for the more severe nocturnaldesaturation observed in the former group. It has been shown that theseverity of desaturation during nocturnal apnoeas correlates well withthe degree of obesity 14 and with the resulting changes inpulmonary function, especially the decrease in ERV. 15 The lower values of maximal Sa O 2 at thebeginning of the night in the PAH+ group may also account for the moresevere nocturnal hypoxaemia in the PAH+ group. Indeed, lying supine hasbeen shown to result in a sharp decrease in ERV in obese patients and aworsening of ventilation-perfusion mismatch. 14 The role of obesity as an aetiological factor in the pathogenesis ofpulmonary hypertension in SAS has been much debated. Weitzenblum et al 5 and Krieger et al 16 did not find anysignificant difference in body weight in patients with and without PAH.In two more recent studies Laks etal 9 and Chaouat etal 7 found that PAH+ patients had a higher BMI thanPAH- patients. This difference was statistically significant only inthe study by Chaouat et al , but thesuggested predictive equation of PAP took no account of BMI. The main mechanism of PAH in our patients is probably the greaterseverity of nocturnal hypoxaemia during apnoeas which induces vasoconstriction in small size pulmonary arteries, resulting in transitory peaks of PAH concomitant with apnoeas. 17 Theseverity and duration of nocturnal desaturations probably leads toremodelling and restructuring of the walls of the pulmonary arteriolesresulting in permanent daytime pulmonary hypertension. This has beendemonstrated in rats submitted to intermittent hypoxia for 4-8 hoursper day. 18 In a necropsy study on 20 obese subjects, halfof whom had presented with SAS, Ahmed etal 19 found muscularisation of arterioles with adiameter of <100 µm and moderate hypertrophy of muscle cells of thepulmonary arterial media. Our hypothesis is that more severe andprolonged nocturnal desaturation may result in remodelling of pulmonaryarterial walls which ultimately leads to permanent PAH. It has been shown that inter-individual differences in the magnitude ofthe pulmonary vascular response to hypoxia may account for the variabledevelopment of chronic pulmonary hypertension in subjects exposed tohigh altitude. 20 Marked inter-subject differences in thepulmonary pressure responses have been also reported in normalsubjects, in patients with COPD, and in patients withSAS. 21 22 In a recent study Sajkov etal 23 showed that the occurrence of PAH in patientswith SAS was associated with an increased pulmonary vascular responseto hypoxia. One may therefore speculate that repeated increases in PAPduring sleep apnoea may lead to pulmonary vascular remodelling andchronic PAH in patients with a genetically determined exaggeratedpressor response to hypoxia. This study shows that SAS may be complicated by PAH in the absence ofCOPD and severe daytime hypoxaemia. Our data do not support thehypothesis that sleep apnoea is an independent risk factor in thedevelopment of PAH. We have also shown that the severity of obesity andthe associated changes in lung function play an important part in thepathogenesis of PAH in patients with SAS. References Top Abstract Introduction Methods Results Discussion References 1. Tilkian AG,Guilleminault C,Schroeder JS, et al . Hemodynamics in sleep-induced apnea. Ann Intern Med 1976; 85 :714-719 [Medline] . 2. Bonsignore MR,Marrone O,Insalaco G, et al . The cardiovascular effects of obstructive sleep apnoeas: analysis of pathogenic mechanisms. Eur Respir J 1994; 7 :786-805 [Abstract/ Free Full Text] . 3. Bradley TD. Right and left ventricular functional impairment and sleep apnea. Clin Chest Med 1992; 13 :459-479 [Medline] . 4. Fletcher EC,Schaaf JW,Miller J, et al . Long-term cardiopulmonary sequelae in patients with sleep apnea and chronic lung disease. Am Rev Respir Dis 1987; 135 :525-533 [Medline] . 5. Weitzenblum E,Krieger J,Apprill M, et al . Daytime pulmonary hypertension in patients with obstructive sleep apnea syndrome. Am Rev Respir Dis 1988; 138 :345-349 [Medline] . 6. Sajkov D,Cowie RJ,Thornton AT, et al . Pulmonary hypertension and hypoxemia in obstructive sleep apnea syndrome. Am J Respir Crit Care Med 1994; 149 :416-422 [Abstract] . 7. Chaouat A,Weitzenblum E,Krieger J, et al . Pulmonary hemodynamics in the obstructive sleep apnea syndrome. Results in 220 consecutive patients. Chest 1996; 109 :380-386 [Abstract/ Free Full Text] . 8. Bradley TD,Rutherford R,Grossman RF, et al . Role of daytime hypoxemia in the pathogenesis of right heart failure in the obstructive sleep apnea syndrome. Am Rev Respir Dis 1985; 131 :835-839 [Medline] . 9. Laks L,Lehrhaft B,Grunstein RR, et al . Pulmonary hypertension in obstructive sleep apneoa. Eur Respir J 1995; 8 :537-541 [Abstract/ Free Full Text] . 10. Weber K,Podszus T,Krupp O, et al . Prevalence of pulmonary hypertension (PH) in patients with obstructive sleep apnea. Sleep Res 1990; 19 :308 (abstract). 11. Sanner BM,Doberauer C,Konermann M, et al . Pulmonary hypertension in patients with obstuctive sleep apnea syndrome. Arch Intern Med 1997; 157 :2483-2487 [Abstract] . 12. Kessler R,Chaouat A,Weitzenblum E, et al . Pulmonary hypertension in the obstructive sleep apnoea syndrome: prevalence, causes and therapeutic consequences. Eur Respir J 1996; 9 :787-794 [Abstract/ Free Full Text] . 13. Quanjer PH. Standardized lung function testing. Bull Eur Physiopathol Respir 1983; 19 :1-95 [Medline] . 14. Series F,Cormier Y,La Forge J. Role of lung volumes in sleep apnoea-related oxygen desaturation. Eur Respir J 1989; 2 :26-30 [Abstract] . 15. Ray CS,Sue DY,Bray G, et al . Effects of obesity on respiratory function. Am Rev Respir Dis 1983; 128 :501-506 [Medline] . 16. Krieger J,Sforza E,Apprill M, et al . Pulmonary hypertension, hypoxemia, and hypercapnia in obstructive sleep apnea patients. Chest 1989; 96 :729-737 [Abstract] . 17. Coccagna G,Mantovani M,Brignani F, et al . Continuous recording of the pulmonary and systemic arterial pressure during sleep in syndromes of hypersomnia with periodic breathing. Bull Eur Physiopathol Respir 1972; 8 :1159-1172 . 18. Kay JM,Suyama KL,Keane PM. Effect of intermittent normoxia on muscularization of pulmonary arterioles induced by chronic hypoxia in rats. Am Rev Respir Dis 1981; 123 :454-458 [Medline] . 19. Ahmed Q,Chung-Park M,Tomashefski J. Cardiopulmonary pathology in patients with sleep apnea/obesity hypoventilation syndrome. Hum Pathol 1997; 28 :264-269 [Medline] . 20. Krieger BP,de la Hoz RE. Altitude-related pulmonary disorders. Crit Care Clin 1999; 15 :265-280 [Medline] . 21. Weitzenblum E,Schrijen F,Mohan-Kumar T, et al . Variability of the pulmonary vascular response to acute hypoxia in chronic bronchitis. Chest 1988; 94 :772-778 [Abstract] . 22. Laks L,Lehrhaft B,Grunstein RR, et al . Pulmonary artery pressure response to hypoxia in sleep apnea. Am J Respir Crit Care Med 1997; 155 :193-198 [Abstract] . 23. Sajkov D,Wang T,Saunders NA, et al . Daytime pulmonary hemodynamics in patients with obstructive sleep apnea without lung disease. Am J Respir Crit Care Med 1999; 159 :1518-1526 [Abstract/ Free Full Text] . © 2000 by Thorax This article has been cited by other articles: ( Search Google Scholar for Other Citing Articles ) R. J. Barst, M. McGoon, A. Torbicki, O. Sitbon, M. J. Krowka, H. Olschewski, and S. Gaine Diagnosis and differential assessment of pulmonary arterial hypertension J. Am. Coll. Cardiol., June 16, 2004;43(12_Suppl_S):40S - 47S. [Abstract] [Full Text] [PDF] J. Zielinski Effects of intermittent hypoxia on pulmonary haemodynamics: animal models versus studies in humans Eur. Respir. J., January 1, 2005;25(1):173 - 180. [Abstract] [Full Text] [PDF] E. Weitzenblum and A. Chaouat Hypoxic pulmonary hypertension in man: what minimum daily duration of hypoxaemia is required? Eur. Respir. J., August 1, 2001;18(2):251 - 253. [Full Text] [PDF] C. W. Atwood Jr, D. McCrory, J. G. N. Garcia, S. H. Abman, and G. S. Ahearn Pulmonary Artery Hypertension and Sleep-Disordered Breathing: ACCP Evidence-Based Clinical Practice Guidelines Chest, July 1, 2004;126(1_suppl):72S - 77S. [Abstract] [Full Text] [PDF] D. S. Hui, F. W. Ko, J. P. Fok, M. C. Chan, T. S. Li, B. Tomlinson, and G. Cheng The Effects of Nasal Continuous Positive Airway Pressure on Platelet Activation in Obstructive Sleep Apnea Syndrome Chest, May 1, 2004;125(5):1768 - 1775. [Abstract] [Full Text] J. o-D. L. Lattimore, D. S. Celermajer, and I. Wilcox Obstructive sleep apnea and cardiovascular disease J. Am. Coll. Cardiol., May 7, 2003;41(9):1429 - 1437. [Abstract] [Full Text] [PDF] S. Boyer and V. Kapur Obstructive Sleep Apnea: Its Relevance in the Care of Diabetic Patients Clin. Diabetes, July 1, 2002;20(3):126 - 132. [Abstract] [Full Text] [PDF] J. W. H. Fung, T. S. T. Li, D. K. L. Choy, G. W. K. Yip, F. W. S. Ko, J. E. Sanderson, and D. S. C. Hui Severe Obstructive Sleep Apnea Is Associated With Left Ventricular Diastolic Dysfunction Chest, February 1, 2002;121(2):422 - 429. [Abstract] [Full Text] [PDF] This Article Abstract Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this link to a friend Similar articles in this journal Similar articles in PubMed Add article to my folders Download to citation manager Google Scholar Articles by Bady, E Articles by Laaban, J-P Articles citing this Article PubMed PubMed Citation Articles by Bady, E Articles by Laaban, J-P Related Collections Sleep Apnea HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

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