scholarly journals Respon Inflamasi Pada Perokok Pasif Di Kecamatan Pahandut Kota Palangka Raya Ditinjau Dari Jumlah Leukosit Dan Jenis Leukosit

2018 ◽  
Vol 1 (2) ◽  
pp. 31
Author(s):  
Rinny Ardina
Keyword(s):  
Free Radicals ◽  
Inflammatory Response ◽  
Blood Cell ◽  
Cell Count ◽  
Cigarette Smoke ◽  
White Blood Cell Count ◽  
White Blood Cell ◽  
Blood Cell Count ◽  
Cross Sectional ◽  
Hematology Analyzer

Proporsi perokok pasif di Indonesia mencapai 40,5 persen dan 78,4 persen perokok pasif banyak terpapar asap rokok di dalam rumah.Setiap hembusan asap rokok mengandung 1015 radikal bebas oksidatif dan nikotinpenyebab leukositosis di dalam darah sebagai bentuk respon inflamasi.Jenis leukosit penunjuk inflamasi akibat asap rokok diawali neutrofilia, neutropenia, limfositosis, limfopenia dan monositosis sebagai bentuk respon inflamasi. Analisis deskriptif dengan rancangan cross sectional digunakan untuk memberikan gambaran respon inflamasi ditinjau dari jumlah leukosit dan jenis leukosit pada perokok pasif yang tinggal di kecamatan Pahandut kota Palangka Raya. Sampel yang diperoleh sebanyak 30 orang diambil dengan teknik Purposive Sampling dimulai dengan observasi, pembagian lembar inform consent, wawancara, pengisian kuesioner, pengambilan sampel darah dan pemeriksaan laboratorium menggunakan hematology analyzer dan apusan darah tepi. Data yang diperoleh dimuat dalam bentuk tabel dan dianalisis dan dideskripsikan dalam bentuk persentase (%). Pada 5 orang (17%) terjadi leukositosis, 2 orang (6%) neutropenia, 1 orang (3%) neutrofilia, 1 orang (3%) limfopenia, dan 6 orang (20%) limfositosis. Leukositosis menunjukkan penanda adanya perubahan imun sistemik, dimana selanjutnya terjadi rekrutmen sel inflamasi diantaranya neutrofil dan limfosit. Radikal bebas dan nikotin memicu inflamasi ditandai dengan neutrofilia dengan limfopenia relatif pada awal inflamasi dan selanjutnya berkembang menjadi limfositosis dengan neutropenia relatif.Proportion of passive smokers in Indonesia reached 40,5% and 78,4% of them were exposure of cigarette smoke in the house. Each puff of cigarette smoke contains 1015 of oxidative free radicals and nicotine that causes leukocytosis in the blood where it found as an inflammatory response. Either free radicals or nicotine can also cause of neutrophilia, neutropenia, lymphocytosis, lymphopenia, and monocytosis. This study aimed to overview of the inflammatory response in terms of white blood cell count and differential counting of leukocytes in passive smokers (housewives) who live in the district of Pahandut, Palangka Raya. Descriptive analysis with cross sectional design was used in this study. Samples obtained by 30 people were taken with Purposive Sampling technique. Procedure of collecting data starts from observation, distribution of informed consent, interview, answered of questionnaire, blood sampling and laboratory examination using hematology analyzer for measured of white blood cell count and peripheral blood smear for measured of differential counting of leukocytes. The data obtained were analyzed and described in percentage (%). This study found 5 people (17%) of leukocytosis, 2 people (6%) of neutropenia, 1 person (3%) of neutrophilia, 1 person (3%) of lymphopenia, and 6 people (20%) of lymphocytosis. Leukocytosis occurs because of the mechanism of leukocytes recruitment into inflammatory tissues and the types of leukocyte that increased are neutrophils and lymphocytes. Free radicals and nicotine play a major role in triggering inflammation. Acute inflammation cause of exposure of cigarette smoke characterized by neutrophilia and relative lymphopenia in the blood and it will be develop into chronic inflammation that characterized by lymphocytosis and relative neutropenia.

scholarly journals Efek Merokok Berat terhadap Jumlah Leukosit dan Jenis Leukosit pada Pria Usia Produktif di Kelurahan Tanjung Pinang Kota Palangka Raya

2019 ◽  
Vol 1 (2) ◽  
pp. 34-40
Author(s):  
Rinny Ardina ◽  
Nada Soraya
Keyword(s):  
Blood Cell ◽  
Cell Count ◽  
White Blood Cell Count ◽  
White Blood Cell ◽  
Leukocyte Count ◽  
Sampling Technique ◽  
Blood Cell Count ◽  
Differential Leukocyte Count ◽  
Cross Sectional ◽  
Heavy Smoking

Prevalence of productive men smokers in Kalimantan Tengah in 2013 has been reached 64.9% with a mean of smoking about 12.3 cigarettes a day. Cigarette smoke contains 1015 of oxidative free radicals which can cause oxidative stress. It will trigger of activation of inflammatory genes and increase of cytokines release by increasing of leukocytes and activate some of the differential leukocytes. Continual inflammation can cause atherosclerosis and coronary heart disease. This study aimed to determine the effects of heavy smoking on white blood cell count and differential leukocyte count in productive men in Kelurahan Tanjung Pinang, Palangka Raya. This study used a descriptive observational method with a cross-sectional design. The sample obtained by 28 people with purposive sampling technique with criteria: men, active smoker, smoking more than ten years, working as a farmer, fish farmer, or laborer, and willing to become a respondent. White blood cell count and differential leukocyte count were analyzed by an automatic method using Hematology Analyzer. The results showed that 3.6% of active smokers had high white blood cell count and others had low white blood cell count (3.6% ). Whereas differential leukocyte count showed that 2 persons had high of eosinophils (7.10%), 5 people had low of eosinophils (17.9%), one person had little of neutrophils (3.6%), 2 persons had high of lymphocytes (7.20%), 10 people had little of lymphocytes (35.7%), and 15 people had high of monocytes (53.6%). To reduce the risks, preventive and educative actions from medical personnel are needed for active smokers and their families.

scholarly journals Diagnosis of Appendicitis in Patients with a Normal White Blood Cell Count; A Cross-Sectional Study

2018 ◽  
Vol 6 (2) ◽  
pp. 128-132 ◽  
Author(s):  
Sadettin Er ◽  
Bülent Çomçalı ◽  
Ahmet Soykurt ◽  
Bülent Cavit Yüksel ◽  
Mesut Tez
Keyword(s):  
Blood Cell ◽  
Cell Count ◽  
White Blood Cell Count ◽  
White Blood Cell ◽  
Cross Sectional Study ◽  
Sectional Study ◽  
Blood Cell Count ◽  
Cross Sectional ◽  
Normal White Blood Cell

scholarly journals Survival After Endovascular Aneurysm Sealing Compared With Endovascular Aneurysm Repair

2021 ◽  
pp. 152660282110250
Author(s):  
Aleksandra C. Zoethout ◽  
Arshad Sheriff ◽  
Clark J. Zeebregts ◽  
Andrew Hill ◽  
Michel M. P.J. Reijnen ◽  
...  
Keyword(s):  
Platelet Count ◽  
Inflammatory Response ◽  
Blood Cell ◽  
Cell Count ◽  
White Blood Cell Count ◽  
White Blood Cell ◽  
Endovascular Aneurysm Repair ◽  
Blood Cell Count ◽  
Aneurysm Repair

Introduction Endovascular aneurysm sealing (EVAS) is a sac-filling device with a blunted systemic inflammatory response compared to conventional endovascular aneurysm repair (EVAR), with a suggested impact on all-cause mortality. This study compares mortality after both EVAS and EVAR. Materials and Methods This is a retrospective observational study including data from 2 centres, with ethical approval. Elective procedures on asymptomatic infrarenal aneurysms performed between January 2011 until April 2018 were enrolled. Laboratory values (serum creatinine, haemoglobin, white blood cell count, platelet count) were measured pre- and postoperatively and at 1 and 2 years, respectively. Mortality and cause of death were recorded during follow-up. Results A total of 564 patients were included (225 EVAS, 369 EVAR), after propensity score matching there were 207 patients in both groups. Baseline characteristics were similar, except for larger neck angulation and more pulmonary disease in the EVAR group. The median follow-up time was 49 (EVAS) and 44 (EVAR) months. No significant differences regarding creatinine and haemoglobin were observed. Preoperative white blood cell count was higher in the EVAR group (p=0.011), without significant differences during follow-up. Median platelet count was lower in the EVAR group preoperatively (p=0.001), but was significantly higher at 1 year follow-up (p=0.003). There were 43 deaths within the EVAS group (20.8%) and 52 within the EVAR group (25.1%) (p=0.293). Of these, 4 were aneurysm related (EVAS n=3, EVAR n=1; p=0.222) and 14 cardiovascular (EVAS n=6, EVAR n=8, p=0.845). For the EVAS cohort, survival was 95.5% at 1 year and 74.9% at 5 years. For the EVAR cohort, this was 93.3% at 1 year and 75.5% at 5 years. No significant differences were observed in causes of death. Conclusion This study showed comparable survival rates through 5 years between EVAS and EVAR with a tendency toward higher inflammatory response in the EVAR patients through the first 2 years.

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