Gastric involvement of sarcoidosis in a patient with multiple lung nodules.

Sarcoidosis is a granulomatous disorder mostly could involve intrathoracic structures. The gastric involvement is rare and the symptoms may be non-specific. We herein report a case of a 56-year-old female patient who was admitted due to chest tightness and discomfort. Computed tomography (CT) of the thorax revealed bilaterally nodular lesions in the lower lobes of the lung and pleural effusion on the left side. Positron emission tomography/CT showed lung nodules and gastric involvement with mesenteric lymphadenomegalies with pathological uptake of 18F-fluoro-2-deoxy-d-glucose. Pathological examination of the lung biopsy taken by thoracotomy demonstrated non-caseating granulomas. The gastric biopsies taken by endoscopy also showed non-caseating granulomas consistent with a diagnosis of sarcoidosis.

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.

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.

Lung function and IFN-gamma levels in the sera of silica-exposed workers.

Excessive exposure to respirable particles of crystalline silica is an occupational health problem in developing countries and can cause a variety of pulmonary diseases, such as silicosis, chronic obstructive pulmonary disease (COPD), and malignancy, in susceptible hosts. In addition to the well-documented role of pulmonary macrophages, lymphocytes occasionally have been suggested to influence the pneumoconiotic process, but their potential role is not clearly understood. Interferon-gamma (IFN-gamma), a lymphocyte cytokine, is recognized as the most important cytokine in converting macrophages from a resting to an activated state. The aim of the present study was to investigate serum IFN-gamma levels and pulmonary function changes in silica-exposed workers and in silicosis. Twenty-seven silica workers (aged 35.6 +/- 8.2 years with 5.11 +/- 2.98 years exposure duration) and 18 unexposed office workers (aged 33.8 +/- 12 years) were included in the study. Mean spirometry parameters and smoking history were comparable to the values of the office workers, but COPD prevalence was higher in the silica-exposed group, and the age-adjusted ratio was more sensitive than fixed quotient criteria for airway obstruction. We found silicosis in 4 silica workers. The mean serum IFN-gamma level was increased in silica-exposed workers (10.22 +/- 22.68 pg/mL) although it was undetectable in all office workers and even in the workers with silicosis. Evaluating pulmonary function tests (PFT) using an age-adjusted quotient may prevent underestimation of airflow limitation, especially in the young population with risk factors. Although serum IFN-gamma may increase initially in response to silica, low levels of IFN-gamma in later stages may be considered a risk factor for silicosis because this cytokine downregulates the fibroblast responses to transforming growth factor-beta (TGF-beta) and decreases collagen production. Additional research to determine the exact role of this potent cytokine may offer insight into the pathogenesis of silicosis.

Microalbuminuria, von Willebrand factor and fibrinogen levels as markers of the severity in COPD exacerbation.

In COPD, the systemic effects of the disease reflect the structural and/or biochemical alterations occurring in the structures or organs other than the lungs in relation to the characteristics of the primary disease. The disorders of endothelial structures due to COPD may lead vascular pathologies, such as ischemic heart disease, stroke, to occur more commonly in those with COPD. On consideration of the fact that the vascular endothelium is a major site in which the systemic effect of the inflammation occurs, should von Willebrand Factor, a clotting factor of endothelium origin, and the plasma level of fibrinogen vary with the severity of the disease in COPD, the variability of arterial blood gas values, and the stability or exacerbation of the disease? Considering the fact that microalbuminuria is an indirect manifestation of the renal endothelial permeability and/or renal perfusion; should there be an association between microalbuminuria and the severity of COPD? Therefore, in order to assess the effect of the systemic inflammation in COPD on the vascular endothelium, we compared the levels of the plasma vWF, fibrinogen, 24-h urine microalbuminuria of those with stable COPD (33 patients) and exacerbation of COPD (26 patients) with those of the controls (16 healthy subjects). The mean age was 63.42 -/+ 10.29, 68.00 -/+ 9.77 and 59.63 -/+ 14.10 years in SCOPD, COPDAE, and CG, respectively. The level of microalbuminuria was found to increase significantly in COPDAE group, compared to that of the controls (P = 0.004). When we investigated the relation between smoking burden and microalbuminuria, vWF, fibrinogen levels, the amount of consumption and positive relationship were found significant. (r = 0.336, P = 0.003 between smoking pack-years and vWF, r = 0.403, P = 0.001 between smoking pack-years and fibrinogen, and r = 0.262, P = 0.02 between smoking pack-years and microalbuminuria). The levels of vWF and fibrinogen are AECOPD > SCOPD > CG, with the highest being in AECOPD, and the difference among the groups was statistically significant. The relationship between the level of hypoxemia and microalbuminuria, fibrinogen and vWF was found to be significant (r = -0.360, P = 0.005 between oxygen saturation and microalbuminuria, r = -0.359, P = 0.005 between the level of PaO(2) and fibrinogen, and r = -0.336, P = 0.009 between PaO(2) and vWF). In conclusion, the levels of plasma vWF, fibrinogen, and microalbuminuria may be helpful in grading the severity of COPD exacerbation. The related increase in these markers may represent a possible pathophysiological mechanism behind the increased vascular morbidity of patients with COPD and detecting indirectly the endothelial dysfunction as a manifestation of systemic outcomes due to COPD and in detecting earlier the cases in which the risk for developing the associated complications are higher. We suggest that further studies are necessary to investigate the impact of antithrombotic treatment on microalbuminuria, plasma vWF and fibrinogen as markers of endothelial dysfunction coexisting COPD exacerbation.

[The effect of spinal anesthesia on pulmonary function tests in old patients]. / Yasli hastalarda spinal anestezi uygulamasinin solunum fonksiyon testlerine etkisi.

Pulmonary function test (PFT) results are mainly dependent on age, sex, height, weight, pulmonary mechanics disturbances and cooperation of the subjects. The position and anesthesia type may also influence the PFT results. In this study we aimed to evaluate spirometric changes in old and young patients who performed spinal anesthesia. Fifty patients performed spinal anesthesia were randomized in two groups: Group 1 (n= 25) aged 60-85 years old and group 2 (n= 25) aged 20-59 years old. After electrocardiography, noninvasive blood pressure and peripheral oxygen saturation (SpO2) monitorization, spinal anesthesia using 0.5% hyperbaric bupivacain from L 3-4 intervertebral space was applied. Sensory block levels, hemodynamics and PFT such as forced vital capacity (FVC), forced expiratory volume/1 second (FEV(1)), peak expiratory flow (PEF), and forced expiratory flow at the 25 and 75% of the pulmonary volume (FEF(25-75)) were performed before and after spinal anesthesia in 10th, 40th and 100th minutes in supine and 30 degrees head position using hand type spirometry. Wilcoxon paired two tests statistical analysis was used to compare PFT changes of the subjects. Mean arterial blood pressure levels and spirometric measurements of FVC, FEV(1) and FEF25-75 decrease with respect to basal values in 40th minutes was significant in old patients whom spinal anesthesia was over Th6 level but in young patients the changes were not significant. PFT decrement probabilities should be taken in account in old patients supposing for spinal anesthesia and be paid attention for high level spinal blocks in risk group 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.

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.