Energetic etiologies of acute pancreatitis: A report of five cases

Table 1 Patient characteristics

Pt	Age	Gender	Type of exposure	Time gap between exposure and pancreatitis	Duration of exposure	Severity of pancreatits	TG	IgG4	Confounding factors
1	40s	F	TENS	Narrow	Short	Mild	Nl	Nl3	CCB and PPI
2	30s	F	IENS	Narrow	Unk	Mild	Unk	Unk	Unk2
3	50s	F	TENS	Narrow	Long	Severe	Nl	Nl3	None1
4	40s	M	Energy drink	Narrow	Consumed Rockstar™ prior to 2 unexplained episodes	Both mild	Nl	Nl	Initial episode due to alcohol, but abstinent for 1 yr prior to these 2 episodes

¹No medications, no alcohol, no gallstones (by transabdominal and intraoperative, but not endoscopic, ultrasound), there was no evidence for or against genetic causes and pancreas divisum;

²No alcohol, and no gallstones (by transabdominal but not endoscopic ultrasound), but the patient could not recall her medication history;

³Total IgG, not IgG4, was sent. Pt: Patient; Nl: Normal; Unk: Unknown; TG: Triglyceride level; TENS: Transcutaneous electrical nerve stimulation; F: Female; M: Male; CCB: Calcium-channel blocker; PPI: Proton-pump inhibitor; IENS: Implanted electrical nerve stimulator.

Table 2 List of observations associating electrical nerve stimulations and the development of acute pancreatitis

	Ref.
Observation
All cases reported here were considered idiopathic	N/A
There was a strong temporal association of exposure and AP	N/A
There was a directly proportional relationship between duration of exposure and severity of subsequent AP	N/A
Neurogenic inflammation is increasingly recognized to play a role in development of AP, with sensory nerves in particular being considered a final common pathway in AP	[24,30,39,40]
TRPV1 and TRPA1 expression and function in pancreatic afferent neurons increases and blocking this pathway attenuates pancreatitis in a mouse model of AP	[25,26]
Over-stimulation of nerves associated with pancreatic disease (decrease in pancreatic blood flow and DNA synthesis) in rats	[34]
Neural cross talk between the duodenum and pancreas (duodeno-pancreatic reflex at T6-T13) can promote AP in a rat model	[41]
Possibly contradictory observations
Stimulation by electroacupuncture of dorsal segmental points corresponding to levels that innervate pancreas (by splanchnic nerves; T9-T11) causes decrease in fasting blood glucose	[33]
Electroacupuncture protects against CCK-induced AP in rats	[31]
Electroacupuncture to paraumbilical point ST25 (dermatome T10) down-regulates pro-inflammatory cytokines (TNFα, IL-6) and attenuates the morphological damage to pancreas in a rat model of AP	[32]

AP: Acute pancreatitis; N/A: Not available; TNF: Tumor necrosis factor; IL- 6: Interleukin- 6; TRPV1: Transient receptor potential vanilloid 1; TRPA1: Transient receptor potential cation channel, subfamily A, member 1; CCK: Cholecystokinin.