A narrative review of acute pancreatitis and its diagnosis, pathogenetic mechanism, and management

Abstract

Acute pancreatitis (AP) is an inflammatory disease that can progress to severe acute pancreatitis (SAP), which increases the risk of death. AP is characterized by inappropriate activation of trypsinogen, infiltration of inflammatory cells, and destruction of secretory cells. Other contributing factors may include calcium (Ca 2+ ) overload, mitochondrial dysfunction, impaired autophagy, and endoplasmic reticulum (ER) stress. In addition, exosomes are also associated with pathophysiological processes of many human diseases and may play a biological role in AP. However, the pathogenic mechanism has not been fully elucidated and needs to be further explored to inform treatment. Recently, the treatment guidelines have changed; minimally invasive therapy is advocated more as the core multidisciplinary participation and "step-up" approach. The surgical procedures have gradually changed from open surgery to minimally invasive surgery that primarily includes percutaneous catheter drainage (PCD), endoscopy, small incision surgery, and video-assisted surgery. The current guidelines for the management of AP have been updated and revised in many aspects. The type of fluid to be used, the timing, volume, and speed of administration for fluid resuscitation has been controversial. In addition, the timing and role of nutritional support and prophylactic antibiotic therapy, as well as the timing of the surgical or endoscopic intervention, and the management of complications still have many uncertainties that could negatively impact the prognosis and patients' quality of life. Consequently, to inform clinicians about optimal treatment, we aimed to review recent advances in the understanding of the pathogenesis of AP and its diagnosis and management.

Familial chylomicronemia syndrome due to a heterozygous deletion of the chromosome 8 treated with the apoCIII inhibitor volanesorsen

“…In the past, treatment of FCS patients was limited to very strict dietary fat restriction and avoidance of alcohol and certain medications. [ 3 , 11 ] Plasmapheresis has been tried in some FCS cases. [ 12 ] In the presence of diabetes, intravenous administration of insulin is required.…”

Factors Affecting the Imaging Preference of Acute Pancreatitis Patients in the Emergency Department: A Retrospective Study on 63 Cases

“…The increase in the accessibility and usability of CT creates a trend for physicians to refer to this examination more frequently for research purposes. An advanced CT scan is the most effective method for diagnosing acute pancreatitis and pancreatic necrosis, with typical features on cross-sectional imaging such as pancreatic enlargement, pancreatic edema, uneven density, peripancreatic fat shift, and fluid collection 11 .…”

“…Moreover, some studies have reported that although abdominal CT can identify pancreatitis in the early phase of the disease course, it will not contribute to the diagnostic sensitivity and may be negative if performed too early [13][14][15] . However, it is accepted that CT imaging can be used if the possibility of necrotizing pancreatitis is suspected in severe cases 8,11,16,17 . As a result of all these, the use of CT remains limited unless there are other conditions that should be evaluated in the differential diagnosis of acute pancreatitis cases in emergency services 8 In the study conducted by Yardan et al 9 , 52 (85.2%) of the patients with acute pancreatitis in the emergency department underwent abdominal CT, and 32 (61.5%) of the patients who were performed abdominal CT had mild clinical manifestations, 20 (38.5%) had severe.…”

A narrative review of a type of pancreatitis worthy of attention: acute pancreatitis associated with pancreatic tumors—current problems and future thinking

“…The cellular events important to the pathogenesis of AP include pathological calcium signaling (10)(11)(12), premature trypsinogen activation within macrophages and acinar cells (13)(14)(15), mitochondrial dysfunction (16,17), endoplasmic reticulum (ER) stress (18,19), impaired autophagy, and impaired unfolded protein response (UPR) (17). These events are caused by usual acinar cell toxins, such as nicotine, alcohol, and bile acids.…”