Can the ADO Index Be Used as a Predictor of Mortality from COVID-19 in Patients with COPD?

Background: Several studies have shown that the risk of mortality due to COVID-19 is high in patients with COPD. However, evidence on factors predicting mortality is limited. Research Question: Are there any useful markers to predict mortality in COVID-19 patients with COPD?. Study Design and Methods: A total of 689 patients were included in this study from the COPET study, a national multicenter observational study investigating COPD phenotypes consisting of patients who were followed up with a spirometry-confirmed COPD diagnosis. Patients were also retrospectively examined in terms of COVID-19 and their outcomes. Results: Among the study patients, 105 were diagnosed with PCR-positive COVID-19, and 19 of them died. Body mass index (p= 0.01) and ADO (age, dyspnoea, airflow obstruction) index (p= 0.01) were higher, whereas predicted FEV1 (p< 0.001) and eosinophil count (p= 0.003) were lower in patients who died of COVID-19. Each 0.755 unit increase in the ADO index increased the risk of death by 2.12 times, and each 0.007 unit increase in the eosinophil count decreased the risk of death by 1.007 times. The optimum cut-off ADO score of 3.5 was diagnostic with 94% sensitivity and 40% specificity in predicting mortality. Interpretation: Our study suggested that the ADO index recorded in the stable period in patients with COPD makes a modest contribution to the prediction of mortality due to COVID-19. Further studies are needed to validate the use of the ADO index in estimating mortality in both COVID-19 and other viral respiratory infections in patients with COPD.

Chronic obstructive pulmonary disease phenotypes in Turkey: the COPET study-a national, multicenter cross-sectional observational study.

BACKGROUND: While mortality rates decrease in many chronic diseases, it continues to increase in COPD. This situation has led to the need to develop new approaches such as phenotypes in the management of COPD. We aimed to investigate the distribution, characteristics and treatment preference of COPD phenotypes in Turkey. METHODS: The study was designed as a national, multicenter, observational and cross-sectional. A total of 1141 stable COPD patients were included in the analysis. RESULTS: The phenotype distribution was as follows: 55.7% nonexacerbators (NON-AE), 25.6% frequent exacerbators without chronic bronchitis (AE NON-CB), 13.9% frequent exacerbators with chronic bronchitis (AE-CB), and 4.8% with asthma and COPD overlap (ACO). The FEV1 values were significantly higher in the ACO and NON-AE than in the AE-CB and AE NON-CB (p < 0.001). The symptom scores, ADO (age, dyspnoea and FEV1 ) index and the rates of exacerbations were significantly higher in the AE-CB and AE NON-CB phenotypes than in the ACO and NON-AE phenotypes (p < 0.001). Treatment preference in patients with COPD was statistically different among the phenotypes (p < 0.001). Subgroup analysis was performed in terms of emphysema, chronic bronchitis and ACO phenotypes of 1107 patients who had thoracic computed tomography. A total of 202 patients had more than one phenotypic trait, and 149 patients showed no features of a specific phenotype. DISCUSSION: Most of the phenotype models have tried to classify the patient into a certain phenotype so far. However, we observed that some of the patients with COPD had two or more phenotypes together. Therefore, rather than determining which phenotype the patients are classified in, searching for the phenotypic traits of each patient may enable more effective and individualized treatment.

[Investigation of the presence of human metapneumovirus in patients with chronic obstructive pulmonary disease and asthma and its relationship with the attacks]. / Kronik Obstrüktif Akciger Hastaligi ve Astimi Olan Hastalarda Insan Metapnömovirus Varliginin Arastirilmasi ve Hastalik Ataklari ile Iliskisi.

Human metapneumovirus (hMPV), an enveloped RNA virus classified in Paramyxoviridae family, was first characterized in 2001 from children with acute respiratory tract infection. Recent studies have suggested hMPV to play a role in chronic obstructive pulmonary disease (COPD) and asthma attacks. The aims of this study were to investigate the frequency of hMPV in patients with COPD and asthma, its effects on the severity of the attacks and the relationship between demographical and clinical factors. A total of 123 patients, including 66 with COPD (45 were in attack and 21 were stable) and 57 with asthma (33 were in attack and 24 were under control) diagnosed according to the criteria of Global Initiative for Chronic Obstructive Lung Disease and the Global Strategy for Asthma Management and Prevention, respectively, were included in the study. Nasopharyngeal lavage samples collected from all of the patients have been evaluated for the presence of hMPV-RNA by using a reverse transcriptase-polymerase chain reaction (RT-PCR) targeting F gene region of the virus. hMPV-RNA positivity rates in patients with COPD and asthma were observed as 30.3% (20/66) and 31.6% (18/57), respectively, and the difference between the groups were not statistically significant (p= 1.00). When patients were compared according to their disease status, hMPV was detected in 31.1% (14/45) of patients with COPD attack and 28.6% of stable patients (p> 0.05). These rates were found as 36.4% (12/33) and 25% (6/24) in patients with asthma attack and controlled asthma, respectively (p> 0.05). Although the virus detection rates in patients with COPD and asthma attacks (26/78; 33.3%) were higher than the patients with stable/controlled disease (12/45; 26.7%), the difference was not found as statistically significant (p= 0.57). The detection rate of hMPV-RNA was 26.1% in patients who can be treated at home and hospital without any need of intensive care and mechanical ventilation, while this rate was 36.4% in patients with COPD attack who require intensive care and mechanical ventilation (p= 0.67). Similarly, hMPV-RNA was detected more frequently in asthma patients with moderate and severe attacks (45%) than in patients with mild attacks (23.1%); however this difference was also not statistically significant (p= 0.28). No association of hMPV-RNA detection and demographical and clinical characteristics (age, gender, medical history, smoking status, allergy, COPD severity, asthma severity, the severity of attacks, using inhaled steroid, fever) of the patients could be demonstrated (p> 0.05), except the severity of the disease in patients with asthma (p= 0.02). In conclusion, further studies with large number of cases are needed to elucidate the role of hMPV in the occurrence and severity of COPD and asthma attacks.

[Determination of the cytokine gene polymorphism and genetic susceptibility in tuberculosis patients]. / Tüberküloz hastalarinda sitokin gen polimorfizmi ve genetik yatkinligin belirlenmesi.

Tuberculosis (TB) is a complicated disease in which biological, socioeconomical and environmental factors play role. Since only 10% of the individuals infected with Mycobacterium tuberculosis develop active disease, it has been suggested that host genetic factors may influence the risk for the development of TB. In this study, we aimed to investigate the presence and role of single nucleotide polymorphisms in the gene regions responsible for cytokine production, since these factors are considered to be associated with susceptibility or resistance to disease development. Single nucleotide polymorphisms were investigated by Amplification Refractory Mutational System (ARMS) Polymerase Chain Reaction (PCR) and PCR-Restriction Fragment Length Polymorphism (RFLP) methods. The presence of single nucleotide polymorphisms were analyzed in tumor necrosis factor alpha (TNF-α) gene promoter -308 G>A (rs1800629) region, interferon gamma (IFN-γ) gene +874 T>A (rs61923114) region, interleukin (IL)-12B p40 gene 1188 A>C (rs3212227) region, IL-10 gene promoter -1082 G>A (rs1800896) region and IL-4 gene promoter -590 C>T (rs2243250) region. A total of 84 patients (71 male, 13 female; mean age: 32.57 ± 15.94 years) whose clinical samples yielded M.tuberculosis complex growth, and 110 healthy blood donors (93 male, 17 female; mean age: 29.40 ± 11.56 years) as control group were included in this study. Of the patients, 76 (90.5%) were diagnosed as pulmonary and 8 (9.5%) as extrapulmonary TB. While 79 (94.1%) patients were newly diagnosed as TB, 5 (5.9%) patients had a TB history (relapsed TB). It was detected that acid-fast bacilli (AFB) were positive in 58 (69%) patients. According to the single nucleotide polymorphism results, gene frequencies could not be compared for TNF-a gene promoter -308 G>A region since healthy controls were in Hardy-Weinberg equilibrium while the patients were not. There were no statistically significant differences in allele and genotype distribution between the patients and healthy controls in IFN-γ gene +874 T>A region, IL-12B p40 gene 1188 A>C region, IL-10 gene promoter -1082 G>A region and IL-4 gene promoter -590 C>T region (p> 0.05). There were also no statistically significant differences between AFB positive (n= 58) and negative (n= 26) patients, and AFB positive (n= 56) and negative (n= 20) pulmonary TB patients (p> 0.05). In conclusion, no statistically significant differences were found associated with the susceptibility or resistance to TB with single nucleotide polymorphisms in the gene regions responsible for cytokine production in the study population. Only some of the single nucleotide polymorphisms of the gene regions responsible for cytokine release were investigated in our study. Therefore further detailed studies to investigate the polymorphisms in the genes that control the cytokine release and receptors specific for these cytokines, should be conducted. Although this study was performed in a relatively small sized population, these findings might provide a significant contribution to the epidemiologic data about the molecular immunology of TB in Turkey.

Lung function impairment in women aged over 40 years: The critical role of abdominal obesity.

SUMMARY: It is known that obesity causes to impairment of pulmonary functions. This impairment worsens with aging. There are studies about obesity showing that the uses of abdominal measurements instead of BMI are more accurate.: PURPOSE: The aim of our study is to investigate the correlation of waist circumference in the women aged over 40 years with obesity to the respiratory function tests and chest expansion. MATERIALS AND METHODS: In our study, BMI, waist circumference and chest expansion of 64 women over 40-year old were measured and the values obtained were compared with the results of respiratory function tests. RESULTS: There was a positive correlation between the age of the patients with waist circumference and DLCO/VA. A negative correlation was found between the age and MVV. The weight increase was associated with an increase in waist circumference and DLCO/VA. It was observed that waist circumference and DLCO/VA were increased and chest expansion was decreased when BMI was increased. A positive correlation was determined between MVV and the other respiratory function parameters, FEV1, FVC, FEV1/FVC and FIVC (p < 0.01). Similarly, the increase in DLCO was found to be correlated with the values of FEV1, FVC and FIVC. FIVC was correlated only with FEV1 and FVC. CONCLUSION: In this study, it was observed that respiratory function tests of women over 40-year old with obesity were associated with anthropometric measurements. But, studies with larger sample sizes and prospective studies are needed to provide more accurate information about the importance of DLCO/VA for the assessment of pulmonary function in obese women.

CYP2C19 gene polymorphism may be a risk factor for bronchial asthma.

OBJECTIVE: The aim of the present study was to investigate whether the genetic polymorphism of CYP2C19 plays a role in susceptibility to bronchial asthma. SUBJECTS AND METHODS: 104 healthy individuals who visited our hospital, including hospital staff, and 97 patients with bronchial asthma (62 atopic and 35 nonatopic) participated in this study. CYPC19*2 and CYP21C9*3 alleles were detected by using LightCycler and CYP2C19 mutation detection kits by real-time PCR with LightCycler. RESULTS: The CYP2C19*3 genotype was found to be the wild type in all cases, and in the control group, the CYP2C19*2 heterozygous genotype had a 2.46-fold increased risk of bronchial asthmacompared with the CYPC19*2 homozygous wild genotype in the control group(p = 0.01, OR = 2.46, 95% CI 1.24-4.88). CONCLUSION: Our data suggest that the CYP2C19*2 heterozygous genotype may be involved in the development of bronchial asthma.

The association between polymorphic genotypes of glutathione S-transferases and COPD in the Turkish population.

Although smoking is regarded as the most important causal factor in chronic obstructive pulmonary disease (COPD), only 10-20% of smokers develop symptomatic COPD, which indicates the presence of genetic predisposing factors in its pathogenesis. This study investigates the association between gene polymorphysims of glutathione S-transferases (GSTs) and COPD. Blood samples were taken from 149 patients and 150 healthy controls. Polymorphisms of GSTT1, GSTM1, and GSTP1 were genotyped using Real-Time PCR. Multivariate logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals between specific genotypes and COPD. There was no difference in the frequencies of the genotypes of GSTM1 and GSTT1 between the groups, but the GSTP1 Ile/Ile genotype was significantly higher in the patients than in the controls (61.1% vs. 38%). GSTP1 Ile/Val and Val/Val genotypes were associated with a decreased risk of COPD when compared to the Ile/Ile genotype (2.12-fold and 4-fold, respectively). Thus we suggest that the Val allele of GSTP1 may have a protective effect for development of COPD. Furthermore, when we evaluated the association between GSTP1 genes and smoking status, smokers with the GSTP1 Ile allele had an increased risk for the development of COPD. Among the combinations of the genotypes, the combination of GSTM1, GSTT1 null, and GSTP1 Val/Val was associated with the maximal increased risk (12-fold) of COPD. Thus to explain the ethiopathogenesis of COPD, investigation of a single gene family is inadequate. Based on our results and the previous data, further studies should be focused on the GSTP1 gene and the interactions with other genes such as polymorphisms of N-acetyltransferases, GSTM1 and GSTT1, microsomal epoxide hydrolase, and allelic variants of cytochrome P450.

[MMP-9 and TIMP-1 levels in the sputum of patients with chronic obstructive pulmonary disease and asthma]. / Kronik obstrüktif akciger hastalari ve astimlilarda indükte balgamda MMP-9 ve TIMP-1 düzeyleri.

Chronic obstructive pulmonary disease (COPD) and asthma are associated with morphological changes in airway and lung and metalloproteinases are tought to play a role in this destruction. The aim of this study is to compare the levels of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinases (TIMP)-1 in the airways of COPD and asthma patients in stable period. We measured MMP-9 and TIMP-1 levels in the induced sputum of 20 asthma, 22 COPD patients in stable period and 15 healthy controls. MMP-9 and TIMP-1 levels were measured by using ELISA kits. MMP-9 and TIMP-1 levels were higher in patient groups than the controls. In COPD patients MMP-9 and TIMP-1 were significantly higher than the controls (respectively; p= 0.0001, p= 0.0001). Similarly, in asthma patients MMP-9 and TIMP-1 levels were higher than the controls (respectively; p= 0.005, p= 0.002). However, while there were no significant difference in MMP-9 levels between the patient groups (p= 0.29), TIMP-1 levels were significantly higher in COPD patients (96.2 +/- 58.2 versus 52.8 +/- 52 microg/mg protein, respectively, p= 0.0001). Atopic asthma patients TIMP-1 levels were slightly higher than non-atopic asthma patients (p> 0.05). There was no significant correlation between FEV(1) and MMP-9 or TIMP-1 levels in all groups. Although known pathogenetic differences in COPD and asthma, the increases in protease-antiprotease levels in both two patient groups may be associated with bronchial and parenchimal morphological changes. New treatment strategies which are focused on modulating of increased protease-antiprotease levels may be give a hope to patients with COPD and asthma.

Relationship between N-acetyl transferase-2 gene polymorphism and risk of bronchial asthma.

There are still uncertainties as to the mechanism of many pathological conditions, among them allergic diseases. It has been suggest that acetylation rate may be a factor that influences the development of allergic diseases. The aim of the present study was to investigate further whether the genetic polymorphism of the NAT2 plays a role in susceptibility to bronchial asthma disease. Ninety-seven patients with bronchial asthma (atopic n= 62; non-atopic n= 35) and 104 healthy individuals were participated in this study. DNA was extracted from the leucocyte by high pure template preparation kit. NAT2*5A, NAT2*6A, NAT2*7A/B and NAT2*14A polymorphisms of NAT2 were detected by using LightCycler-NAT2 mutation detection kit by real time PCR with LightCycler instrument. We found that mutant NAT2*5A (OR= 3.84, 95% CI= 1.08-13.6) and NAT2*6A (OR= 5.27, 95% CI= 1.06-26.05) genotype could be associated with a high risk for the development of bronchial asthma according to the genotype. After grouping phenotype, the risk for bronchial asthma was more than two times higher (OR= 2.7, 95% CI= 1.07-6.97) in individuals with the slow NAT2*5A acetylator phenotype compared to the fast phenotype. Our study suggests that the NAT2 slow acetylators may be a determinant in susceptibility to asthma disease. This finding may have implications for the theories for the pathogenesis of the disease as well as for therapeutic aspects.

Cranial optic nerve involvements in patients with severe COPD.

OBJECTIVE: The relationship between neuropathy and increased morbidity in patients with COPD is clear, but few studies have assessed cranial neuropathies, especially optic nerve involvement, in COPD patients. We evaluated peripheral involvement of the optic nerve and determined factors influencing this condition in patients with severe COPD. METHODOLOGY: Twenty-eight patients, mean age 59.4 +/- 9.4 years, diagnosed with severe stable COPD according to the GOLD criteria, and 20 age- and gender-matched healthy individuals, mean age 55.6 +/- 8.5 years, were included in the study. All subjects underwent visual evoked potential (VEP) assessment together with detailed clinical and laboratory examination to exclude concurrent risk factors for neuropathy. RESULTS: VEP assessment showed significant abnormalities in COPD patients (82.1%) (commonly amplitude abnormalities) when compared with healthy controls. CONCLUSIONS: The optic nerve is often involved in patients with severe COPD, possibly as part of a polyneuropathy, and this is related to acidosis, hypercarbia and airway obstruction, independent of disease duration, smoking and age. These results should be taken into consideration when determining management strategies for these patients.

Glutathione-S-transferase gene polymorphisms (GSTT1, GSTM1, GSTP1) as increased risk factors for asthma.

OBJECTIVES: Asthma is a complex multifactorial disease with an obvious genetic predisposition, immunological aberration, and involvement of noxious environmental factors. Polymorphisms of the glutathione-S-transferase (GST) genes are known risk factors for some environmentally-related diseases. In the present study, the hypothesis that polymorphisms in the GSTT1, GSTM1 and GSTP1 genes are associated with atopic and nonatopic asthma was examined. METHODOLOGY: The study population consisted of 103 unrelated healthy individuals and 101 patients with bronchial asthma (64 atopic, 37 nonatopic). Asthma was diagnosed according to the American Thoracic Society statement. Genotyping of polymorphisms in the GSTT1, GSTM1 and GSTP1 genes was performed using real time polymerase chain reaction with a Light Cycler instrument and hybridization probes in combination with the Light Cycler DNA master hybridization probes kit. RESULTS: Patients with atopic asthma (34.4%) had a higher prevalence of the GSTT1 null genotype than the nonatopic asthma patients (13.5%; OR = 3.83; 95% CI, 1.24-11.78). Asthma patients (63.4%) had a higher prevalence of the GSTM1 null genotype than the control group (40.8%; OR = 2.34; 95% CI, 1.31-4.20). Subjects with the GSTP1 homozygous Val/Val genotype had a 3.55-fold increased risk of having atopic asthma compared to nonatopic asthma (OR = 3.55; 95% CI, 1.10-12.56). CONCLUSIONS: These results suggest that the GSTT1 and GSTM1 null genotypes and the GSTP1 Val/Val polymorphism may play important roles in asthma pathogenesis. It is possible that intermediate electrophilic metabolites, arising in the first phase of detoxification, are not metabolized by GST enzymes in asthmatic patients and are not excreted. These intermediate metabolites may damage cells and generate oxidative stress, and so contribute to the pathogenesis of asthma.

[The nitrosative effect of peripheral ischemia-reperfusion on lung and preventive of caffeic acid phenethyl ester]. / Periferik iskemi reperfüzyonun akcigerdeki nitrozatif etkileri ve "caffeic acid phenethyl ester" in koruyucu rolü.

Ischemia-reperfusion (IR) is characterized by microvascular disfunction and this involves both direct effected organ and remote organ by systemic inflammatory response. These remote effects of IR are most frequently observed in the lung and cardiovascular system. In this study we aim to determine lung damage which induced IR, and endothelial and microvascular disfunction using nitrosative markers. Previous studies suggest that caffeic acid phenethyl ester (CAPE) has some antioxidant effects. Therefore, we also investigated whether it has a role associated with nitric oxide during IR condition. Twenty-two adult male Wistar rats were divided into three groups: control (n= 7), IR (n= 7), and CAPE + IR (n= 8). 8 h IR period was performed on right hindlimb in the IR and the CAPE with IR group. In the CAPE with IR group, animals received CAPE 10 microM 1 h before the reperfusion. At the end of the reperfusion period, blood, bronchoalveolar lavage (BAL) and lung tissue were obtained, and were used for biochemical and histopathological examination. There was a significantly elevation in serum nitrate, BAL MPO, and leukocyte infiltration in the lung in the IR group compared to the CAPE + IR group. But, serum nitrite and lung 3-NT levels were not different between these groups. While nitrate (p< 0.0001), MPO (p< 0.0001) and leukocyte infiltration (chi2= 27.163, p= 0.0001), reduce by using CAPE before reperfusion, tissue 3-NT levels did not change. In conclusion, peripheral IR leads to systemic inflammatory responses and endothelial disfunction-induced NO production, and these harmful effects may reduced by CAPE.

The effects of the caffeic acid phenethyl ester (CAPE) on erythrocyte membrane damage after hind limb ischaemia-reperfusion.

Reactive oxygen species have been implicated in pathogenesis injury after ischaemia-reperfusion (I/R). Caffeic Acid Phenethyl Ester (CAPE), an active component of honeybee propolis extract, exhibits antioxidant and anti-inflammatory properties. The aim of this study was to investigate the effects of CAPE on erythrocyte membrane damage after hind limb I/R. Rats were divided into two groups: I/R and I/R with CAPE pre-treatment. They were anaesthetized with intramuscular ketamine 100 mg kg(-1). A 4-h I/R period was performed on the right hind limb of all animals. In the CAPE-treated group, animals received CAPE 10 microm by intraperitoneal injection 1 h before the reperfusion. At the end of the reperfusion period, a midsternotomy was performed. A 5-ml blood sample was withdrawn from the ascending aorta for biochemical assays. Serum and erythrocyte membrane MDA levels were significantly lower in the CAPE-treated group when compared to the I/R group ( p = 0.001 and p<0.001, respectively). Erythrocyte membrane Na(+)-K(+) ATPases activity in the CAPE-treated group was significantly higher than the I/R group ( p<0.001). In conclusion, CAPE seems to be effective in protecting against oxidative stress. Therefore, we suggest that in order to decrease I/R injury, pre-administration of CAPE may be a promising agent for a variety of conditions associated with I/R.

Massive pleural effusion in an 18-year-old girl with Ewing sarcoma.

Ewing sarcoma is a bone tumour that commonly appears between ages five and 10 in the diaphysis of the long bones and predominantly presents with pain and swelling. The case of an 18-year-old girl who presented with back pain, cough, dyspnea, weakness and fever is described. Chest radiograph showed a homogenous density in the middle and inferior zones of the right hemithorax. Thoracic computed tomography revealed a diffuse pleural effusion and a 6.99 cm x 4.45 cm solid mass composed of lobulated, small cystic lesions and calcifications in the right hemithorax. Biochemical analysis of pleural fluid showed hemorrhagic effusion and exudate. A pleural needle biopsy demonstrated solid uniform tumour cells with narrowed cytoplasm, round nuclei and uncertain nucleoli. All of the tumour cell cytoplasms stained with CD99. The pathological examination supported Ewing sarcoma. Three-phase Tc-99m methylene diphosphonate scintigraphy of the whole body showed pathological tracer uptake in a broad area of the eighth costal bone and in smaller areas of the ninth and 10th costal bones. This case is reported because Ewing sarcoma is a rare cause of pleural effusion in clinical practice among younger adults.

Use of acute phase proteins in pleural effusion discrimination.

The differentiation between exudates and transudates is fundamental when investigating the cause of pleural effusions. Acute-phase proteins could be potentially useful markers in this discrimination. In the attempt to define diagnostic criteria for the differentiation of pleural exudates from transudates, we measured alpha 1 acid glycoprotein, C-reactive protein, haptoglobin, ceruloplasmin and transferrin in pleural effusions and serum in patients with pleural effusions of various etiologoies. We measured the concentrations of the above proteins in the serum and pleural fluid of 80 (54 exudate, 26 transudate) consecutive patients by immunoturbidometrical methods. Pleural effusion acute phase proteins were elevated in the patients with exudate compared to patients with transudate (p< 0.001 for all). In receiver operator characteristic analysis showed that pleural fluid ceruloplasmin levels and the ratio pleural fluid/serum transferrin were superior to the others. Using the optimum cut-off point of 0.16 g/L pleural fluid ceruloplasmin achieves a sensitivity of 92% with a specificity of 85%. In addition to, the optimum cut-off point for pleural fluid/serum transferrin ratio was 0.4 with sensitivity and specificity of 92% and 80%. When using together these parameters sensitivity and specificity were increased (95%, 85%). In differential diagnosis, none of these proteins were significantly different in subgroups of pleural exudate. We conclude that when using together ceruloplasmin levels in pleural fluid and the ratio of pleural to serum transferrin have a high sensitivity and specificity in discrimination of exudative pleural effusions.

Respiratory muscle strength but not BASFI score relates to diminished chest expansion in ankylosing spondylitis.

Pulmonary function is altered in ankylosing spondylitis (AS) owing mainly to the restriction of chest wall involvement (limited chest expansion). The objective of this study was to investigate the relationship between chest expansion, respiratory muscle strength (MIP, MEP) maximum voluntary ventilation (MVV), and BASFI score in patients with AS. Twenty-three male patients with definite AS and 21 age-matched healthy male controls were recruited for the study. Patients with AS were assessed for functional status by BASFI. Measurement of chest expansion and lumbar spinal flexion (modified Schober) method was performed in all subjects. Pulmonary function tests were performed by spirometry. Respiratory muscle strength was evaluated by a mouth-pressure meter (MPM). Body mass index (kg/m(2)) was recorded in all individuals. Chest expansion and modified Schober measurement were significantly lower in AS patients (p<0.05). Pulmonary function tests revealed restrictive lung disease. The mean BASFI score suggested good functional capacity in the AS group. The respiratory muscle strength and MVV were also lower in AS (p<0.05). The chest expansion was correlated with MIP and MEP values (r=0.491; p=0.02, r=0.436; p=0.05). Chest expansion was also correlated negatively with disease duration (r=-0.502; p=0.03). In addition, there was no correlation between chest expansion and BASFI score (r=-0.076; p=0.773). This study demonstrates that functional status (BASFI) is not influenced by the limitation of chest wall movement. It may be as a result of the maintenance of moderate physical activity during active life in patients with AS.

Pulmonary muscle strength, pulmonary function tests, and dyspnea in women with major depression.

OBJECTIVE: To evaluate the subjective sensation of dyspnea compared with pulmonary function tests, pulmonary muscle strength, and chest expansion in depressed women and control subjects free of cardiorespiratory disease. METHODS: Thirty female patients with major depression (MD) and 30 age-matched female control subjects were included in the study. All subjects were assessed by pulmonary function tests (spirometry) and pulmonary muscle strength measurement (maximum inspiratory and expiratory pressures [MIP and MEP]) by mouth pressure meter (MPM). Chest expansion was measured, and body mass index (kg/m(2)) (BMI) was calculated. The Health Assessment Questionnaire (HAQ) was used to evaluate the activities of daily living, and a dyspnea score was used to determine dyspnea severity. RESULTS: There were no significant differences between groups regarding pulmonary function tests, pulmonary muscle strength, and chest expansion. HAQ scores were significantly lower in women, and dyspnea was higher with MD compared with controls (p < 0.05). BMI was also lower in depressed patients (p < 0.05). CONCLUSIONS: The subjective sensation of dyspnea is increased in women with MD in the presence of normal lung function and is associated with the level of anxiety rather than that of depression.

Is chest expansion a determinant of pulmonary muscle strength in primary fibromyalgia?

OBJECTIVE: To examine the possible relationship between chest expansion and pulmonary muscle strength in patients with primary fibromyalgia (PFM). METHODS: Forty-one consecutive women with PFM were compared with age and body mass index matched 40 healthy women concerning pulmonary function tests, chest expansion, and maximum respiratory pressures indicating pulmonary muscle strength, and endurance (MVV). Pain was scored according to a visual analog scale (VAS). Chest pain was scored on a 10 point scale. RESULTS: There was no significant difference between the two groups regarding chest expansion (P > 0.05). Maximum inspiratory and expiratory pressures (MIP, MEP) were lower in fibromyalgia patients than controls (P < 0.05). However, chest expansion and dyspnea score were insignificant between groups (P > 0.05). CONCLUSION: Reduced maximum respiratory pressures (MIP, MEP) may result from isometric type pulmonary muscle dysfunction as a result of low physical performance in fibromyalgia patients, despite insignificant finding of chest expansion and dyspnea score according to controls.

HRCT evaluation of the accessory fissures of the lung.

INTRODUCTION: The purpose of this study was to classify the accessory fissures of the lung and to assess their frequency by using high-resolution CT. METHODS AND PATIENTS: HRCT scans of 115 patients were prospectively reviewed. 1 mm thin sections were obtained at 10 mm intervals with a scan time of 1.9 s. The fissure and its relationship to the segmental bronchovascular structures were then evaluated on transverse sections. RESULTS: Forty-four accessory fissures were detected in 35 of 115 patients. The most common accessory fissure was the inferior accessory fissure (12%). The second most common accessory fissure was the left minor fissure (8%). The right superior accessory fissure (5%), the accessory fissure between the medial and lateral segments of the right middle lobe (5%), and the accessory fissure between the superior and inferior segments of the lingula (5%) were seen in equal frequencies. Also, intersegmental accessory fissures, namely the fissure between the anterobasal and laterobasal of both the right (1%) and the left (2%) lower lobes were detected. We found only one subsegmental accessory fissure. DISCUSSION AND CONCLUSION: The inferior accessory fissure and the left minor fissure were the most common accessory fissures in our study.

Leptin and TNF-alpha levels in patients with chronic obstructive pulmonary disease and their relationship to nutritional parameters.

BACKGROUND: Leptin is a protein mainly secreted by adipocytes, and the major function of leptin was its role in body weight regulation. In humans, there was a strong correlation between leptin and nutritional parameters, such as body mass index (BMI) and fat mass (FM). Administration of recombinant leptin to OB/OB mice, which have a genetic defect in leptin production, reduces food intake, increases energy expenditure, and decreases body weight. It is suggested that increased levels of circulating leptin levels may contribute to anorexia and weight loss in pathologic conditions including chronic obstructive pulmonary disease (COPD). Recent studies have provided evidence for a link between leptin and proinflammatory cytokines such as TNF-alpha. OBJECTIVE: This study aimed to detect serum leptin and TNF-alpha levels in COPD patients without weight loss during stable disease and acute exacerbation, and to investigate relationships between leptin, TNF-alpha and nutritional parameters at different stages of the disease. MATERIAL AND METHODS: 26 stable COPD patients, 16 COPD patients with acute exacerbation and 15 control subjects participated in this study. To eliminate the effects of sex differences, all patients and controls were male. BMI, percent ideal body weight, percent FM, sum of skinfold thickness and serum leptin and TNF-alpha levels were measured in all participants. Leptin and TNF-alpha levels were measured by ELISA. RESULTS: Serum leptin and TNF-alpha levels were significantly higher in the patients experiencing exacerbation than in the stable patients and controls. Although leptin levels were lower and TNF-alpha levels were higher in the stable patient group than in the controls, these differences were not statistically different. Leptin levels were significantly correlated with the nutritional parameters in both control and stable groups. However, in patients with acute exacerbation, a correlation between leptin and nutritional parameters was not found. There was no significant relationship between TNF-alpha and nutritional parameters in the three groups. In addition, while there was no correlation between leptin and TNF-alpha levels in the stable and control groups, a significant positive correlation was observed in patients with exacerbation. CONCLUSION: In conclusion (1) elevated TNF-alpha levels may be related to increased inflammation in patients, (2) circulating TNF-alpha levels were associated with increased leptin levels and (3) although leptin and nutritional parameters were correlated in the stable COPD patients, the correlation was weaker compared to controls, and during an exacerbation it disappeared completely. Therefore, inappropriately increased levels of leptin and TNF-alpha noted during recurrent acute exacerbations in patients with COPD may lead to changes in nutritional parameters and body weight in the course of the disease.