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Thematische Bibliographien / Inflammatory response syndrome / Zeitschriftenartikel

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Zeitschriftenartikel zum Thema „Inflammatory response syndrome“

Autor: Grafiati

Veröffentlicht am 15. Februar 2025

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1

Williams, John G., und Ronald V. Maier. „The Inflammatory Response“. Journal of Intensive Care Medicine 7, Nr. 2 (März 1992): 53–66. http://dx.doi.org/10.1177/088506669200700203.

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Inflammation is a critical component of the normal healing process. In the patient with extensive injury or infection, however, this same process may lead to organ dysfunction and failure as seen in adult respiratory distress syndrome and multiple organ failure syndrome. In this article we review: (1) the evolution of current concepts of inflammation; (2) individual elements of the host response to inflammatory stimuli; and (3) current strategies for the prevention and treatment of adult respiratory distress syndrome and multiple organ failure syndrome. From the Department of Surgery, University of Washington School of Medicine, Harborview Medical Center, Seattle, WA.

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2

Botwinski, Carol. „Systemic Inflammatory Response Syndrome“. Neonatal Network 20, Nr. 5 (August 2001): 21–28. http://dx.doi.org/10.1891/0730-0832.20.5.21.

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Despite advances in perinatal care in the past decade, sepsis and its complications continue to present problems for the neonate, remaining a major cause of neonatal morbidity and mortality. Sepsis research is focusing on how the neonate (host) responds to bacteria. The newborn may develop a systemic reaction to bacteria that induces the release of substances known as inflammatory mediators. Termed the systemic inflammatory response syndrome (SIRS), this reaction is believed to be responsible for the signs and symptoms of sepsis. This article introduces the neonatal nurse to SIRS, providing an overview of various inflammatory mediators and cytokines, their clinical consequences, and potential new therapies in the management of SIRS.

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3

Ahmed, Najma, und Nicolas Christou. „SYSTEMIC INFLAMMATORY RESPONSE SYNDROME“. Shock 5 (Juni 1996): S39–42. http://dx.doi.org/10.1097/00024382-199606001-00008.

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4

Ahmed, Najma, und Nicolas Christou. „SYSTEMIC INFLAMMATORY RESPONSE SYNDROME“. Shock 6, Supplement (Oktober 1996): S39—S42. http://dx.doi.org/10.1097/00024382-199610001-00008.

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5

Adams-Chapman, Ira, und Barbara J. Stoll. „Systemic inflammatory response syndrome“. Seminars in Pediatric Infectious Diseases 12, Nr. 1 (Januar 2001): 5–16. http://dx.doi.org/10.1053/spid.2001.19230.

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6

Davies, M. G., und P. O. Hagen. „Systemic inflammatory response syndrome“. British Journal of Surgery 84, Nr. 7 (Juli 1997): 920–35. http://dx.doi.org/10.1002/bjs.1800840707.

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7

Angood, Peter B. „Pancreatitis inflammatory response syndrome (PIRS)? Can there be another inflammatory response syndrome?“ Critical Care Medicine 27, Nr. 12 (Dezember 1999): 2832–33. http://dx.doi.org/10.1097/00003246-199912000-00041.

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8

van der Poll, Tom, und Joost C. M. Meijers. „Systemic Inflammatory Response Syndrome and Compensatory Anti-Inflammatory Response Syndrome in Sepsis“. Journal of Innate Immunity 2, Nr. 5 (2010): 379–80. http://dx.doi.org/10.1159/000318190.

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9

Vanourny, Jaime, und Brian L. Swick. „Sweet Syndrome With Systemic Inflammatory Response Syndrome“. Archives of Dermatology 148, Nr. 8 (01.08.2012): 969. http://dx.doi.org/10.1001/archdermatol.2012.766.

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10

Ansari, Shuaib, Irfan Murtaza Shahwani, Zeeshan Ali, Syed Zulfiquar Ali Shah und Faisal Shahab. „SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS)“. Professional Medical Journal 22, Nr. 03 (10.03.2015): 293–98. http://dx.doi.org/10.29309/tpmj/2015.22.03.1343.

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Systemic inflammatory response syndrome (SIRS) is a generalized disorder,immune response to infection which results in disturbed microcirculation, visceral perfusion andultimately visceral failure. Objectives: To determine the frequency of systemic inflammatoryresponse syndrome in patients with liver cirrhosis. Design: Cross sectional descriptive.Period: Six months study. Setting: At Liaquat University Hospital Hyderabad. Patients andmethods: All the patients with liver cirrhosis for 06 months duration admitted in the ward werefurther evaluated for systemic inflammatory response syndrome. The data was analyzed inSPSS 16 and the frequency and percentage was calculated. Results: During six months studyperiod, total 100 cirrhotic subjects were studied for SIRS. The mean ± SD for age in all (100)cirrhotic patients was 45.74 ± 7.537. The mean temperatures was 40.42±0.32 where as it was39.72±0.43 and 38.92±0.11 in male and female population respectively. The mean heart beatwas 128.42±6.74 where as it was 115.83±8.93 and 120.62±5.53 in male and female populationrespectively. The mean respiratory rate was 25.31±3.52 where as it was 23.52±2.31 and26.63±3.21 in male and female population respectively. The mean white blood cell count was28.81±4.51 where as it was 23.74±4.73 and 30.83±5.73 respectively. The SIRS was observedin 70% subjects of which 47(67.1%) were males and 23(32.9%) were females (p=0.04). Majorityof SIRS subjects were 30-39 years of age and male population was predominant (p=0.03). Thegender distribution in relation to severity of liver disease was statistically significant (p=0.05)while the SIRS in relation statical analysis. Conclusions: The systemic inflammatory responsesyndrome occurs in patients with liver cirrhosis.

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Meeran, Hanif, und Mark Messent. „The systemic inflammatory response syndrome“. Trauma 3, Nr. 2 (April 2001): 89–100. http://dx.doi.org/10.1177/146040860100300203.

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12

Balk, Robert A. „Systemic inflammatory response syndrome (SIRS)“. Virulence 5, Nr. 1 (13.11.2013): 20–26. http://dx.doi.org/10.4161/viru.27135.

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13

Fein, Alan M. „Systemic Inflammatory Response Syndrome (SIRS)“. Clinical Pulmonary Medicine 2, Nr. 3 (Mai 1995): 189. http://dx.doi.org/10.1097/00045413-199505000-00008.

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14

GOTSCH, FRANCESCA, ROBERTO ROMERO, JUAN PEDRO KUSANOVIC, SHALI MAZAKI-TOVI, BETH L. PINELES, OFFER EREZ, JIMMY ESPINOZA und SONIA S. HASSAN. „The Fetal Inflammatory Response Syndrome“. Clinical Obstetrics and Gynecology 50, Nr. 3 (September 2007): 652–83. http://dx.doi.org/10.1097/grf.0b013e31811ebef6.

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15

Meeran, H., und M. Messent. „The systemic inflammatory response syndrome“. Trauma 3, Nr. 2 (01.04.2001): 89–100. http://dx.doi.org/10.1191/146040801678227932.

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16

Gomez, Ricardo, Roberto Romero, Fabio Ghezzi, Bo Hyun Yoon, Moshe Mazor und Stanley M. Berry. „The fetal inflammatory response syndrome“. American Journal of Obstetrics and Gynecology 179, Nr. 1 (Juli 1998): 194–202. http://dx.doi.org/10.1016/s0002-9378(98)70272-8.

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17

Robertson, Charles M., und Craig M. Coopersmith. „The systemic inflammatory response syndrome“. Microbes and Infection 8, Nr. 5 (April 2006): 1382–89. http://dx.doi.org/10.1016/j.micinf.2005.12.016.

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18

Bone, Roger C. „The Systemic Inflammatory Response Syndrome“. Clinical Immunotherapeutics 1, Nr. 5 (Mai 1994): 369–77. http://dx.doi.org/10.1007/bf03258514.

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19

Weigand, Markus A., Christian Hörner, Hubert J. Bardenheuer und Axel Bouchon. „The systemic inflammatory response syndrome“. Best Practice & Research Clinical Anaesthesiology 18, Nr. 3 (September 2004): 455–75. http://dx.doi.org/10.1016/j.bpa.2003.12.005.

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20

Cavaillon, Jean-Marc, und Minou Adib-Conquy. „Compensatory anti-inflammatory response syndrome“. Thrombosis and Haemostasis 101, Nr. 01 (2009): 36–47. http://dx.doi.org/10.1160/th08-07-0421.

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SummaryThe concept of ‘Compensatory anti-inflammatory response syndrome’ (CARS) was proposed in 1997 by Roger Bone (1941–1997) to qualify the consequences of the counter-regulatory mechanisms initiated to limit the overzealous inflammatory process in patients with infectious (sepsis) or non-infectious systemic inflammatory response syndrome (SIRS). One major consequence of CARS is the modification of the immune status that could favour the enhanced susceptibility of intensive care patients to nosocomial infections. Indeed, most animal ‘two-hit’ models illustrate an enhanced sensitivity to infection after a first insult. However, this observation is highly dependent on the experimental procedure. Numerous functions of circulating leukocytes are altered in sepsis and SIRS patients, as well as in animal models of sepsis or SIRS. However, this is rather a reprogramming of circulating leukocytes, since there is not a global defect of the immune cells functions. Furthermore, within tissues, leukocytes are rather primed or activated than immunosuppressed. Thus, CARS may be considered as an adapted compartmentalized response with the aim to silence some acute proinflammatory genes, and to maintain the possible expression of certain genes involved in the anti-infectious process.

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21

Balk, R. A. „The systemic inflammatory response syndrome“. JAMA: The Journal of the American Medical Association 274, Nr. 2 (12.07.1995): 127b—127. http://dx.doi.org/10.1001/jama.274.2.127b.

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22

Balk, Robert A. „The Systemic Inflammatory Response Syndrome“. JAMA: The Journal of the American Medical Association 274, Nr. 2 (12.07.1995): 127. http://dx.doi.org/10.1001/jama.1995.03530020045021.

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23

Zhuk, S. I., und O. D. Shchurevska. „The Fetal Inflammatory Response Syndrome (Clinical lecture)“. Reproductive health of woman, Nr. 1 (23.03.2022): 37–43. http://dx.doi.org/10.30841/2708-8731.1.2022.258136.

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The article highlights the problem of fetal inflammatory response syndrome (FIRS) in modern conditions. This term has been introduced into the clinical practice to describe the systemic activation of the innate or acquired immune system of the fetus. FIRS can occur in response to infection or inflammation and is divided into two types depending on the type of immune response. FIRS I and II types are different clinical syndromes and correspond to acute and chronic inflammatory processes.The main pathophysiological mechanisms and clinical features of different variants of FIRS are described. Fetuses with this syndrome have signs of multiorgan damage. The consequences of FIRS are a high rate of complications in newborns: sepsis, congenital pneumonia, intraventricular hemorrhage, periventricular leukomalacia, cerebral palsy, neurosensory deafness, necrotic enterocolitis and others. The detailed description of fetal organs and systems damage by FIRS is presented. In further life, such children are at risk of long-term complications. This syndrome can also be the cause of unexplained antenatal fetal death.Laboratory diagnostic criteria for FIRS type I include elevated levels of interleukin-6 and acute phase reagents. Histologically there are the signs of funiculitis or chorionic vasculitis.The marker of FIRS type II is the chemotactic chemokine CXCL10, which simulates maternal antifetal rejection.The article presents the basic mechanisms of the immune response in FIRS. In this type of pathology there are chronic inflammatory lesions of the placenta which are determined by histological study (chronic chorioamnionitis, vilitis of unknown etiology, chronic deciduitis).

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24

Matthews, P. C., und S. M. Willatts. „Sweet's syndrome associated with systemic inflammatory response syndrome“. Intensive Care Medicine 24, Nr. 10 (20.10.1998): 1106–9. http://dx.doi.org/10.1007/s001340050724.

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25

Otheo, Enrique, Purificación Ros, José L. Vázquez, Rosario Carrillo, Ramón Moreno, Soledad Maldonado und Isabel Martos. „Systemic inflammatory response syndrome associated with Sweet’s syndrome“. Pediatric Critical Care Medicine 3, Nr. 2 (April 2002): 190–93. http://dx.doi.org/10.1097/00130478-200204000-00020.

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26

Galkin, A. A., und V. S. Demidova. „NEUTROPHILS AND SYSTEMIC INFLAMMATORY RESPONSE SYNDROME“. Wounds and wound infections. The prof. B.M. Kostyuchenok journal 2, Nr. 2 (16.12.2015): 25. http://dx.doi.org/10.17650/2408-9613-2015-2-2-25-31.

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27

Wolf, Ido, Meir Mouallem, Shmuel Rath und Zvi Farfel. „Clopidogrel-Induced Systemic Inflammatory Response Syndrome“. Mayo Clinic Proceedings 78, Nr. 5 (Mai 2003): 618–20. http://dx.doi.org/10.4065/78.5.618.

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28

Moore, Lesley. „Systemic inflammatory response syndrome – an overview“. Veterinary Nursing Journal 31, Nr. 1 (14.12.2015): 18–21. http://dx.doi.org/10.1080/17415349.2015.1113150.

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29

Dellinger, R. Phillip. „Dynamic Systemic Inflammatory Response Syndrome Monitoring“. Critical Care Medicine 44, Nr. 12 (Dezember 2016): 2285–86. http://dx.doi.org/10.1097/ccm.0000000000002112.

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30

Forster, Christopher J., Brian M. Cohee, Robert N. Wood-Morris und Joshua D. Hartzell. „Nitrofurantoin-Induced Systemic Inflammatory Response Syndrome“. American Journal of the Medical Sciences 338, Nr. 4 (Oktober 2009): 338–40. http://dx.doi.org/10.1097/maj.0b013e3181abd9f6.

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31

Barraviera, B. „Systemic inflammatory response syndrome in envenoming“. Toxicon 35, Nr. 1 (Januar 1997): 13–14. http://dx.doi.org/10.1016/s0041-0101(96)00126-2.

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32

Graninger, W., und C. Wenisch. „Pentoxifylline in Severe Inflammatory Response Syndrome“. Journal of Cardiovascular Pharmacology 25 (1995): S134—S138. http://dx.doi.org/10.1097/00005344-199500252-00028.

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33

Purvis, Deanna, und Rebecca Kirby. „Systemic Inflammatory Response Syndrome: Septic Shock“. Veterinary Clinics of North America: Small Animal Practice 24, Nr. 6 (November 1994): 1225–47. http://dx.doi.org/10.1016/s0195-5616(94)50136-0.

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34

Rangel-Frausto, M. Sigfrido. „The Systemic Inflammatory Response Syndrome-Reply“. JAMA: The Journal of the American Medical Association 274, Nr. 2 (12.07.1995): 127. http://dx.doi.org/10.1001/jama.1995.03530020045022.

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35

Milic, Dragan, Miljko Pejic, Sasa Zivic, Aleksandar Karanikolic, Slobodan Jovanovic und Milan Radojkovic. „Systemic inflammatory response syndrome in surgical patients with sepsis“. Srpski arhiv za celokupno lekarstvo 132, Nr. 5-6 (2004): 182–86. http://dx.doi.org/10.2298/sarh0406182m.

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Systemic inflammatory response syndrome and sepsis are common in surgically treated patients. Systemic inflammatory response syndrome represents a major factor of morbidity and mortality in these patients. The pathogenesis of these syndromes has been increasingly clarified. The objective of this review is to present an overview of our current understanding of the physiology underlying these conditions. <br><br><font color="red"><b> This article has been retracted. Link to the retraction <u><a href=http://dx.doi.org/10.2298/SARH1206269U>10.2298/SARH1206269U</a><u></b></font>

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36

KAWAI, Shin, Susumu SAKAYORI und Hiroyuki KOBAYASHI. „The Role of IL-10 in Patients with SIRS (Systemic Inflammatory Response Syndrome)“. Journal of the Japanese Association for Infectious Diseases 69, Nr. 7 (1995): 765–71. http://dx.doi.org/10.11150/kansenshogakuzasshi1970.69.765.

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37

Shrestha, Manisha, und Anand Kumar. „SYSTEMIC INFLAMMATORY RESPONSE SYNDROME: THE CURRENT STATUS“. Journal of Universal College of Medical Sciences 6, Nr. 1 (20.11.2018): 56–61. http://dx.doi.org/10.3126/jucms.v6i1.21732.

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Systemic inflammatory response syndrome (SIRS) is a frequent and serious problem faced by clinicians in day to day practice and is a major factor of intensive care morbidity and mortality. The American College of Chest Physicians and the American Society of Critical Care Medicine in 1991 published definitions and criteria for systemic inflammatory response syndrome. Since then many researches have been undertaken to better understand the pathophysiology of systemic inflammatory response syndrome and to determine the accuracy of its diagnostic criteria. The criteria set by the 1991 consensus is still popularly used today. However, with the current knowledge on this matter many researchers have put forward the need of refinement in the criteria of systemic inflammatory response syndrome defined by 1991 consensus. This article aims to review the epidemiology, etiology, pathophysiology, laboratory diagnosis, treatment and the current views regarding SIRS.Journal of Universal College of Medical SciencesVol. 6, No. 1, 2018, Page: 56-61

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38

Retnoningrum, Dwi, Meita Hendrianingtyas, Hermawan Istiadi und Ardhea Jaludamascena. „Correlation between Prolactin Serum with Neutrophil Lymphocyte Ratio (NLR) in Systemic Inflammatory Response Syndrome“. Diponegoro International Medical Journal 2, Nr. 1 (10.03.2021): 10–13. http://dx.doi.org/10.14710/dimj.v2i1.9546.

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Background: Systemic inflammatory response syndrome (SIRS) is a state of systemic inflammatory activation by various causes. SIRS have a high mortality rate. Prolactin is known to regulate cellular function of immune system. Neutrophil-lymphocyte ratio (NLR) is simple, cost effective and easy parameter that currently used as inflammation marker.Objective: The aims of this study is to determine the correlation between prolactin serum with NLR in SIRS patients.Methods: A cross sectional study was conducted on 50 clinically SIRS patients. Prolactin serum was measured by enzyme linked immunosorbent assay (ELISA) and NLR was calculated manually from absolute neutrophil and lymphocyte count measured by automatic hematology analyzer. Non-parametric Spearman test was used to analyze the correlation between prolactin with NLR.Results: Median value of serum prolactin level was 11.32 ng/mL (2.76-194.81), whereas the mean value NLR was 16.36 ± 11.58. The correlation between prolactin levels with NLR was r = 0.345, p = 0.014.Conclusion: There is a weak positive significant correlation between prolactin with neutrophil lymphocyte ratio in SIRS

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McGarry, Molly R., Meredith W. Wagner und Barry M. Wall. „Systemic Inflammatory Response Syndrome Secondary to Nitrofurantoin“. Journal of Investigative Medicine High Impact Case Reports 9 (Januar 2021): 232470962098461. http://dx.doi.org/10.1177/2324709620984610.

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Nitrofurantoin is considered optimal treatment for acute uncomplicated cystitis by the Infectious Diseases Society of America and is being increasingly recommended due to microbial resistance to sulfamethoxazole/trimethoprim and various fluoroquinolone antibiotics. Adverse effects of nitrofurantoin are generally considered mild, with gastrointestinal complaints being the most common. However, there have been isolated case reports describing a more severe systemic inflammatory response syndrome–like reaction, which leads to diagnostic challenges and treatment complications. We report the case of a patient with repeat episodes of systemic inflammatory response syndrome secondary to nitrofurantoin, which was initially attributed to recurrent urinary tract infections.

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吴, 娱. „Prenatal Diagnosis of Fetal Inflammatory Response Syndrome“. Advances in Clinical Medicine 12, Nr. 02 (2022): 1260–66. http://dx.doi.org/10.12677/acm.2022.122184.

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41

Кабанова, А. А., И. О. Походенько-Чудакова, С. А. Кабанова und Н. В. Дорошенко. „Odontogenic Phlegmon and Systemic Inflammatory Response Syndrome“. Стоматология. Эстетика. Инновации, Nr. 1 (13.04.2022): 93–99. http://dx.doi.org/10.34883/pi.2022.6.1.010.

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Цель. Выявить особенности течения одонтогенных флегмон челюстно-лицевой области при развитии синдрома системного воспалительного ответа.Материалы и методы. В проспективном обсервационном исследовании приняли участие 62 пациента, находившихся на стационарном лечении в отделении челюстно-лицевой хирургии Витебской областной клинической больницы в период 2016– 2018 гг. Все пациенты были разделены на 2 группы: группа 1 – пациенты с синдромом системного воспалительного ответа (ССВО) (34 человека), группа 2 – пациенты без синдрома системного воспалительного ответа (28 человек). Выполнено сравнение клинических показателей, а также ряда показателей крови пациентов при развитии ССВО и без него.Результаты. Проведенный анализ ряда показателей сыворотки крови, клинических показателей течения раневого процесса в зависимости от наличия синдрома системного воспалительного ответа у пациентов с одонтогенными флегмонами челюстно-лицевой области показал, что уровень прокальцитонина, аланинаминотрансферазы в крови, а также фагоцитарный индекс могут быть использованы в качестве прогностических критериев развития воспалительного процесса.Заключение. Дальнейший поиск предикторов распространения инфекционно-воспалительных процессов одонтогенной этиологии должен быть продолжен, что позволит повысить эффективность проводимого лечения и снизить количество тяжелых осложнений. Purpose. To identify the features of maxillofacial odontogenic phlegmons with the development of systemic inflammatory response syndrome.Materials and methods. A prospective observational study involved 62 patients who were hospitalized in the Department of Maxillofacial Surgery of the Vitebsk Regional Clinical Hospital in the period 2016–2018. All patients were divided into 2 subgroups: group 1 – patients with systemic inflammatory response syndrome (34 people), group 2 – patients without systemic inflammatory response syndrome (28 people). The comparison of clinical parameters, as well as a number of blood parameters of patients with the development of SIRS and without it, was carried out.Results. The analysis of a number of blood serum parameters, clinical indicators of the course of the wound process, depending on the presence of a systemic inflammatory response syndrome in patients with maxillofacial odontogenic phlegmons, showed that the level of procalcitonin, alanine aminotransferase in the blood, as well as the phagocytic index could be used as prognostic criteria for inflammation development.Conclusion. Further search for predictors of the infectious spread and inflammatory processes of odontogenic etiology should be continued, which will increase the effectiveness of the treatment and reduce the number of severe complications.

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Smajic, Jasmina, Lejla Tupkovic, Samir Husic, Selma Avdagic, Samir Hodzic und Semir Imamovic. „Systemic Inflammatory Response Syndrome in Surgical Patients“. Medical Archives 72, Nr. 2 (2018): 116. http://dx.doi.org/10.5455/medarh.2018.72.116-119.

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43

Jairam, Abhishek, Ping Song, Nirav B. Patel und Michael S. Wong. „Pressure Sores and Systemic Inflammatory Response Syndrome“. Annals of Plastic Surgery 80 (Mai 2018): S308—S310. http://dx.doi.org/10.1097/sap.0000000000001378.

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44

King, Landon S., und Hamid Rabb. „Muscling in on systemic inflammatory response syndrome*“. Critical Care Medicine 32, Nr. 5 (Mai 2004): 1233–34. http://dx.doi.org/10.1097/01.ccm.0000125516.53007.00.

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Katsuya, Inada, Endo Shigeatsu, Nakae Hajime, Kikuchi Mitsuru, Inoue Yoshihiro, Taniguchi Shigeru und Masao Yoshida. „ENDOTOXEMIA IN SIRS (SYSTEMIC INFLAMMATORY RESPONSE SYNDROME“. Shock 4, Supplement (Dezember 1995): 50. http://dx.doi.org/10.1097/00024382-199512001-00197.

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