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1.  Underrecognized comorbidities of chronic obstructive pulmonary disease 
COPD is associated with different comorbid diseases, and their frequency increases with age. Comorbidities severely impact costs of health care, intensity of symptoms, quality of life and, most importantly, may contribute to life span shortening. Some comorbidities are well acknowledged and established in doctors’ awareness. However, both everyday practice and literature searches provide evidence of other, less recognized diseases, which are frequently associated with COPD. We call them underrecognized comorbidities, and the reason why this is so may be related to their relatively low clinical significance, inefficient literature data, or data ambiguity. In this review, we describe rhinosinusitis, skin abnormalities, eye diseases, different endocrinological disorders, and gastroesophageal reflux disease. Possible links to COPD pathogenesis have been discussed, if the data were available.
PMCID: PMC4507790  PMID: 26203239
COPD; comorbidities; rhinosinusitis; endocrinological disorders; GERD
2.  Mycobacterium tuberculosis as a sarcoid factor? A case report of family sarcoidosis 
Patient: Male, 26
Final Diagnosis: Sarcoidosis
Symptoms: Disseminated lung parenchymal changes
Medication: —
Clinical Procedure: —
Specialty: Pulmonology
Rare disease
Sarcoidosis is a granulomatous inflammatory disease that is induced by unknown antigen(s) in a genetically susceptible host. Although the direct link between Mycobacterium tuberculosis (MTB) infection and sarcoidosis can be excluded on the basis of a current knowledge, the non-infectious mechanisms may explain the causative role of mycobacterial antigens. The co-incidence of tuberculosis (TB) and sarcoidosis, and higher incidence of mycobacterial DNA in biological samples of sarcoid patients, have been reported by many authors.
Case Report:
We present a case in which MTB infection in 1 family member triggered a sarcoid reaction in the infected subject and 2 other non-infected family members. We discuss different aspects of diagnosis and differentiation, as well as up-to-date hypotheses on the possible mechanisms leading to sarcoid inflammation in patients exposed to MTB.
This case series documents the possibility of familial spreading of sarcoidosis, and points to MTB as a potential etiological factor.
PMCID: PMC4026149  PMID: 24847413
Tuberculosis; Mycobacterium Tuberculosis; Sarcoidosis
3.  The selected genetic polymorphisms of metalloproteinases MMP2, 7, 9 and MMP inhibitor TIMP2 in sarcoidosis 
Increased activity of metalloproteinases may play a role in the initiation and propagation of inflammation in sarcoidosis, and may also be one of the factors responsible for the development of lung fibrosis. The aim of this study was to verify whether polymorphisms of MMP2 C-735T, MMP7 A-181G, MMP9 T-1702A and tissue inhibitor of metalloproteinase (TIMP)2 G-418C predispose to sarcoidosis.
The study included 139 patients with sarcoidosis and 100 healthy subjects. MMPs and TIMP2 mRNA were measured in peripheral blood lysate using real-time RT-PCR. DNA for genetic polymorphism was extracted from peripheral blood by GTC method. Protein concentrations in peripheral blood lysates were measured by ELISA, and MMP2 and 9 activities in BAL fluid were estimated by gel zymography.
TT genotype in MMP9 T-1702A was more frequent in sarcoidosis (p<0.0001, OR=13.71, 95% CI 7.02–26.80) and resulted in higher expression of MMP9 mRNA (p<0.0001). No differences were found between TT and AT/AA patients in terms of radiological stage, lung function test parameters, activity markers and the presence/absence of Löfgren syndrome. There were no differences in the distribution of MMP2, MMP7 and TIMP2 polymorphisms. Messenger RNAs, as well as protein concentrations of MMP2, 7, 9, and TIMP2 were elevated in patients with sarcoidosis (p<0.0001 for each).
The TT homozygotes of MMP9 T-1702A genotype may be predisposed to sarcoidosis. Elevated MMP2, 7, 9, and TIMP2 mRNAs suggest their inducibility.
PMCID: PMC3539463  PMID: 21959615
sarcoidosis; metalloproteinases; genetic polymorphism
4.  Exhaled breath 8-isoprostane as a marker of asthma severity 
Oxidative stress is a non-specific feature of airway inflammation in asthmatics. 8-Isoprostane (8-IP), a prostaglandin-F2α isomer, is a relatively new marker of oxidative stress and may be measured in exhaled breath condensate (EBC) of patients with asthma. This research study aimed to evaluate the usefulness of EBC 8-IP as a marker of severity and control of severe adult asthma.
Material and methods
Twenty-seven severe, never-smoking asthmatics were studied. According to positive or negative reversibility testing, this group was subdivided into reversible and irreversible asthma groups. All participants were observed for 8 weeks during which they completed daily diary observations including day and night symptoms, number of awakenings, peak expiratory flow (PEF) variability, daily rescue medication usage and oral steroids consumption. They attended the clinic 3 times and on these occasions spirometry assessments, EBC collection and asthma control tests (ACT) were done. Two control groups were included: 11 healthy never-smokers and 16 newly diagnosed and never-treated, non-smoking mild asthmatics.
There were no statistically significant differences between severe asthma and healthy control or never-treated asthma groups in concentrations of EBC 8-IP (median and interquartile range: 4.67; 2.50-27.92 vs. 6.93; 2.5-12.98 vs. 3.80; 2.50-10.73, respectively). No correlations were found between EBC 8-IP and asthma control parameters, such as ACT results, night and day symptoms, consumption of rescue medication, percentage of days free of oral steroids, PEF diurnal variation, lung function test results, forced expiratory volume in the 1 s reversibility, and markers of systemic inflammation.
Our study results suggest that EBC 8-IP measurements are not useful for asthma monitoring.
PMCID: PMC3400897  PMID: 22852009
8-isoprostane; exhaled breath condensate; oxidative stress; severe asthma
5.  Exhaled eicosanoids and biomarkers of oxidative stress in exacerbation of chronic obstructive pulmonary disease 
Eicosanoids and oxidants play an important role in inflammation, but their role in chronic obstructive pulmonary disease (COPD) is uncertain. In this study we hypothesized that levels of exhaled leukotrienes, prostaglandins and biomarkers of oxidative stress are increased in infectious exacerbations of COPD and that they decrease after antibiotic therapy.
Material and methods
Cysteinyl-leukotrienes (LTs), leukotriene B4 (LTB4), prostaglandin E4, hydrogen peroxide (H2O2) and 8-isoprostane were measured in exhaled breath condensate (EBC) in 16 COPD patients with infectious exacerbations (mean age 64 ±12 years, 13 male) on day 1, during antibiotic therapy (days 2-4), 2-4 days after therapy and at a follow-up visit when stable (21-28 days after therapy).
There was a significant fall in concentration of cys-LTs, LTB4 and 8-isoprostane at visit 3 compared to day 1 (cys-LTs: 196.5 ±38.4 pg/ml vs. 50.1 ±8.2 pg/ml, p < 0.002; LTB4: 153.6 ±25.5 pg/ml vs. 71.9 ±11.3 pg/ml, p < 0.05; 8-isoprostane: 121.4 ±14.6 pg/ml vs. 56.1 ±5.2 pg/ml, p < 0.03, respectively). Exhaled H2O2 was higher on day 1 compared to that at visits 2 and 3 (0.74 ±0.046 µM vs. 0.52 ±0.028 µM and 0.35 ±0.029 µM, p < 0.01 and p < 0.01, respectively). Exhaled PGE2 levels did not change during exacerbations of COPD. Exhaled eicosanoids and H2O2 in EBC measured at the follow-up visit (stable COPD) were significantly higher compared to those from healthy subjects.
We conclude that eicosanoids and oxidants are increased in infectious exacerbations of COPD. They are also elevated in the airways of stable COPD patients compared to healthy subjects.
PMCID: PMC3361040  PMID: 22662001
chronic obstructive pulmonary disease; exhaled eicosanoids; 8-isoprostane; exhaled breath condensate
6.  Exhaled 8-isoprostane in sarcoidosis: relation to superoxide anion production by bronchoalveolar lavage cells 
Inflammation Research  2010;59(12):1027-1032.
This study was designed to examine the mutual relationship between 8-isoprostane in exhaled breath condensate (EBC) and superoxide anion generation by bronchoalveolar lavage fluid (BALF) cells in patients with sarcoidosis.
About 29 patients with sarcoidosis, 34 healthy never smokers (control group for EBC) and 15 healthy never smokers (control group for BAL) were examined. EBC was collected directly before bronchoscopy. 8-Isoprostane was measured by ELISA, and superoxide anion by colorimetry.
Exhaled breath condensate 8-isoprostane is increased in sarcoidosis (median, 25–75 percentile): 2.50; 2.50–3.90 versus 6.20; 2.50–16.95 pg/ml, p ≤ 0.05). Spontaneous superoxide anion release from BALF cells was significantly elevated only in patients with a high percentage of lymphocytes in BALF (6.42 ± 1.24 vs. 23.52 ± 4.30 nmol/106 cells, p ≤ 0.01). There were no correlations between 8-isoprostane and spontaneous or stimulated superoxide anion release.
We confirmed higher concentrations of EBC 8-isoprostane in sarcoidosis and higher spontaneous release of superoxide anion from BALF cells in patients with sarcoidosis. The increase of EBC 8-isoprostane is not directly related to superoxide anion released from BALF cells.
PMCID: PMC2978317  PMID: 20521080
Bronchoalveolar lavage; Exhaled breath condensate; Oxidative stress; Sarcoidosis; Superoxide anion
7.  Rhinosinusitis in COPD: symptoms, mucosal changes, nasal lavage cells and eicosanoids 
The coexistence of upper airways disease with chronic obstructive pulmonary disease (COPD) is not well documented. The aim of this research was to assess sino-nasal inflammation in COPD by various tools, and look for the impact on quality of life, relation to smoking, disease severity and systemic inflammation. Current and ex-smokers with COPD (n = 42) and healthy never-smokers (n = 21) were included in this study. COPD severity was assessed by GOLD criteria and BODE index. Markers of systemic inflammation were measured. Nasal symptoms and general quality of life were assessed using the questionnaires; sino-nasal questionnaire (SNAQ-11) and St. George's Respiratory Questionnaire (SGRQ). Nasal endoscopy and saccharine test were performed. Nasal lavages were collected for cytological examination and eicosanoids (cysteinyl leukotrienes, leukotriene B4, 8-isoprostane). Symptoms and endoscopic scores were higher in COPD (P ≤ 0.0001). Only SGRQ symptoms subscore correlated with SNAQ-11 (r = 0.34, P = 0.035). Mucociliary clearance was impaired only in current smokers (9.91 ± 0.49 versus 13.12 ± 0.68 minutes, P ≤ 0.001). 8-isoprostane was higher in COPD smokers compared to the controls (0.17 ± 0.04 versus 0.34 ± 0.09 pg/g protein, P < 0.05). Endoscopic score and mucociliary of impairment patients who currently smoked cigarettes correlated with concentrations of 8-isoprostane. None of the parameters correlated with disease severity and markers of systemic inflammation. We provide evidence of upper airways disease in COPD, which appears to be related more to patients who currently smoke than to disease severity.
PMCID: PMC2898086  PMID: 20631813
chronic obstructive pulmonary disease; eicosanoids; nasal lavage; rhinitis; smoking; upper airways disease
8.  Exhaled 8-isoprostane as a prognostic marker in sarcoidosis. A short term follow-up 
8-Isoprostane (8-IP) is a marker of lipid peroxidation. Elevated concentrations have been reported in BAL fluid and exhaled breath condensate (EBC) in sarcoidosis (S). To validate the prognostic value of this marker we tested whether: 1. high initial EBC 8-IP predispose to more severe disease; 2. low initial concentrations increase a chance of early remission; 3. remissions are connected with the decrease of EBC 8-IP.
40 patients (S) have been examined initially (V1) and after 8.5 ± 0.5 months (V2). EBC 8-IP concentrations were measured by ELISA. Chest X-ray, lung function test, serum ACE and Ca2+ concentrations, 24 hrs Ca2+loss, abdominal ultrasonography, symptoms evaluation were performed.
We confirmed higher concentrations of 8-IP in EBC of patients with sarcoidosis (p = 0.001). Relative risk (RR) of persistence of disease at V2 when initial 8-IP was above 20 pg/mL was 1.04, and the frequency distributions estimated by χ2 test were not significantly different. A chance (RR) of early complete remission when V1 8-IP was below DL, was 3.33 (p = 0.04 by χ2 test). A significant decrease of 8-IP at V2 was observed only in patients who received treatment (p = 0.03), but not in those with spontaneous remission.
We come to the conclusion, that low initial 8-IP may be a positive prognostic factor. A decrease of 8-IP in treated patients reflects a non-specific effect of treatment and is not related to mere regression of disease.
PMCID: PMC2882362  PMID: 20420721

Results 1-8 (8)