Search

Immune-related sclerosing cholangitis (irSC) is relatively rare and its clinical characteristics are not well known. In this study, we aimed to summarize the clinical features of irSC. Clinical data were collected retrospectively from 1,393 patients with advanced malignancy treated with immune-checkpoint inhibitors (ICIs) between August 2014 and October 2021. We analyzed patients with immune-related adverse events of liver injury (liver-irAEs) and compared irSC and non-irSC groups. Sixty-seven patients (4.8%) had a liver-irAE (≥ grade 3) during the follow-up period (median, 262 days). Among these, irSC was observed in eight patients (11.9%). All patients in the irSC group were treated with anti-PD-1/PD-L1 antibodies. Compared with the non-irSC group, the irSC group showed mainly non-hepatocellular liver injury (87.5 % vs 50.8 %, P = 0.065), and had elevated serum inflammatory markers (e.g., CRP and NLR) and biliary enzymes (e.g., GGTP and ALP) at the onset of liver-irAEs. Furthermore, most patients with irSC had abdominal pain. In the non-irSC group, the liver injury of 23 patients improved only with the discontinuation of ICIs, and 22 patients improved with medication including prednisolone (PSL). Conversely, almost all patients (n=7) in the irSC group were treated with PSL, but only two patients experienced an improvement in liver injury. We found that irSC is characterized by a non-hepatocellular type of liver injury with abdominal pain and a high inflammatory response and is refractory to treatment. Further examination by imaging is recommended to detect intractable irSC in cases with these characteristics.

Background: IgG4-Sclerosing Cholangitis (IgG4-SC) is an uncommon clinical entity that has an uncertain prognosis and incompletely defined clinical management pathway. Existing data are predominantly from Japanese populations with limited data from Western countries. We sought to describe the presentation, management and outcomes of an Australian IgG4-SC population Methods: Retrospective data collection from major liver centres affiliated with the ALA Clinical Research Network with site selection based on an affirmative response to an expression of interest Patients were included as IgG4-SC if they fulfilled the criteria for definite or probable IgG4-SC according to the IgG4-SC 2012 clinical diagnostic criteria Baseline demographic and biochemical data were obtained in addition to treatment response Follow-up data included disease progression, relapse, development of malignancy and survival Results: 53 patients from 18 institutions met the inclusion criteria (M/F 40/13; Age 64 2+/-1 9 year [range 14.5 - 84.1 years]). Caucasian (68%) and Asian (28%) A previous diagnosis of PSC had been made in 3 (6%) subjects and a suspected biliary tract malignancy or pancreatic tumour in 5 (9%) Three subjects had evidence of cirrhosis The most frequent presenting symptom was jaundice (62%) and abdominal pain (32%) and 34% had co-existing diabetes mellitus Bilirubin (80+/-13mumol/L), ALT (267+/-43 U/L) and IgG4 (6.2+/-0.8 g/L) were significantly elevated at diagnosis and 38% had Ca19-9 > 37 kU/L (range 1-2248 kU/L). The bile duct lesion was: Type 1 (distal bile duct stricture only; 57%), Type 2A (13%), Type 2B (2%), Type 3 (13%) and Type 4 (9%) IgG4-SC was associated with other IgG4-related diseases, most commonly: autoimmune pancreatitis (AIP) (55%), dacryoadenitis/sialadenitis (15%) 87% received prednisolone as initial treatment and 60% achieved remission while a further 19% experienced a partial response with a median time to best response of 3 4 months Endoscopic dilatation was p

Background: IgG4-Sclerosing Cholangitis (IgG4-SC) is an uncommon clinical entity that has an uncertain prognosis and incompletely defined clinical management pathway. Existing data are predominantly from Japanese populations with limited data from Western countries. We sought to describe the presentation, management and outcomes of an Australian IgG4-SC population Methods: Retrospective data collection from major liver centres affiliated with the ALA Clinical Research Network with site selection based on an affirmative response to an expression of interest Patients were included as IgG4-SC if they fulfilled the criteria for definite or probable IgG4-SC according to the IgG4-SC 2012 clinical diagnostic criteria Baseline demographic and biochemical data were obtained in addition to treatment response Follow-up data included disease progression, relapse, development of malignancy and survival Results: 53 patients from 18 institutions met the inclusion criteria (M/F 40/13; Age 64 2+/-1 9 year [range 14.5 - 84.1 years]). Caucasian (68%) and Asian (28%) A previous diagnosis of PSC had been made in 3 (6%) subjects and a suspected biliary tract malignancy or pancreatic tumour in 5 (9%) Three subjects had evidence of cirrhosis The most frequent presenting symptom was jaundice (62%) and abdominal pain (32%) and 34% had co-existing diabetes mellitus Bilirubin (80+/-13mumol/L), ALT (267+/-43 U/L) and IgG4 (6.2+/-0.8 g/L) were significantly elevated at diagnosis and 38% had Ca19-9 > 37 kU/L (range 1-2248 kU/L). The bile duct lesion was: Type 1 (distal bile duct stricture only; 57%), Type 2A (13%), Type 2B (2%), Type 3 (13%) and Type 4 (9%) IgG4-SC was associated with other IgG4-related diseases, most commonly: autoimmune pancreatitis (AIP) (55%), dacryoadenitis/sialadenitis (15%) 87% received prednisolone as initial treatment and 60% achieved remission while a further 19% experienced a partial response with a median time to best response of 3 4 months Endoscopic dilatation was p

Cholestasis comprises aetiologically heterogeneous conditions characterized by accumulation of bile acids in the liver that actively contribute to liver damage. Sirtuin 1 (SIRT1) regulates liver regeneration and bile acid metabolism by modulating farnesoid X receptor (FXR); we here investigate its role in cholestatic liver disease. We determined SIRT1 expression in livers from patients with cholestatic disease, in two experimental models of cholestasis, as well as in human and murine liver cells in response to bile acid loading. SIRT1-overexpressing (SIRToe) and hepatocyte-specific SIRT1-KO (knockout) mice (SIRThep-/-) were subjected to bile duct ligation (BDL) and were fed with a 0.1% DDC (3,5-diethoxycarbonyl-1,4-dihydrocollidine) diet to determine the biological relevance of SIRT1 during cholestasis. The effect of NorUDCA (24-norursodeoxycholic acid) was tested in BDL/SIRToe mice. We found that SIRT1 was highly expressed in livers from cholestatic patients, mice after BDL, and Mdr2 knockout mice (Mdr2(-/-)) animals. The detrimental effects of SIRT1 during cholestasis were validated in vivo and in vitro. SIRToe mice showed exacerbated parenchymal injury whereas SIRThep-/- mice evidenced a moderate improvement after BDL and 0.1% DDC feeding. Likewise, hepatocytes isolated from SIRToe mice showed increased apoptosis in response to bile acids, whereas a significant reduction was observed in SIRThep-/- hepatocytes. Importantly, the decrease, but not complete inhibition, of SIRT1 exerted by norUDCA treatment correlated with pronounced improvement in liver parenchyma in BDL/SIRToe mice. Interestingly, both SIRT1 overexpression and hepatocyte-specific SIRT1 depletion correlated with inhibition of FXR, whereas modulation of SIRT1 by NorUDCA associated with restored FXR signaling. Conclusion: SIRT1 expression is increased during human and murine cholestasis. Fine-tuning expression of SIRT1 is essential to protect the liver from cholestatic liver damage.

Cholestasis comprises aetiologically heterogeneous conditions characterized by accumulation of bile acids in the liver that actively contribute to liver damage. Sirtuin 1 (SIRT1) regulates liver regeneration and bile acid metabolism by modulating farnesoid X receptor (FXR); we here investigate its role in cholestatic liver disease. We determined SIRT1 expression in livers from patients with cholestatic disease, in two experimental models of cholestasis, as well as in human and murine liver cells in response to bile acid loading. SIRT1-overexpressing (SIRToe) and hepatocyte-specific SIRT1-KO (knockout) mice (SIRThep-/-) were subjected to bile duct ligation (BDL) and were fed with a 0.1% DDC (3,5-diethoxycarbonyl-1,4-dihydrocollidine) diet to determine the biological relevance of SIRT1 during cholestasis. The effect of NorUDCA (24-norursodeoxycholic acid) was tested in BDL/SIRToe mice. We found that SIRT1 was highly expressed in livers from cholestatic patients, mice after BDL, and Mdr2 knockout mice (Mdr2(-/-)) animals. The detrimental effects of SIRT1 during cholestasis were validated in vivo and in vitro. SIRToe mice showed exacerbated parenchymal injury whereas SIRThep-/- mice evidenced a moderate improvement after BDL and 0.1% DDC feeding. Likewise, hepatocytes isolated from SIRToe mice showed increased apoptosis in response to bile acids, whereas a significant reduction was observed in SIRThep-/- hepatocytes. Importantly, the decrease, but not complete inhibition, of SIRT1 exerted by norUDCA treatment correlated with pronounced improvement in liver parenchyma in BDL/SIRToe mice. Interestingly, both SIRT1 overexpression and hepatocyte-specific SIRT1 depletion correlated with inhibition of FXR, whereas modulation of SIRT1 by NorUDCA associated with restored FXR signaling. Conclusion: SIRT1 expression is increased during human and murine cholestasis. Fine-tuning expression of SIRT1 is essential to protect the liver from cholestatic liver damage.

Cholestasis comprises aetiologically heterogeneous conditions characterized by accumulation of bile acids in the liver that actively contribute to liver damage. Sirtuin 1 (SIRT1) regulates liver regeneration and bile acid metabolism by modulating farnesoid X receptor (FXR); we here investigate its role in cholestatic liver disease. We determined SIRT1 expression in livers from patients with cholestatic disease, in two experimental models of cholestasis, as well as in human and murine liver cells in response to bile acid loading. SIRT1-overexpressing (SIRToe) and hepatocyte-specific SIRT1-KO (knockout) mice (SIRThep-/-) were subjected to bile duct ligation (BDL) and were fed with a 0.1% DDC (3,5-diethoxycarbonyl-1,4-dihydrocollidine) diet to determine the biological relevance of SIRT1 during cholestasis. The effect of NorUDCA (24-norursodeoxycholic acid) was tested in BDL/SIRToe mice. We found that SIRT1 was highly expressed in livers from cholestatic patients, mice after BDL, and Mdr2 knockout mice (Mdr2(-/-)) animals. The detrimental effects of SIRT1 during cholestasis were validated in vivo and in vitro. SIRToe mice showed exacerbated parenchymal injury whereas SIRThep-/- mice evidenced a moderate improvement after BDL and 0.1% DDC feeding. Likewise, hepatocytes isolated from SIRToe mice showed increased apoptosis in response to bile acids, whereas a significant reduction was observed in SIRThep-/- hepatocytes. Importantly, the decrease, but not complete inhibition, of SIRT1 exerted by norUDCA treatment correlated with pronounced improvement in liver parenchyma in BDL/SIRToe mice. Interestingly, both SIRT1 overexpression and hepatocyte-specific SIRT1 depletion correlated with inhibition of FXR, whereas modulation of SIRT1 by NorUDCA associated with restored FXR signaling. Conclusion: SIRT1 expression is increased during human and murine cholestasis. Fine-tuning expression of SIRT1 is essential to protect the liver from cholestatic liver damage.

Cholestasis comprises aetiologically heterogeneous conditions characterized by accumulation of bile acids in the liver that actively contribute to liver damage. Sirtuin 1 (SIRT1) regulates liver regeneration and bile acid metabolism by modulating farnesoid X receptor (FXR); we here investigate its role in cholestatic liver disease. We determined SIRT1 expression in livers from patients with cholestatic disease, in two experimental models of cholestasis, as well as in human and murine liver cells in response to bile acid loading. SIRT1-overexpressing (SIRToe) and hepatocyte-specific SIRT1-KO (knockout) mice (SIRThep-/-) were subjected to bile duct ligation (BDL) and were fed with a 0.1% DDC (3,5-diethoxycarbonyl-1,4-dihydrocollidine) diet to determine the biological relevance of SIRT1 during cholestasis. The effect of NorUDCA (24-norursodeoxycholic acid) was tested in BDL/SIRToe mice. We found that SIRT1 was highly expressed in livers from cholestatic patients, mice after BDL, and Mdr2 knockout mice (Mdr2(-/-)) animals. The detrimental effects of SIRT1 during cholestasis were validated in vivo and in vitro. SIRToe mice showed exacerbated parenchymal injury whereas SIRThep-/- mice evidenced a moderate improvement after BDL and 0.1% DDC feeding. Likewise, hepatocytes isolated from SIRToe mice showed increased apoptosis in response to bile acids, whereas a significant reduction was observed in SIRThep-/- hepatocytes. Importantly, the decrease, but not complete inhibition, of SIRT1 exerted by norUDCA treatment correlated with pronounced improvement in liver parenchyma in BDL/SIRToe mice. Interestingly, both SIRT1 overexpression and hepatocyte-specific SIRT1 depletion correlated with inhibition of FXR, whereas modulation of SIRT1 by NorUDCA associated with restored FXR signaling. Conclusion: SIRT1 expression is increased during human and murine cholestasis. Fine-tuning expression of SIRT1 is essential to protect the liver from cholestatic liver damage.

Mesenchymal stem cells (MSCs) represent a valuable cell source in regenerative medicine, and large numbers of MSCs can be isolated from the amnion noninvasively. Sclerosing cholangitis is a chronic cholestatic disease and characterized by progressive biliary destruction leading to cirrhosis. Many factors are involved in the development of sclerosing cholangitis; however, effective medical therapy is not established. We investigated the effects of human amnion-derived MSCs (hAMSCs) and conditioned medium (CM) obtained from hAMSC cultures in rats with sclerosing cholangitis. Sclerosing cholangitis was induced via the intragastric administration of 100 mg/kg alpha-naphthylisothiocyanate (ANIT) twice weekly for 4 weeks. One million hAMSCs or 200 mu L of CM were intravenously administered on days 15 and 22. Rats were sacrificed on day 29 and evaluated via histological, immunohistochemical, and mRNA expression analyses. hAMSC transplantation and CM administration significantly improved the histological score. In addition, these two interventions significantly improved biliary hyperplasia, peribiliary fibrosis, and inflammation in Glisson's sheath. Accordingly, CK19, MMP-9, and TNF-alpha, and MCP-1 expression in the liver was also decreased by hAMSC and CM administration. In conclusion, hAMSC and CM administration ameliorated biliary hyperplasia, peribiliary fibrosis, and inflammation in a rat model of sclerosing cholangitis. hAMSCs and CM may represent new modalities for treating sclerosing cholangitis.

Mesenchymal stem cells (MSCs) represent a valuable cell source in regenerative medicine, and large numbers of MSCs can be isolated from the amnion noninvasively. Sclerosing cholangitis is a chronic cholestatic disease and characterized by progressive biliary destruction leading to cirrhosis. Many factors are involved in the development of sclerosing cholangitis; however, effective medical therapy is not established. We investigated the effects of human amnion-derived MSCs (hAMSCs) and conditioned medium (CM) obtained from hAMSC cultures in rats with sclerosing cholangitis. Sclerosing cholangitis was induced via the intragastric administration of 100 mg/kg alpha-naphthylisothiocyanate (ANIT) twice weekly for 4 weeks. One million hAMSCs or 200 mu L of CM were intravenously administered on days 15 and 22. Rats were sacrificed on day 29 and evaluated via histological, immunohistochemical, and mRNA expression analyses. hAMSC transplantation and CM administration significantly improved the histological score. In addition, these two interventions significantly improved biliary hyperplasia, peribiliary fibrosis, and inflammation in Glisson's sheath. Accordingly, CK19, MMP-9, and TNF-alpha, and MCP-1 expression in the liver was also decreased by hAMSC and CM administration. In conclusion, hAMSC and CM administration ameliorated biliary hyperplasia, peribiliary fibrosis, and inflammation in a rat model of sclerosing cholangitis. hAMSCs and CM may represent new modalities for treating sclerosing cholangitis.

Introduction: Endotoxins, in the form of lipopolysaccharides (LPS), are potent inducers of biliary injury. However the mechanism by which injury develops remains unclear. We hypothesized that hepatic macrophages are pivotal in the development of endotoxin-induced biliary injury and that no injury would occur in their absence.Material and methods: Clodronate liposomes were used to deplete macrophages from the liver. Forty-eight rats were equally divided across six study groups: sham operation (sham), liposome treatment and sham operation (liposomes + sham), 1 mg/kg LPS i.p. (LPS), liposome treatment and LPS administration (liposomes + LPS), hepatic ischaemia-reperfusion injury with LPS administration (IRI + LPS) and liposome treatment followed by IRI + LPS (liposomes + IRI + LPS). Following 6 h of reperfusion, blood, bile, and liver tissue was collected for further analysis. Small bile duct injury was assessed, serum liver tests were performed and bile composition was evaluated. The permeability of the blood-biliary barrier (BBB) was assessed using intravenously administered horseradish peroxidase (HRP).Results: The presence of hepatic macrophages was reduced by 90% in LPS and IRI + LPS groups pre-treated with clodronate liposomes (P <0.001). Severe small bile duct injury was not affected by macrophage depletion, and persisted in the liposomes + IRI + LPS group (50% of animals) and liposomes + LPS group (75% of animals). Likewise, BBB impairment persisted following macrophage depletion. LPS-induced elevation of the chemokine Mcp-1 in bile was not affected by macrophage depletion.Conclusions: Depletion of hepatic macrophages did not prevent development of biliary injury following LPS of LPS-enhanced IRI. Cholangiocyte activation rather than macrophage activation may underlie this injury. This article is part of a Special Issue entitled: Cholangiocytes in Health and Diseaseedited by Jesus Banales, Marcc Marzioni, Nicholas LaRusso and Peter Ja

Introduction IgG4 related sclerosing cholangitis is a novel disease entitywhich, while often associated with autoimmune pancreatitis, can presentin isolation. We describe two patients diagnosed with IgG4 related sclerosingcholangitis with contrasting clinical presentations and treatmentcourse.Case 1: A 43 year-old man was referred in Dec 2010 with painlessobstructive jaundice. He reported a 9-month history of 20 kg loss ofweight, right upper quadrant pain, fevers and deranged liver function tests.The patient had left sided proptosis, bilateral submandibular and parotidgland enlargement. An abdominal CT demonstrated mass lesions of thekidneys, liver, pancreas and gall bladder. MRCP confirmed a common bileduct stricture measuring 15 mm in length. The serum IgG4 level wasmarkedly elevated at 17.6 g/L (normal range: 0.04-0.86 g/L). The patienthad a laparoscopic cholecystectomy for the purpose of histopathologicaldiagnosis. This demonstrated multiple pseudo tumours of the gall bladder,which stained 80% positive for IgG4. Treatment with oral corticosteroidresulted in clinical and radiological remission of the patient's pseudotumours, lymphadenopathy and biliary stricture. Disease remission hasbeen maintained with azathioprine for 6 months.Case 2: A 73 year-old man presented with a 4-month history of painlessobstructive jaundice and 12 kg loss of weight. CT cholangiogram demonstrateda 2 cm hilar mass associated with a CBD stricture suspicious fora cholangiocarcinoma of the porta hepatis. Cytology on EUS guided FNAshowed benign cells. The biliary stricture and presumed cholangiocarcinomawere treated by right hemi-hepatectomy and the bile duct reconstructedwith roux-en-y limb. Histopathology of the resected lesionshowed a 20 mm x 12 x 20 mm mass with a moderate infiltration oflympho-plasmacytic cells. IgG4 immunostain of the specimen showed thatthe majority of plasma cells were IgG4 positive. The patient has not beentreated with corticosteroids as there has been no evidence

Introduction IgG4 related sclerosing cholangitis is a novel disease entitywhich, while often associated with autoimmune pancreatitis, can presentin isolation. We describe two patients diagnosed with IgG4 related sclerosingcholangitis with contrasting clinical presentations and treatmentcourse.Case 1: A 43 year-old man was referred in Dec 2010 with painlessobstructive jaundice. He reported a 9-month history of 20 kg loss ofweight, right upper quadrant pain, fevers and deranged liver function tests.The patient had left sided proptosis, bilateral submandibular and parotidgland enlargement. An abdominal CT demonstrated mass lesions of thekidneys, liver, pancreas and gall bladder. MRCP confirmed a common bileduct stricture measuring 15 mm in length. The serum IgG4 level wasmarkedly elevated at 17.6 g/L (normal range: 0.04-0.86 g/L). The patienthad a laparoscopic cholecystectomy for the purpose of histopathologicaldiagnosis. This demonstrated multiple pseudo tumours of the gall bladder,which stained 80% positive for IgG4. Treatment with oral corticosteroidresulted in clinical and radiological remission of the patient's pseudotumours, lymphadenopathy and biliary stricture. Disease remission hasbeen maintained with azathioprine for 6 months.Case 2: A 73 year-old man presented with a 4-month history of painlessobstructive jaundice and 12 kg loss of weight. CT cholangiogram demonstrateda 2 cm hilar mass associated with a CBD stricture suspicious fora cholangiocarcinoma of the porta hepatis. Cytology on EUS guided FNAshowed benign cells. The biliary stricture and presumed cholangiocarcinomawere treated by right hemi-hepatectomy and the bile duct reconstructedwith roux-en-y limb. Histopathology of the resected lesionshowed a 20 mm x 12 x 20 mm mass with a moderate infiltration oflympho-plasmacytic cells. IgG4 immunostain of the specimen showed thatthe majority of plasma cells were IgG4 positive. The patient has not beentreated with corticosteroids as there has been no evidence

BACKGROUND: Primary sclerosing cholangitis (PSC) is commonly associated with inflammatory bowel disease (IBD) and characterized by fibrosing inflammatory destruction of biliary ducts. The pathogenesis of PSC remains unknown, but immunological, bacterial, viral, and toxic factors play a role in a genetically susceptible host. We hypothesized that CC-type chemokine receptor 5 (CCR5) would be an interesting candidate gene for susceptibility to PSC from its chromosomal location within the IBD susceptibility locus on 3p21, as well as from a functional perspective. We therefore investigated the role of the functional 32-bp deletion in this gene (CCR5-Delta32) with regard to susceptibility to PSC. METHODS: A total of 110 patients with PSC, 56 with concomitant IBD (23 with Crohn's disease, 28 with ulcerative colitis, 5 with indeterminate colitis), were collected. All of the subjects were genotyped for CCR5-Delta32 with polymerase chain reaction amplification, followed by detection on ethidium bromide-stained agarose gel. Genotypes and allele frequencies were compared with a cohort of IBD patients without PSC (n = 400) and healthy control subjects (n = 362). RESULTS: The frequency of the CCR5-Delta32 mutation in PSC (6.8%) was significantly lower compared with IBD (12.6%; P = 0.016) and healthy control subjects (12.2%, P = 0.026), suggesting a protective effect of this mutation on PSC. None of the PSC patients with severe disease necessitating liver transplantation (n = 17) carried CCR5-Delta32. CONCLUSIONS: Because an intact CCR5 receptor is needed for internalization of specific pathogens and homing of memory T lymphocytes to the liver, we hypothesize that a deficient expression of this receptor resulting from the CCR5-Delta32 variant may protect against PSC.

Patients with acquired immunodeficiency syndrome (AIDS) can develop biliary and pancreatic disorders, like sclerosing cholangitis and acute pancreatitis. Chronic pancreatic changes are rare and only poorly described. In this study, we report our endoscopic retrograde cholangiopancreatography (ERCP) findings in 20 patients with AIDS, focusing on pancreatographic changes. ERCP findings from 20 patients with advanced disease were analyzed. Patients with history of chronic alcoholism were ruled out. ERCP findings were correlated to the coexistence of an opportunistic infection and the taking of antiviral therapies. Bile duct and pancreatic duct abnormalities were observed in 11 (55%) of 20 and seven (37%) of 19 patients, respectively. Bile duct lesions were mainly sclerosing cholangitis, and chronic pancreatic alterations consisted of side-branch involvement (n = 4), multiple and diffuse strictures of the main duct (n = 1), and diffuse dilatation of the main pancreatic duct (n = 2). The presence of an opportunistic infection was correlated with sclerosing cholangitis but not with chronic pancreatic changes. Similarly, there was no association between the finding of an abnormal cholangiogram and the presence of pancreatic alterations. This population of patients with AIDS had a significant proportion (37%) of chronic pancreatic ductal changes, which do not seem to be related to morphologic alterations and/or opportunistic infections of the biliary tract., Journal Article, info:eu-repo/semantics/published

Patients with acquired immunodeficiency syndrome (AIDS) can develop biliary and pancreatic disorders, like sclerosing cholangitis and acute pancreatitis. Chronic pancreatic changes are rare and only poorly described. In this study, we report our endoscopic retrograde cholangiopancreatography (ERCP) findings in 20 patients with AIDS, focusing on pancreatographic changes. ERCP findings from 20 patients with advanced disease were analyzed. Patients with history of chronic alcoholism were ruled out. ERCP findings were correlated to the coexistence of an opportunistic infection and the taking of antiviral therapies. Bile duct and pancreatic duct abnormalities were observed in 11 (55%) of 20 and seven (37%) of 19 patients, respectively. Bile duct lesions were mainly sclerosing cholangitis, and chronic pancreatic alterations consisted of side-branch involvement (n = 4), multiple and diffuse strictures of the main duct (n = 1), and diffuse dilatation of the main pancreatic duct (n = 2). The presence of an opportunistic infection was correlated with sclerosing cholangitis but not with chronic pancreatic changes. Similarly, there was no association between the finding of an abnormal cholangiogram and the presence of pancreatic alterations. This population of patients with AIDS had a significant proportion (37%) of chronic pancreatic ductal changes, which do not seem to be related to morphologic alterations and/or opportunistic infections of the biliary tract., Journal Article, info:eu-repo/semantics/published

The study determined predictive factors for postoperative complications and outcome after ileal pouch-anal anastomosis in patients with ulcerative colitis and primary sclerosing cholangitis. Patients with ulcerative colitis and primary sclerosing cholangitis treated by colectomy and ileostomy are at high risk of troublesome bleeding from peristomal varices. Postoperative complications and outcome were assessed in 40 patients with ulcerative colitis and sclerosing cholangitis who received in ileal pouch-anal anastomosis between January 1981 and February 1990. Immediate postoperative and remote ileoanal anastomosis-related complications were high but related directly to the severity of liver disease. No patient had perianastomotic anal bleeding. In patients with both ulcerative colitis and primary sclerosing cholangitis, ileal pouch-anal anastomosis is safe and is not associated with perianastomotic bleeding.