Clinical Chronic Pancreatitis

Walter G. Park

Disclosures

Curr Opin Gastroenterol. 2016;32(5):415-421. 

In This Article

Abstract and Introduction

Abstract

Purpose of review To summarize observations in clinical chronic pancreatitis in the past year.

Recent findings A predisposing genetic mutation was identified in 67% of cases of pediatric chronic pancreatitis. A novel susceptibility gene involving a hybrid allele is associated with idiopathic chronic pancreatitis. ABO blood type B and FUT2 nonsecretor status is associated with asymptomatic hyperlipasemia and chronic pancreatitis. Alcohol consumption impairs cystic fibrosis transmembrane conductance regulator (CFTR) activity leading to decreased bicarbonate secretion and patients with susceptible CFTR mutations can develop clinical pancreatitis. Computed tomography imaging findings in chronic pancreatitis correlate poorly with pain patterns. Endoscopic ultrasound features correlate poorly with fibrosis. Circulating epithelial cells are present in chronic pancreatitis patients but not healthy volunteers. Surgery is superior to endoscopic treatment in providing durable pain relief (>5 years). Repetitive pancreatic duct stent placements and chronic narcotic use are preoperative predictors of poor outcome after total pancreatectomy with islet cell auto transplantation.

Summary Novel genetic mutations for idiopathic chronic pancreatitis are being identified. Alcohol impairs CFTR activity and may explain a mechanism for pancreatitis. Current imaging modalities correlate poorly with clinical pain presentation and fibrosis in chronic pancreatitis. Novel imaging modalities are needed. As total pancreatectomy with islet cell auto transplantation grows, rigorous outcomes analysis is needed to drive patient selection.

Introduction

Chronic pancreatitis is characterized by progressive inflammation and fibrosis of the pancreas. Clinically, it is challenging to encounter due to the various causes, the variable clinical presentations, the suboptimal correlation between available diagnostic imaging and functional testing and clinical symptoms, and the challenge in getting reliable and well tolerated histological tissue. These factors, including the overall low prevalence of the disease, create formidable barriers for advancing clinical care and research. Despite this, novel observations have been made in the past year to provide hope for better diagnostics and treatments.

Comments

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