Chronic Pancreatitis Medication
- Author: Jason L Huffman, MD; Chief Editor: BS Anand, MD more...
No curative treatment for chronic pancreatitis exists. Medical therapy is determined primarily by symptoms. If no anatomic explanation for abdominal pain can be found, medical therapy can be attempted. This therapy includes pain control with analgesic agents and a trial of noncoated pancreatic enzymes.
The use of exogenous pancreatic enzymes to reduce pain is linked to the hypothesis that pancreatic stimulation by food causes pain. Cholecystokinin (CCK) is one of the possible mediators of this response.
Initial therapy consists of acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs). For severe, refractory pain, narcotic analgesics often are required, starting with the least potent agents and progressing to more potent formulations as necessary.
Acetaminophen is the drug of choice for pain in patients with documented hypersensitivity to aspirin or NSAIDs, those with upper GI disease, and those who are taking oral anticoagulants.
These medications provide control of moderate to severe pain.
This drug combination is indicated for moderate to severe pain.
Acetaminophen with codeine (Tylenol-3)
This drug combination is indicated for treatment of mild to moderate pain.
Tramadol inhibits ascending pain pathways, altering the perception of and response to pain. It also inhibits the reuptake of norepinephrine and serotonin.
Nonsteroidal Anti-Inflammatory Drugs
NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.
Naproxen is indicated for relief of mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.
These NSAIDs inhibit prostaglandin synthesis by decreasing cyclooxygenase activity, decreasing formation of prostaglandin precursors.
Ketorolac is an intravenously administered NSAID and a very powerful analgesic. It inhibits prostaglandin synthesis by decreasing activity of the enzyme cyclooxygenase, which results in decreased formation of prostaglandin precursors. In turn, this results in reduced inflammation.
Ibuprofen is usually the drug of choice for treatment of mild to moderate pain, if no contraindications exist. It inhibits inflammatory reactions and pain by decreasing the activity of the enzyme cyclo-oxygenase, resulting in inhibition of prostaglandin synthesis.
Celecoxib inhibits primarily cyclooxygenase-2 (COX-2). COX-2 is considered an inducible isoenzyme; it is induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, celecoxib does not inhibit the COX-1 isoenzyme; thus, GI toxicity may be decreased. The increased cost of celecoxib must be weighed against the benefit of avoidance of GI bleeds. Seek the lowest dose of celecoxib for each patient.
Hormones can be used for the reduction of pancreatic exocrine secretion.
Octreotide has an 8 ̶ amino acid sequence containing the active portion of somatostatin. In a study, subcutaneous injection of octreotide 3 times daily at 200mcg provided pain relief in 66% of patients. Note that 35% of the control group also experienced pain relief.
In addition to alleviating coexistent depression, tricyclic antidepressants may ameliorate pain and potentiate the effects of opiates.
This agent is an analgesic for certain chronic and neuropathic pain.
Clomipramine is a dibenzazepine compound belonging to the family of TCAs. The drug inhibits the membrane pump mechanism responsible for the uptake of norepinephrine and serotonin in adrenergic and serotonergic neurons.
Clomipramine affects serotonin uptake while it affects norepinephrine uptake when converted into its metabolite desmethylclomipramine. It is believed that these actions are responsible for its antidepressant activity.
Doxepin increases the concentration of serotonin and norepinephrine in the CNS by inhibiting their reuptake by presynaptic neuronal membrane. It inhibits histamine and acetylcholine activity and has proven useful in the treatment of various forms of depression associated with chronic pain.
Nortriptyline has demonstrated effectiveness in the treatment of chronic pain.
This is the original TCA used for depression. These agents have been suggested to act by inhibiting reuptake of noradrenaline at synapses in central descending pain-modulating pathways located in the brainstem and spinal cord.
Pancreatic Enzyme Supplements
These are used as dietary supplementation to aid digestion in patients with pancreatic enzyme deficiency. Several preparations are available. The aim is to provide at least 30,000 units of lipase. Because the cost of different preparations is variable, consider the unit price of the enzyme supplement based on the lipase content.
Uncoated pancrelipase is used to treat painful chronic pancreatitis based on the following rationale. Serum CCK levels are higher in patients with severe chronic pancreatitis, ductal or parenchymal hypertension is believed to cause pain, increased CCK levels stimulate pancreatic secretion (which increases ductal hypertension and exacerbates pain), and exogenous pancreatic enzyme supplements trigger a negative feedback inhibition.
Pancrelipase assists in the digestion of protein, starch, and fat. Nonenteric-coated products are used for pain caused by pancreatitis (ie, Viokace) in combination with a proton pump inhibitor. The enteric-coated products may be used for restoration of digestion and absorption.
Vege SS, Ziring B, Jain R, Moayyedi P, for the Clinical Guidelines Committee. American Gastroenterological Association Institute guideline on the diagnosis and management of asymptomatic neoplastic pancreatic cysts. Gastroenterology. 2015 Apr. 148(4):819-22. [Medline].
Kaufman M, Singh G, Das S, Concha-Parra R, Erber J, Micames C, et al. Efficacy of endoscopic ultrasound-guided celiac plexus block and celiac plexus neurolysis for managing abdominal pain associated with chronic pancreatitis and pancreatic cancer. J Clin Gastroenterol. 2010 Feb. 44(2):127-34. [Medline].
Gadroy FX, Ponchon T, Roda R, et al. Endoscopic treatment of chronic pancreatitis: long-term results. Gastrointest Endosc. Apr 2006. 63(5):AB312.
Cahen DL, Gouma DJ, Nio Y, et al. Endoscopic versus surgical drainage of the pancreatic duct in chronic pancreatitis. N Engl J Med. 2007 Feb 15. 356(7):676-84. [Medline].
Büchler MW, Martignoni ME, Friess H, Malfertheiner P. A proposal for a new clinical classification of chronic pancreatitis. BMC Gastroenterol. 2009 Dec 14. 9:93. [Medline]. [Full Text].
Pezzilli R. Etiology of chronic pancreatitis: has it changed in the last decade?. World J Gastroenterol. 2009 Oct 14. 15(38):4737-40. [Medline]. [Full Text].
Kawa S, Hamano H, Ozaki Y, et al. Long-term follow-up of autoimmune pancreatitis: characteristics of chronic disease and recurrence. Clin Gastroenterol Hepatol. 2009 Nov. 7(11 Suppl):S18-22. [Medline].
Schmitt F, Le Henaff G, Piloquet H, et al. Hereditary pancreatitis in children: surgical implications with special regard to genetic background. J Pediatr Surg. 2009 Nov. 44(11):2078-82. [Medline].
Ooi CY, Dorfman R, Cipolli M, et al. Type of CFTR mutation determines risk of pancreatitis in patients with cystic fibrosis. Gastroenterology. 2011 Jan. 140(1):153-61. [Medline].
Tezuka K, Makino T, Hirai I, Kimura W. Groove pancreatitis. Dig Surg. 2010. 27(2):149-52. [Medline].
Saftoiu A, Popescu C, Cazacu S, et al. Power Doppler endoscopic ultrasonography for the differential diagnosis between pancreatic cancer and pseudotumoral chronic pancreatitis. J Ultrasound Med. 2006 Mar. 25(3):363-72. [Medline]. [Full Text].
Kalb B, Martin DR, Sarmiento JM, Erickson SH, Gober D, Tapper EB, et al. Paraduodenal Pancreatitis: Clinical Performance of MR Imaging in Distinguishing from Carcinoma. Radiology. 2013 Nov. 269(2):475-81. [Medline].