The Levels of Serum Biomarkers in Stable Asthma Patients with Comorbidities.

The effects of comorbidities on systemic inflammation markers in stable asthmatics and the consequences of such effects have not been well evaluated. We aimed to evaluate the effect of comorbidities on clinical manifestations and systemic inflammation in asthmatic patients under control. The study group consisted of asthmatic patients who applied to our pulmonology outpatient clinic and volunteered to participate. 120 clinically stable asthma patients (71 females and 49 males) and 35 healthy controls (19 females and 16 males) with similar age, gender, and body mass index distributions were admitted to the study. The levels of osteopontin, interleukin 6 (IL-6), interleukin 8 (IL-8), interleukin 13 (IL-13), eosinophilic cationic protein, adiponectin, and high-sensitivity C-reactive protein of the individuals were evaluated using commercial ELISA kits by taking venous blood samples. Of 120 asthmatic subjects, 47 (39, 2%) had comorbidities and allergic rhinitis (15%) coexisted most frequently. Other comorbidities associated with asthma were gastroesophageal reflux, sinusitis, hypertension, diabetes, gastritis, and peptic ulcus respectively. There was no physician-diagnosed comorbidity in the control group. The levels of IL-6 and IL-8 were found higher in asthma group with comorbidities when compared to those with no comorbidities (p were 0.032 and 0.046, respectively). Comorbidities interfere with the diagnosis and treatment of asthma, besides affecting the disease control. Our findings suggest the possibility of the impact of comorbidities on systemic inflammation markers, especially IL-6 and IL-8. To evaluate the impact of comorbidities on asthma control and systemic markers, further studies are needed.

Left ventricular dysfunction in relation with systemic inflammation in chronic obstructive pulmonary disease patients.

BACKGROUND/AIMS: Most important cause of mortality in chronic obstructive pulmonary disease (COPD) patients is known to be cardiovascular disease (CVD). The objective of the present study was to evaluate the echocardiographic parameters in COPD patients with or without pre-diagnosed CVD and to investigate the relationship between echocardiographic parameters and systemic inflammation markers. METHODS: A total of 60 stable COPD patients (23 patients with CVD, group 1; 37 patients without CVD, group 2) and 21 healthy controls (group 3) were included in the study. Six-minute walking test (6MWT), COPD assessment test (CAT), and Body mass index, airflow Obstruction, Dyspnea, and Exercise (BODE) index results were recorded. High-sensitivity C-reactive protein (HsCRP), interleukin 8 (IL-8), fetuin-A, Clara cell protein (CCL-16), N-terminal pro-brain natriuretic peptide levels were studied in serum. Parameters of left and right ventricular systolic and diastolic function were measured by echocardiography. RESULTS: Patients with COPD had higher levels of systemic inflammation markers and lower level of inflammation inhibitor fetuin-A. When three groups were compared, group 1 had lower 6MWT result. HsCRP was highest in group 2 while other inflammatory markers were similar in groups 1 and 2. Regarding echocardiographic parameters, left ventricular ejection fraction (LVEF) was lower and left ventricle end-diastolic diameter (LVED), left ventricle end-systolic diameter (LVES) diameters were higher in group 1. The aortic diameter was higher in COPD patients. Fetuin-A was correlated with diameter of aorta and LVES. LVEF, LVED, and LVES were found to be correlated with functional parameters of COPD cases. CONCLUSION: In COPD, left ventricular functions are affected as well as right ventricle before prominent clinical findings of cardiac disease and these echocardiographic parameters correlate with functional parameters of COPD patients.

The role of molds in the relation between indoor environment and atopy in asthma patients.

BACKGROUND: The effect of mold fungi to allergic sensitization is not well-known. We aimed to evaluate the role of molds in the relation between indoor environment and atopy in asthmatics. MATERIALS AND METHODS: The air samples obtained from 66 stable asthmatics and 35 control subject's houses were sprayed into Sabouraud dextrose agar. Allergy skin testing were performed in both groups. The temperature and humidity of each house were measured. RESULTS: The incidence of atopy was similar in cases (59.1%) and controls (51.4%). The average amount of mold was 35.9 CFU/m(3) and 34.3 CFU/m(3), respectively. The number of household residents was positively correlated with the amount of molds. There was no difference in the amount of mold with respect to dosage of inhaler corticosteroids as well as symptom levels in asthmatics. The most frequently encountered allergens were Dermatophagoides farinae/Dermatophagoides pteronyssinus, grass/weeds and molds. Spending childhood in a village was more common among atopics. CONCLUSION: Living environment during the childhood might affect atopy and asthma. Based on the identification of molds as the second most frequent allergen after mites in our study population, assessment of mold sensitization as well as in forming patients about ways to avoid them seem likely to contribute to the effective management of uncontrolled asthma.

Teratoma during Pregnancy with Positive Estrogen and Progesterone Receptors and Elevated Ca19-9 Antigen Levels.

We present a 27-year-old female patient admitted with an anterior mediastinal mass. She complained of chest discomfort and hemoptysis which began seven months prior. She had given birth five months prior. Thoracic X-ray showed an anterior mediastinal mass. Thorax computed tomography (CT) confirmed a well-defined anterior mediastinal mass with 13 × 12 cm diameter, extending to the right hemithorax. It was composed of cystic spaces and discrete areas like soft tissue and fat. Serum Ca 19-9 level was elevated. CT features were consistent with a mature teratoma. During median sternotomy, the tumor revealed adhesions to the right lung and the right subclavian artery. Histologically, the tumor was diagnosed as a mature teratoma. Estrogen and progesterone receptors were detected to be positive in the resected tissue. We conclude that alterations in hormone levels during pregnancy might be the cause of rapid tumor growth which leads to hemoptysis.

Adipokines and systemic inflammation in weight-losing lung cancer patients.

BACKGROUND: Cancer cachexia is a devastating condition leading to loss of function and independence, decreased performance status, decreased quality of life, and poor prognosis. Adipokines play a role in a wide variety of physiological or pathological processes, including immunity and inflammation, in addition to having significant effects on metabolism and lipogenesis. The objective of the present study was to investigate the relationship of adipokines and systemic inflammation in weight-losing advanced-stage non-small-cell lung cancer (NSCLC) patients. METHODS: Sixty-three male NSCLC patients (stages III and IV) and 25 age- and sex-matched controls were included. NSCLC patients were further divided into subgroups as those with a>5% weight loss in last 6 months and those who did not. Serum leptin, adiponectin, and TNF-α concentrations were measured by ELISA using commercially available kits. RESULTS: The positive acute-phase reactants (APR) CRP, leukocyte, ferritin, thrombocyte, and fibrinogen were higher in the NSCLC group. Serum albumin level (which is a negative APR) was lower in the cancer group, whereas there was no difference in transferrin level between the groups. TNF-α and leptin concentrations were similar in the cancer group and the control group, whereas adiponectin was lower in the cancer group. There was a difference in thrombocyte and transferrin levels between patients with and without weight loss, whereas CRP, TNF-α, and adiponectin levels were similar. Leptin was lower in weight-losing cancer patients. However, there was no correlation between adipokines and markers of systemic inflammation. CONCLUSION: These results revealed a lack of association between adipokine levels and systemic inflammation with cancer cachexia.

The clinical importance of bone metabolic markers in detecting bone metastasis of lung cancer.

AIM: The aim of this study was to evaluate the role of bone metabolic markers in clinical evaluation of bone metastasis of lung cancer. MATERIALS AND METHODS: Sixty-five male patients with lung cancer were included in this trial, 77% of whom were diagnosed as having non-small cell lung cancer and 20% were small cell lung cancer. The presence of bone metastasis was investigated by whole-body bone scintigraphy via Tc-99m mostly (80%) and, in some cases, PET/CT (positron emission tomography and computerized tomography) which was performed for staging. Bone-specific alkaline phosphatase (BALP) and osteocalcin were measured in serum of the patients as markers of bone formation. N-terminal telopeptide (NTX) and ß-form of C terminal telopeptide (ß-CTX) were studied as bone destruction markers. RESULTS: The cases were divided into two groups according to the presence of bone metastasis. Twenty-three patients (35%) had bone metastasis. Serum levels of total ALP, BALP and NTX were significantly higher in the group with bone metastasis (p < 0.05). Osteocalcin and ß-CTX levels were not significantly different between two groups. According to ROC-curve analysis, at the threshold value of 22.38 µg/L, the sensitivity of BALP was 60.87% and the specificity was 69.05%. Similarly, at the threshold value of 25.69 nmol BCE, the sensitivity of NTX was 90.24% and the specificity was 43.4%. CONCLUSION: Bone metabolic markers are considered noninvasive, useful and cost-effective. However, more prospective studies are needed in order to use them for evaluation of bone metastasis in lung cancer.

Osteopontin as a marker of weight loss in lung cancer.

Although the role of osteopontin (OPN) in tumorigenesis and invasiveness is well-known, its role in systemic consequences of lung cancer has not been studied yet. The objective of the current study was to assess the value of osteopontin as a marker of weight loss in relation to systemic inflammation in non-small cell lung cancer (NSCLC) patients. A total of 63 male NSCLC patients (stage III and IV) and 25 age and sex-matched controls were included. The NSCLC patients were further divided into subgroups depending on whether they had > 5% weight loss in the last 6 months or not. Serum OPN and TNF-α concentrations were measured by ELISA using commercially available kits. Serum C-reactive protein (CRP) concentration was measured by the turbidimetric method. OPN (p = 0.001) and CRP (p < 0.001) concentrations were significantly higher in lung cancer patients compared to controls whereas TNF-α concentrations were similar in cancer and control groups (p = 0.063). There were 33 NSCLC patients (52.4%) with weight loss. Serum OPN concentration was found to be higher in this weight-losing group (p = 0.042). CRP concentration was also higher in the weight-losing group but the difference was not statistically significant (p = 0.246). TNF-α concentrations were similar in both subgroups (p = 0.094). In correlation tests, there was a positive correlation between OPN and CRP (r = 0.299, p = 0.044), but no correlation was detected between OPN and TNF-α (r = − 0.009, p = 0.930). A negative correlation was detected between OPN and BMI (r = − 0.246, p = 0.048). In addition to being an indicator of systemic inflammation in lung cancer patients, osteopontin may also be an indicator of weight loss.

Adiponectin as a biomarker of systemic inflammatory response in smoker patients with stable and exacerbation phases of chronic obstructive pulmonary disease.

BACKGROUND AND OBJECTIVE: Adiponectin is an adipose tissue-derived specific protein that has a role in energy homeostasis, that has a protective role against the development of insulin resistance and atherosclerosis and that exhibits anti-inflammatory properties. We investigated serum adiponectin as a biomarker of systemic inflammatory response and its relation with leptin, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and nitric oxide (NO) in chronic obstructive pulmonary disease (COPD) patients. MATERIAL AND METHODS: We studied 36 male patients with COPD (15 stable and 21 exacerbated) and 17 age and sex-matched healthy subjects. The adiponectin and leptin levels were measured by enzyme-linked immunosorbent assay. Serum CRP levels were measured using the nephelometric method. ESR was determined using the Westergren method and NO by the cadmium reduction method. RESULTS: Adiponectin levels in COPD patients were significantly higher than those in control subjects (p<0.001), whereas there were no differences in leptin or NO levels. Serum levels of CRP, ESR and adiponectin were significantly higher in the exacerbated COPD patients compared to the stable group (p<0.001, p = 0.033 and p = 0.024, respectively), whereas the differences in leptin and NO levels were not significant. Serum levels of adiponectin were not correlated with FEV(1), FEV(1)/FVC, dyspnoea score, BMI or other inflammatory parameters in the stable COPD group. CRP and ESR correlated negatively with FEV(1) in the stable COPD group. CONCLUSIONS: Adiponectin may be a marker of low-grade systemic inflammatory response in COPD. A further rise in serum adiponectin in the exacerbation period denotes that this may also be a biomarker of the exacerbation phase as well as CRP and ESR.

Biomarkers of systemic inflammation in stable and exacerbation phases of COPD.

Apart from the deleterious effects on the lungs, chronic obstructive pulmonary disease (COPD) should be considered a complex, systemic disease involving several organs and systems. The nature and course of systemic inflammation in COPD is important since there is a potential for anti-inflammatory therapy. The objective of the current study was to assess biomarkers of systemic inflammation in stable and exacerbation phases of COPD patients as compared to healthy controls. We also investigated the course of these biomarkers after COPD exacerbation to evaluate their usefulness for disease monitoring. Eighty-three stable patients with moderate to very severe COPD, 20 patients in exacerbation phase, and 30 subjects with normal pulmonary function were included. Serum tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and nitric oxide (NO) levels were measured once in stable COPD patients and controls and three times in the COPD exacerbation group during follow-up. TNF-alpha and IL-6 levels were higher than in controls in both stable and exacerbation groups. Although NO was not higher in the stable COPD group than in controls, it was higher in the exacerbation group. In follow-up after the exacerbation period, significant alteration was not detected in cytokine or NO levels compared to admission. Raised serum levels of TNF-alpha and IL-6 support their use as biomarkers of the systemic inflammatory response in stable COPD patients. However, the circulating biomarkers we have studied are not found to be useful either as indicators of COPD exacerbation or for monitoring recovery after exacerbation.

The value of C-reactive protein as a marker of systemic inflammation in stable chronic obstructive pulmonary disease.

BACKGROUND: Systemic aspects of chronic obstructive pulmonary disease (COPD) include oxidative stress and altered circulating levels of inflammatory mediators and acute-phase proteins. C-reactive protein (CRP) reflects total systemic burden of inflammation in several disorders and has been shown to upregulate the production of proinflammatory cytokines. The aim of this study was to evaluate circulating CRP levels to determine the value of CRP as a biomarker of systemic inflammation and as an indicator of malnutrition or severity of COPD in stable COPD patients in comparison to the proinflammatory cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). METHODS: Thirty-five male patients with stable COPD and 30 age- and sex-matched subjects with normal pulmonary function were admitted to the study. Serum CRP levels were measured using a commercially available kit with the turbidimetric method. Serum TNF-alpha and IL-6 concentrations were measured with ELISA kits. RESULTS: Sixty percent of the patients had severe or very severe and 40% moderate COPD. Serum CRP was significantly higher in stable COPD patients than in control subjects (p<0.001), while TNF-alpha and IL-6 concentrations were not statistically different. Serum TNF-alpha was higher in severe or very severe COPD patients (p=0.046). When the COPD patients with a low BMI were compared to those with a normal-to-high BMI, there was a significant difference in CRP (p=0.034) and TNF-alpha (p=0.037). CONCLUSION: The present study confirms that circulating CRP levels are higher in stable COPD patients and may thus be regarded as a valid biomarker of low-grade systemic inflammation. In addition, CRP is significantly higher in COPD patients with a low BMI and thus, together with TNF-alpha, may be considered an indicator of malnutrition in COPD patients.

Correlates of non-thyroidal illness syndrome in chronic obstructive pulmonary disease.

Non-thyroidal illness syndrome (NTIS) is frequently detected in chronic, systemic diseases. The objectives of the current study is to assess the alterations of thyroid hormones during exacerbation period, recovery of exacerbation and stable phase of chronic obstructive pulmonary disease (COPD) and correlates of these hormonal alterations. A total of 83 stable COPD patients, 20 patients with acute exacerbation and 30 control subjects were evaluated. TT3, fT3, TT3/TT4 levels of both stable and exacerbation COPD groups were lower than control subjects. TSH was also decreased during exacerbation period. In follow-up of COPD exacerbation group, TSH, TT3, fT3 and TT3/TT4 were found to be increased in measurements on the day of discharge from hospital and after 1 month, compared to baseline values. TT3 and TT3/TT4 were lower in severe COPD; whereas TSH, fT3, TT3 and TT3/TT4 were lower in patients with severe hypoxemia. IL-6 and TNF-alpha were higher in both stable and exacerbation phase COPD groups and IL-6 was correlated to TT3 in stable COPD. As a result, there are significant alterations in thyroid hormones of stable COPD patients, which are related to severity of disease and hypoxemia. The hormonal changes are more significant during exacerbation and partially regress after 1 month when the disease is stabilized. We conclude that COPD patients should not be evaluated for thyroid disease during exacerbation of the disease, and thyroid function alterations during stable phase of the disease should be considered cautiously, since thyroid function abnormalities in non-thyroid illness may mimic or mask biochemical abnormalities observed in true thyroid disease.

Correlates of erectile dysfunction in moderate-to-severe chronic obstructive pulmonary disease patients.

OBJECTIVE AND BACKGROUND: Erectile dysfunction (ED) has important negative effects on male quality of life and self-esteem. The aim of this study was to acquire an insight into the sexual status of COPD patients. METHODS: Ninety-five male patients aged 48-75 years, with moderate-to-severe stable COPD, and 30 age-matched subjects with normal pulmonary function were included. After clinical evaluation and measurement of serum sex hormones and TNF-alpha concentration, subjects were asked to answer the International Index of Erectile Function (IIEF) questionnaire as a method to diagnose and classify ED. RESULTS: Varying degrees of ED were detected in 87% of COPD patients and 83% of controls. Although the total percentages of subjects with various severities of ED seemed similar, moderate and severe ED was 57% in COPD group and 20% in control subjects, suggesting a more severe course of ED in COPD patients. ED score of COPD patients was not correlated with age, smoking burden, duration of COPD, FEV1%, PaO2, PaCO2, serum dehydroepiandrosterone-sulphate, testosterone or estradiol levels. When patients were subgrouped according to severity of ED, serum TNF-alpha concentration, used as a marker of systemic inflammatory status in COPD, was significantly higher in patients with moderate-to-severe ED compared with mild-moderate ED. CONCLUSION: The present study showed that ED is frequent and more severe in COPD patients than age-matched controls. Chronic systemic inflammation is likely to play a role in ED in COPD; the role of TNF-alpha should be evaluated further. Patients with COPD need comprehensive management including a detailed sexual evaluation.

Role of arterial blood gas abnormalities in oedema formation in COPD.

OBJECTIVE: Renal and hormonal abnormalities, manifesting as oedema or hyponatraemia, are often seen in patients with COPD. The aim of this study was to investigate the effect of airflow obstruction and arterial blood gas abnormalities on oedema formation in COPD patients. METHODOLOGY: A total of 58 COPD patients hospitalized for treatment of COPD exacerbation were admitted to the study. Of these, 38 patients had peripheral oedema (group 1) and 20 patients had no oedema (group 2). RESULTS: The mean age was 68 +/- 9 years in group 1 and 68 +/- 8 years in group 2. On the first day of admission, serum urea was 29.18 +/- 12.25 mg/dL and creatinine was 1.62 +/- 0.46 mg/dL in group 1, while urea was 15.50 +/- 4.59 mg/dL and creatinine was 1.07 +/- 0.10 mg/dL in group 2. Hyponatraemia occurred in five patients (13%) in group 1 and one patient (5%) in group 2. There was no difference in severity of airflow obstruction in the two groups; FEV1 was 44 +/- 15% of predicted and FEV1/FVC was 53 +/- 14 in group 1, while FEV1 was 45 +/- 16% of predicted and FEV1/FVC was 54 +/- 20 in group 2. There were statistically significant differences in pH (7.32 vs. 7.39; P= 0.013) and in PaCO2 (62 +/- 10 mmHg vs. 42 +/- 6; P= 0.048) for group 1 compared with group 2. PaO2 (62 +/- 17 mmHg vs. 82 +/- 27) and SaO2 (87 +/- 9%vs. 90 +/- 13) were found to be lower in group 1 compared with group 2 but the difference did not reach statistical significance. CONCLUSION: Alterations in pH and PaCO2 (respiratory acidosis and hypercapnia) appear to have more prominent roles than hypoxaemia in oedema formation in COPD patients.

Trace elements as a component of oxidative stress in COPD.

OBJECTIVE: The purpose of this study was to assess the serum concentrations of those trace elements that act as a component of oxidative stress in COPD patients. Clinically stable COPD outpatients (n = 26) and healthy controls (n = 24) were studied. METHODOLOGY: Serum concentrations of copper (Cu) and zinc (Zn) were determined using a Varian Spectra AA220 flame atomic absorption spectrophotometer. Serum concentration of iron (Fe) was measured by the ferene assay, using a commercially available kit (IL Test Iron) with the ILAb 900 autoanalyser. The lipid peroxidation product malondialdehyde (MDA) in serum samples was measured spectrophotometrically in terms of TBARS (thiobarbituric acid reactive substances). RESULTS: The serum MDA concentration in COPD patients was found to be similar to the control group (0.68 +/- 0.15 nmol/mL vs 0.62 +/- 0.13 nmol/mL, respectively; P= 0.163). The serum concentrations of the trace elements in both study groups were in the normal reference range. There was no difference in Fe concentration between COPD patients and the control group (0.81 +/- 0.38 micro g/mL vs 0.92 +/- 0.41 micro g/mL; P= 0.360). Copper concentrations were higher (1.06 +/- 0.26 microg/mL vs 0.92 +/- 0.19 microg/mL; P <0.040); while zinc was lower in the COPD group compared to the controls (0.83 +/- 0.25 microg/mL vs 1.03 +/- 0.23 microg/mL; P= 0.006). Serum Zn concentrations were lower in the severe COPD patients compared to mild-moderate COPD patients (P = 0.038). CONCLUSION: The results of this study indicate that there are alterations in serum concentrations of trace elements in COPD patients, suggesting that they may play a role in the pathophysiology of this disease by virtue of their role in oxidative stress. We recommend further studies on the role of trace elements in the pathophysiology of COPD, their association with markers of oxidant/antioxidant status and on the clinical significance of their deficiency.

Determinants of BMI in patients with COPD.

OBJECTIVE: COPD is characterized by significant chronic inflammation that is evident not only in the pulmonary compartment but also in the circulation. Peripheral blood features of COPD include markers of oxidative stress and altered circulating levels of inflammatory mediators and acute-phase proteins. The presence of a systemic inflammatory response may influence quality of life by giving rise to weight loss, muscle wasting and tissue depletion. The aim of the present study was to evaluate the determinants of body mass and the value of serum tumour necrosis factor alpha (TNF-alpha) as a marker of weight loss in COPD patients, and to correlate this with the burden of oxidative stress as measured by serum malonyldialdehyde (MDA) levels. METHODOLOGY: Fifty-two male COPD patients (mean age 62.55 +/- 6.81 years) were studied. After anthropometric measurements and standard spirometry, serum TNF-alpha concentration was measured by enzyme-linked immunosorbent assay using an hTNF-alpha kit, and MDA was studied spectrophotometrically using the Yoshioka-Kawada method. RESULTS: The mean BMI was 24.82 +/- 3.46. BMI was lower than normal (< 19) in six patients. Mean serum TNF-alpha concentration was 14.99 +/- 8.98 pg/mL and MDA was 0.93 +/- 0.13 nmol/L. There was no significant correlation between serum MDA and TNF concentrations (P = 0.140). Serum TNF-alpha and MDA concentrations were not correlated with severity of airflow obstruction or degree of hypoxaemia (P > 0.05 for all). BMI was negatively correlated with burden of smoking (pack-years) (r = -0.392, P= 0.004); but not with pulmonary function, degree of hypoxaemia, serum TNF-alpha or MDA levels. BMI was significantly lower in current smokers than ex-smokers (P = 0.041); however, serum MDA and TNF levels were similar in both groups. CONCLUSION: The results of this study indicate that body mass is related to smoking status (both pack-years and continuance of smoking) in COPD; however, serum TNF-alpha concentration does not seem to be a good marker of weight loss in these patients.

Should chronic obstructive pulmonary disease outpatients be routinely evaluated for trace elements?

We searched for serum concentrations of trace elements and correlated them to malondialdehyde (MDA), which is an indirect marker of oxidative stress, in order to clarify if routine evaluation is necessary in chronic obstructive pulmonary disease (COPD) outpatients. Serum concentrations of copper (Cu), zinc (Zn), and magnesium (Mg) were determined by atomic absorption spectrophotometry and iron (Fe) by a ILLab 1800 autoanalyzer with ILLab test kits. Serum MDA concentrations were detected in terms of TBARS (thiobarbituric acid reactive substances) spectrophotometrically. Serum Cu, Zn, Mg, Fe, and MDA concentrations in patient and control groups were all in the normal reference range. The results respectively were as follows: Cu:123 +/- 29.2 and 122.2 +/- 23.4 microg/dL; Zn: 87.8 +/- 17.8 and 96.9 +/- 12.9 microg/dL; Mg: 2.3 +/- 0,5 and 2.04 +/- 0.28 mg/dL; Fe: 73.8 +/-35.5 and 80.7+/-51.2 microg/dL; MDA: 1.09+/-0.11 and 0.95+/-0.06 nmol/L. MDA was not correlated to Cu, Zn, Mg, or Fe (p>0.05 for all). The serum Zn concentration of COPD group was lower than the control group (p=0.042), whereas the Mg concentration was higher (p=0.021). There was no statistical difference in other study parameters. Oxidative stress was not increased in clinically stable, regularly treated COPD patients. Although there was no deficiency in trace elements (Cu, Fe, Mg, and Zn), serum Zn was close to the lower limit of the reference value. There is no need for routine evaluation of trace elements in clinically stable, regularly treated COPD outpatients.

Should COPD patients be routinely evaluated for bone mineral density?

There are many factors that increase the risk of osteoporosis, including smoking, malnutrition, vitamin D deficiency, hypogonadism, limited physical activity due to chronic disease, and corticosteroid therapy in chronic obstructive pulmonary disease (COPD). The aim of this study was to investigate bone mineral density (BMD) in COPD outpatients receiving regular therapy in order to clarify whether they were suitable candidates for bone mass screening. Twenty-eight male, clinically stable COPD patients (mean age, 63 +/- 9 years) and 20 male volunteer subjects with normal pulmonary function, as a control group (mean age, 63 +/- 5 years) were admitted to the study. The BMD of the COPD patients and control subjects was measured by dual X-ray absorptiometry (Hologic QDR-4000). Pulmonary function tests and arterial blood gas analyses of COPD patients revealed moderate-degree airway obstruction with mild hypoxemia and normal pH. Rates of 42% and 67% for lumbar and femoral osteopenia, respectively, and 35%, and 10% for lumbar and femoral osteoporosis, respectively, were detected in the COPD patients; whereas the rates of lumbar and femoral osteopenia were 40% and 50%, respectively, and the rates of lumbar and femoral osteoporosis were 40% and 15%, respectively, in the control subjects. There was no statistically significant difference between the BMD values of the COPD and control groups. Lumbar BMD was 0.871 g/cm(2) in the COPD patients and 0.853 g/cm(2) in the control group (P = 0.682); femoral BMD was 0.790 g/cm(2) in the COPD patients and 0.795 g/cm(2) in the control group (P = 0.909). Bone density was correlated with the degree of airway obstruction and arterial blood pH. In conclusion, the BMD values of COPD patients were not different from those of control subjects of the same age group. We conclude that the risk of osteoporosis is not increased in appropriately treated patients with moderate-degree COPD, and there is no indication for bone mass screening in this group.

Erythrocyte fragility is not altered in stable chronic obstructive pulmonary disease with normal arterial pH.

The aim of this study is to investigate if erythrocyte fragility is altered in chronic obstructive pulmonary disease (COPD) due to oxidative stress. Fasting blood samples were collected into both plain tubes and tubes with K(3) EDTA and analyzed in two hours for hematologic indexes and erythrocyte osmotic fragility (EOF). Malondialdehyde (MDA) concentrations in serum were detected in terms of TBARS (thiobarbituric acid reactive substances), spectrophotometrically. Thirty-nine clinically stable male COPD patients with mean age 67+/-8 were prospectively studied. The control subjects consisted of healthy males with mean age 64+/-12. Pulmonary function tests of COPD patients revealed severe airway obstruction whereas they were normal for control group. Normal pH with mild hypoxemia and hypercapnia were detected in arterial blood gas analyses. Hemoglobin, haematocrit and mean corpuscular volume values of two groups were similar. Mean serum MDA concentration was 1.09+/-0.11 micromol/l in COPD patients and 0.95+/-0.06 micromol/l in the control group (p=0.336). EOF was 33.06+/-1.24% in COPD group and 33.17+/-1.55% in controls (p=0.453). There was no correlation between EOF and MDA concentrations of COPD patients (r=-0.18, p=0.924). EOF and MDA did not correlate with severity of COPD (p>0.05). We conclude that markers of oxidative stress are not increased and erythrocyte osmotic fragility is not altered in stable COPD patients with normal arterial pH.

Cavitary necrobiotic nodule imitating malignant lung disease in a patient without articular manifestations of rheumatoid arthritis.

Pulmonary involvement is a serious complication of rheumatoid arthritis (RA) and may be seen as airway disease, rheumatoid nodules, interstitial lung disease, and pleurisy. However, cavitary rheumatoid nodules without articular manifestations are rare. We describe a male patient presenting with pleurisy and multiple rheumatoid necrobiotic nodules in the absence of arthritis or subcutaneous nodules. One of the nodules was quite large (5 x 8 cm in diameter) and cavitary, imitating bronchial carcinoma radiologically and bronchoscopically. Definite histopathologic diagnosis was obtained by open lung biopsy. The patient was given methylprednisolone and methotrexate, and significant regression was observed in clinical and radiologic findings. He has been followed for 14 months with no articular manifestations yet, receiving 4 mg/d methylprednisolone and 20 mg/wk methotrexate. The diagnosis of rheumatoid pulmonary involvement without articular manifestations can be difficult. Rheumatoid nodules may imitate bronchial carcinoma, or bronchial carcinoma may coexist in RA patients. Open lung biopsy may be necessary for differential diagnosis of pulmonary lesions in RA.