The Experts below are selected from a list of 231 Experts worldwide ranked by ideXlab platform
Prodromos Hytiroglou - One of the best experts on this subject based on the ideXlab platform.
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Toxic hepatic injury mimicking Ascending Cholangitis: is Pyrus amygdaliformis to blame?
Virchows Archiv : an international journal of pathology, 2008Co-Authors: Despoina Televantou, Emmanouil Sinakos, Evangelos Akriviadis, Prodromos HytiroglouAbstract:Cholestatic hepatic injury can be caused by a number of drugs and herbal remedies [1, 3, 5]. Occasionally, drugs that cause cholestasis, such as amoxicillin-clavulanate, chlorpromazine, and erythromycin are associated with acute purulent inflammation of the intrahepatic bile ducts, mimicking acute (Ascending) Cholangitis [3]. We present a case of acute cholestatic toxic liver injury with histologic features of Ascending Cholangitis and a possible association with ingestion of forest fruit. The patient is a 55-year-old man, who presented with a 3-day history of marked jaundice. There was no abdominal pain, fever, or history of medications, except for a 5-day course of a cephalosporin antibiotic taken 2 months prior to presentation. On physical examination, there were no findings apart from jaundice. The patient was carefully interviewed regarding potential toxins, and he admitted recent consumption of Pyrus amygdaliformis fruit (also known as “wild pears” in Greece). In detail, he admitted consuming approximately 0.5 kg of raw fruit daily, during the week prior to presentation. He also admitted previous exposure to the same fruit, but that was sporadic and in much smaller quantities. Laboratory findings on his first day of hospitalization were as follows: hemoglobin, 15.4 g/dl; white blood cell count, 7,370 per milliliter; platelets, 275,000 per milliliter; glucose, 118 mg/dl; urea, 27 mg/dl; creatinine, 1.1 mg/dl; bilirubin, 10.6 mg/dl; direct bilirubin, 7.0 mg/dl; aspartate aminotransferase (AST), 195 U/L (normal,
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toxic hepatic injury mimicking Ascending Cholangitis is pyrus amygdaliformis to blame
Virchows Archiv, 2008Co-Authors: Despoina Televantou, Emmanouil Sinakos, Evangelos Akriviadis, Prodromos HytiroglouAbstract:Cholestatic hepatic injury can be caused by a number of drugs and herbal remedies [1, 3, 5]. Occasionally, drugs that cause cholestasis, such as amoxicillin-clavulanate, chlorpromazine, and erythromycin are associated with acute purulent inflammation of the intrahepatic bile ducts, mimicking acute (Ascending) Cholangitis [3]. We present a case of acute cholestatic toxic liver injury with histologic features of Ascending Cholangitis and a possible association with ingestion of forest fruit. The patient is a 55-year-old man, who presented with a 3-day history of marked jaundice. There was no abdominal pain, fever, or history of medications, except for a 5-day course of a cephalosporin antibiotic taken 2 months prior to presentation. On physical examination, there were no findings apart from jaundice. The patient was carefully interviewed regarding potential toxins, and he admitted recent consumption of Pyrus amygdaliformis fruit (also known as “wild pears” in Greece). In detail, he admitted consuming approximately 0.5 kg of raw fruit daily, during the week prior to presentation. He also admitted previous exposure to the same fruit, but that was sporadic and in much smaller quantities. Laboratory findings on his first day of hospitalization were as follows: hemoglobin, 15.4 g/dl; white blood cell count, 7,370 per milliliter; platelets, 275,000 per milliliter; glucose, 118 mg/dl; urea, 27 mg/dl; creatinine, 1.1 mg/dl; bilirubin, 10.6 mg/dl; direct bilirubin, 7.0 mg/dl; aspartate aminotransferase (AST), 195 U/L (normal, <37 U/L); alanine aminotransferase (ALT), 315 U/L (normal, <45 U/L); alkaline phosphatase (AP), 878 U/L (normal, <258 U/L); gamma-glutamine transpeptidase, 187 U/L (normal, <55 U/L); lactate dehydrogenase, 482 U/L (normal, <480 U/L); international normalized ratio, 1.05; and erythrocyte sedimentation rate (first hour), 39 mm. Viral and autoimmune markers, including HBsAg, anti-HBc IgM, anti-HAV IgM, anti-HCV, antinuclear antibodies, antimitochondrial antibodies, anti-smooth muscle antibodies, c-ANCA, and p-ANCA were negative. Abdominal CT scan showed no abnormalities. Treatment with intravenous ceftriaxone (2 g daily) was initiated. An endoscopic retrograde cholangiopancreatography (ERCP) was performed. There were no strictures or other pathologic findings in the common bile duct and the main pancreatic duct, except for a small amount of bile sludge that was removed through the ampulla. During hospitalization there was no evidence of renal or pulmonary dysfunction. The patient underwent laparoscopic cholecystectomy on the third day of hospitalization. A needle liver biopsy was also obtained. Laboratory findings on the day of surgery included: AST, 207 U/L; ALT, 463 U/L; AP, 759 U/L; bilirubin, 11.5 mg/dl; and direct bilirubin, 8.1 mg/dl. Histologic examination of the liver biopsy showed moderate portal inflammatory infiltrates consisting of Virchows Arch (2008) 453:413–415 DOI 10.1007/s00428-008-0663-0
Ted Mcdermott - One of the best experts on this subject based on the ideXlab platform.
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Ascending Cholangitis: rare presentation of a ruptured right-sided renal angiomyolipoma.
Journal of surgical case reports, 2017Co-Authors: Stefanie M Croghan, Orla Mccormack, Anna L Walsh, Ted McdermottAbstract:We report the case of a 46-year-old female who presented to the Emergency Department with acute, painful obstructive jaundice, with evidence of secondary Ascending Cholangitis. Surprisingly, imaging revealed the clinical picture to be caused not by hepatobiliary pathology, but by external compression of the biliary tree from a ruptured renal angiomyolipoma (AML) of the right kidney. The patient remained haemodynamically stable and conservative management saw resolution of biliary obstruction. We believe this to be the first report of a renal AML presenting in this way. This report highlights the diverse spectrum of presentations of renal angiomyolipomas.
Despoina Televantou - One of the best experts on this subject based on the ideXlab platform.
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Toxic hepatic injury mimicking Ascending Cholangitis: is Pyrus amygdaliformis to blame?
Virchows Archiv : an international journal of pathology, 2008Co-Authors: Despoina Televantou, Emmanouil Sinakos, Evangelos Akriviadis, Prodromos HytiroglouAbstract:Cholestatic hepatic injury can be caused by a number of drugs and herbal remedies [1, 3, 5]. Occasionally, drugs that cause cholestasis, such as amoxicillin-clavulanate, chlorpromazine, and erythromycin are associated with acute purulent inflammation of the intrahepatic bile ducts, mimicking acute (Ascending) Cholangitis [3]. We present a case of acute cholestatic toxic liver injury with histologic features of Ascending Cholangitis and a possible association with ingestion of forest fruit. The patient is a 55-year-old man, who presented with a 3-day history of marked jaundice. There was no abdominal pain, fever, or history of medications, except for a 5-day course of a cephalosporin antibiotic taken 2 months prior to presentation. On physical examination, there were no findings apart from jaundice. The patient was carefully interviewed regarding potential toxins, and he admitted recent consumption of Pyrus amygdaliformis fruit (also known as “wild pears” in Greece). In detail, he admitted consuming approximately 0.5 kg of raw fruit daily, during the week prior to presentation. He also admitted previous exposure to the same fruit, but that was sporadic and in much smaller quantities. Laboratory findings on his first day of hospitalization were as follows: hemoglobin, 15.4 g/dl; white blood cell count, 7,370 per milliliter; platelets, 275,000 per milliliter; glucose, 118 mg/dl; urea, 27 mg/dl; creatinine, 1.1 mg/dl; bilirubin, 10.6 mg/dl; direct bilirubin, 7.0 mg/dl; aspartate aminotransferase (AST), 195 U/L (normal,
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toxic hepatic injury mimicking Ascending Cholangitis is pyrus amygdaliformis to blame
Virchows Archiv, 2008Co-Authors: Despoina Televantou, Emmanouil Sinakos, Evangelos Akriviadis, Prodromos HytiroglouAbstract:Cholestatic hepatic injury can be caused by a number of drugs and herbal remedies [1, 3, 5]. Occasionally, drugs that cause cholestasis, such as amoxicillin-clavulanate, chlorpromazine, and erythromycin are associated with acute purulent inflammation of the intrahepatic bile ducts, mimicking acute (Ascending) Cholangitis [3]. We present a case of acute cholestatic toxic liver injury with histologic features of Ascending Cholangitis and a possible association with ingestion of forest fruit. The patient is a 55-year-old man, who presented with a 3-day history of marked jaundice. There was no abdominal pain, fever, or history of medications, except for a 5-day course of a cephalosporin antibiotic taken 2 months prior to presentation. On physical examination, there were no findings apart from jaundice. The patient was carefully interviewed regarding potential toxins, and he admitted recent consumption of Pyrus amygdaliformis fruit (also known as “wild pears” in Greece). In detail, he admitted consuming approximately 0.5 kg of raw fruit daily, during the week prior to presentation. He also admitted previous exposure to the same fruit, but that was sporadic and in much smaller quantities. Laboratory findings on his first day of hospitalization were as follows: hemoglobin, 15.4 g/dl; white blood cell count, 7,370 per milliliter; platelets, 275,000 per milliliter; glucose, 118 mg/dl; urea, 27 mg/dl; creatinine, 1.1 mg/dl; bilirubin, 10.6 mg/dl; direct bilirubin, 7.0 mg/dl; aspartate aminotransferase (AST), 195 U/L (normal, <37 U/L); alanine aminotransferase (ALT), 315 U/L (normal, <45 U/L); alkaline phosphatase (AP), 878 U/L (normal, <258 U/L); gamma-glutamine transpeptidase, 187 U/L (normal, <55 U/L); lactate dehydrogenase, 482 U/L (normal, <480 U/L); international normalized ratio, 1.05; and erythrocyte sedimentation rate (first hour), 39 mm. Viral and autoimmune markers, including HBsAg, anti-HBc IgM, anti-HAV IgM, anti-HCV, antinuclear antibodies, antimitochondrial antibodies, anti-smooth muscle antibodies, c-ANCA, and p-ANCA were negative. Abdominal CT scan showed no abnormalities. Treatment with intravenous ceftriaxone (2 g daily) was initiated. An endoscopic retrograde cholangiopancreatography (ERCP) was performed. There were no strictures or other pathologic findings in the common bile duct and the main pancreatic duct, except for a small amount of bile sludge that was removed through the ampulla. During hospitalization there was no evidence of renal or pulmonary dysfunction. The patient underwent laparoscopic cholecystectomy on the third day of hospitalization. A needle liver biopsy was also obtained. Laboratory findings on the day of surgery included: AST, 207 U/L; ALT, 463 U/L; AP, 759 U/L; bilirubin, 11.5 mg/dl; and direct bilirubin, 8.1 mg/dl. Histologic examination of the liver biopsy showed moderate portal inflammatory infiltrates consisting of Virchows Arch (2008) 453:413–415 DOI 10.1007/s00428-008-0663-0
J S Dooley - One of the best experts on this subject based on the ideXlab platform.
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Review article: antibiotic prophylaxis for endoscopic retrograde cholangiopancreatography (ERCP)
Alimentary pharmacology & therapeutics, 1999Co-Authors: J M Subhani, C Kibbler, J S DooleyAbstract:This review examines the evidence for antibiotic prophylaxis in endoscopic retrograde cholangiopan-creatography (ERCP), and provides detailed advice about suitable antibiotic regimens in appropriate high-risk patients. Ascending Cholangitis and infective endocarditis are potential complications of endoscopic ERCP. The pathophysiology of these two complications is quite separate and different sub-groups of patients require prophylaxis with appropriate antibiotic regimens. Ascending Cholangitis results from bacterial infection of an obstructed biliary system, usually from enteric Gram-negative microorganisms, resulting in bacteraemia. There is incomplete drainage of the biliary system after ERCP in up to 10% of patients who require stenting. Antibiotics started in these patients will probably reduce the frequency of Cholangitis by 80%. If antibiotics are restricted to this group, approximately 90% of all patients having an ERCP will avoid antibiotics, but 80% of cholangitic episodes will be prevented. Infective endocarditis may result from the bacteraemia caused at the time of the ERCP in patients with an abnormal heart valve. Antibiotic prophylaxis, in particular covering alpha-haemolytic streptococci, should be started before the procedure in this defined high-risk group.
M. J. Schmalz - One of the best experts on this subject based on the ideXlab platform.
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The role of surveillance endoscopic retrograde cholangiopancreatography in preventing episodic Cholangitis in patients with recurrent common bile duct stones
Endoscopy, 1998Co-Authors: D. J. Geenen, Joseph E. Geenen, F. M. Jafri, Walter J. Hogan, M. F. Catalano, Gk Johnson, M. J. SchmalzAbstract:Background and Study Aims: Approximately 2-7% of patients who have undergone previous removal of bile duct stones have recurrence often presenting as Ascending Cholangitis. The aim of this study was to identify the incidence, clinical presentation, and objective findings in this group of patients. Additionally, the effect of surveillance endoscopic retrograde cholangiopancreatography (ERCP) in preventing Cholangitis, was studied. Patients and Methods: Two thousand and ninety-six patients who underwent ERCP for cholelithiasis were studied with 45 of these patients being identified as having recurrent common bile duct stones. Of the 45, 13 had two or more recurrences without having any obvious predisposing factors. The mean age of the 13 patients was 57 years. The characteristics of 13 patients were reviewed, including sphincterotomy size, liver function tests, and contrast drainage time. Results: All 13 patients with recurrent stones presented with Ascending Cholangitis. Stones were found to be soft, brown and accompanied by a large amount of sludge. The common bile duct in all 13 patients was noted to be dilated and had notable, widely patent sphincterotomes. There was significant delayed drainage in 77% of these patients. Yearly surveillance ERCPs were performed in the 13 patients, the incidence of acute Cholangitis episodes per patient decreased from 2 to 0.6 with a four-year follow-up. Conclusion: In a subgroup of patients with multiple common bile duct stone recurrences, annual surveillance ERCP with stone removal decreases the incidence of recurrent episodes of Ascending Cholangitis as well as its associated morbidity and mortality.
