Abstract
Most patients with sepsis have underlying co-morbidities. Co-existing disease is typically thought to influence the pathophysiology and outcome of sepsis by reducing physiological reserve. Certainly this is true: A patient with chronic obstructive pulmonary disease (COPD) will tolerate pneumonia less well than a patient with previously healthy lungs. Additionally, many chronic disease states (or their treatments) alter the pre-existing inflammatory and immune milieu. This effect ranges from the obvious (as in the case of patients taking immunosuppressant therapy) to the underappreciated (as in the inflammatory dysregulation associated with obesity). In seeking explanations for differences in the host response to infection, much has been made of the possible effects of genetic variability. However, subtle variations in the underlying state of the immune and inflammatory systems have received little attention.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Yende S, Tuomanen EI, Wunderink R, et al (2005) Preinfection systemic inflammatory markers and risk of hospitalization due to pneumonia. Am J Respir Crit Care Med 172:1440–1446
Glibetic MD, Baumann H (1986) Influence of chronic inflammation on the level of mRNA for acute-phase reactants in the mouse liver. J Immunol 137:1616–1622
Hotchkiss RS, Karl IE (2003) Medical progress: The pathophysiology and treatment of sepsis. N Engl J Med 348:138–150
Angus DC, Linde-Zwirble WT, Lidicker J, Clermont G, Carcillo J, Pinsky MR (2001) Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care. Crit Care Med 29:1303–1310
Koivula I, Sten M, Makela PH (1994) Risk factors for pneumonia in the elderly. Am J Med 96:313–320
LaCroix AZ, Lipson S, Miles TP, White L (1989) Prospective study of pneumonia hospitalizations and mortality of U.S. older people: the role of chronic conditions, health behaviors, and nutritional status. Public Health Rep 104:350–360
Baik I, Curhan GC, Rimm EB, Bendich A, Willett WC, Fawzi WW (2000) A prospective study of age and lifestyle factors in relation to community-acquired pneumonia in US men and women. Arch Intern Med 160:3082–3088
Fessler BJ (2002) Infectious diseases in systemic lupus erythematosus: risk factors, management and prophylaxis. Best Pract Res Clin Rheumatol 16:281–291
Zandman-Goddard G, Shoenfeld Y (2005) Infections and SLE. Autoimmunity 38:473–485
D’Aiuto F, Parkar M, Andreou G, et al (2004) Periodontitis and systemic inflammation: control of the local infection is associated with a reduction in serum inflammatory markers. J Dent Res 83:156–160
De Nardin E (2001) The role of inflammatory and immunological mediators in periodontitis and cardiovascular disease. Ann Periodontol 6:30–40
Seinost G, Wimmer G, Skerget M, et al (2005) Periodontal treatment improves endothelial dysfunction in patients with severe periodontitis. Am Heart J 149:1050–1054
Bajestan MN, Radvar M, Afshari JT, Naseh MR, Arab HR (2006) Interleukin-6 production by cultured peripheral blood monocytes before and after stimulation by E. Coli lipopolysaccharide in Iranian patients with aggressive periodontitis. Med Sci Monit 12:CR393–CR396
von Dossow, V, Schilling C, Beller S, et al (2004) Altered immune parameters in chronic alcoholic patients at the onset of infection and of septic shock. Crit Care 8:R312–R321
Sander M, Irwin M, Sinha P, Naumann E, Kox WJ, Spies CD (2002) Suppression of interleukin-6 to interleukin-10 ratio in chronic alcoholics: association with postoperative infections. Intensive Care Med 28:285–292
Chen NG, Abbasi F, Lamendola C, et al (1999) Mononuclear cell adherence to cultured endothelium is enhanced by hypertension and insulin resistance in healthy nondiabetic volunteers. Circulation 100:940–943
Dorffel Y, Latsch C, Stuhlmuller B, et al (1999) Preactivated peripheral blood monocytes in patients with essential hypertension. Hypertension 34:113–117
Hilgers KF (2002) Monocytes/macrophages in hypertension. J Hypertens 20:593–596
Yaegashi M, Jean R, Zuriqat M, Noack S, Homel P (2005) Outcome of morbid obesity in the intensive care unit. J Intensive Care Med 20:147–154
Cottam DR, Mattar SG, Barinas-Mitchell E, et al (2004) The chronic inflammatory hypothesis for the morbidity associated with morbid obesity: implications and effects of weight loss. Obes Surg 14:589–600
Vachharajani V, Vital S (2006) Obesity and sepsis. J Intensive Care Med 21:287–295
Azevedo ZM, Luz RA, Victal SH, et al (2005) Increased production of tumor necrosis factoralpha in whole blood cultures from children with primary malnutrition. Braz J Med Biol Res 38:171–183
van der Vaart H, Postma DS, Timens W, ten Hacken NH (2004) Acute effects of cigarette smoke on inflammation and oxidative stress: a review. Thorax 59:713–721
Laan M, Bozinovski S, Anderson GP (2004) Cigarette smoke inhibits lipopolysaccharideinduced production of inflammatory cytokines by suppressing the activation of activator protein-1 in bronchial epithelial cells. J Immunol 173:4164–4170
Miller LG, Goldstein G, Murphy M, Ginns LC (1982) Reversible alterations in immunoregulatory T cells in smoking. Analysis by monoclonal antibodies and flow cytometry. Chest 82: 526–529
Oudijk EJ, Lammers JW, Koenderman L (2003) Systemic inflammation in chronic obstructive pulmonary disease. Eur Respir J Suppl 46:5s–13s
Osborne MJ, Stansby GP (1992) Cigarette smoking and its relationship to inflammatory bowel disease: a review. J R Soc Med 85:214–216
Crabtree TD, Pelletier SJ, Gleason TG, Pruett TL, Sawyer RG (1999) Gender-dependent differences in outcome after the treatment of infection in hospitalized patients. JAMA 282:2143–2148
Beery TA (2003) Sex differences in infection and sepsis. Crit Care Nurs Clin North Am 15:55–62
Marriott I, Bost KL, Huet-Hudson YM (2006) Sexual dimorphism in expression of receptors for bacterial lipopolysaccharides in murine macrophages: a possible mechanism for genderbased differences in endotoxic shock susceptibility. J Reprod Immunol 71:12–27
Krabbe KS, Pedersen M, Bruunsgaard H (2004) Inflammatory mediators in the elderly. Exp Gerontol 39:687–699
Walston J, McBurnie MA, Newman A, et al (2002) Frailty and activation of the inflammation and coagulation systems with and without clinical comorbidities: results from the Cardiovascular Health Study. Arch Intern Med 162:2333–2341
Shephard RJ (2002) Cytokine responses to physical activity, with particular reference to IL-6: sources, actions, and clinical implications. Crit Rev Immunol 22:165–182
Zheng H, Patel M, Hryniewicz K, Katz SD (2006) Association of extended work shifts, vascular function, and inflammatory markers in internal medicine residents: a randomized crossover trial. JAMA 296:1049–1050
Fishman JA, Rubin RH (1998) Infection in organ-transplant recipients. N Engl J Med 338:1741–1751
Safdar A, Armstrong D (2001) Infectious morbidity in critically ill patients with cancer. Crit Care Clin 17:531–viii
Blumberg N, Triulzi DJ, Heal JM (1990) Transfusion-induced immunomodulation and its clinical consequences. Transfus Med Rev 4:24–35
Almog Y, Shefer A, Novack V, et al (2004) Prior statin therapy is associated with a decreased rate of severe sepsis. Circulation 110:880–885
Elsayed E, Becker RC (2003) The impact of heparin compounds on cellular inflammatory responses: a construct for future investigation and pharmaceutical development. J Thromb Thrombolysis 15:11–18
Watson DW, Kim YB (1963) Modification of host responses to bacterial endotoxins. I. Specificity of pyrogenic tolerance and the role of hypersensitivity in pyrogenicity, lethality, and skin reactivity. J Exp Med 118:425–446
Randow F, Syrbe U, Meisel C, et al (1995) Mechanism of endotoxin desensitization: involvement of interleukin 10 and transforming growth factor beta. J Exp Med 181:1887–1892
Cavaillon JM, Adib-Conquy M (2006) Bench to bedside review: Endotoxin tolerance as a model of immune deactivation in sepsis. Crit Care 10:233
White JC, Nelson S, Winkelstein JA, Booth FV, Jakab GJ (1986) Impairment of antibacterial defense mechanisms of the lung by extrapulmonary infection. J Infect Dis 153:202–208
Steinhauser ML, Hogaboam CM, Kunkel SL, Lukacs NW, Strieter RM, Standiford TJ (1999) IL-10 is a major mediator of sepsis-induced impairment in lung antibacterial host defense. J Immunol 162:392–399
Meduri GU, Kanangat S, Stefan J, Tolley E, Schaberg D (1999) Cytokines IL-1beta, IL-6, and TNF-alpha enhance in vitro growth of bacteria. Am J Respir Crit Care Med 160:961–967
Cundell DR, Gerard NP, Gerard C, Idanpaan-Heikkila I, Tuomanen EI (1995) Streptococcus pneumoniae anchor to activated human cells by the receptor for platelet-activating factor. Nature 377:435–438
Clark J, Vagenas P, Panesar M, Cope AP (2005) What does tumour necrosis factor excess do to the immune system long term? Ann Rheum Dis 64:70–76
Yende S, Kong L, Weissfeld L, et al (2006) Inflammatory markers prior to hospital discharge predict subsequent mortality after community acquired pneumonia. Proc Am Thorac Soc 3:A836 (abst)
Benjamim CF, Hogaboam CM, Kunkel SL (2004) The chronic consequences of severe sepsis. J Leukoc Biol 75:408–412
Author information
Authors and Affiliations
Rights and permissions
Copyright information
© 2007 Springer Science + Business Media Inc.
About this paper
Cite this paper
Reade, M.C., Milbrandt, E.B., Angus, D.C. (2007). The Impact of Chronic Disease on Response to Infection. In: Intensive Care Medicine. Yearbook of Intensive Care and Emergency Medicine, vol 2007. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-49433-1_18
Download citation
DOI: https://doi.org/10.1007/978-3-540-49433-1_18
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-540-49432-4
Online ISBN: 978-3-540-49433-1
eBook Packages: MedicineMedicine (R0)