A Revised Treatment Approach for Hospitalized Patients with Eosinophilic and Neutrophilic Exacerbations of Chronic Obstructive Pulmonary Disease.

OBJECTIVES: The choice of treatment according to the inflammation type in acute exacerbation of chronic obstructive pulmonary disease (AECOPD) has been of recent interest. This study investigated the role of novel biomarkers, hospital outcomes, and readmission rates in the first month in patients with eosinophilic or neutrophilic AECOPD. MATERIALS AND METHODS: We conducted a retrospective observational cohort study in a Chest Teaching Hospital with hospitalized AECOPD patients. Subjects' characteristics, hemogram results, C-reactive protein (CRP), neutrophil/lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR), platelet/mean platelet volume (PLT/MPV), length of hospital stay, mortality, and steroid use were recorded. Eosinophilic AECOPD defined as peripheral blood eosinophilia (PBE) was >2% and neutrophilic AECOPD as PBE ≤2%. Readmission within 28 days of discharge was recorded. RESULTS: Of 2727(31.5% females) patients, eosinophilic AECOPD was found in 510 (18.7%) patients. Leucocytes, CRP, NLR, and PLR were significantly higher in neutrophilic AECOPD than in eosinophilic AECOPD (p<0.001). Steroid use and mortality rate were 45% and 0.6% in eosinophilic AECOPD and 71%, and 1.4% in neutrophilic AECOPD, respectively (p=0.001, p=0.19). Age >75 years, albumin <2.5 g/dL, CRP >50 mg/dL, and PLT/MPV <20×103 were found to be risks factors for hospital mortality (p<0.05 each). Readmission rates within 28 days of discharge were 5% (n=136), and this rate was higher in eosinophilic AECOPD patients not taking steroids (p<0.001). CONCLUSION: NLR, PLR, and CRP levels were higher in neutrophilic AECOPD compared with eosinophilic AECOPD. These markers decreased with treatment in neutrophilic AECOPD. A PLT/MPV ratio of <20×103 resulted in an increased mortality rate. Thus, appropriate steroid therapy may reduce readmission rates in the first 28 days after discharge in eosinophilic AECOPD.

Neutrophil to lymphocyte ratio is a better indicator of COPD exacerbation severity in neutrophilic endotypes than eosinophilic endotypes.

Background: Complete blood count parameters provide novel inflammatory markers, namely neutrophil to lymphocyte ratio (NLR) and platelet to lymphocyte ratio (PLR). We aimed to assess any differences in these novel inflammatory markers according to exacerbation severity in patients with COPD in both eosinophilic and neutrophilic endotypes. Method: This retrospective cross-sectional study was conducted at a tertiary education hospital. Previously diagnosed COPD patients admitted to the hospital with acute COPD exacerbation (AECOPD) were enrolled into the study. Patients were grouped according to COPD endotype, eosinophilic (peripheral blood eosinophil rate ≥2%) and neutrophilic (peripheral blood eosinophil rate <2%), and further subdivided according to place of admission (outpatient clinic, ward, or intensive care unit [ICU]) as an indicator of disease severity. Complete blood count, biochemistry, C-reactive protein (CRP), NLR, PLR, and platelet to mean platelet volume values were recorded from an electronic hospital database system and compared among all groups. Results: Of the 10,592 patients included in the study, 7,864 were admitted as outpatients, 2,233 to the wards, and 495 to ICU. Neutrophilic COPD patients (n=6,536, 62%) had increased inflammatory markers compared with eosinophilic COPD patients (n=4,056, 38%); median NLR was 5.11 vs 2.62 (P<0.001), PLR was 175.66 vs 130.00 (P<0.001), and CRP was 11.6 vs 7.7 (P<0.001). All values increased relative to admission to the outpatient clinic, ward, or ICU: median NLR was 3.20, 6.33, and 5.94, respectively, median PLR was 140.43, 208.46, and 207.39, respectively, and median CRP was 6.4, 15.0, and 22.8, respectively. The median NLR values of patients in outpatients/ward/ICU increased in neutrophilic and eosinophilic endotypes: 4.21/7.57/8.60 (P<0.001) and 2.50/3.43/3.42 (P=0.81), respectively. CRP showed a similar increased pattern according to severity of AECOPD endotypes. Conclusion: In COPD exacerbation, the inflammatory markers show different increases in each COPD endotypes. These findings may be crucial for defining exacerbation endotypes, the severity of exacerbation, and treatment response during follow-up in COPD patients.

The impact of exposure to biomass smoke versus cigarette smoke on inflammatory markers and pulmonary function parameters in patients with chronic respiratory failure.

PURPOSE: The aim of this study was to evaluate the impact of exposure to biomass smoke vs cigarette smoke on serum inflammatory markers and pulmonary function parameters in patients with chronic respiratory failure (CRF). PATIENTS AND METHODS: A total of 106 patients with CRF divided into age and gender-matched groups of cigarette-smoke exposure (n=55, mean [SD] age: 71.0 [12.0] years, 92.7% were females) and biomass smoke exposure (n=51, mean [SD] age: 73.0 [11.0] years, 94.1% were females) were included in this retrospective study. Data on patient demographics (age and gender), inflammatory markers, including neutrophil-to-lymphocyte ratio, C-reactive protein, platelet/mean platelet volume ratio, arterial blood gas analysis, and pulmonary function test findings, including forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and FEV1/FVC were obtained from medical records. RESULTS: Carbon dioxide partial pressure levels were significantly higher in the biomass smoke exposure than in the cigarette smoke exposure group (mean [SD] 51.0 [8.0] vs 47.0 [8.0] mmHg, p=0.026, respectively). Spirometry revealed similarly low levels for FEV1 (%) (38.0 [16.0] vs 40.0 [12.0]%) and FVC (%) (45.0 [19.0] vs 39.0 [19.0]%) in cigarette-smoke and biomass smoke exposure groups, whereas biomass smoke exposure was associated with significantly higher FEV1/FVC (75.0 [14.0] vs 58.0 [12.0]%, p=0.001), lower FVC (mL) (mean [SD] 744.0 [410.0] vs 1,063.0 [592.0] mL, p=0.035) and lower percentage of patients with FEV1/FVC <70% (36.8% vs 82.0%, p<0.001) than cigarette smoke exposure. CONCLUSION: Our findings indicate similarly increased inflammatory markers and abnormally low pulmonary function test findings in both biomass smoke exposure and cigarette smoke exposure groups, emphasizing the adverse effects of biomass smoke exposure on lungs to be as significant as cigarette smoke exposure. Association of biomass smoke exposure with higher likelihood of FEV1/FVC ratio of >70% and more prominent loss of vital capacity than cigarette smoke exposure seems to indicate the likelihood of at least 18 years of biomass exposure to be sufficiently high to be responsible for both obstructive and restrictive pulmonary diseases.

Analysis of Age Distribution and Disease Presentation of 1269 Patients with Sarcoidosis.

OBJECTIVE: While the incidence of sarcoidosis peaks between 20 and 39 years, it is comparatively low in elderly subjects. We sought to determine whether there are age-dependent differences in the demographic and laboratory characteristics of patients with sarcoidosis. MATERIALS AND METHODS: We retrospectively collected information from our database using the International Classification of Disease (ICD) diagnostic code D86 between 2008 and 2014. Patients were divided into three groups: 20-39 years old (Group 1), 40-59 years old (Group 2), and 60-80 years old (Group 3). RESULTS: A total of 3988 patients with code of D86 were included in the study. After the exclusion of non-eligible patients, the number of cases in Groups 1, 2, and 3 were 276, 641, and 352, respectively. The groups were compared according to demographic characteristics, ICD diagnostic codes, and laboratory parameters. The ratio of female patients was significantly higher in Group 3 than in Groups 1 and 2 (p=0.000). There was no difference in diagnostic codes of the ICD subgroups between groups (p=0.19). While the level of blood-urea nitrogen was significantly higher in Group 3 patients than in other groups (p=0.000), serum angiotensin-converting enzyme (ACE) values were found to be significantly low in Group 3 (p=0.010). The mean ACE values did not differ between females and males (50.8±39.3 and 59.1±45.5 mg/dL, respectively) (p=0.18). CONCLUSION: The majority of patients with sarcoidosis were female in all age groups and pulmonary sarcoidosis was the most common presentation of the disease. Elderly patients (≥60 years) with sarcoidosis had lower serum ACE levels than younger patients.

The utility of inflammatory markers to predict readmissions and mortality in COPD cases with or without eosinophilia.

BACKGROUND: COPD exacerbations requiring hospitalization increase morbidity and mortality. Although most COPD exacerbations are neutrophilic, approximately 10%-25% of exacerbations are eosinophilic. AIM: We aimed to evaluate mortality and outcomes of eosinophilic and non-eosinophilic COPD exacerbations and identify new biomarkers that predict survival. METHODS: A retrospective observational cohort study was carried out in a tertiary teaching hospital from January 1, 2014 to November 1, 2014. All COPD patients hospitalized with exacerbations were enrolled in the study at their initial hospitalization and followed-up for 6 months after discharge. Electronic data were collected from the hospital database. Subjects' characteristics, hemogram parameters, CRP levels, neutrophil-to-lymphocyte ratio (NLR), platelet-to-mean platelet volume ratio on admission and discharge, length of hospital stay (days), readmissions, and mortality were recorded. Patients were grouped according to peripheral blood eosinophil (PBE) levels: Group 1, >2% PBE, eosinophilic; Group 2, non-eosinophilic ≤2%. Patient survival after hospital discharge was evaluated by Kaplan-Meier survival analysis. RESULTS: A total of 1,704 patients hospitalized with COPD exacerbation were included. Approximately 20% were classified as eosinophilic. Six-month mortality was similar in eosinophilic and non-eosinophilic groups (14.2% and 15.2%, respectively); however, the hospital stay length and readmission rate were longer and higher in the non-eosinophilic group (P<0.001 and P<0.01, respectively). CRP and NLR were significantly higher in the non-eosinophilic group (both P<0.01). The platelet-to-mean platelet volume ratio was not different between the two groups. Cox regression analysis showed that survival was negatively influenced by elevated CRP (P<0.035) and NLR (P<0.001) in the non-eosinophilic group. CONCLUSION: Non-eosinophilic patients with COPD exacerbations with high CRP and NLR values had worse outcomes than eosinophilic patients. PBE and NLR can be helpful markers to guide treatment decisions.

Eosinophilic Lung Disease: Accompanied with 12 Cases.

OBJECTIVES: Eosinophilic lung diseases are a rare group of heterogeneous diseases characterized by the increase of the eosinophil ratio in airways and lung parenchyma. In our clinic, patients diagnosed with eosinophilic lung disease were evaluated with their clinical features and prognoses. MATERIAL AND METHODS: In our clinic, 12 cases that were diagnosed and followed up for eosinophilic lung disease [eosinophilic granulomatosis with polyangiitis (EGPA, Churg-Strauss syndrome) (n=4), chronic eosinophilic pneumonia (CEP) (n=7), and simple pulmonary eosinophilia (Löffler's syndrome) (n=1)] were retrospectively evaluated. RESULTS: Of the 12 cases, 8 were females, and the average age was 43 (28-72) years. All cases were undergoing bronchodilator therapy with asthma diagnosis (2 months-40 years). Additionally, 4 of the cases had sinusitis, and 1 had allergic rhinitis. The most common complaints of the patients were difficulty in breathing and coughing, and the duration of complaints was a median of 2 months. Peripheral eosinophilia and total IgE elevation were present during the admission of all cases; additionally, leucocyte elevation was recorded in 10 of them, anemia in 4 of them, and thrombocytosis in 4 of them. Moreover, 43% of the recorded DLCO values were lower than normal. Of the 10 cases that underwent bronchoalveolar lavage (BAL), the eosinophil ratio was above 25% in 7 subjects. Of the 8 cases that underwent transbronchial biopsy, eosinophil-involving infiltration was detected in 6 subjects. Additional findings in cases diagnosed with EGPA were nasal polyposis (n=1), sinusitis (n=2), polyneuropathy (n=1), cardiac involvement (n=2), and skin involvement in biopsy (n=1). Spontaneous recovery was observed in the patient diagnosed with simple pulmonary eosinophilia during the follow-up that was performed based on the history and laboratory and BAL results of the patient. Prednisolone treatment was started for all cases, except for simple pulmonary eosinophilia, and their controls were performed. Relapse was observed in eight cases (EGPA: 4, CEP: 4); during the relapse treatment of one case diagnosed with EGPA, exitus occurred. One case rejected treatment despite the presence of peripheral eosinophilia, and the other cases are being followed-up without medication. CONCLUSION: Given that the clinical pictures in pulmonary eosinophilia syndromes are on a wide spectrum, a specific diagnosis is important. Progression may differ in each patient, and a close follow-up is necessary during and after the treatment.