- ICH GCP
- US Clinical Trials Registry
- Klinisk forsøg NCT00786591
Study of New Biological Markers for Prediction of Severe Acute Pancreatitis
27. december 2012 opdateret af: Medicine, National University Hospital, Singapore
Clinical Evaluation of Novel Biological Markers for the Prediction of Severe Acute Pancreatitis
Acute pancreatitis refers to inflammation of the pancreas and is associated with sudden onset of severe abdominal pain, often accompanied by transient systemic manifestations, including fever.
In the majority of cases, the inflammatory process is self limiting and patient recovers uneventfully; however, in about 20% to 30% of the cases, a protracted clinical course ensues and the disease may progress to a severe necrotizing form, often triggering a systemic inflammatory response syndrome during which time, acute respiratory distress syndrome, renal failure, shock, and disseminated intravascular coagulation may occur.
In the worst sequelae, multiple organ dysfunctions may follow and death supervene.
The clinical outcome of patients suffering from severe acute pancreatitis depends to a great extent on the early diagnosis and prediction of severity and timely therapeutic intervention to prevent local and systemic complications.
However, the course of the disease is often difficult to predict from the outset.
Currently, there is still no single clinical or laboratory test that can be considered the "gold standard" for diagnosis and/or assessment of severity of acute pancreatitis.
For a disease that may progress rapidly without apparent sign, the ideal marker for the prediction of disease severity in a patient would be one that is measurable rapidly and easily, besides being able to fulfill all the other criteria required of a good biological marker.
To identify such a potential marker for acute pancreatitis requires understanding of the pathophysiological process underlying the rapid progression of a fulminant course of the disease.
Although much remains to be elucidated, recent studies in animals have suggested that inflammatory mediators substance P and hydrogen sulfide may play critical roles.
This study will evaluate if inflammatory mediators substance P and hydrogen sulfide are upregulated early on in the disease process, and if the levels of their elevation predict disease severity.
Studieoversigt
Status
Afsluttet
Betingelser
Undersøgelsestype
Observationel
Tilmelding (Faktiske)
75
Kontakter og lokationer
Dette afsnit indeholder kontaktoplysninger for dem, der udfører undersøgelsen, og oplysninger om, hvor denne undersøgelse udføres.
Studiesteder
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Singapore, Singapore, 119074
- National University Hospital
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Deltagelseskriterier
Forskere leder efter personer, der passer til en bestemt beskrivelse, kaldet berettigelseskriterier. Nogle eksempler på disse kriterier er en persons generelle helbredstilstand eller tidligere behandlinger.
Berettigelseskriterier
Aldre berettiget til at studere
18 år og ældre (Voksen, Ældre voksen)
Tager imod sunde frivillige
Ingen
Køn, der er berettiget til at studere
Alle
Prøveudtagningsmetode
Ikke-sandsynlighedsprøve
Studiebefolkning
Patients with clinical presentation suggestive of acute pancreatitis
Beskrivelse
Inclusion Criteria:
The patient should fulfill all of the following criteria:
- The subject should be at least 18 years of age.
- Clinical features compatible with acute pancreatitis.
- First symptoms of acute pancreatitis not more than 72 hours before enrolment.
- Serum amylase level above 480 U/dl (normal 60-160 U/dl or 2-hour urinary amylase greater than 1120 U (normal 280 U).
- Serum lipase levels greater than 2 U (normal < 1 U).
- Patient has signed consent form regarding participation in the study.
Exclusion Criteria:
The patient should not present any of the following criteria:
- Symptoms of acute pancreatitis present for more than 72 hours
- Clinical evidence of sepsis or other inflammatory diseases.
- Clinical evidence of disorders/disease known to affect endogenous regulation of substance P, e.g. asthma, immune-complex-mediated lung injury, arthritis.
- Age under 18 years
- Pregnancy
Studieplan
Dette afsnit indeholder detaljer om studieplanen, herunder hvordan undersøgelsen er designet, og hvad undersøgelsen måler.
Hvordan er undersøgelsen tilrettelagt?
Design detaljer
- Observationsmodeller: Case-Control
- Tidsperspektiver: Fremadrettet
Kohorter og interventioner
Gruppe / kohorte |
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Acute Pancreatitis Patients
Patients presenting with clinical features compatible with acute pancreatitis
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Control
Preoperative patients going for elective cholecystectomy
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Hvad måler undersøgelsen?
Primære resultatmål
Resultatmål |
Tidsramme |
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Levels of substance P and hydrogen sulfide in blood measured 6-hourly over a time course of 3 days
Tidsramme: On admission to hospital, blood sampling will be done every 6 hours for 3 days
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On admission to hospital, blood sampling will be done every 6 hours for 3 days
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Sekundære resultatmål
Resultatmål |
Tidsramme |
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Disease severity index derived from: (i) Ranson score; (ii) Acute Physiology and Chronic Health Evaluation (APACHE) II scores; (iv) Glasgow and (v) Multi-Organ System Failure (MOSF) Score
Tidsramme: Within 3 days of hospital admission
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Within 3 days of hospital admission
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Samarbejdspartnere og efterforskere
Det er her, du vil finde personer og organisationer, der er involveret i denne undersøgelse.
Publikationer og nyttige links
Den person, der er ansvarlig for at indtaste oplysninger om undersøgelsen, leverer frivilligt disse publikationer. Disse kan handle om alt relateret til undersøgelsen.
Generelle publikationer
- Tamizhselvi R, Moore PK, Bhatia M. Hydrogen sulfide acts as a mediator of inflammation in acute pancreatitis: in vitro studies using isolated mouse pancreatic acinar cells. J Cell Mol Med. 2007 Mar-Apr;11(2):315-26. doi: 10.1111/j.1582-4934.2007.00024.x.
- Bhatia M, Zhi L, Zhang H, Ng SW, Moore PK. Role of substance P in hydrogen sulfide-induced pulmonary inflammation in mice. Am J Physiol Lung Cell Mol Physiol. 2006 Nov;291(5):L896-904. doi: 10.1152/ajplung.00053.2006. Epub 2006 Jun 23.
- Hegde A, Bhatia M. Neurogenic inflammation in acute pancreatitis. JOP. 2005 Sep 10;6(5):417-21.
- Lau HY, Wong FL, Bhatia M. A key role of neurokinin 1 receptors in acute pancreatitis and associated lung injury. Biochem Biophys Res Commun. 2005 Feb 11;327(2):509-15. doi: 10.1016/j.bbrc.2004.12.030.
- Grady EF, Yoshimi SK, Maa J, Valeroso D, Vartanian RK, Rahim S, Kim EH, Gerard C, Gerard N, Bunnett NW, Kirkwood KS. Substance P mediates inflammatory oedema in acute pancreatitis via activation of the neurokinin-1 receptor in rats and mice. Br J Pharmacol. 2000 Jun;130(3):505-12. doi: 10.1038/sj.bjp.0703343.
- Bhatia M, Saluja AK, Hofbauer B, Frossard JL, Lee HS, Castagliuolo I, Wang CC, Gerard N, Pothoulakis C, Steer ML. Role of substance P and the neurokinin 1 receptor in acute pancreatitis and pancreatitis-associated lung injury. Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4760-5. doi: 10.1073/pnas.95.8.4760.
Datoer for undersøgelser
Disse datoer sporer fremskridtene for indsendelser af undersøgelsesrekord og resumeresultater til ClinicalTrials.gov. Studieregistreringer og rapporterede resultater gennemgås af National Library of Medicine (NLM) for at sikre, at de opfylder specifikke kvalitetskontrolstandarder, før de offentliggøres på den offentlige hjemmeside.
Studer store datoer
Studiestart
1. juni 2006
Primær færdiggørelse (Faktiske)
1. juli 2009
Studieafslutning (Faktiske)
1. juli 2009
Datoer for studieregistrering
Først indsendt
4. november 2008
Først indsendt, der opfyldte QC-kriterier
4. november 2008
Først opslået (Skøn)
6. november 2008
Opdateringer af undersøgelsesjournaler
Sidste opdatering sendt (Skøn)
31. december 2012
Sidste opdatering indsendt, der opfyldte kvalitetskontrolkriterier
27. december 2012
Sidst verificeret
1. december 2012
Mere information
Begreber relateret til denne undersøgelse
Yderligere relevante MeSH-vilkår
Andre undersøgelses-id-numre
- D/05/194
Disse oplysninger blev hentet direkte fra webstedet clinicaltrials.gov uden ændringer. Hvis du har nogen anmodninger om at ændre, fjerne eller opdatere dine undersøgelsesoplysninger, bedes du kontakte register@clinicaltrials.gov. Så snart en ændring er implementeret på clinicaltrials.gov, vil denne også blive opdateret automatisk på vores hjemmeside .