Acute pancreatitis is an inflammatory disease of the pancreas. Acute abdominal pain is the most common symptom, and increased concentrations of serum amylase and lipase confirm the diagnosis. Pancreatic injury is mild in 80% of patients, who recover without complications. The remaining patients have a severe disease with local and systemic complications. Acute pancreatitis is a hypercatabolic state resulting in rapid loss of body weight, fat and protein. Nutritional support is an integral part of patient care and is started early in the course of disease. Patients with mild to moderate disease (80% of patients) do not require enteral nutrition (EN) or parenteral nutrition(PN), as they will begin oral feeding within 4 days of presentation. Nutritional support is needed for severe disease, EN is preferred over PN, and use PN when EN is contraindicated or not feasible. Most groups have used nasojejunal feeding, which has difficulties in maintenance of the tube position and patency. Nasogastric feeding in severe AP has shown little difference in terms of clinical outcome from nasojejunal feeding. In this review, we review the role, methods, and clinical implications of nutritional supports in acute pancreatitis and also present recently recommended standard guidelines.

십이지장 벽내혈종은 70-75%는 복부 둔상에 의해 발생하며 그 외 항응고제 사용이나 혈액응고장애에 의한 자발적 출혈, 치료적 내시경 시술 후 합병증의 증례가 보고되었으나 췌장염에 의한 증례는 드물다. 75세 남자가 전복부통증, 오심, 구토로 내원하여 시행한 전산화 단층촬영과 상부 위장관 내시경에서 급성 알코올성 췌장염으로 인해 발생한 십이지장 벽내혈종이 관찰되었으며 내과적 보존 치료로 급성 췌장 염을 치료하여 벽내혈종까지 흡수되었다. 이는 급성 알코올 성 췌장염에서 십이지장 벽내혈종이 발생할 수 있으며 수술 적 치료를 시행하지 않고 내과적 보존적 치료를 초 치료로 시행해 볼 수 있는 임상경과를 보여주기에 저자들은 이를 보고한다.

In the initial genetic studies about pancreatitis in Korea, gene mutations were thought to be rare. However, the recent findings of PRSS1, SPINK1, and CFTR mutations in patients with idiopathic chronic pancreatitis or inherited cases of chronic pancreatitis are much more common than originally predicted. Therefore, it is important to identify underlying genetic background in idiopathic chronic pancreatitis to avoid progression and development of complications. In addition, concentrated and strict follow-up must be given to the patients because of very high risk of pancreatic cancer. However, it is also true that studies about genetics in pancreatitis were not enough to compare with Western studies. Accordingly, further large scale studies are necessary to find other unknown possible genes that could be related to the chronic and hereditary pancreatitis.

Autoimmune pancreatitis should be differentiated from pancreatobiliary cancers because they often have similar clinical features and images. Accurate and practical diagnostic algorithm for AIP is important to avoid unnecessary surgery and delayed treatment. International Consensus Diagnostic Criteria for AIP suggested that diagnostic algorithms and the practical patterns considerably vary worldwide. Patients with clinically suspected AIP can be categorized into patients with typical features of AIP and patients with indeterminate features based on CT findings. Serology and other organ involvement can be used as collateral evidence of AIP. If a patient presents with diffuse pancreatic enlargement but is lack of collateral evidence, pancreatogram could be useful. If a patient has obstructive jaundice, biliary drainage and endobiliary biopsy are recommended. Duodenal papillary biopsy for IgG4 immunostain can be used during ERCP. In case of atypical imaging findings, EUS-guided FNA/biopsy is recommended to exclude pancreatic cancer and to obtain the suggestive findings of AIP. If type 2 is clinically suspected, EUS-guided core biopsy is required for the definite diagnosis. Short-term steroid trial can be performed to confirm the diagnosis of AIP when pancreatobiliary cancer workup shows negative results. However, clinical practice in diagnosing AIP varies depending on the local expertise, facilities, cost, prevalence of AIP and its subtypes.

The diagnosis of autoimmune pancreatitis (AIP) is clinically challenging because it is a rare disease, which closely mimics more common pancreaticobiliary malignancies in its presentation such as obstructive jaundice and pancreatic mass. The price of misdiagnosis is high because AIP diagnosed as pancreatic cancer can lead to unnecessary surgery for the benign disease, and cancer diagnosed as AIP can delay potentially curative surgery. There is no single ideal diagnostic test for AIP; hence one has to use a set of diagnostic criteria to distinguish it from other diseases. International consensus diagnostic criteria (ICDC) and algorithm for AIP have been proposed by a consensus of expert opinion in 2011. The concept of the Japan pancreas society (JPS) 2011 criteria took basic concepts of both the Japanese previous criteria and type 1 in the ICDC as much as possible. However, the ICDC are very complex to remember and definition of level 1 and 2 are not evidence based in some criteria. The revised JPS criteria are simpler than ICDC but further evaluation is necessary in other than Japan. So, further research is required to establish easy, ideal and practical diagnostic criteria.

감염성 췌장괴사의 고전적인 치료는 개복 수술이었다. 하지만 개복 수술 후 합병증, 사망률의 유의한 증가가 보고되면서 항생제와 보존적 치료가 일차적 치료로서 우선적으로 선택되고 있다. 보존 치료에 반응이 없는 경우에는 다양한 경로를 통한 배액법 및 괴사제거술 등의 최소 침습시술이 대두되고 있으며, 이러한 최소 침습 시술의 선택은 환자의 임상 양상, 보존적 치료에 대한 치료 반응, 괴사 조직과 위장관의 해부학적 위치 관계에 대한 정확한 평가 및 그에 따른 시술 방법의 선택이 이루어져야 한다. 저자들은 급성 감염성 췌장 괴사에서 항생제 등의 보존적 치료와 경피적 배액술을 시행하였으나 치료반응이 없는 환자에서 경피적 내시경적 괴사 제거술을 통한 성공적인 괴사 치료1예를 경험하였기에 보고하는 바이다.

Genetic factors are increasingly found as potential causes of children with acute recurrent pancreatitis (ARP) or chronic pancreatitis (CP). Representative genes include cationic trypsinogen, serine protease 1 (PRSS1), serine protease inhibitor Kazal type 1 (SPINK1), cystic fibrosis transmembrane conductance regulator (CFTR), chymotrypsin C (CTRC) and calcium sensing receptor (CASR) genes, etc. In Korean children, PRSS1 and SPINK1 genes have been most commonly studied, while CFTR mutations were reported in one patient to date. We report a case of a 13-year-old male adolescent with CP with CFTR mutations. Since he was first diagnosed with idiopathic acute pancreatitis (IAP) based on laboratory and computed tomographic findings, he was admitted with ARP and CP over four times in a year at the secondary and tertiary hospital. No etiology was detected by several examinations including magnetic resonance cholangiopancreatography (MRCP), endosco-pic retrograde cholangiopancreatography (ERCP), endoscopic ultrasonography (EUS) with fine needle aspiration (FNA) biopsy and genetic test including PRSS1 and SPINK1. Although he had no typical symptoms associated with cystic fibrosis (CF), CFTR mutations were detected with additional gene examination. Testing for CFTR mutations should be concerned in pediatric patients with APR and CP without other identified causes.