Muzaffer METİNTAŞ, İrfan UÇGUN, Mustafa KOLSUZ

Toplum kökenli pnömonilerde hastalık şiddeti ile akut faz reaktanları arasındaki ilişki

Toplum kökenli pnömoniler (TKP), mortalite ve morbiditesi nedeniyle önemli bir klinik problem olmaya devam etmektedir. TKP'li hastalar hastaneye yatış gerekliliği, hastalığın şiddeti, ek hastalık varlığı ve yaşına göre 4 grup altında incelenir. Akut faz reaktanları, doku zedelenmesi ve infeksiyona karşı sistemik fizyolojik bir cevap olarak salgılanır. Bunların en önemlileri C-reaktif proteindir (CRP). Biz bu çalışmamızda pnömoninin şiddeti ile hastaların başvuru dönemindeki ve tedavi sonrasındaki CRP, fıibrinojen ve eritrosit sedimentasyon hızı (ESR) arasındaki ilişkiyi araştırdık. Hastaların 64 (%64)'ü erkek, 36 (%36)'sı kadın, ortalama yaş 49.3 yıl idi. Hastaların 40 (%40)'ında ek hastalık mevcuttu, en sık olarak kronik obstrüktif akciğer hastalığı (%14) ve diabetes mellitus (%11) saptandı. Hastaların 10 (%10)'u öldü. Başvuru döneminde tüm hastaların CRP düzeyleri yüksekti. Pnömoninin şiddeti, CRP düzeyi ve lökosit sayı yüksekliği ile ilişkili bulundu, ESR ve fibrinojende ise bu ilişki gözlenmedi. Mortal seyreden olguların CRP düzeyleri daha yüksekti ve bu istatistiksel olarak anlamlı idi.

The relations between levels of acute phase reactants and severity of community acquired pneumonia

Community acquired pneumonia (CAP) continous to be a major clinical problem in terms of morbidity and mortality. Patients presenting with CAP were divided into one of four pneumonia groups based on the need for hospitalization, severity of illness, presence of coexisting disease and age. The acute-phase response is the physiological systemic response to tissue injury and infection. The most important one is C-reactive protein (CRP). We investigate the relations between severity of pneumonia and levels of acute phase proteins, such as CRP, fibrinogen and erythrocyte sedimentation rate (ESR) at initial presentation and at the end of the therapy. One hundred patients were included in the study. The mean age was 49.3 years; 64 patients (64%) were male and 36 patients (36%) were female. Forty patients (40%) had chronic disease, the most frequent being chronic obstructive pulmonary disease (14%) and diabetes mellitus (11%). Ten patients were died during their hospital stay. On admission, all patients had elevated CRP levels. The severity of disease was associated with admission levels of CRP and white blood cells, but not with ESR and fibrinogen. In the patients who died of pneumonia, CRP levels were statisticaly higher than who improved.

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1. American Thoracic Society. Guidelines for the initial management of adults with community acquired pneumonia: Diagnosis, assessment of severity, and initial antimicrobial therapy. Am Rev Respir Dis 1993; 48: 1418-26.
2. Ekim N, Köktürk O ue ark. Toplum kökenli pnömoni: Tanı ue tedaui rehberi. Toraks Derneği Pnömoniler Tanı ue Tedaui Rehberi 1998; 3: 2-14.
3. British Thoracic Society Research Committee. Community acquired pneumonia in adults in British hospitals in 1982-1983: A survey of aetiology, mortality, prognostic factors and outcome. Q J Med 1987; 62: 195-220.
4. Steel DM, Whitehead AS. The major acut phase reactants: C-reactive protein, serum amyloid P component and serum amyloid A protein. Immunology Today 1994; 15: 80-8.
5. Smith RP, Lipworth BJ, Cree IA, et al. C-reactiue protein: A clinical .marker in community acquired pneumonia. Chest 1995; 108: 1288-91.
6. Smith RP, Lipworth BJ. C-reactiue protein in simple community acquired pneumonia. Chest 1995; 107: 1028-31.
7. Jaye DL, Waites KB. Clinical applications of C-reactive protein in pediatrics. Pediatr Infect Dis J 1997; 16: 735-47.
8. Topçu F, Kaya K, özcan C ue ark. Pnömonİierde tanı ue tedavinin takibinde CRP. Solunum Hastalıkları 1997; 8: 375-9.
9. Hedlund J, Hansson LO. Procalcitonin and C-reactive protein leveis in community acquired pneumonia: Correlation with etiology and prognosis. Infection 2000; 28; 68-73.
10. Povoa P, Almelda E, Moreira P, et al. C-reactive protein as an indicator of sepsis. Intensive Care Med 1998; 24: 1052-6.
11. Knaus WA, Draper EA, Wagner DP, Zimmerman JE. APACHE II: A seuerity of disease classification system. Crit Care Med 1985; 13: 818-29.
12. Daley J, Jencks S, Draper D, et al. Predicting hospital associated mortality for medicare patients. JAMA 1988; 260:3617-24.
13. Padley SPG, Rubens MB. Pulmonary infections. In: Sutlon D (ed). Textbook of Radiology and Imaging, 6th ed. Churchill Livingstone, 1998: 421-49.
14. Wimberley N, Faling JL, Barlett JG. A fiberoptic bronchoscopy tecnique to obtain uncontamined lower airway secretion for bacterial culture. Am Rev Respir Dis 1979; 119: 337-43.
15. Almirall J, Bolibar I, Balanzo X, Gonzalez CA. Risk factors for community acquired pneumonia in adults: A population-based case-control study. Eur Respir J 1999; 13: 349-55.
16. Campbell GD. Overview of community acquired pneumonia: Prognosis and clinical features. Pneumonia: Pathogenesis, diagnosis and management. Med Clin North Am 1994; 78: 1035-48.
17. Korppi M, Heiskanen-Kosma T, Leinonen M. White blood cells, C-reactive protein and erytrocyte sedimentation rate in pneumococcal pneumonia in children. Eur Respir J 1997; 10: 1125-9.
18. Kosmas EN, Baxevanis CN, Papamichail M, Kordossis T. Daily variation in circulating cytokines and acute-phase proteins correlates with clinical and laboratory indices in community acquired pneumonia. Eur J Clin Invest 1997:27:308-15.
19. Peltola H, Jaakkola M. Serious bacterial infections: C-reactive protein as a serial index of seuerity. Clinical Pediatrics 1988; 27: 532-7.
20. Adnet F, Borron SW, Vicaut E, et al. Value of C-reactiue protein in the detection of bacterial contamination at the time of presentation in drug-induced aspiration pneumonia. Chest 1997; 112: 466-71.