Relationship between parenchymal involvement and obstructive sleep apnea in subjects with sarcoidosis

IntroductionIncreased obstructive sleep apnea (OSA) incidence has been reported in sarcoidosis. However, no research has been conducted to determine the relation between OSA and pulmonary parenchymal involvement in sarcoidosis

Vocal Cord Paralysis and Hypercapnic Respiratory Failure in a Patient with Familial Amyloidotic Polyneuropathy

We herein report a patient case with familial amyloidotic polyneuropathy (FAP) who presented with vocal cord paralysis (VCP). A 60-year-old man with FAP (Gly89Gln) presented with hoarseness and snoring for the previous two years. A chest X-ray demonstrated cardiomegaly and bilateral diaphragmatic elevation. The findings of a restrictive pattern on spirometry and daytime hypercapnia were consistent with respiratory muscle weakness related to neuropathy [ forced expiratory volume (FEV1): 38%, forced vital capacity (FVC): 39%, FEV1/FVC: 77, partial pressure of arterial oxygen (PaO2): 80 mmHg, partial pressure of carbon dioxide in arterial blood (PaCO2): 52 mmHg]. An ear-nose-throat examination showed VCP. Polysomnography revealed severe obstructive sleep apnea (OSA). FAP may cause OSA by VCP and hypercapnic respiratory failure by respiratory muscle weakness. Therefore, an ear-nose-throat examination, spirometry, arterial blood gases analysis and polysomnography are important for these patients

Clinical Predictors of Obesity Hypoventilation Syndrome in Obese Subjects With Obstructive Sleep Apnea

BACKGROUND: Arterial blood gas (ABG) analysis is not a routine test in sleep laboratories due to its invasive nature. Therefore, the diagnosis of obesity hypoventilation syndrome (OHS) is underestimated. We aimed to evaluate the differences in subjects with OHS and pure obstructive sleep apnea (OSA) and to determine clinical predictors of OHS in obese subjects. METHODS: Demographics, body mass index (BMI), Epworth Sleepiness Scale score, polysomnographic data, ABG, spirometric measurements, and serum bicarbonate levels were recorded. RESULTS: Of 152 obese subjects with OSA (79 females/73 males, mean age of 50.3 +/- 10.6 y, BMI of 40.1 +/- 5.6 kg/m(2), 51.9% with severe OSA), 42.1% (n = 64) had OHS. Subjects with OHS had higher BMI (P = .02), neck circumference (P 27 mmol/L as the cutoff gives a satisfactory discrimination for the diagnosis of OHS (sensitivity of 76.6%, specificity of 74.6%, positive predictive value of 54.5%, negative predictive value of 88.9%). A nadir S-pO2 of = 27 mmol/L and/or a nadir S-pO2 of < 80% as a screening measure, only 3 of 64 subjects with OHS were missed. CONCLUSIONS: Serum bicarbonate level and nadir saturation were independent predictive factors for the diagnosis of OHS. (C) 2015 Daedalus Enterprise

Vocal Cord Paralysis and Hypercapnic Respiratory Failure in a Patient with Familial Amyloidotic Polyneuropathy

We herein report a patient case with familial amyloidotic polyneuropathy (FAP) who presented with vocal cord paralysis (VCP). A 60-year-old man with FAP (Gly89Gln) presented with hoarseness and snoring for the previous two years. A chest X-ray demonstrated cardiomegaly and bilateral diaphragmatic elevation. The findings of a restrictive pattern on spirometry and daytime hypercapnia were consistent with respiratory muscle weakness related to neuropathy [ forced expiratory volume (FEV1): 38%, forced vital capacity (FVC): 39%, FEV1/FVC: 77, partial pressure of arterial oxygen (PaO2): 80 mmHg, partial pressure of carbon dioxide in arterial blood (PaCO2): 52 mmHg]. An ear-nose-throat examination showed VCP. Polysomnography revealed severe obstructive sleep apnea (OSA). FAP may cause OSA by VCP and hypercapnic respiratory failure by respiratory muscle weakness. Therefore, an ear-nose-throat examination, spirometry, arterial blood gases analysis and polysomnography are important for these patients

Leptin and adiponectin levels in obstructive sleep apnea phenotypes

Objective: To examine the serum levels of leptin and adiponectin in different obstructive sleep apnea (OSA) phenotypes. Methods: Obese patients who were admitted to our sleep laboratory were included. All patients underwent spirometry, daytime arterial blood gas analysis, polysomnography and transthoracic echocardiography. Serum levels of adiponectin and leptin were recorded. Results: Analysis included 146 OSA patients (81 females, 65 males, age: 49.8 +/- 10.7 years, body mass index:40.3 +/- 4.9kg/m(2), 47.9% severe OSA, 42.5% severe obesity). Females had higher leptin and adiponectin levels (p<0.001;p<0.001, respectively). Leptin levels were higher in patients with severe obesity (p<0.001). Severe OSA patients had lower leptin and adiponectin levels (p=0.023;p=0.035, respectively). Conclusion: Adipokine levels were different especially in OSA patients with severe obesity, female gender and severe OSA

Fractional Exhaled Nitric Oxide Measurement in Pulmonary Hypertension: A Follow-Up Study

Pulmonary hypertension (PH) is a fatal disease although significant improvements in treatment are achieved. Easily implemented and noninvasive prognostic techniques are needed while following-up these patients. The aim was to investigate the role of fractional exhaled nitric oxide (FeNO) in follow-up for patients with PH. In this longitudinal study, patients with pulmonary arterial hypertension (PAH) and chronic thromboembolic PH (CTEPH) who were seen in PH Outpatient Clinic, Istanbul Faculty of Medicine, Istanbul University, were enrolled in the study. Echocardiography, 6-minute walking test, brain natriuretic peptide, and FeNO measurements were performed, and World Health Organization functional class was evaluated to all patients at baseline, and third, and sixth months. Right-heart catheterization and pulmonary function tests at the time of diagnosis were recorded. The study comprised 31 patients (23 women, 8 men; mean age: 53.4 +/- 17.1 years) with PAH (n = 19) and CTEPH (n = 12) and 80 healthy controls. Patients with PH had lower FeNO values than the control group (16.5 ppb vs 19.8 ppb; P < .05). Fractional exhaled nitric oxide values did not change during follow-up and did not correlate with other follow-up measures except tricuspid annular plane systolic excursion values. Fractional exhaled nitric oxide was higher in the idiopathic PAH subgroup at baseline and at third month than patients with PAH associated with other diseases. Fractional exhaled nitric oxide did not change in patients who had clinical deterioration. As a conclusion; Patients with PH had lower FeNO values than healthy controls, but FeNO did not change significantly during follow-up. Large-scale studies with prolonged follow-up periods are needed to understand the role of FeNO in the follow-up of the patients with PH