RESUMO
We present the case of a 64-year-old man who, after a first episode of acute pancreatitis, was readmitted 20 days later due to severe epigastric pain and later an episode of upper gastrointestinal bleeding in the form of hematemesis and melena with hemodynamic instability. An urgent gastroscopy was performed at that time, revealing a probable gastrointestinal fistula in the duodenal bulb with an adherent clot without active bleeding at that time, so an urgent CT angiography was performed that revealed a necrotic peripancreatic collection with the presence of active bleeding inside from the pancreatoduodenal artery. Urgent arteriography identified an image compatible with arterial pseudoaneurysm dependent on the pancreaticoduodenal artery branch, which was successfully embolized. Unfortunately, the patient died a few hours later as a result of septic shock secondary to an infected pancreatic collection.
Assuntos
Falso Aneurisma , Pancreatite , Masculino , Humanos , Pessoa de Meia-Idade , Pancreatite/complicações , Falso Aneurisma/complicações , Falso Aneurisma/diagnóstico , Doença Aguda , Hemorragia Gastrointestinal/complicações , Duodeno/irrigação sanguíneaRESUMO
BACKGROUND AND AIMS: Controversial data have been reported regarding the prevalence of Non-Alcoholic Fatty Liver Disease (NAFLD) in Inflammatory Bowel Disease (IBD) population and IBD-related risk factors. The aim of the study was to assess the prevalence and risk factors associated with NAFLD and liver fibrosis in IBD participants compared with non-IBD controls. METHODS: Cross-sectional, case-control study including 741 IBD cases and 170 non-IBD controls, matched by sex and age. All participants underwent liver ultrasound, transient elastography and laboratory tests. A logistic regression multivariable analysis was performed adjusting for classic metabolic risk factors and history of systemic steroid use. RESULTS: The prevalence of NAFLD and significant liver fibrosis was 45 % and 10 % in IBD group, and 40 % and 2.9 % in non-IBD group (p = 0.255 and 0.062, respectively). Longer IBD duration (aOR 1.02 95% CI (1.001-1.04)) and older age at IBD diagnosis (aOR 1.02 95 % CI (1.001-1.04)) were independent risk factors for NAFLD in IBD group. Crohn´s Disease was an independent risk factor for significant liver fibrosis in participants with IBD and NAFLD (aOR 3.97 95 % CI (1.78-8.96)). NAFLD occurred at lower BMI levels in IBD group with NAFLD compared to non-IBD group with NAFLD (aOR 0.92 95 % CI (0.87-0.98)). CONCLUSIONS: Although we found no differences in the prevalence of NAFLD and liver fibrosis between IBD group and non-IBD group, our findings suggest that liver fibrosis progression should be closely monitored in patients with concomitant CD and NAFLD, more in particular in those with long standing active disease.
Assuntos
Doença de Crohn , Doenças Inflamatórias Intestinais , Hepatopatia Gordurosa não Alcoólica , Humanos , Hepatopatia Gordurosa não Alcoólica/epidemiologia , Doença de Crohn/complicações , Doença de Crohn/epidemiologia , Estudos de Casos e Controles , Estudos Transversais , Fatores de Risco , Doenças Inflamatórias Intestinais/complicações , Cirrose Hepática/complicações , PrevalênciaRESUMO
Chronic inflammation in patients with Inflammatory Bowel Disease (IBD) leads to an increased risk of colorectal cancer, small bowel cancer, intestinal lymphoma and cholangiocarcinoma. However, treatments for IBD have also been associated with an increased risk of neoplasms. Patients receiving Thiopurines (TPs) have an increased risk of hematologic malignancies, non-melanoma skin cancer, urinary tract neoplasms and cervical cancer. Anti-TNFs have been associated with a higher risk of neoplasms, mainly lymphomas and melanomas; however, the data are controversial, and some recent studies do not confirm the association. Nevertheless, other biologic agents, such as ustekinumab and vedolizumab, have not shown an increased risk of any neoplasm to date. The risk of malignancies with tofacitinib exists, but its magnitude and relationship with previous treatment with TPs is not defined, so more studies from daily clinical practice are needed. Although biologic therapy seems to be safe for patients with current cancer or a prior history of cancer, as has been demonstrated in other chronic inflammatory conditions, prospective studies in this specific population are needed. Until that time, it is crucial to manage such conditions via the combined clinical expertise of the gastroenterologist and oncologist.
RESUMO
The aim of the systematic review is to assess the prevalence and risk factors of liver fibrosis in patients with Inflammatory Bowel Disease (IBD) and Non-Alcoholic Fatty Liver Disease (NAFLD) and to discuss the role of liver fibrosis in the progression to hepatocellular carcinoma (HCC). We performed a structured search in PubMed, Web of Science, Embase, and Scopus up to 3 March 2023 to identify observational studies reporting liver fibrosis in patients with NAFLD and IBD. Quality of studies was assessed using the Newcastle-Ottawa Scale (NOS) score. A total of 23 studies met our inclusion criteria, including 629,781 patients. A total of 10 cross-sectional, 3 case-control, and 10 cohort studies were included. Fourteen studies had a NOS score ≥ 7 points. NAFLD was diagnosed in 2162/6332 (34.1%) IBD participants. However, NAFLD diagnosis was established in 924/2962 (31.2%) healthy individuals without IBD. Advanced liver fibrosis was found in 116 (11.6%) of 992 IBD patients with NAFLD. Most studies found an association between NAFLD and classic cardiovascular risk factors such as older age, male sex, higher BMI, diabetes, hypertension and dyslipidemia. In addition, metabolic syndrome features were also associated with an increased risk of significant and advanced liver fibrosis. Although no strong association between NAFLD and IBD therapy was reported, some studies associated NAFLD with IBD diagnosis, Crohn's Disease, a complicated course of IBD, disease activity, and IBD duration. Advanced liver fibrosis was also associated with Crohn's disease in several studies. In conclusion, NAFLD and advanced liver fibrosis are prevalent and clinically relevant extraintestinal manifestations, so its diagnosis and potential progression to HCC should be carefully considered in daily clinical practice.
RESUMO
Presentamos el caso de un varón de 64 años quien, tras un primer episodio de pancreatitis aguda necrotizante, reingresa a los 20 días por cuadro de dolor epigástrico intenso y posteriormente episodio de hemorragia digestiva alta en forma de hematemesis y melenas con inestabilización hemodinámica. Se realiza en ese momento gastroscopia urgente objetivándose probable fistula gastrointestinal en bulbo duodenal con coágulo adherido sin sangrado activo en ese momento por lo que se realiza angio-TC urgente que revela colección peripancreática necrótica con presencia de sangrado activo en su interior, procedente de la arteria pancreatoduodenal. La arteriografía urgente identificó imagen compatible con pseudoaneurisma arterial dependiente de la rama de arteria pancreatoduodenal, que fue embolizada con éxito. Desgraciadamente el paciente falleció en las horas posteriores, como consecuencia de un shock séptico secundario a colección pancreática infectada.
We present the case of a 64-year-old man who, after a first episode of acute pancreatitis, was readmitted 20 days later due to severe epigastric pain and later an episode of upper gastrointestinal bleeding in the form of hematemesis and melena with hemodynamic instability. An urgent gastroscopy was performed at that time, revealing a probable gastrointestinal fistula in the duodenal bulb with an adherent clot without active bleeding at that time, so an urgent CT angiography was performed that revealed a necrotic peripancreatic collection with the presence of active bleeding inside from the pancreatoduodenal artery. Urgent arteriography identified an image compatible with arterial pseudoaneurysm dependent on the pancreaticoduodenal artery branch, which was successfully embolized. Unfortunately, the patient died a few hours later as a result of septic shock secondary to an infected pancreatic collection.