Pain in chronic pancreatitis: managing beyond the pancreatic duct

Abstract

Chronic pancreatitis (CP) continues to be a clinical challenge. Persistent or recurrent abdominal pain is the most compelling symptom that drives patients to seek medical care. Unfortunately, in spite of using several treatment approaches in the clinical setting, there is no single specific treatment modality that can be earmarked as a cure for this disease. Traditionally, ductal hypertension has been associated with causation of pain in CP; and patients are often subjected to endotherapy and surgery with a goal to decompress the pancreatic duct. Recent studies on humans (clinical and laboratory based) and experimental models have put forward several mechanisms, including neuroimmune alterations, which could be responsible for pain. This might explain the partial or no response to single modality treatment in a significant proportion of patients. The current review discusses the recent concepts of pain generation in CP and evidence based therapeutic approaches (other than ductal decompression) to handle persistent or recurrent pain. We focus primarily on parenchymal and neural components; and discuss the role of antioxidants and the existing controversies, drugs that interfere with neural transmission, pancreatic enzyme supplementation, celiac neurolysis, and pancreatic resection procedures. The review concludes with the treatment approach that we follow at our institute.

Keywords: Antioxidant micronutrients; Chronic pancreatitis; Neuroplasticity; Nociception; Pain; Pancreatic enzymes; Pregabalin.

Figures

Figure 1

Schematic diagram representing neuroimmune mechanisms of pain in patients with chronic pancreatitis. The TrkA receptors (for nerve growth factor, NGF) are expressed on the sensory and sympathetic nerve fibres, p75 (for brain derived neurotropic factor, BDNF) on the perineurium and glial cell line-derived neurotrophic factor receptor α3 (GFRα3) (for Artemin) on the Schwann cell nuclei and intrapancreatic ganglia. The receptor expression is mediated by inflammation involving inflammatory cells and neural elements.

Figure 2

Schematic representation of the conceptual framework of pain mechanisms in chronic pancreatitis.

Figure 3

Management approach for recurrent and/or persistent pain in patients with chronic pancreatitis at the Asian Institute of Gastroenterology. SSRIs: Selective serotonin reuptake inhibitors; NERI: Norepinephrine reuptake inhibitor; NSAIDs: Nonsteroidal anti-inflammatory drugs.