Stavros Tryfon

How common is sleep-disordered breathing in patients with idiopathic pulmonary fibrosis?

Background and aimThe frequency of obstructive sleep apnea–hypopnea syndrome (OSAHS) in patients with idiopathic pulmonary fibrosis (IPF) remains controversial. The aim of this study was to assess the frequency of OSAHS in newly diagnosed IPF patients and to identify possible correlations with body mass index and pulmonary function testing parameters.Materials and methodsThirty-four newly diagnosed IPF patients were included. All subjects underwent attended overnight PSG. None of the included subjects was under any of the currently available IPF treatments or nocturnal supplemental oxygen therapy.ResultsTotal apnea–hypopnea index (AHI) was <5, 5–15, and ≥15/h of sleep in 14 (41%), 15 (44%), and five patients (15%), respectively. REM AHI was statistically significant correlated with TLC [Total lung capacity] (p = 0.03, r = −0.38). Diffusing capacity of the lung for carbon monoxide was correlated with mean oxygen saturation during sleep (p = 0.02, r = 0.39).ConclusionsSleep-disordered breathing seems frequent, although remains usually under diagnosed in IPF patients. A decrease in TLC, reflecting the severity of pulmonary restriction, might predispose IPF patients in SDB, especially during the vulnerable REM sleep period.

Sleep Apnea Syndrome and Diastolic Blood Pressure Elevation during Exercise

Background: Several studies assessing the role of obstructive sleep apnea syndrome (OSAS) as an independent risk factor for hypertension have produced conflictingresults. Although the sleep apnea syndrome is associated with hypertension, there are no references regarding the blood pressure response of normotensive OSAS patients during exercise. Study Objectives: The aim of this study was to investigate the relationship between diastolic blood pressure (DBP) response during exercise and the severity of OSAS. Methods: We performed exercise testing a day after polysomnography in 17 normotensive males who were admitted for the first time because of OSAS and in 10 normal subjects who were members of the same families. During maximal incremental exercise test (bicycle ergometry) oxygen consumption (VO2) and the DBP were estimated at rest and at peak exercise. VO2 was also measured when DBP were 100 and 110 mm Hg. Results: At peak exercise DBP was significantly higher in OSAS patients (115.3 ± 9.2 mm Hg) than in normal subjects (101 ± 8.4 mm Hg, p < 0.01). OSAS patients reached a DBP of 110 mm Hg with a significantly lower VO2 than normal subjects (1,881.5 ± 703.4 vs. 1,972.3 ± 108.6 ml/min, p = 0.045). VO2 was not different between the two groups at a DBP of 100 mm Hg (1,211.2 ± 371.7 vs. 1,536.6 ± 267.2 ml/min, p = 0.089) but OSAS patients had a significantly lower heart rate than normals (111.2 ± 13 vs. 118.6 ± 27.6, p = 0.009). None of the aspects of quality of life, according to the Nottingham Health Profile Questionnaire, Part 1, were significantly different between patients and normal subjects. Conclusions: Normotensive OSAS patients develop DBP elevation at an earlier stage during exercise compared to normal subjects. This hypertensive response was not correlated with the severity (apnea-hypopnea index, oxygen desaturation parameters) of OSAS. DBP elevation could be a limiting factor of physical performance in this group of patients.

Hering-Breuer Reflex in Normal Adults and in Patients with Chronic Obstructive Pulmonary Disease and Interstitial Fibrosis

Background: It has been suggested that the Hering-Breuer reflex (HBR) is unimportant in adults during normal tidal breathing and that it is elicited only if tidal volume is increased above a certain critical threshold. Objective: The aim of this study was (1) to study the occurrence of the HBR in adults with normal pulmonary function and (2) to examine if changes in lung mechanics have any effect on the HBR. Methods: We examined 11 adults with normal pulmonary function, 8 patients with chronic destructive pulmonary disease (COPD) and 3 with interstitial fibrosis (IF). All subjects were lightly sedated with fentanyl, intubated and ventilated with a Servo-900 ventilator. Inspiratory and expiratory flow (and after integration, volume) and mouth pressure were recorded from the endotracheal tube with a pneumotachograph and a pressure transducer. Pressure support ventilation was applied in all patients and functional residual capacity (FRC) was measured with the N2 washout method. Mean (Temean) and maximal expiratory time (Temax) were determined for each individual for 20 breaths. Following several breaths to establish a stable baseline the airway was occluded at end inspiration by a shutter. A positive HBR was interpreted as longer Teocc than Temax (Teocc/Temax, %). Occlusion was maintained until negative airway pressure occurred and the occlusion time (Teocc) was measured. We attempted occlusions after the addition of 5 cm H2O positive end-expiratory pressure (PEEP) and subsequently with 10, 15 and 20 cm H2O PEEP. Teocc was measured of progressively larger lung volumes. To examine the HBR sensitivity in the three groups, we plotted the lung volumes of occlusion against the corresponding Teocc/Temax. Results: The ratio Teocc/Temax increased from 167.5 ± 82.5 at normal FRC to 474 ± 200.2 s (PEEP20). On the contrary, in patients with COPD, Teocc/Temax increased from 125.2 ± 34 to 193.7 ± 74.2 (p < 0.05). Conclusions: The HBR was positive in all subjects. COPD patients were found to be less sensitive to volume changes when compared with normal controls and with IF patients.

Sodium valproate as a cause of recurrent transudative pleural effusion: a case report

IntroductionThere are few reported cases of neutrophilic pleural effusions associated with valproic acid therapy. Most of them are of eosinophilic exudates with or without blood eosinophilia.Case presentationThis case study describes a 70-year-old man with recurrent episodes of eosinophilic transudative pleural effusions associated with sodium valproate treatment. The recurrence of effusion after re-administration of the drug is strongly suggestive of an association between them. To the best of our knowledge, this is the first reported case with a pleural effusion with these characteristics caused by sodium valproate.ConclusionThis is the first report in the literature, with a full understanding of the etiology but with an unknown drug mechanism. This case report is of interest to different medical specialists (such as pulmonologists, neurologists, cardiologists) and pharmacologists.

Penetration of azithromycin in experimental pleural empyema fluid.

There were no data about the extent of azithromycin penetration into the empyemic pleural fluid in humans and in experimental animals. An empyema was created via the intrapleural injection of an Escherichia coli solution into the pleural space of New Zealand white rabbits. After an empyema was verified by thoracocentesis, 24h post inoculation, azithromycin (15 mg/kg) was administered intravenously. Antibiotic levels were determined in samples of pleural fluid and blood serum, collected serially at 2, 8, 24, 48 and 72 h, after administration. Azithromycin levels were estimated using an HPLC analytical method with fluorimetric detection. Azithromycin penetrated well into the empyemic pleural fluid, exhibiting a slower onset and decline compared to the corresponding blood serum levels. Equilibration between pleural fluid and blood serum compartments seemed to occur at 2h, with peak pleural fluid levels (C(maxpf) of 0.48 microg/ml) occurring 24h post administration and decreasing thereafter. Azithromycin peak serum concentration (C(maxserum) of 0.24 microg/ml) was observed 2h after administration and, thereafter, serum antibiotic levels remained lower than the corresponding pleural fluid ones. The area under the concentration versus time curve (AUC) and terminal half-life (T(1/2)) of azithromycin was three- to six fold and twofold higher, respectively, in the pleural fluid compared to the blood serum compartment. After intravenous administration, azithromycin penetrated well into the empyemic pleural fluid, exhibiting pleural fluid levels that are inhibitory for most erythromycin-sensitive pathogens causing empyema.

Acute effect of smoking on plasma Obestatin levels

BackgroundSmoking and smoking cessation are considered to be associated with weight changes. We have recently shown that smoking acutely increases plasma levels of ghrelin, a known orexigenic hormone.Obestatin is a peptide encoded by the ghrelin gene, which opposes ghrelin effects on food intake. We conducted a study in adult volunteers measuring plasma levels of obestatin immediately after initiation of smoking.Methods31 volunteers (mean age 32.2 ± 9.2 years and mean BMI 25.7 ± 4.1), 17 smokers and 14 non-smokers, were enrolled in our study. The 2 groups were matched in age and BMI. Plasma obestatin concentrations were determined at baseline (T0), 2 (T2), 5 (T5), 15 (T15), and 60 (T60) minutes after the initiation of smoking.ResultsIn all 31 subjects, no significant difference in the mean values of plasma obestatin levels was observed from baseline at T2, T5, T15 and T60 after initiation of smoking (overall p = 0.15). However, a trend for higher obestatin levels was noted in smokers vs non-smokers (overall p = 0.069), which was not related to the pack-years.ConclusionOn the contrary with ghrelins response after smoking initiation, there is no such an acute response of plasma obestatin levels.

Pharmacokinetics of Linezolid and Ertapenem in experimental parapneumonic pleural effusion

ObjectiveTo determine the extent of linezolid and ertapenem penetration into the empyemic fluid using a rabbit model of empyema.MethodsAn empyema was created via the intrapleural injection of Escherichia coli bacteria (ATCC 35218) into the pleural space of New Zealand white rabbits. After an empyema was verified by thoracocentesis, 24 hours post inoculation, linezolid (10 mg/kg) and ertapenem (60 mg/kg) were administered intravenously into 10 and 8 infected empyemic rabbits, respectively. Antibiotic levels were determined in samples of pleural fluid and blood serum, collected serially at 1, 2, 4, 6 and 8 hours, after administration each of the two antibiotics.ResultsLinezolid as well as ertapenem penetrate well into the empyemic pleural fluid, exhibiting a slower onset and decline compared to the corresponding blood serum levels. Equilibration between blood serum and pleural fluid compartments seems to occur at 1.5 hours for both linezolid and ertapenem, with peak pleural fluid levels (Cmaxpf of 2.02 ± 0.73 «mu»g/ml and Cmaxpf of 3.74 ± 1.39 «mu»g/ml, correspondingly) occurring 2 hours post antibiotics administration and decreasing very slowly thereafter. The serum concentrations for both antibiotics were significantly lower from the corresponding pleural fluid ones during the 8 hours collecting data, with the exception of samples collected at the 1st hour (Cmaxserum of 2.1 ± 1.2 «mu»g/ml for linezolid and Cmaxserum of 6.26 ± 2.98 «mu»g/ml for ertapenem).ConclusionPleural fluid levels of both antibiotics are inhibitory for common specified pathogens causing empyema.

Excessive Muscle Paralysis Due to Pulmonary Carcinoid —A Case Report

We present the case of a 58-year-old woman with a renin secreting typical bronchopulmonary carcinoid. This patient showed hypotension, constipation and fatigue due to extensive hypokaliemia (K = 1.9 meq/L). Aldosterone (102.7 ng/100 mL) and renin (46 ng/mL) were excessively elevated at that time, but cortisol level was normal. Routine chest roentgenography and computed tomography revealed a nodular lesion in the upper left lung lobe, which was suspicious for a neurosecretory pulmonary tumor. The final diagnosis was made by using bronchoscopic procedures and the histologically diagnosis was compatible as a typical pulmonary carcinoid. The tumor was resected curatively, and the renin and aldosterone level became normal. A year after the patient looks healthy.

Successful management of drug-induced hypercapnic acidosis with naloxone and noninvasive positive pressure ventilation

A 74-year-old man was referred to our hospital due to deteriorating level of consciousness and desaturation. His Glasgow Coma Scale was 6, and his pupils were constricted but responded to light. Chest radiograph was negative for significant findings. Arterial blood gas evaluation on supplemental oxygen revealed severe acute on chronic respiratory acidosis: pH 7.15; PCO2, 133 mm Hg; PO2,64 mm Hg; and HCO3, 31 mmol/L. He regained full consciousness (Glasgow Coma Scale, 15) after receiving a 0.4 mg dose of naloxone, but because of persistent severe respiratory acidosis (pH 7.21; PCO2, 105 mm Hg), he was immediately commenced on noninvasive positive pressure ventilation (NIV) displaying a remarkable improvement in arterial blood gas values within the next few hours. However, in the days that followed, he remained dependent on NIV, and he was finally discharged on a home mechanical ventilation prescription. In cases of drug-induced respiratory depression, NIV should be regarded as an acceptable treatment, as it can provide ventilatory support without the increased risks associated with invasive mechanical ventilation.

Serratia pneumonia presenting as hemoptysis in a patient with sarcoidosis: a case report

Introduction Serratia marcescens is a Gram-negative bacillus which belongs to the family Enterobacteriaceae. It is a facultative anaerobe and produces red pigment at room temperature. It naturally occurs in soil and water as well as the intestines, and it is responsible for nosocomial infections. There have been few reports about community acquired pneumonia of Serratia. Case presentation This report presents a 37-year-old man with hemoptysis, fever, and shortness of breath. The clinical and laboratory examinations revealed that the patient had pseudohemoptysis due to S. marcescens pneumonia, on an immunocompromised pattern, because of the coexistence of sarcoidosis (stage 1). Conclusion Appropriate antibiotic therapy for Serratia was administered, and the patient’s symptoms regressed. The patient is healthy and asymptomatic after 1-year follow-up. To the best of the authors’ knowledge, this is the first reported case of a pseudohemoptysis in a patient with pulmonary sarcoidosis.