Complications of acute pancreatitis

Balthazar, Emil J.

doi:10.1016/s0033-8389(02)00043-x

Cited by 133 publications

(75 citation statements)

References 63 publications

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“…Necrosis and saponification of adipose tissue, particularly in the retroperitoneum, are typically observed in AP patients (35). Macroscopic and histologic observation of adipose tissue obtained from ob/ob mice injected with IL-12 plus IL-18 revealed the presence of numerous foci of necrotic adipose tissue with saponification, which were rarely observed in WT mice (Fig.…”

Section: Resultsmentioning

confidence: 86%

Interleukin-18, together with interleukin-12, induces severe acute pancreatitis in obese but not in nonobese leptin-deficient mice

Sennello¹,

Fayad²,

Pini³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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Obesity is associated with increased severity of acute pancreatitis (AP). The cytokines IL-18 and IL-12 are elevated in patients with AP, and IL-18 levels are high in obesity. We aimed to develop a pathologically relevant model to study obesity-associated severe AP. Lean WT and obese leptin-deficient ob/ob mice received two injections of IL-12 plus IL-18. Survival, pancreatic inflammation, and biochemical markers of AP were measured. Dosing with IL-12 plus IL-18 induced 100% lethality in ob/ob mice; no lethality was observed in WT mice. Disruption of pancreatic exocrine tissue and acinar cell death as well as serum amylase and lipase levels were significantly higher in ob/ob than in WT mice. Edematous AP developed in WT mice, whereas obese ob/ob mice developed necrotizing AP. Adipose tissue necrosis and saponification were present in cytokine-injected ob/ob but not in WT mice. Severe hypocalcemia and elevated acute-phase response developed in ob/ob mice. The cytokine combination induced high levels of regenerating protein 1 and pancreatitis-associated protein expression in the pancreas of WT but not of ob/ob mice. To differentiate the contribution of obesity to that of leptin deficiency, mice received short-and long-term leptin replacement therapy. Shortterm leptin reconstitution in the absence of major weight loss did not protect ob/ob mice, whereas leptin deficiency in the absence of obesity resulted in a significant reduction in the severity of the pancreatitis. In conclusion, we developed a pathologically relevant model of AP in which obesity per se is associated with increased severity.cytokines ͉ inflammation ͉ obesity ͉ pancreas A cute pancreatitis (AP) is an inflammatory disorder that ranges from interstitial edema to confluent necrosis and hemorrhage. In severe cases, progress to circulatory shock, acute lung injury, renal failure, and eventual death may occur (1). Despite some controversy, numerous studies have demonstrated that obesity is associated with increased risk of the severe form of AP and with development of life-threatening complications (2-8). However, the mechanism by which increased adiposity worsens AP remains unknown.Leptin, a protein mainly produced by adipocytes, is a critical regulator of appetite (9). Leptin exerts important regulatory effects on inflammation (10). In the context of AP, the role of leptin remains controversial. In patients with AP, a correlation between serum leptin and disease severity has been reported by some investigators but not by others (11,12). Although in animal models administration of leptin decreases AP severity (13-16), more severe disease is present in leptin-deficient ob/ob and leptin receptordeficient db/db mice as well as leptin-receptor mutant fa/fa rats (17, 18). However, the differential effect of obesity versus leptin deficiency has not been fully investigated.IL-12 and IL-18 are two proinflammatory cytokines that drive the Th1 cell response, characterized by high levels of IFN-␥ (19). Both cytokines are mainly produced by monocytes/macrophages....

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Section: Resultsmentioning

confidence: 86%

Interleukin-18, together with interleukin-12, induces severe acute pancreatitis in obese but not in nonobese leptin-deficient mice

Sennello¹,

Fayad²,

Pini³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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“…Arterial erosion or pseudoaneurysms, ischaemic complications, and gastritis are the most common causes for a hemorrhage. Bleeding as a result of LSPH is even more dangerous because of the difficulty of diagnosis, treatment decision, and high recurrence rate (Balthazar, 2002). In the present study, we reported a case of LSPH caused by acute pancreatitis which suffered from fatal GI bleeding because of local gastric varices and failed to respond to medical therapy.…”

Section: Discussionmentioning

confidence: 60%

Acute pancreatitis associated left-sided portal hypertension with severe gastrointestinal bleeding treated by transcatheter splenic artery embolization: a case report and literature review

et al. 2013

J. Zhejiang Univ. Sci. B

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Left-sided portal hypertension (LSPH) followed by acute pancreatitis is a rare condition with most patients being asymptomatic. In cases where gastrointestinal (GI) bleeding is present, however, the condition is more complicated and the mortality is very high because of the difficulty in diagnosing and selecting optimal treatment. A successfully treated case with severe GI bleeding by transcatheter splenic artery embolization is reported in this article. The patient exhibited severe uncontrollable GI bleeding and was confirmed as gastric varices secondary to LSPH by enhanced computed tomography (CT) scan and CT-angiography. After embolization, the bleeding stopped and stabilized for the entire follow-up period without any severe complications. In conclusion, embolization of the splenic artery is a simple, safe, and effective method of controlling gastric variceal bleeding caused by LSPH in acute pancreatitis.

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“…Ölümlerin %2-10'u akut pankreatitin komplikasyonlar› sonucunda meydana gelir (12). Yaflam› tehdit eden komplikasyonlar hemen daima fliddetli akut pankreatitde oluflur (13 Bu komplikasyonlar görüldükleri döneme göre erken (2-3 gün), orta (2-5 hafta) ve geç (aylar-y›llar) olarak s›n›fland›r›-l›rlar (Tablo 5).…”

Section: Komplikasyonlarunclassified

Akut pankreatitde tedavi

Dışıbeyaz¹

2015

Endoskopi Gastrointestinal

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Toplumdaki insidans› 100.000'de 5-20 olan akut pankreatitin en s›k nedeni %80 olguda alkol ve safra tafl› migrasyonudur. Olgular›n büyük ço¤unlu¤u hafif formda olup, sadece k›sa süreli hospitalizasyonla düzelebilirken, az bir k›sm› ciddi mortalitiye de neden olabilen fliddetli formda görülür. fiiddetli formlarda tedavi mutlak yo¤un bak›m koflullar›nda yap›lmal› ve hasta çok yak›ndan izlenmelidir. Bu nedenle bu amaçla gelifltirilmifl indeksler kullan›la-rak fliddetli formun önceden tan›nmas› çok önemlidir. Tedavi medikal ve giriflimsel (endoskopik/cerrahi) olmak üzere ikiye ayr›labilir. S›v› replasman›, a¤r› kontrolü, tromboz proflaksisi, antibiyotik proflaksisi, enteral beslenme, O 2 tedavisi medikal tedavide önemliyken, endoskopik retrograd kolanjiyopankreatografi ile biliyer pankreatitde tafl ekstraksiyonu, pankreas divisumda stent yerlefltirilmesi, sfinkter oddi disfonksiyonunda sfinkterotomi ve ayr›ca endoskopik/cerrahi nekroz debridman›, pseudokist drenaj› uygulanabilecek giriflimsel yöntemlerdir.The prevalence of acute pancreatitis in population is estimated as 100.000/5-20 and alcohol and bile stone migration are considered as causes in 80% of cases. Disease has a mild course in most cases and patients recover with a short term hospitalization. In minority of patients, disease has a severe course that may cause death eventually. Patients in last form should be treated in ICU and be monitored very closely. Therefore estimating the severity of the disease early in the course, using several severity indexes which is developed for this purpose is very important. The treatment includes medical and interventional (surgical / endoscopic) modalities. Fluid replacement, pain control, antibiotic prophylaxis , enteral feeding, thrombosis prophlaxis and O 2 support are considered as essentials of medical treatment. Invasive methods are consist of biliary stone extraction , stenting in pancreas divisium, sphincterotomy in Sphyncter of Oddi Dysfunction via endoscopic retrograde cholangiopancreatography and endoscopic or surgical debridman in pancreatic necrosis and pseudocyst drainage.

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Complications of acute pancreatitis

Cited by 133 publications

References 63 publications

Interleukin-18, together with interleukin-12, induces severe acute pancreatitis in obese but not in nonobese leptin-deficient mice

Interleukin-18, together with interleukin-12, induces severe acute pancreatitis in obese but not in nonobese leptin-deficient mice

Acute pancreatitis associated left-sided portal hypertension with severe gastrointestinal bleeding treated by transcatheter splenic artery embolization: a case report and literature review

Akut pankreatitde tedavi

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