Non-malignant Portal Vein Thrombosis Research Articles

Transjugular portal vein recanalization with creation of intrahepatic portosystemic shunt (PVR-TIPS) in patients with chronic non-cirrhotic, non-malignant portal vein thrombosis.

To determine safety and efficacy of transjugular portal vein recanalization with creation of intrahepatic portosystemic shunt (PVR-TIPS) in patients with chronic non-cirrhotic, non-malignant portal vein thrombosis (PVT). This retrospective study includes 17 consecutive patients with chronic non-cirrhotic PVT (cavernous transformation n = 15). PVR-TIPS was indicated because of variceal bleeding (n = 13), refractory ascites (n = 2), portal biliopathy with recurrent cholangitis (n = 1), or abdominal pain (n = 1). Treatment consisted of a combination of transjugular balloon angioplasty, mechanical thrombectomy, and-depending on extent of residual thrombosis-transjugular intrahepatic portosystemic shunt and additional stenting of the portal venous system. Recanalization was successful in 76.5 % of patients despite cavernous transformation in 88.2 %. Both 1- and 2-year secondary PV and TIPS patency rates were 69.5 %. Procedure-related bleeding complications occurred in 2 patients (intraperitoneal bleeding due to capsule perforation, n = 1; liver hematoma, n = 1) and resolved spontaneously. However, 1 patient died due to subsequent nosocomial pneumonia. During follow-up, 3 patients with TIPS occlusion and PVT recurrence experienced portal hypertensive complications. PVR-TIPS is safe and effective in selected patients with chronic non-cirrhotic PVT. Due to technical complexity and possible complications, it should be performed only in specialized centers with high experience in TIPS procedures.

Association of Nonmalignant Portal Vein Thrombosis and Outcomes after Transjugular Intrahepatic Portosystemic Shunt in Patients with Cirrhosis.

Purpose To assess the effects of preexisting nonmalignant portal vein thrombosis (PVT) on mortality, clinical relapse, shunt dysfunction, and overt hepatic encephalopathy (HE) after transjugular intrahepatic portosystemic shunt (TIPS) placement. Materials and Methods This retrospective study was approved by the institutional ethics committee, and written informed consent was obtained from all patients. From March 2001 to December 2014, 1171 consecutive patients with cirrhosis (762 men, 409 women; mean age, 50.0 years ± 12.8) and PVT (n = 212; 18%) or without PVT (n = 959; 82%) who underwent TIPS placement were included. The association between PVT and outcomes after TIPS placement was measured by using Fine and Gray competing risk regression model after adjusting for important baseline characteristics or by using propensity score. The Wald test was used to assess the homogeneity of the effects of PVT across different strata (stratified PVT according to the stages, degrees, and extents) and major subgroups. Results During a median follow-up period of 28.4 months, 507 (43%) patients died, 373 (32%) experienced clinical relapse, 217 (19%) developed shunt dysfunction, and 475 (41%) experienced overt HE. Compared with patients without PVT, patients with PVT had a similar risk of mortality (adjusted hazard ratio, 0.82; 95% confidence interval [CI]: 0.63, 1.09; P = .17), clinical relapse (adjusted hazard ratio, 1.24; 95% CI: 0.92, 1.69; P = .15), shunt dysfunction (adjusted hazard ratio, 1.03; 95% CI: 0.70, 1.51; P = .43), and overt HE (adjusted hazard ratio, 0.88; 95% CI: 0.70, 1.11; P = .29). Furthermore, the effects of PVT were consistent across the relevant strata and subgroups. Conclusion There was no evidence that preexisting PVT was associated with an improved or worsened outcome after TIPS. © RSNA, 2017 Online supplemental material is available for this article.

Transjugular local thrombolysis with/without TIPS in patients with acute non-cirrhotic, non-malignant portal vein thrombosis

Background & aimsTherapeutic anticoagulation is the standard treatment in patients with acute non-cirrhotic portal vein thrombosis (PVT). In critically ill patients, anticoagulation only may not suffice to achive rapid and stable recanalization. This study evaluates efficacy and safety of transjugular interventional therapy in acute non-cirrhotic PVT. MethodsThis retrospective study includes 17 consecutive patients with acute noncirrhotic, non-malignant PVT. Main indication for interventional therapy was imminent intestinal infarction (n=10). Treatment consisted of a combination of transjugular thrombectomy, local fibrinolysis and – depending on thrombus resolution – transjugular intrahepatic portosystemic shunt. ResultsRecanalization was successful in 94.1%. One- and two-year secondary PV patency rates were 88.2%. Major complications (n=3) resolved spontaneously in all but one patient (heparin induced thrombocytopenia type 2 with intestinal infarction). Symptoms improved in all patients. However, segmental bowel resection had to be performed in two (11.8%). During a median follow-up of 28.6 months, no patient experienced portal hypertensive complications. Presence of JAK2 V617F mutation predicted both short-term and long-term technical success. ConclusionsTransjugular recanalization is safe and effective in patients with acute non-cirrhotic, non-malignant PVT. It should be considered especially in patients with imminent bowel infarction and low likelihood of recanalization following therapeutic anticoagulation. Patients with JAK2 mutation ought to be followed meticulously.

Occult myeloproliferative neoplasms: not so occult any more

Non-cirrhotic, non-malignant portal vein thrombosis (PVT) is commonly secondary to inherited or acquired prothrombotic states. However, even after extensive workup, 25% of patients with PVT have no apparent prothrombotic aetiology...

Anticoagulation in non-malignant portal vein thrombosis is associated with improved hepatic function

Non-malignant portal vein thrombosis (PVT) is common in patients with chronic liver disease. Anticoagulation (AC) increases chances of recanalization and may also improve liver function in cirrhotic patients.

Efficacy and safety of treatment of acute nonmalignant portal vein thrombosis with subcutaneous fondaparinux in patients with cirrhosis and marked thrombocytopenia

Efficacy and safety of treatment of acute nonmalignant portal vein thrombosis with subcutaneous fondaparinux in patients with cirrhosis and marked thrombocytopenia

GI ischemia in patients with portal vein thrombosis: a prospective cohort study

GI ischemia is a concerning adverse event of portal vein thrombosis (PVT). Minimally invasive techniques, such as visible light spectroscopy (VLS), have greatly improved the ability to diagnose GI ischemia. The aim of this study was to assess the clinical presentation and characteristics of GI ischemia in patients with PVT. Patients with noncirrhotic, nonmalignant PVT were included in this prospective cohort study. Clinical symptoms of GI ischemia were assessed by a structured questionnaire, VLS, and radiologic evaluation of the mesenteric vasculature. VLS measurements were compared with those in patients with cirrhosis and with a reference population. We included 15 patients with chronic PVT and 1 patient with acute PVT (median age 46.1 years [interquartile range [IQR], 30.9-53.7]; 44% male). Decreased mucosal oxygenation in at least 1 location of the GI tract was found in 12 patients (75%). Compared with the reference population (median 60.0 [IQR, 56.2-61.7]), VLS measurements were mostly decreased in the descending duodenum in patients with PVT (median 55.5 [IQR, 52.3-58.8]; P = .02) and patients with cirrhosis (median 52.0 [IQR, 46.5-54.0], P = .003). Symptoms typical for GI ischemia, such as postprandial pain and exercise-induced pain, were reported in 10 patients (63%) with PVT. In patients with extension of thrombosis into the superior mesenteric vein and splenic vein and/or presence of hypercoagulability, decreased VLS measurements were observed compared with historical control subjects. In patients with chronic PVT, GI ischemia is frequent. VLS enables objective and quantitative determination of GI mucosal ischemia. Onset of abdominal symptoms such as postprandial pain should prompt the physician to re-evaluate extent, cause, and treatment of PVT.

P0165 : Non-malignant portal vein thrombosis in patients with cirrhosis. Response to treatment

P0165 : Non-malignant portal vein thrombosis in patients with cirrhosis. Response to treatment

Natural course of nonmalignant partial portal vein thrombosis in cirrhotic patients.

Background/Aim:Portal vein thrombosis (PVT) has a high incidence in patients with liver cirrhosis and determines a poor prognosis of hepatic disease. The aim of our study was to define the natural course of partial PVT in cirrhotic patients, including survival and decompensation rates.Patients and Methods:We performed a prospective, cohort study, in a tertiary referral center. There were 22 cirrhotic patients with partial nonmalignant PVT, without anticoagulant treatment, who were followed-up between January 2011 and October 2013. All patients were evaluated by Doppler abdominal ultrasound and computed tomography. Kaplan–Meier method was used to determine the difference in clinical events between the study subgroups.Results:After a mean follow-up period of 20.22 months, partial PVT improved in 5 (22.73%), was stable in 11 (50%), and worsened in 6 (27.27%) patients. Hepatic decompensation rate at 6 and 18 months was higher in patients with worsened PVT than in those with stable/improved PVT (50% vs. 25%, P < 0.0001 and 100% vs. 56.25%, P < 0.0001, respectively). The survival rate at 6 months was 66.66% in worsened PVT group vs. 81.25% (P = 0.005) in stable/improved group, and 16.66% vs. 81.25% (P < 0.0001) at 18 months, respectively. Multivariate analysis showed that Model of End-Life Disease was the independent predictor of hepatic decompensation [hazard ratio (HR) 1.42; 95% confidence interval (CI): 1.08−1.87, P = 0.012] and survival (HR 1.76; 95% CI: 1.06−2.92, P = 0.028).Conclusions:Nonmalignant partial PVT remained stable/improved in over half of cirrhotic patients and aggravated in more than one fourth in whom it negatively influenced the survival and decompensation rates.

Combined Surgical and Interventional Therapy of Acute Portal Vein Thrombosis without Cirrhosis: A New Effective Hybrid Approach for Recanalization of the Portal Venous System

Acute portomesenteric venous thrombosis represents a rare event, but is associated with severe and potentially lethal complications. Portal vein thrombosis (PVT) usually develops in the main trunk reaching left or right hepatic branches and can extend to the superior mesenteric vein and/or splenic vein. Noncirrhotic, nonmalignant, or nontransplant PVT is rarely a solitary disease and mostly a consequence of hypercoagulability or hypofibrinolysis. Other underlying causes for acute PVT are abdominal trauma and septic conditions, such as pancreatitis. In addition, surgical interventions, such as splenectomy in particular, as well as other local factors can lead to acute PVT. Clinical symptoms of acute PVT are mostly unspecific and variable, which makes an accurate clinical diagnosis difficult. Most patients present with acute abdominal pain, nausea, diarrhea, or ileus symptoms, but some patients are even asymptomatic. For diagnosis of PVT, Doppler ultrasound and contrast-enhanced CT are the most common imaging techniques that detect intrahepatic and extrahepatic PVT explicitly. Additional information, for example, the extent of thrombosis (mesenteric veins) and underlying or concomitant findings, such as bowel ischemia or congestion, is provided by a contrastenhanced CT scan that also allows distinguishing acute from chronic PVT. Management of acute PVT can include anticoagulation, regional or systemic thrombolysis, thrombectomy, or a combination of these treatments, with the aim to

Prevalence of paroxysmal nocturnal hemoglobinuria in Chinese patients with Budd‐Chiari syndrome or portal vein thrombosis

Routine screening for paroxysmal nocturnal hemoglobinuria (PNH) in patients with Budd-Chiari syndrome (BCS) or portal vein thrombosis (PVT) has been recommended in Western countries. However, little is known about whether the routine screening test should be necessary in Chinese patients with BCS or PVT. We conducted a prospective observational study to examine the prevalence of PNH in these patients. Patients with primary BCS or non-malignant PVT who were consecutively admitted to our department or regularly followed up between September 2009 and December 2011 were eligible for the study and detected the expression of CD55 and CD59 on erythrocytes and granulocytes. The CD55 or CD59 deficiency was considered as the proportion of erythrocytes or granulocytes with normal expression of CD55 or CD59 was less than 90%. PNH was diagnosed by both CD55 and CD59 deficient clone at flow cytometry of peripheral blood cells. CD55 and/or CD59 deficiencies were found in 1.6% (2/127) of patients with primary BCS, 1.0% (1/100) of non-malignant and non-cirrhotic patients with PVT, and 4.7% (4/85) of cirrhotic patients with PVT. Only one patient had both CD55 and CD59 deficiencies on granulocytes. But he had been diagnosed with PNH before BCS. Paroxysmal nocturnal hemoglobinuria was very rare in Chinese patients with BCS or PVT, suggesting that routine screening for PNH should not be indiscriminately performed in such patients.

CT features of non-malignant portal vein thrombosis: A pictorial review

Portal vein thrombosis (PVT) is a rare clinical entity in general population, but a relatively frequent entity in liver cirrhosis. Severe PVT-related complications are potentially lethal, such as ischemic intestinal infarction and complications of portal hypertension. Additionally, occlusive PVT can not only increase the incidence of variceal rebleeding, but also significantly decrease the cirrhotic patients' survival. Based on the clinical significance of PVT, early diagnosis is very critical to allow for rapid establishment of appropriate treatment and improvement of prognosis. Dynamic CT scan is an important diagnostic modality of PVT. The objective of this pictorial review is to illustrate various CT features of non-malignant portal vein thrombosis and its associated abnormalities. Evolution of portal vein thrombosis, such as stage, degree, and extension of thrombus, can be evaluated according to CT demonstrations, which is helpful to timely adopt appropriate treatment modality. Other associated CT findings include the dilation of collateral veins around the obstructed portion of portal vein and the hepatic perfusion and morphology abnormalities.

Prospective evaluation of anticoagulation and transjugular intrahepatic portosistemic shunt for the management of portal vein thrombosis in cirrhosis

There is no established management algorithm for portal vein thrombosis (PVT) in cirrhotic patients. The aim of our study was to prospectively evaluate anticoagulation and transjugular intrahepatic portosystemic shunt (TIPS) to treat PVT. Cirrhotics with non-malignant PVT were included. Low weight molecular heparin anticoagulation was considered in all; TIPS was indicated if thrombosis progressed or anticoagulation was contraindicated. Patients who were not anticoagulated nor received TIPS served as controls. Fifty-six patients (of whom 21 controls) were included. PVT was occlusive in 11/35, with extension to the superior mesenteric or splenic vein in 13/35. In the study group 33 patients were anticoagulated, with a recanalization rate of 36% (12/33) compared with 1/21 among controls. A time interval between appearance of thrombosis and anticoagulation < 6 months predicted chance of repermeation. Thrombus progression occurred in 15/21 non anticoagulated patients and in 5/33 anticoagulated patients (P < 0.001). TIPS was placed in six patients. There were five variceal bleedings and two intestinal venous ischaemia episodes in the control group, compared with one variceal bleeding episode in the study group. In cirrhotics with PVT, a treatment algorithm using anticoagulation and TIPS achieves a good chance of complete repermeation, reduces portal hypertensive complications, and decreases the rate of thrombosis progression.

Long-term follow-up of patients with portal vein thrombosis and myeloproliferative neoplasms.

Myeloproliferative neoplasms (MPNs) are frequently identified as an underlying cause in patients with non-cirrhotic portal vein thrombosis (PVT). The aim of this study was to describe the long-term outcome of patients with PVT and MPN. A cohort study was performed including all adult patients referred to our hospital between 1980 and 2008 with non-cirrhotic, non-malignant PVT and confirmed MPN. A total of 44 patients (70% female) were included, with a median age at PVT-diagnosis of 48 years (range 18-79). In 31 patients (70%) PVT was the first manifestation of an MPN. Additional risk factors for thrombosis were present in 20 patients (45%). Median follow-up was 5.8 years (range 0.4-21). Twenty-three patients (52%) were treated with oral anticoagulants after diagnosis of PVT, of whom 15 (34%) received long-term therapy. During follow-up, 17 patients (39%) experienced at least one episode of gastrointestinal bleeding. Additional thrombotic events occurred in 12 patients (27%). Twelve patients (27%) had progression of the underlying MPN. Seventeen patients (39%) died at a median age of 64 years (range 30-88). Death was directly related to end-stage MPN in eight patients (47%) and to a new thrombotic event in three patients (18%). No patients died from gastrointestinal bleeding. PVT is often the presenting symptom of an underlying MPN, highlighting the need for thorough screening for this disease. Recurrent thrombosis is a common and severe complication in patients with PVT and MPN. Mortality is primarily related to the underlying MPN and not to complications of portal hypertension.

Extrahepatic Portal Biliopathy: Proposed Etiology on the Basis of Anatomic and Clinical Features

To compare the anatomic and clinical features in patients with chronic portal vein thrombosis (PVT) to determine why some patients develop portal biliopathy (PB) while most do not and propose an etiology for PB. This project satisfied HIPAA regulations and received institutional review board approval for a retrospective review without the need for consent. From 100 patients with PVT, 60 were extracted who had chronic, nonmalignant PVT, after exclusion of those with sclerosing cholangitis, liver transplants, choledocholithiasis, or portosystemic shunts. Clinical and imaging data from 19 patients with biliary dilatation (PB group) were compared with data from 41 patients without biliary dilatation (no-PB group). Statistical analysis was performed with the Fisher exact test for categorical variables or the Wilcoxon rank-sum test for numerical and ordered categorical variables. P values of .05 or less were considered to indicate a significant difference. The etiology of PVT differed between the groups (P < .001); cirrhosis was infrequently seen in the PB group (two of 19, 11%) but was common in the no-PB group (31 of 41, 76%). Only two of 33 (6%) patients with cirrhosis and PVT had PB. Extension of PVT into the mesenteric veins was significantly more common in the PB group (18 of 19, 95%) than in the no-PB group (one of 41, 2%) (P < .001). Compared with the no-PB group, patients in the PB group had more acute angulation of the bile duct (median, 110° vs 128°; P = .008), less frequent gastroesophageal varices (three of 19 [16%] vs 20 of 41 [49%], P = .021), and a smaller mean coronary vein diameter (median, 5 vs 6 mm; P = .014). Noncirrhotic patients with hypercoagulable states tend to develop PB when PVT extends to the splenomesenteric veins. A possible etiology is the formation of specific peribiliary venous pathways responsible for bile duct compression and tethering.

Portal vein thrombosis in Egyptian patients with liver cirrhosis: Role of methylenetetrahydrofolate reductase C677T gene mutation

The pathogenesis of non-malignant portal vein thrombosis (PVT) in cirrhotic patients is not clearly defined. This case-control study aimed to investigate the role of methylenetetrahydrofolate reductase (MTHFR) C677T gene mutation in the pathogenesis of PVT in Egyptian cirrhotic patients. Plasma homocysteine was measured and MTHFR C677T gene mutation was detected in 76 cirrhotic patients (21 with PVT, 55 without PVT) and 20 healthy controls. The frequency of CC genotype (wide type) in cirrhotic patients with PVT was lower than controls and cirrhotics without PVT. However, the frequency of TT genotype (homozygous mutation) was elevated in cirrhotic patients with PVT as compared to controls and those without PVT. Cirrhotic patients with PVT had significantly higher homocysteine than those without PVT. Cirrhotic patients with TT genotype are at a significant risk for PVT (odds ratio = 7.7, 95% confidence interval, 1.50-42.81) when compared with CC genotype. Moreover, subjects carrying TT genotype had a higher homocysteine than those carrying CC genotype. The TT genotype of MTHFR is associated with an increased risk of PVT in Egyptian cirrhotic patients. Hyperhomocysteinemia could be considered as a relatively new risk factor for PVT in cirrhotic patients and plasma homocysteine should be investigated particularly in patients with PVT of unexplained etiology. The important clinical implication is that the readily available therapy of folate, vitamin B6 and B12 supplementation may reduce homocysteine and prevent further thrombotic complications in cirrhotic patients carrying the TT genotype.

Systematic review: portal vein thrombosis in cirrhosis

As current imaging techniques in cirrhosis allow detection of asymptomatic portal vein thrombosis during routine ultrasonography, more patients with cirrhosis are diagnosed with portal vein thrombosis. Although a consensus on noncirrhotic extra-hepatic portal vein thrombosis has been published, no such consensus exists for portal vein thrombosis with cirrhosis. To perform a systematic review of nonmalignant portal vein thrombosis in cirrhosis in terms of prevalence, pathogenesis, diagnosis, clinical course and management. Studies were identified by a search strategy using MEDLINE and EMBASE. Portal vein thrombosis is encountered in 10-25% of cirrhotics. In terms of pathophysiology, cirrhosis is no longer considered a hypocoagulable state; rather than a bleeding risk in cirrhosis, various clinical studies support a thrombotic potential. Clinical findings of portal vein thrombosis in cirrhosis vary from asymptomatic disease to a life-threatening condition at first presentation. Optimal management of portal vein thrombosis in cirrhosis is currently not addressed in any consensus publication. Treatment strategies most often include the use of anticoagulation, while thrombectomy and transjugular intrahepatic portosystemic shunts are considered second-line options. Portal vein thrombosis in cirrhosis has many unresolved issues, which are often the critical problems clinicians encounter in their everyday practice. We propose a possible research agenda to address these unresolved issues.

S1847 Hyperhomocyteinemia As a New Risk Factor for Unexplaned Portal Vein Thrombosis in Cirrhotic Patients in Eygpt

Background/ Aims: Portal vein thrombosis (PVT) in patients with liver cirrhosis is usually associated with hepatocellualar carcinoma. The pathogenesis of non-malignant PVT in cirrhotics has not been specifically studied and risk factors of PVT in this group of patients are still poorly understood. The aim of this study was to ascertain the prevalence and the significance of hyperhomocyteinemia among other risk factors in the development of PVT in cirrhotic patients. Patients and methods: Fifty two subjects were included in this study. Forty two cirrhotic patients; among them 21 had PVT and 21 had liver cirrhosis without PVT. Ten healthy subjects were included as controls. Plasma levels of homocysteine, antithrombin III, protein C and protein S were measured. Factor V Leiden was determined and methylenetetrahydrofolate reductase (MTHFR) C677T gene mutation was detected. Results: Our results revealed that plasma levels of protein C, protein S and antithrombin III were lower in cirrhotic patients with PVT than in those without PVT and controls. Plasma homocysteine level was higher among cirrhotics with PVT compared to those without PVT and controls. Factor V Leiden was detected only in 10% of controls and in 9.52% of cirrhotics with and without PVT whereas MTHFR gene mutation TT (homozygous) was detected in 23.81% of cirrhotics with PVT and not found in other groups. Conclusion: Heyperhomocyteinemia could be considered as a newly recognized risk factor for PVT in cirrhotic patients and should be routinely measured particularly when the etiology of PVT is unclear. These results could be clinically important due to the readily available therapy of folate, vitamin B6 and B12 supplementation that may reduce homocysteine and prevent further thrombotic complications.

S1848 A Kidney Function Determined Treatment Algorithm for Administration of Albumin in the Management of Spontaneous Bacterial Peritonitis (SBP)

Background/ Aims: Portal vein thrombosis (PVT) in patients with liver cirrhosis is usually associated with hepatocellualar carcinoma. The pathogenesis of non-malignant PVT in cirrhotics has not been specifically studied and risk factors of PVT in this group of patients are still poorly understood. The aim of this study was to ascertain the prevalence and the significance of hyperhomocyteinemia among other risk factors in the development of PVT in cirrhotic patients. Patients and methods: Fifty two subjects were included in this study. Forty two cirrhotic patients; among them 21 had PVT and 21 had liver cirrhosis without PVT. Ten healthy subjects were included as controls. Plasma levels of homocysteine, antithrombin III, protein C and protein S were measured. Factor V Leiden was determined and methylenetetrahydrofolate reductase (MTHFR) C677T gene mutation was detected. Results: Our results revealed that plasma levels of protein C, protein S and antithrombin III were lower in cirrhotic patients with PVT than in those without PVT and controls. Plasma homocysteine level was higher among cirrhotics with PVT compared to those without PVT and controls. Factor V Leiden was detected only in 10% of controls and in 9.52% of cirrhotics with and without PVT whereas MTHFR gene mutation TT (homozygous) was detected in 23.81% of cirrhotics with PVT and not found in other groups. Conclusion: Heyperhomocyteinemia could be considered as a newly recognized risk factor for PVT in cirrhotic patients and should be routinely measured particularly when the etiology of PVT is unclear. These results could be clinically important due to the readily available therapy of folate, vitamin B6 and B12 supplementation that may reduce homocysteine and prevent further thrombotic complications.

Corrigenda

Alimentary Pharmacology & TherapeuticsVolume 27, Issue 6 p. 528-529 Free Access Corrigenda This article corrects the following: Review article: appropriate use of corticosteroids in Crohn’s disease P. M. IRVING, R. B. GEARRY, M. P. SPARROW, P. R. GIBSON, Volume 26Issue 3Alimentary Pharmacology & Therapeutics pages: 313-329 First Published online: May 25, 2007 First published: 20 February 2008 https://doi.org/10.1111/j.1365-2036.2008.03608_1.xAboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat In Ref.1, Figure 1 contained an error in which Finland was shown in yellow colour (availability of infliximab, 0–25%), where it should have been shown in blue colour (availability of infliximab, 76–100%). The corrected Figure 1 is printed below. Figure 1Open in figure viewerPowerPoint Gastroenterologists’ perceptions of availability of infliximab in their own countries. As the information was not made available by the manufacturer or distributor of infliximab, gastroenterologists around the world were contacted and asked to estimate what proportion of their country’s population had access to infliximab to induce remission for active Crohn’s disease. African gastroenterologists provided data for more than one country. References 1 Irving PM, Gearry RB, Sparrow MP, Gibson PR. Review article: appropriate use of corticosteroids in Crohn’s disease. Aliment Pharmacol Ther 2007; 26: 313– 29. 2 Campisi G, Di Liberto C, Iacono G, et al. Oral pathology in untreated coelic disease. Aliment Pharmacol Ther 2007; 26: 1529– 36. 3 Manolakopoulos S, Bethanis S, Koutsounas S, et al. Long-term therapy with adefovir dipivoxil in hepatitis B e antigen-negative patients developing resistance to lamivudine. Aliment Pharmacol Ther 2008; 27: 266– 73. 4 Spaander VM, Van Buuren HR, Janssen HL. Review article: the management of non-cirrhotic non-malignant portal vein thrombosis and concurrent portal hypertension in adults. Aliment Pharmacol Ther 2007; 26 (Suppl. 2): 203– 9. Volume27, Issue6March 2008Pages 528-529 FiguresReferencesRelatedInformation