Therapeutic effect of rupatadine against l-arginine-induced acute pancreatitis in rats: role of inflammation.

Acute pancreatitis (AP) is an abrupt inflammatory disorder causing high morbidity and mortality. As AP is an insidious medical emergency, a curative modality is required instead of a preventive measure. Thus, we investigated the possible curative effect of rupatadine on a rat model of AP. Rupatadine is a potent histamine receptor 1 (H1R) and platelet-activating factor (PAF) blocker. We used four groups of six Wistar rats as follows: the control group received vehicle; the rupatadine control group received rupatadine as 6 mg/kg orally; the AP group received l-arginine intraperitoneally, and the treatment group received rupatadine at 1, 6, and 24 h after l-arginine injection. The levels of serum amylase, pancreatic oxidative parameters, and pancreatic cytokines were measured. PAF, histamine, and myeloperoxidase levels were determined in the pancreas. Histopathological and immunohistochemical examinations were performed to determine nuclear factor kappa-B (NF-κB) and caspase 3 expressions. Oxidative damage and severe inflammation were detected in the pancreas of the AP group. Rupatadine reduced the oxidative damage and the levels of proinflammatory cytokines, PAF, histamine, myeloperoxidase, NF-κB, and caspase 3 expressions. It restored the pancreatic acini to almost normal condition. Rupatadine induced important anti-inflammatory and antiapoptotic effects against l-arginine-induced AP.

Reorienting of pramipexole as a promising therapy for acute pancreatitis in a rat model by suppressing TLR4\NF-κB p65\NLRP3 inflammasome signaling.

Acute pancreatitis (AP), a disorder of global importance, has a growing incidence and prevalence, particularly in the Western world. Its complications include pseudocysts and chronic pancreatitis. Pramipexole (PMX), a D2/3 receptor selecting agonist used in Parkinsonism, was reported to have anti-inflammatory effects. This study explored the potential curative role of PMX in an l-arginine-induced acute pancreatitis rat model in addition to a possible mechanistic pathway. Rats were divided randomly into three groups: control, l-arginine, and l-arginine + PMX. Seven days after AP induction, rats were decapitated and estimated for serum amylase, lipase, glucose, pancreatic inflammatory mediators toll-like receptor-4, nuclear factor κ B p65, serum tumor necrosis factor-α, NOD-, LRR and pyrin domain- containing protein 3 (NLRP3) inflammasome, caspase-1, interleukin 1ß, oxidative biomarkers malondialdehyde, myeloperoxidase, nitrite/nitrate, reduced glutathione, and the apoptotic marker caspase-3, with pancreatic histopathological changes. l-arginine-mediated AP was proved by elevated serum lipase and amylase and pancreatic inflammatory, oxidative, and apoptotic markers with infiltration of inflammatory cells using hematoxylin and eosin stain. PMX improved all these adverse signs of AP greatly. PMX might be considered an innovative therapy for AP due to its remarkable antioxidant, antiapoptotic, and anti-inflammatory effects, which are attributed to the suppression of the NLRP3 inflammasome and its downstream inflammatory cytokines.

Trimethylamine N-oxide promotes hyperlipidemia acute pancreatitis via inflammatory response.

Trimethylamine N-oxide (TMAO), a metabolite of gut microbiota, is involved in the regulation of lipid metabolism and inflammatory response; however, the role of TMAO in hyperlipidemia acute pancreatitis (HAP) is not clear. In this study, HAP mice were used as an animal model to explore the effects and possible mechanism of TMAO on HAP, which may provide new ideas for the treatment of HAP. Results found that the levels of triglycerides, total cholesterol, low-density lipoprotein cholesterol, nonestesterified fatty acid, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, α-amylase, TMAO, and flavin-containing monooxygenase 3 were significantly increased, the levels of high-density lipoprotein cholesterol and insulin were significantly decreased, and there was an obvious pancreatic injury and inflammatory response in the model group. The choline analogue 3,3-dimethyl-1-butanol (DMB) treatment reversed the changes of serum biochemical parameters, alleviated the pancreatic tissue injury, and reduced the levels of inflammatory cytokines. Further studies of toll-like receptor (TLR)/p-glycoprotein 65 (p65) pathway found that the expressions of TLR2, TLR4, and p-p65/p65 in the model group were significantly increased, which was more obvious after Escherichia coli (Migula) Castellani & Chalmers treatment, while activation of the TLR/p65 pathway was inhibited by DMB. The results indicated that TMAO promotes HAP by promoting inflammatory response through TLR/p65 signaling pathway, suggesting that TMAO may be a potential target of HAP.

[Multivisceral pancratic cytosteatonecrosis found at autopsy]. / Cytostéatonécrose multiviscérale d'origine pancréatique, de découverte autopsique.

INTRODUCTION: Pancreatic cytosteatonecrosis is a rare condition associated with various pancreatic diseases such as acute or chronic pancreatitis and pancreatic cancer. We report a case of pancreatic cytosteatonecrosis discovered at autopsy. OBSERVATION: This is a young man, 29 years old, alcoholic, non-smoker, who consulted for abdominal pain, vomiting, fever (38°). Renal ultrasound showed signs of acute renal failure, with severe anemia at 6g/dl and hyperleukocytosis. Lipasemia has not been tested. The treatment combined hemodialysis, punctures of effusions, analgesics, antibiotics and diuretics. The death occurred after 45 days of hospitalization. The medical autopsy requested showed an abdominal cavity dotted with multiple whitish, chalky, "candle-stained" nodules scattered throughout the peritoneum. Microscopy confirmed the diagnosis by showing large areas of adiponecrosis associated with polymorphic, diffuse leukocyte infiltrates and calcifications. CONCLUSION: This observation is original by the discovery at autopsy of one of the major complications of acute pancreatitis. This situation is dramatic because the death could be avoided. You have to think about it in order to ask for the dosage of lipasemia. The "digestion" of pancreatic enzymes are responsible for intra-pancreatic and peri-pancreatic complications. Chronic alcoholism and cholelithiasis are the main risk factors.

[Acute pancreatitis under acitretin]. / Pancréatite aiguë sous acitrétine.

INTRODUCTION: Retinoids are vitamin A derivatives with numerous indications in dermatology. Acute pancreatitis is a rare adverse effect of systemic retinoids. We report a case occurring during acitretin treatment for psoriasis. PATIENTS AND METHODS: A 27-year-old male patient with no history of diabetes, obesity, alcohol consumption or medication consulted for extensive pustular psoriasis. The lipid balance and liver tests were normal. The patient was treated with acitretin at a dose of 25mg/d. Four days after the start of treatment, the patient was admitted to the surgical emergency room for piercing epigastric pain with vomiting of bile, without transit problems. Serum lipase was 20 times the normal value (1278 IU/L). CRP was raised at 155mg/L and triglycerides were normal at 0.66g/L. Ranson's score was 1 and the abdominal scan revealed Balthazar Grade B pancreatitis with a small amount of peritoneal effusion. The ultrasound examination showed absence of gall stones, without dilation of either the intra- or extra-hepatic bile ducts. Acitretin was discontinued due to its possible causative role. The patient was treated by means of parenteral feeding, strict fasting and a proton-pump inhibitor, and a good clinical outcome with gradual normalization of serum lipase and CRP was achieved in 10 days. The patient was subsequently treated with infliximab for psoriasis, with good results. DISCUSSION: In the event of acute abdominal pain in a patient treated with retinoids, a diagnosis of acute pancreatitis should be considered. This complication can occur in the absence of hypertriglyceridemia.

Role of Wnt/ß-catenin pathway agonist SKL2001 in Caerulein-induced acute pancreatitis.

The goal of this study was to clarify the protective role of the Wnt/ß-catenin pathway agonist SKL2001 in a rat model of Caerulein-induced acute pancreatitis. AR42J cells and rats were divided into 4 groups: control, Caerulein, SKL2001 + Caerulein, and SKL2001 + control. Cell apoptosis was examined using flow cytometry. Hematoxylin-eosin staining was performed to observe pathological changes in pancreatic and small intestinal tissues. Inflammatory cytokines were detected by enzyme-linked immunosorbent assay (ELISA), while genes related to the Wnt/ß-catenin pathway were quantified using quantitative real-time PCR. In vitro results showed that Caerulein promoted cell necrosis, inhibited the Wnt/ß-catenin pathway, and increased the level of inflammatory cytokines. However, SKL2001 reduced cell necrosis and inflammatory cytokines and activated the Wnt/ß-catenin pathway. Additionally, in vivo results demonstrated the accumulation of fluid (i.e., edema), hemorrhage, inflammation and necrosis of the pancreatic acini occurred 6 h after the final Caerulein induction, with the damage reaching a maximal level 12 h after the final Caerulein induction; meanwhile, the Wnt/ß-catenin pathway was evidently inhibited with an enhanced level of inflammatory cytokines. The aforementioned damage was further aggravated 12 h later. Nevertheless, the pancreatic and small intestinal tissue damages were alleviated in Caerulein-induced rats treated with SKL2001. In conclusion, activation of the Wnt/ß-catenin pathway could inhibit Caerulein-induced cell apoptosis and inflammatory cytokine release, thus improving pancreatic and intestinal damage in rats with acute pancreatitis.

[Cholangitis with granulocytic epithelial lesion: a new entity with a specific treatment]. / La cholangite à lésion épithéliale granulocytique : une nouvelle entité avec un traitement spécifique.

Herein, we report a case of cholangitis with granulocytic epithelial lesion associated with pancreatitis in a 22-year-old patient. The association of bile duct lesions and pancreatitis is usually very suggestive of IgG4 related disease. However, in our case, we found no IgG4 tissue infiltration and we found a granulocytic epithelial on the liver biopsy. Recently, cholangitis with granulocytic epithelial lesion was described in the literature. This entity is identified in 2 % of patients with sclerosing cholangitis. Patients are more likely children or young adults and often have an associated inflammatory bowel disease or rarely a pancreatitis. It is defined by the presence of neutrophilic bile duct lesions on a liver biopsy. Although rare, the diagnosis of cholangitis with granulocytic epithelial lesion is important because of its excellent response to immunosuppressive treatment.

[An IgG4-related pancreatitis mimicking an adenocarcinoma: A case report]. / Une pancréatite auto-immune à IgG4 simulant un adénocarcinome : à propos d'un cas.

Type 1 auto-immune pancreatitis (type 1 AIP) is the pancreatic manifestation of IgG4-related systemic disease (IgG4-RD). This disease has recently been individualized and is characterized by elevated serum IgG4 levels and extrapancreatic lesions with common histologic characteristic: dense infiltration of lymphocytes, IgG4-positive plasma cells and storiforme fibrosis. Obliterative phlebitis is frequently detected. The pancreas is frequently involved in this disease. As approach to the pancreas for histological examination is generally difficult, AIP is diagnosed using a combination of clinical, serological, morphological and histopathological features. In pseudotumoral cases, AIP can be misdiagnosed as pancreatic cancer. Since AIP responds dramatically to steroid therapy, accurate diagnosis of AIP can avoid unnecessary laparotomy or pancreatic resection. We report here a case of a patient who underwent surgery for presumed pancreatic cancer. The final diagnosis was type 1 AIP.

Unusual course of the aberrant right hepatic artery running through the pancreatic parenchyma during modified Frey's procedure.

We report a variation of an aberrant right hepatic artery arising from the superior mesenteric artery and crossing into pancreatic head without other hepatic artery substitution. The variant was discovered during radiological examinations in a patient with symptomatic chronic pancreatitis requiring Frey's procedure with reinsertion of the common bile duct into the pancreatic head. An aberrant right hepatic artery arising from the superior mesenteric artery is present in 10 to 20% of case and its course is usually retro-pancreatic. The course of this artery into the pancreatic head is uncommon and can be present up to 10% in case of ARHA. Knowledge of an aberrant right hepatic artery crossing into the pancreatic head is important before pancreatic surgery in order to avoid surgical complications, especially for liver necrosis.

[Acute pancreatitis induced by valproic acid]. / Pancréatite aiguë induite par l'acide valproïque.

INTRODUCTION: We describe the case of an adult man aged 49, without personal antecedents, or family psychiatric history, treated for bipolar disorder since 1995 and stabilised in the last 8 years by valproic acid, who presented in January 2010 an acute drug-induced pancreatitis. Drug-induced pancreatitis has been described since 1955. It may be induced by more than 260 various molecules, as well as by valproic acid, which remains underreported in the literature because there is a problem of imputability. BACKGROUND: The prevalence of acute drug-induced pancreatitis is set between 1 and 2 %. However, it must remain as an exclusion diagnosis after conducting an exhaustive etiological investigation that will, notably, eliminate bilary and alcoholic causes. The most incriminated drugs are the inhibitors of the conversion enzyme, sulfa drugs, non-steroidal anti-inflammatory, diuretics and anticonvulsants, including valproic acid. In Tunisia, the prescription of valproic acid is increasing in bipolar disorder therapy because it is known for its weak toxicity and easy handling. CASE REPORT: The case of our patient, who suffers from an acute Balthazar stage C pancreatitis with severe evolution after the drug was stopped, the imputability of valproic acid was considered strong and the collegial decision between the surgery, pharmacovigilance and psychiatry services maintained the drug-induced origin and consequently stopped the valproic acid. DISCUSSION: This case supports the idea that acute pancreatitis may be induced by valproic acid, even after a prescription lasting for a long period of time, it has no predictable factors and is totally independent of the drug-related dose and of depakine blood levels. There are no predictive factors to the present day, but the evolution is generally good except in rare cases where it may be dangerous. This leads us to think of bipolar patients who are found within weak grounds, such as alcoholics, cancer and HIV positive patients.

[IgG4-related disease: A proteiform pathology with frequent chest manifestations]. / Maladie associée aux IgG4 : une maladie protéiforme aux manifestations thoraciques fréquentes.

INTRODUCTION: While IgG4-related disease (IgG4-RD) was initially described in the early 2000s, its polymorphic clinical manifestations were previously reported under different names ; they have in common the presence of IgG4+ oligoclonal plasma cells and fibrosis. STATE OF THE ART: Ruling out certain differential diagnoses, the diagnosis of IgG4-RD is based on a bundle of clinical, biological and histological features. Chest involvement is variable and can affect the mediastinum, bronchi, parenchyma, pleura and/or, more rarely, bones and (pericardium, aorta, coronary…) vascular structures. The most frequent radiological manifestations are peribronchovascular thickening, mediastinal lymphadenopathy, and nodular or interstitial patterns. Pleural involvement and posterior mediastinal fibrosis are less frequent, while thoracic paravertebral tissue thickening is highly specific. Systemic corticosteroids are the cornerstone of treatment. In case of relapse or as frontline therapy in case of risk factors for relapse and/or poor tolerance of corticosteroids), a steroid-sparing agent (most often rituximab) is added, and biannual maintenance infusions are associated with a lower risk of relapse. PERSPECTIVES: An international consensus has recently led to the development of classification criteria that should standardize the diagnostic approach and homogenize the enrolment of patients in epidemiological as well as therapeutic studies. Other treatments are also under evaluation, including biologics targeting T2 inflammation, CD-19 (inebilizumab, obexelimab), SLAMF7 (elotuzumab) surface proteins, Bruton's tyrosine kinase, and the JAK/STAT pathway. CONCLUSIONS: Substantial progress has been made over recent years in understanding IgG4-RD pathophysiology, and personalized patient care seems to be an achievable medium-term goal.

[Acute pancreatitis as a complication of massive hemolysis in patients on hemodialysis: About three observations]. / Pancréatite aiguë dans le décours d'une hémolyse sévère chez des patients hémodialysés : à propos de trois observations.

Haemolysis is an uncommon complication of haemodialysis which can be serious. We herein report on three patients with kidney failure who developed acute pancreatitis due to mechanical haemolysis during a haemodialysis session. We also review the current literature and discuss putative etiopathogenic mechanisms.

[Management of acute pancreatitis. A literature review]. / Prise en charge de la pancréatite aiguë. Revue de la littérature.

The management of acute pancreatitis is now fairly codified, with specific recommendations developed by expert groups. These recommendations deal in particular with the minimum initial assessment, recognized severity scores, initial medical management with hyperhydration, preventive anticoagulation, early refeeding, delays in imaging and management of complications. In this work, we have tried to bring together the various recommendations, articles and studies dealing with this subject, based more particularly on European recommendations, in order to guide the management of acute pancreatitis in current practice.

Acute pancreatitis and recurrent acute pancreatitis: an exploration of clinical and etiologic factors and outcomes.

OBJECTIVE: To describe the epidemiology and clinical features of acute pancreatitis and recurrent acute pancreatitis in children. METHODS: Observational and retrospective study with an analytical component. Patients were classified into two groups: Acute pancreatitis and recurrent pancreatitis. The relationship with each parameter obtained was analyzed using the chi-squared test, Student's t-test, or the Mann-Whitney U test. RESULTS: There were 130 patients with acute pancreatitis; recurrent pancreatitis was diagnosed in 23.8% of the cases. The most frequent causes were anatomical (29.6%), pharmacological (19.2%), and biliary (14.6%), although in 29.2% etiology was not identified. Fasting lasted 3.5±3.8 days and parenteral nutrition was indicated in 26.9% of the cases for 10.8±11.3 days. A statistical association with anatomical (p=0.02) and pharmacological causes (p=0.01) was found in the recurrent pancreatitis group; no other differences between acute pancreatitis and recurrent pancreatitis groups were observed. The mortality rate was 3.1%, it was not attributable to acute pancreatitis in any cases. CONCLUSION: Acute pancreatitis is associated with a high frequency of acute recurrent pancreatitis. Severity and complications did not show statistically significant differences in this investigation. Anatomical etiologies were the most relevant cause in this cohort. Fasting time and parenteral nutrition use were relevant. Genetics testing is required in this population.

[A jejunal artery pseudoaneurysm ruptured in the jejunal lumen: A rare vascular complication of severe pancreatitis]. / Faux anévrisme rompu d'une artériole jéjunale: une complication rare d'une pancréatite grave.

Jejunal pseudoaneurysm is a rare complication of pancreatitis, usually manifested by digestive bleeding when it ruptures into the digestive lumen. This complication is extremely rare and may be life-threatening. The diagnosis is based on abdominal angiographic computed tomography. Radiology allows therapeutic management through arterial embolization. This case report describes a pseudoaneurysm of jejunal artery that developed as the result of pancreatitis: A 77-year-old man seen in early September 2015 at the emergency department for acute pancreatitis had a pseudocyst infected and spontaneously fistulized into the jejunum lumen. His condition responded initially to symptomatic therapy, and he was discharged. He returned two years later, with digestive bleeding from jejunal pseudoaneurysm that had ruptured into the jejunal lumen. Angiographic embolization was performed as first-line treatment with good outcome. Bleeding more than two years after acute pancreatitis due to rupture of a jejunal pseudoaneurysm is an exceptional complication. Here we report a rare case of digestive hemorrhage caused by jejunal pseudoaneurysm, complicating acute pancreatitis.

Jejum aumenta a gravidade da pancreatite aguda em camundongos: implicações para intervenções pré-operatórias para reduzir as complicações da cirurgia pancreática / Fasting increases the severity of acute pancreatitis in a mouse model: implications for preoperative interventions to reduce complications of pancreatic surgery

ABSTRACT Background: Acute pancreatitis following surgical or endoscopic procedures on the pancreas can compromise the outcome and lead to severe complications and even death. The aim of this study was to determine whether prolonged fasting affects the severity of acute pancreatitis (AP). Methods: Male mice were divided into 4 groups: Group CF (n=5) control animals that fasted for 24 hours; Group CNF (n=5) control animals that did not fast; Group APF (n=7) that fasted for 24 hours and underwent induction of acute pancreatitis (AP) and Group APNF (n=7) that did not fast and underwent AP. Eight hours after AP blood was collected for evaluation of cytokines: IL-1β, IL-6, IL-10, TNF-α and MCP-1. Liver tissue was collected for determination of Malondialdehyde, pancreatic tissue for determination of enzyme content and lung tissue for determination of myeloperoxidase. Results: Significant increase in pancreatic amylase content was observed in group CF and increased serum levels of IL -6, Il-10 and MCP-1 were in group APF. Liver malondialdehyde was also increased in APF animals. APF group showed much more necrosis of the pancreatic acinar cells. Conclusion: In the present study, we observed an increase in the severity of acute pancreatitis with prolonged fasting in a severe acute pancreatitis model. These results suggest that in clinical practice, the preoperative fasting time should be shortened before pancreatic procedures.

RESUMO Contexto: A pancreatite aguda após procedimentos cirúrgicos ou endoscópicos no pâncreas pode comprometer o resultado e levar a complicações graves e até mesmo à morte. O objetivo deste estudo foi determinar se o jejum prolongado afeta a gravidade da pancreatite aguda (PA). Métodos: Camundongos machos foram divididos em 4 grupos: Grupo CF (n=5) animais de controle que jejuaram por 24 horas; Grupo CNF (n=5) animais de controle que não jejuaram; Grupo APF (n=7) que jejuaram por 24 horas e foram submetidos à indução de PA e Grupo APNF (n=7) que não jejuaram e foram submetidos a PA. Oito horas após a PA, o sangue foi coletado para avaliação de citocinas: IL-1β, IL-6, IL-10, TNF-α e MCP-1. O tecido hepático foi coletado para a determinação do malondialdeído, o tecido pancreático para a determinação do conteúdo enzimático e o tecido pulmonar para a determinação da mieloperoxidase. Resultados: Foi observado um aumento significativo no conteúdo de amilase pancreática no grupo CF e um aumento nos níveis séricos de IL-6, Il-10 e MCP-1 no grupo APF. O malondialdeído hepático também aumentou nos animais APF. O grupo APF apresentou muito mais necrose das células acinares pancreáticas. Conclusão: No presente estudo, observamos um aumento na gravidade da pancreatite aguda com o jejum prolongado em um modelo de pancreatite aguda grave. Esses resultados sugerem que, na prática clínica, o tempo de jejum pré-operatório deve ser reduzido antes dos procedimentos pancreáticos.

Avaliação da lactoferrina e da calprotectina como marcadores de inflamação intestinal na pancreatite crônica / Evaluating lactoferrin and calprotectin as markers of intestinal inflammation inchronic pancreatitis

ABSTRACT Background: The treatment of chronic pancreatitis does not consistently solve intestinal abnormalities, and despite the implementation of various therapeutic measures, patients often continue to experience persistent diarrhea. Therefore, it is imperative to recognize that diarrhea may stem from factors beyond pancreatic insufficiency, and intestinal inflammation emerges as a potential contributing factor. Objective: The aim of this study was to assess fecal lactoferrin and calprotectin levels as indicators of intestinal inflammation in patients with chronic pancreatitis experiencing persistent diarrhea. Methods: In this study, 23 male patients with chronic pancreatitis primarily attributed to alcohol consumption and presenting with diarrhea (classified as Bristol stool scale type 6 or 7), underwent a comprehensive evaluation of their clinical and nutritional status. Fecal lactoferrin and calprotectin levels were mea­sured utilizing immunoassay techniques. Results: The average age of the participants was 54.8 years, 43.5% had diabetes, and 73.9% were smokers. Despite receiving enzyme replacement therapy and refraining from alcohol for over 4 years, all participants exhibited persistent diarrhea, accompanied by elevated calprotectin and lactoferrin levels indicative of ongoing intestinal inflammation. Conclusion: The findings of this study underscore that intestinal inflammation, as evidenced by elevated fecal biomarkers calprotectin and lactoferrin, may contribute to explaining the persistence of diarrhea in patients with chronic pancreatitis.

RESUMO Contexto: O tratamento da pancreatite crônica não resolve de forma consistente as anomalias intestinais e, apesar da implementação de várias medidas terapêuticas, os pacientes muitas vezes continuam a apresentar diarreia persistente. Portanto, é imperativo reconhecer que a diarreia pode resultar de fatores além da insuficiência pancreática, e a inflamação intestinal surge como um potencial fator contribuinte. Objetivo: O objetivo deste estudo foi avaliar os níveis fecais de lactoferrina e calprotectina como indicadores de inflamação intestinal em pacientes com pancreatite crônica com diarreia persistente. Métodos: Neste estudo, 23 pacientes do sexo masculino com pancreatite crônica atribuída principalmente ao consumo de álcool e apresentando diarreia (classificada na escala de fezes de Bristol tipo 6 ou 7), foram submetidos a uma avaliação abrangente de seu estado clínico e nutricional. Os níveis fecais de lactoferrina e calprotectina foram medidos utilizando técnicas de imunoensaio. Resultados: A idade média dos participantes foi de 54,8 anos, 43,5% tinham diabetes e 73,9% eram fumantes. Apesar de receber terapia de reposição enzimática e abster-se de álcool por mais de 4 anos, todos os participantes apresentaram diarreia persistente, acompanhada por níveis elevados de calprotectina e lactoferrina, indicativos de inflamação intestinal contínua. Conclusão: Os achados deste estudo ressaltam que a inflamação intestinal, evidenciada pelos biomarcadores fecais elevados calprotectina e lactoferrina, pode contribuir para explicar a persistência da diarreia em pacientes com pancreatite crônica.

Acute pancreatitis and COVID-19: an integrative review of the literature / Pancreatite aguda e COVID-19: uma revisão integrativa da literatura

ABSTRACT The first cases of the COVID-19 disease were identified in late 2019 in China, but it didnt take long for it to become pandemic. At first, it was believed that it was restricted to respiratory symptoms only, until extrapulmonary manifestations were reported worldwide. Acute pancreatitis concomitant with the diagnosis of SARS-CoV-2 infection has been observed in some patients, in the absence of the most common etiologies described in the literature. It is postulated that the presence of the ECA-2 viral receptor in the pancreas is responsible for the direct cellular damage and that the hyperinflammatory state of COVID-19 favors the development of pancreatitis through an immune-mediated mechanism. This study aimed to analyze the correlation between acute pancreatitis and COVID-19 disease as a probable causality factor. An integrative literature review was carried out, including studies published between January 2020 and December 2022 that brought data on patients diagnosed with acute pancreatitis according to the revised Atlanta Classification with a confirmed diagnosis of COVID-19 in the same period. A total of thirty studies were reviewed. Demographic, clinical, laboratory and imaging aspects were analyzed and discussed. It is believed that SARS-CoV-2 was responsible for the development of acute pancreatitis in these patients, due to the absence of other precipitating risk factors, as well as the close temporal relationship between both. Attention should be given to gastrointestinal manifestations in patients affected by COVID-19.

RESUMO Os primeiros casos da doença COVID-19 foram identificados no final de 2019 na China, mas não foi necessário muito tempo para que se tornasse pandêmica. Acreditava-se, a princípio, que ela fosse restrita apenas a sintomas respiratórios, até que manifestações extrapulmonares fossem mundialmente relatadas. Quadros de pancreatite aguda concomitantes ao diagnóstico de infecção por SARS-CoV-2 vêm sendo observados em alguns pacientes, na ausência das etiologias mais comuns descritas na literatura. Postula-se que a presença do receptor viral ECA-2 no pâncreas seja responsável pelo dano celular direto e que o estado hiperinflamatório da COVID-19 favoreça o desenvolvimento da pancreatite por mecanismo imunomediado. Este estudo teve como objetivo analisar a correlação entre pancreatite aguda e a doença COVID-19 como um provável fator de causalidade. Realizou-se uma revisão integrativa da literatura, foram incluídos estudos publicados entre janeiro de 2020 e dezembro de 2022 que trouxessem dados acerca de pacientes diagnosticados com pancreatite aguda conforme a Classificação de Atlanta revisada com diagnóstico confirmado de COVID-19 no mesmo período. Um total de trinta estudos foram revisados. Aspectos demográficos, clínicos, laboratoriais e de imagem foram analisados e discutidos. Acredita-se que o SARS-CoV-2 foi o responsável pelo desenvolvimento de pancreatite aguda nestes pacientes, devido à ausência de demais fatores de risco precipitantes, bem como à estreita relação temporal entre ambos. Uma atenção deve ser dada às manifestações gastrointestinais em pacientes acometidos pela COVID-19.