Gastrointestinal manifestations of hemolytic uremic syndrome: recognition of pancreatitis

Grodinsky, S.; Telmesani, Abdulwahab; Robson, Wm. Lane M.; Fick, Gordon H.; Scott, R. B.

doi:10.1007/bf00857886

Cited by 24 publications

(49 citation statements)

References 2 publications

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“…The microangiopathy caused by E. coli O-157 can also occur in other important organs, such as the brain and heart, with associated complications that include chronic renal failure, encephalopathy, cardiomyopathy, hypertension, and seizures [1,2,3]. Although some surgical gastrointestinal complications during the acute phase in HUS are well known, such as rectal prolapse and intussusception, the occurrence of either colonic perforation or stricture during the post-acute phase of HUS is rare [4,5].…”

Section: Introductionmentioning

confidence: 97%

Colonic stricture secondary to hemolytic uremic syndrome caused by Escherichia coli O-157

et al. 2005

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Shiga toxin-producing Escherichia coli (E. coli) is known to be one of the main causes of hemolytic uremic syndrome (HUS). Of the secondary complications of HUS, colonic stricture is relatively rare. We herein report on a Japanese girl that demonstrated sigmoid colon stricture secondary to HUS caused by an infection of E. coli O-157. Severe HUS occurred after the E. coli O-157 infection, so hemodialysis was performed due to renal failure. However, 1 month after recovery from HUS, abdominal symptoms occurred. A contrast study in the colon revealed a sigmoid colon stricture. The stricture was operatively resected. Thereafter, her postoperative course was uneventful. We also review the occurrence of this complication secondary to HUS in the literature.

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Section: Introductionmentioning

confidence: 97%

Colonic stricture secondary to hemolytic uremic syndrome caused by Escherichia coli O-157

et al. 2005

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“…Hyperglycemia was considered to be significant if a fasting serum glucose value was > 7.8 mmol/1, if any random serum glucose level was >11.1 mmol/l. and if the high glucose level persisted for >48 h. Pancreatitis was defined as a serum lipase or amylase level greater than four times the accepted level of normal, an elevation of serum levels of these enzymes associated with abnormal echogenicity or edema of the pan creas by ultrasound examination, or pathological evidence of pancre atitis found at autopsy [13,14], An elevated white blood cell count (WBC) was defined as > 15 x 109/1. Thrombocytopenia was defined as a platelet count < 100 x 109/l.…”

Section: Methodsmentioning

confidence: 99%

Hyperglycemia in Diarrhea-Associated Hemolytic-Uremic Syndrome

Robson

Leung²,

Brant³

et al. 1995

Nephron

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Hyperglycemia is a recognized complication of diarrhea-associated hemolytic-uremic syndrome (D + HUS). Hyperglycemia developed in 8 (6.6%) of 121 patients with D + HUS. A literature review revealed a further 11 patients with D + HUS who developed hyperglycemia. The mortality rate in this group of patients is high. Hyperglycemia is more common in patients with D + HUS uremic syndrome who are female, who have an elevated white blood cell count on admission, and who develop anuria or a central nervous system complication.

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“…It is well known that jaundice is often associated with hypersecretion of pancreatic juice and enzymes (17) and with acute pancreatitis (9,10,14,15,18,32). Several mechanisms have been suggested to possibly induce pancreatic hypersecretion in jaundice: an increase in circulating gastrointestinal peptide such as CCK and secretin due to impaired metabolism in the diseased liver (7,19,38); an increase in the circulating …”

Section: Discussionmentioning

confidence: 99%

“…We were unable to determine whether conjugated bilirubin has the same effects as unconjugated bilirubin on pancreatic acinar cells due to the lack of an available preparation of conjugated bilirubin. It is possible, however, that unconjugated bilirubin exerts its effects on the exocrine pancreas, because jaundice due to hemolytic diseases as well as liver and biliary tract disease can induce acute pancreatitis (9,10,14,15,18,32). Our study suggests a possible mechanism through which bilirubin induces pancreatic secretion and pancreatic injury by demonstrating the unique amylase-releasing effects of the bilirubin that accumulates in the circulation and/or periacinar space in patients with jaundice.…”

Section: Discussionmentioning

confidence: 99%

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Stimulatory effects of bilirubin on amylase release from isolated rat pancreatic acini

Hirohata

Fujii

Okabayashi

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

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latory effects of bilirubin on amylase release from isolated rat pancreatic acini. Am J Physiol Gastrointest Liver Physiol 282: G249-G256, 2002; 10.1152/ajpgi.00429.2002.-Considered to be an etiologic factor of acute pancreatitis, hypersecretion of pancreatic juice and digestive enzymes is often associated with hyperbilirubinemia. We explored the intracellular mechanisms through which bilirubin affects pancreatic exocrine secretory function by examining the effect of bilirubin on isolated rat pancreatic acini. Bilirubin stimulated amylase release in a concentration-and time-dependent manner, significantly increasing amylase release at concentrations Ͼ5 mg/100 ml and after 15 min of incubation. Coincubation of bilirubin with vasoactive intestinal polypeptide, 8-bromo-cAMP, or A-23187 had a synergistic effect on amylase release, whereas coincubation with CCK-8, carbamylcholine, or 12-O-tetradecanoylphorbol 13-acetate had an additive effect. Bilirubin did not affect acinar cAMP content or Ca 2ϩ efflux. Intracellular Ca 2ϩ pool depletion had no influence on bilirubin-evoked amylase release. The protein kinase C (PKC) inhibitors staurosporine and calphostin C partially but significantly inhibited bilirubin-stimulated amylase release, whereas the PKA inhibitor H-89 did not. The tyrosine kinase (TK) inhibitor genistein, phospholipase A2 (PLA2) inhibitor indoxam, and PLC inhibitor U-73122 also inhibited amylase release. Bilirubin significantly translocated PKC activity from the cytosol to the membrane fraction and activated TK in cytosol and membrane fractions. These results indicate that bilirubin stimulates amylase release by activating PKC and TK in rat pancreatic acini and that PLC and PLA2 partly mediate this process. signal transduction; protein kinase C; tyrosine kinase; phospholipase C; phospholipase A 2

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Gastrointestinal manifestations of hemolytic uremic syndrome: recognition of pancreatitis

Cited by 24 publications

References 2 publications

Colonic stricture secondary to hemolytic uremic syndrome caused by Escherichia coli O-157

Colonic stricture secondary to hemolytic uremic syndrome caused by Escherichia coli O-157

Hyperglycemia in Diarrhea-Associated Hemolytic-Uremic Syndrome

Stimulatory effects of bilirubin on amylase release from isolated rat pancreatic acini

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