Changes in pulmonary function in hyperbaric chamber inside attendants: a case-control study.

BACKGROUND: Inside attendants (IAs) [are] exposed to high pressure during hyperbaric oxygen (HBO2) therapy. The aim of this study was to evaluate the alterations of pulmonary functions in IAs over time. METHODS: IAs in our hyperbaric center constituted the IA group (n=11). A sex- and age-matched control group (n=15) was constituted from hospital staff who had not dived or been exposed to hyperbaric environments before. We measured the respiratory function of all subjects at two time points: 1) at the start of the study; and 2) 12 months after the first measurement. The following parameters were recorded: forced vital capacity (FVC), forced expiratory volume in one second (FEV1), rate of FEV1 to FVC (FEV1/FVC%), forced expiratory flow at 25% to 75% vital capacity (FEF25-75%), forced expiratory flow at 50% vital capacity (FEF50%), forced expiratory flow at 25% vital capacity (FEF25%). RESULTS: Both groups were similar in terms of age, sex, smoking and body mass index. We found that FEV1, FEV1/FVC%, FEF25-75% and FEF50% significantly reduced in both groups after 12 months (p⟨0.05). However, the rate of change in all parameters was similar in both groups (p⟩0.05). In the IA group, the total number of exposures within the 12 months was positively correlated with the rate of reduction in FEF25% (r=0.788, p=0.004). CONCLUSION: Working as an IA does not deteriorate pulmonary function in the short term. However, there is a need for long-term follow-up studies.

Omalizumab as a steroid-sparing agent in chronic eosinophilic pneumonia.

Chronic eosinophilic pneumonia (CEP) is an idiopathic eosinophilic pulmonary disease characterized by an abnormal and marked accumulation of eosinophils in the lung. Common presenting complaints include cough, fever, dyspnea, wheezing, and night sweats. Common laboratory abnormalities are peripheral blood and BAL eosinophilia. The pathognomonic radiographic finding is bilateral peripheral infiltrates. Corticosteroids are the mainstay of therapy, and dramatic improvement follows treatment. Relapses are common, and most patients require prolonged therapy. Side effects associated with chronic corticosteroid therapy must be monitored. Our case was that of a 36-year-old woman who had characteristic clinical and radiologic features. She was treated with corticosteroids but she needed prolonged therapy, and side effects occurred. Because the patient had high IgE levels and a positive skin prick test result, we used omalizumab for the treatment. The patient responded well. To our knowledge, this is the first CEP case in the literature successfully treated with omalizumab.

Serum chitotriosidase activity in pulmonary tuberculosis: response to treatment and correlations with clinical parameters.

BACKGROUND: Chitotriosidase is an accepted marker of macrophage activation. In this study, we investigated serum chitotriosidase levels in pulmonary tuberculosis (PTB). METHODS: Forth-two patients with PTB and 30 healthy subjects were enrolled in the study. The radiological extent of PTB, radiological sequela after treatment, and the degree of smear positivity were assessed. Chitotriosidase levels were measured by a fluorometric method. RESULTS: The serum chitotriosidase levels of the PTB patients were significantly higher than those of the control subjects (39.73±24.97 vs. 9.63±4.55 nmol/mL/h, P<0.001). After completion of the standard 6-month antituberculous treatment, chitotriosidase levels in PTB patients significantly decreased (10.47±4.54 nmol/mL/h, P<0.001). Chitotriosidase levels correlated significantly with the radiological extent of PTB, degree of smear positivity, and post-treatment radiological sequela score (r=0.439, r=0.449, and r=0.337, respectively). CONCLUSIONS: This study demonstrated that serum chitotriosidase levels increase in PTB; therefore, chitotriosidase can be used as a marker of disease activity, severity, and response to treatment.

Serum lactate dehydrogenase levels significantly correlate with radiological extent of disease and spirometric values in patients with silicosis due to denim sandblasting.

BACKGROUND: The aim of the present study was to investigate serum lactate dehydrogenase (LD) levels in patients with silicosis due to denim sandblasting (SDDS) and also to investigate possible correlations between serum LD levels and the degree of radiological extent of disease (RED) and pulmonary function tests. METHODS: Forty-four males with SDDS and 32 healthy male subjects were included in the study. Patients and healthy controls were compared for serum LD levels. Correlations between serum LD levels, RED and spirometric values were investigated. RESULTS: Patients with SDDS had significantly higher serum LD levels than healthy controls. Patients with complicated SDDS had significantly higher serum LD levels than patients with simple SDDS. Significant correlations were found between serum LD levels and RED values. Significant correlations were found between serum LD levels and spirometric parameters. CONCLUSIONS: High serum LD levels might be considered as a marker of pulmonary parenchymal involvement in patients with SDDS. This study also suggests that the increase in serum LD levels might be closely related to the degree of pulmonary involvement in SDDS patients.

Long-term exposure to repetitive hyperbaric oxygen results in cumulative oxidative stress in rat lung tissue.

CONTEXT: Despite its known benefits, hyperbaric oxygen (HBO) is also reported to enhance the production of reactive oxygen species and can cause oxidative stress in several tissues. Previous studies had shown that HBO-induced oxidative stress is directly proportional to both its exposure pressure and duration. Nevertheless, these studies were usually performed with single-session HBO exposure but its clinical use commonly depends on long-term exposure periods. OBJECTIVE: To clarify the oxidative effect of long-term repetitive HBO in the lung tissue of rats. MATERIALS AND METHODS: Male Sprague-Dawley rats were divided into six study groups exposed to consecutive HBO sessions (2.8 atm/90 min) for 5, 10, 15, 20, 30, and 40 days. Animals were sacrificed 24 h after the last HBO session. An additional control group was set to obtain normal data. Lung malondialdehyde (MDA) and carbonylated protein (PCC) levels were determined as measures of oxidative stress along with the activities of the antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase. RESULTS: None of the measured parameters showed any changes among the groups exposed to 5-15 HBO sessions. However, MDA, PCC, and SOD were found to be significantly increased in the 20 to 40 session groups. DISCUSSION AND CONCLUSION: These results indicate that repetitive treatment with HBO may cause oxidative stress in critical tissues including the lung. Although HBO-mediated free radicals are accepted to be responsible for the benefits of this therapeutic modality, especially in cases with prolonged exposure, possible injurious effects of supranormal values of bio-oxidative products need to be considered.

Effect of nail polish and henna on oxygen saturation determined by pulse oximetry in healthy young adult females.

OBJECTIVE: The purpose of this study was to determine the effect of different colour nail polishes and henna on the measurement of oxygen saturation and the differences among the measurements of three pulse oximetry devices. MATERIAL AND METHODS: 33 healthy females with a mean age of 19±1.0 years and no complaints or known disease were included into the study. All the participants applied henna to one of their fingers a day before the study. Just before the study, one finger was left empty as control and the other fingers were dyed using various colours of nail polish (red, blue, beige, purple, brown, white, pink, green, colourless polish, light blue, light green and yellow). There were more than eight colour nail polishes and some fingers were used for the other colours after being completely cleaned. The same brand nail polishes were used for the study. Oxygen saturation measurements were done using three different pulse oximetry devices (device I, II, III) from the control, different colour nail polished and henna applied fingers. The measurements of different devices, different colour nail polishes, henna and control were statistically compared. RESULTS: The mean saturations obtained from blue, beige, purple and white nail polished fingers were significantly lower than those of control and the other coloured fingers. In addition, the mean measurement of device II was significantly lower than those of other devices. CONCLUSION: The results suggest that blue, beige, purple and white nail polished fingers might cause pulse oximetry devices to make incorrect measurements.

[Resistance rates to major anti-tuberculosis drugs in Mycobacterium tuberculosis strains isolated from seven different regions of Turkey in 2003-2006 period]. / Ulkemizin yedi farkli bölgesinden 2003-2006 yillari arasinda izole edilen mycobacterium tuberculosis suslarinin majör antitüberkoloz ilaçlara direnç oranlari.

Multi-drug resistance in Mycobacterium tuberculosis (MDR-TB) is a global problem and has increased especially in areas where tuberculosis control programmes are inefficient. The aim of this study was to detect the resistance rates against isoniazide (INH), rifampisin (RMP), ethambutol (EMB) and streptomycin (SM) in M. tuberculosis strains collected from 7 different regions including 62 cities and sent to Refik Saydam Hygiene Center National Tuberculosis Reference and Research Laboratory. Of the patients included, 7.61% were children, 92.39% were adults; 76.16% were male and 23.84% were female. These strains were isolated from sputum (n = 885, 81.11%), gastric lavage (n = 49, 4.49%), pleural fluid (n = 43, 3.94%), urine (n = 30, 2.74%), bronchoalveolar lavage (n = 22, 2.01%), and other clinical samples (n = 62, 8.46%) such as cerebrospinal fluid, lymph node, abscess material, lung tissue. The susceptibilities of the 1091 M. tuberculosis strains against the major anti-tuberculosis drugs were determined by the proportion method in Lowenstein-Jensen medium. Three hundred ninety two of the isolates were from Central Anatolia, 146 from Black Sea, 419 from Aegean, 28 from Mediterranean, 20 from Marmara, 64 from Eastern Anatolia and 21 from South Eastern Anatolia regions of Turkey. The distribution of the strains according to years were as follows: 88 in 2003, 114 in 2004, 341 in 2005 and 548 in 2006. Resistance to at least one of the drugs tested was found in 264 (14.20%) strains. Overall drug resistance rates to INH, RMP, EMB and SM were 12.3%, 10.1%, 6% and 15.8%, respectively. MDR-TB rate was 10% for this 4 years study period. MDR-TB rate was detected as 13.2%, 9.7%, 10.1% and 9.6% in children, adult, male and female patients, respectively. MDR-TB rate did not exhibit a statistically significant difference in terms of sex, age and study years (p > 0.05). However, this rate showed statistically significant difference in terms of geographical regions (p < 0.05). This study emphasized that regular surveillance of M. tuberculosis resistance to the major anti-tuberculosis drugs will provide valuable data for the effective national control and treatment of tuberculosis.

Reduced left ventricular ejection fraction and sudden cardiac death in patients undergoing revascularization: time to remember the other players of the game.

We strongly believe that relying solely upon ameliorating myocardial ischemia by coronary revascularization may be an inadequate clinical strategy for the prevention of sudden cardiac death (SCD) in dialysis and chronic obstructive pulmonary disease (COPD) patients. More importantly when predicting SCD risk in patients with coronary artery disease one should assess not only left ventricular ejection fraction but also the other clinical parameters such as renal replacement therapy and COPD.

Proanthocyanidin to prevent formation of the reexpansion pulmonary edema.

BACKGROUND: We aimed to investigate the preventive effect of Proanthocyanidine (PC) in the prevention of RPE formation. METHODS: Subjects were divided into four groups each containing 10 rats. In the Control Group (CG): RPE wasn't performed. Then subjects were followed up for three days and they were sacrificed after the follow up period. Samplings were made from tissues for measurement of biochemical and histopathologic parameters. In the Second Group (PCG): The same protocol as CG was applied, except the administration of PC to the subjects. In the third RPE Group (RPEG): Again the same protocol as CG was applied, but as a difference, RPE was performed. In the Treatment Group (TG): The same protocol as RPEG was applied except the administration of PC to the subjects. RESULTS: In RPEG group, the most important histopathological finding was severe pulmonary edema with alveolar damage and acute inflammatory cells. These findings were less in the TG group. RPE caused increased MDA levels, and decreased GPx, SOD and CAT activity significantly in lung tissue. CONCLUSION: PC decreased MDA levels. Oxidative stress plays an important role in pathophysiology of RPE and PC treatment was shown to be useful to prevent formation of RPE.

Epigenetic perturbations in the pathogenesis of mustard toxicity; hypothesis and preliminary results.

Among the most readily available chemical warfare agents, sulfur mustard (SM), also known as mustard gas, has been the most widely used chemical weapon. SM causes debilitating effects that can leave an exposed individual incapacitated for days to months; therefore delayed SM toxicity is of much greater importance than its ability to cause lethality. Although not fully understood, acute toxicity of SM is related to reactive oxygen and nitrogen species, oxidative stress, DNA damage, poly(ADP-ribose) polymerase (PARP) activation and energy depletion within the affected cell. Therefore several antioxidants and PARP inhibitors show beneficial effects against acute SM toxicity. The delayed toxicity of SM however, currently has no clear mechanistic explanation. One third of the 100,000 Iranian casualties are still suffering from the detrimental effects of SM in spite of the extensive treatment. We, therefore, made an attempt whether epigenetic aberrations may contribute to pathogenesis of mustard poisoning. Preliminary evidence reveals that mechlorethamine (a nitrogen mustard derivative) exposure may not only cause oxidative stress, DNA damage, but epigenetic perturbations as well. Epigenetic refers to the study of changes that influence the phenotype without causing alteration of the genotype. It involves changes in the properties of a cell that are inherited but do not involve a change in DNA sequence. It is now known that in addition to mutations, epimutations contribute to a variety of human diseases. Under light of preliminary results, the current hypothesis will focus on epigenetic regulations to clarify mustard toxicity and the use of drugs to correct possible epigenetic defects.

Changes in platelet count and indices in pulmonary tuberculosis.

BACKGROUND: Recent studies show that platelets have important roles in the immune system. Little is known about the clinical significance of platelet indices. Changes in platelet indices, including platelet distribution width (PDW), mean platelet volume (MPV) and plateletcrit, in pulmonary tuberculosis were investigated. METHODS: Platelet indices were quantified in 82 patients with active tuberculosis and 87 patients with inactive or non-tuberculous disease (controls). Radiological extent of the disease was assessed. RESULTS: There were significantly higher PDW (40.9+/-23.5% vs. 27.0+/-14.5%), MPV (10.05+/-2.36 vs. 8.83+/-1.47 fL) and plateletcrit (0.330+/-0166% vs. 0.266+/-0.128%) values in the active tuberculosis group, which decreased significantly with anti-tuberculous therapy. Erythrocyte sedimentation rate and plateletcrit showed significant correlation (r=0.54 and r=0.66) with radiological extent of tuberculosis, while PDW and MPV correlations with radiological extent of tuberculosis were also significant but weaker (r=0.31 and r=0.23). In a subpopulation of controls with pneumonia, which leads to acute phase reaction, PDW, MPV and plateletcrit values were significantly lower than in the tuberculosis group. CONCLUSIONS: We suggest that PDW, MPV and plateletcrit change in tuberculosis and that these changes may not reflect only acute phase reaction and disease activity. The potential role of platelet indices in tuberculosis immunopathogenesis remains to be investigated.

Atopy in patients with bronchiectasis: more than coincidence.

Bronchiectasis is common in developing countries, but its precise underlying mechanism can be detected in only about 40% of the cases. The studies reporting the frequency of atopy and its relation to radiological findings and lung function in bronchiectasis are limited in number, and the results are controversial. The present study was designed to investigate the relationship between atopy and bronchiectasis by means of high resolution computed tomography (HRCT) and pulmonary function tests. Skin prick test, HRCT and pulmonary function tests, including spirometric values of forced expiratory volume in one second (FEV1), FEV1/FVC (forced vital capacity) ratio were performed in 121 bronchiectatic patients of unknown etiology and in 68 healthy controls. Atopy and HRCT scores for the severity of atopy and extent of bronchiectasis respectively were determined for each patient. The rate of atopy (48.8% vs 11.8%) and mean atopy score (14.3 +/- 10.1 mm vs 5.5 +/- 2.1 mm) were significantly higher in patients with bronchiectasis than those in controls. Atopic patients had significantly worse spirometric values and more extended bronchiectasis than non-atopics. There is a significant correlation between atopy and HRCT scores (r = 0.54, p < 0.001), indicating that the more severe atopy is the more extended bronchiectasis. In conclusion, we suggest that the rate of atopy is higher in bronchiectatic patients than that in healthy controls. Bronchiectatic patients with atopy have lower spirometric values and higher HRCT scores. Atopy might be considered as a deteriorating and/or a causative or contributing factor for development of bronchiectasis.