Hereditary pancreatitis medical therapy: Difference between revisions

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==Overview==
==Overview==
There is no treatment for [disease name]; the mainstay of therapy is supportive care.
The goals of management for hereditary pancreatitis include [[pain]] control, management of [[pancreatic insufficiency]] by pancreatic [[Enzyme replacement therapy|enzyme replacement]] and management of [[complications]]. Pain is managed in a stepwise approach of general recommendations, pancreatic [[Enzyme replacement therapy|enzyme replacement]], [[analgesics]] and invasive procedures. General recommendations usually include [[smoking cessation]], cessation of alcohol intake, small meals and [[hydration]]. Medical therapy includes pancreatic enzyme supplementation, [[analgesics]] and [[antioxidants]]. Specialized approaches include celiac nerve block, [[endoscopic]] therapy, [[Lithotripsy|extracorporeal shock wave lithotripsy]] (ESWL), and [[Radiation therapy|radiation]]. [[Steatorrhea]] can be managed by dietary modification, [[lipase]] supplementation, [[vitamin]] supplementation, and [[medium chain triglycerides]] (MCTs). [[Diabetes]] is usually managed with a trial of oral [[Hypoglycemic agent|hypoglycemic agents]] followed by [[Insulin|insulin therapy]].


OR
==Chronic pancreatitis management:==
The goals of management are:
* Pain control
* Management of [[pancreatic insufficiency]] by pancreatic enzyme replacement
* Management of complications<ref name="pmid18319401">{{cite journal |vauthors=Callery MP, Freedman SD |title=A 21-year-old man with chronic pancreatitis |journal=JAMA |volume=299 |issue=13 |pages=1588–94 |year=2008 |pmid=18319401 |doi=10.1001/jama.299.9.jrr80001 |url=}}</ref>


Supportive therapy for [disease name] includes [therapy 1], [therapy 2], and [therapy 3].
== Pain management: ==
Pain is managed in a step-wise approach of:
* General recommendations
* Pancreatic enzyme replacement
* [[Analgesics]]
* Other invasive procedures


OR
=== General recommendations: ===
Most of the patients usually improve following the general recommendations with only a few requiring [[analgesics]].


The majority of cases of [disease name] are self-limited and require only supportive care.
====== (a) Smoking cessation: ======
*[[Smoking cessation]] may:
**Delay the progression of chronic pancreatitis
**Decrease the risk of [[pancreatic cancer]]<ref name="pmid15753536">{{cite journal |vauthors=Maisonneuve P, Lowenfels AB, Müllhaupt B, Cavallini G, Lankisch PG, Andersen JR, Dimagno EP, Andrén-Sandberg A, Domellöf L, Frulloni L, Ammann RW |title=Cigarette smoking accelerates progression of alcoholic chronic pancreatitis |journal=Gut |volume=54 |issue=4 |pages=510–4 |year=2005 |pmid=15753536 |pmc=1774435 |doi=10.1136/gut.2004.039263 |url=}}</ref>


OR
===== (b) Cessation of alcohol intake: =====
*Alcohol cessation may help in symptomatic improvement particularly in alcohol induced chronic pancreatitis.
*Alcohol intake is associated with increased mortality in pateints with alcohol induced chronic pancreatitis.<ref name="pmid7739686">{{cite journal |vauthors=Steer ML, Waxman I, Freedman S |title=Chronic pancreatitis |journal=N. Engl. J. Med. |volume=332 |issue=22 |pages=1482–90 |year=1995 |pmid=7739686 |doi=10.1056/NEJM199506013322206 |url=}}</ref>
====== (c) Small meals: ======
* Dietary preference in chronic pancreatitis should be small meals with low fat content
* [[Medium chain triglycerides|Medium chain triglyceride]] (MCTs) supplementation is particularly helpful because of:
** Its [[antioxidant]] effects
** Minimal increase in plasma [[CCK receptor|CCK]] levels
** It may prevent weight loss in patients


[Disease name] is a medical emergency and requires prompt treatment.
====== (d) Hydration: ======
* Keeping the patients well hydrated may help in preventing the development of acute flares of pancreatitis.


OR
== Medical Therapy: ==


The mainstay of treatment for [disease name] is [therapy].
===1.Pancreatic Enzyme Supplementation:===
* Pancreatic enzyme supplementation is associated with pain alleviation and may be used when the general recommendations fail.
* It decreases the release of [[CCK receptor|CCK]] and thus reduces the stimulation-induced pancreatic pain but mixed results have been observed from various clinical trials.<ref name="pmid7914921">{{cite journal |vauthors=Owyang C |title=Negative feedback control of exocrine pancreatic secretion: role of cholecystokinin and cholinergic pathway |journal=J. Nutr. |volume=124 |issue=8 Suppl |pages=1321S–1326S |year=1994 |pmid=7914921 |doi= |url=}}</ref><ref name="pmid12631450">{{cite journal |vauthors=Singh VV, Toskes PP |title=Medical therapy for chronic pancreatitis pain |journal=Curr Gastroenterol Rep |volume=5 |issue=2 |pages=110–6 |year=2003 |pmid=12631450 |doi= |url=}}</ref><ref name="pmid6825540">{{cite journal |vauthors=Isaksson G, Ihse I |title=Pain reduction by an oral pancreatic enzyme preparation in chronic pancreatitis |journal=Dig. Dis. Sci. |volume=28 |issue=2 |pages=97–102 |year=1983 |pmid=6825540 |doi= |url=}}</ref><ref name="pmid3633631">{{cite journal |vauthors=Halgreen H, Pedersen NT, Worning H |title=Symptomatic effect of pancreatic enzyme therapy in patients with chronic pancreatitis |journal=Scand. J. Gastroenterol. |volume=21 |issue=1 |pages=104–8 |year=1986 |pmid=3633631 |doi= |url=}}</ref><ref name="pmid1289173">{{cite journal |vauthors=Mössner J, Secknus R, Meyer J, Niederau C, Adler G |title=Treatment of pain with pancreatic extracts in chronic pancreatitis: results of a prospective placebo-controlled multicenter trial |journal=Digestion |volume=53 |issue=1-2 |pages=54–66 |year=1992 |pmid=1289173 |doi= |url=}}</ref><ref name="pmid9362186">{{cite journal |vauthors=Brown A, Hughes M, Tenner S, Banks PA |title=Does pancreatic enzyme supplementation reduce pain in patients with chronic pancreatitis: a meta-analysis |journal=Am. J. Gastroenterol. |volume=92 |issue=11 |pages=2032–5 |year=1997 |pmid=9362186 |doi= |url=}}</ref><ref name="pmid6640255">{{cite journal |vauthors=Leung JW, Bowen-Wright M, Aveling W, Shorvon PJ, Cotton PB |title=Coeliac plexus block for pain in pancreatic cancer and chronic pancreatitis |journal=Br J Surg |volume=70 |issue=12 |pages=730–2 |year=1983 |pmid=6640255 |doi= |url=}}</ref><ref name="pmid9721175">{{cite journal |vauthors=Warshaw AL, Banks PA, Fernández-Del Castillo C |title=AGA technical review: treatment of pain in chronic pancreatitis |journal=Gastroenterology |volume=115 |issue=3 |pages=765–76 |year=1998 |pmid=9721175 |doi= |url=}}</ref>
*It is particularly beneficial in the management of patients with idiopathic chronic pancreatitis.<ref name="pmid6202586">{{cite journal |vauthors=Slaff J, Jacobson D, Tillman CR, Curington C, Toskes P |title=Protease-specific suppression of pancreatic exocrine secretion |journal=Gastroenterology |volume=87 |issue=1 |pages=44–52 |year=1984 |pmid=6202586 |doi= |url=}}</ref><ref name="pmid6640255">{{cite journal |vauthors=Leung JW, Bowen-Wright M, Aveling W, Shorvon PJ, Cotton PB |title=Coeliac plexus block for pain in pancreatic cancer and chronic pancreatitis |journal=Br J Surg |volume=70 |issue=12 |pages=730–2 |year=1983 |pmid=6640255 |doi= |url=}}</ref>


OR
=== 2.Analgesics: ===
 
* [[Analgesics]] are usually required when pancreatic enzyme replacement therapy fails to manage pain in chronic pancreatitis.
The optimal therapy for [malignancy name] depends on the stage at diagnosis.
* Pain cycle may be disrupted by:
** [[Opiates]] coupled with [[amitriptyline]] and an [[NSAIDs|NSAID]].<ref name="pmid19796802">{{cite journal |vauthors=Gilron I, Bailey JM, Tu D, Holden RR, Jackson AC, Houlden RL |title=Nortriptyline and gabapentin, alone and in combination for neuropathic pain: a double-blind, randomised controlled crossover trial |journal=Lancet |volume=374 |issue=9697 |pages=1252–61 |year=2009 |pmid=19796802 |doi=10.1016/S0140-6736(09)61081-3 |url=}}</ref><ref name="pmid12077076">{{cite journal |vauthors=Fioramonti J, Bueno L |title=Centrally acting agents and visceral sensitivity |journal=Gut |volume=51 Suppl 1 |issue= |pages=i91–5 |year=2002 |pmid=12077076 |pmc=1867729 |doi= |url=}}</ref>
** [[NPO]] and short-term hospitalization of the patient.


OR
* Long-acting agents, such as continuous [[morphine sulphate]] or [[Fentanyl (transdermal)|fentanyl patch]] are usually recommended for chronic pain management.
* [[Adjuvant therapy]] with [[pregabalin]] is also found to be effective in some clinical trials.<ref name="pmid21683078">{{cite journal |vauthors=Olesen SS, Bouwense SA, Wilder-Smith OH, van Goor H, Drewes AM |title=Pregabalin reduces pain in patients with chronic pancreatitis in a randomized, controlled trial |journal=Gastroenterology |volume=141 |issue=2 |pages=536–43 |year=2011 |pmid=21683078 |doi=10.1053/j.gastro.2011.04.003 |url=}}</ref><ref name="pmid21950372">{{cite journal |vauthors=Graversen C, Olesen SS, Olesen AE, Steimle K, Farina D, Wilder-Smith OH, Bouwense SA, van Goor H, Drewes AM |title=The analgesic effect of pregabalin in patients with chronic pain is reflected by changes in pharmaco-EEG spectral indices |journal=Br J Clin Pharmacol |volume=73 |issue=3 |pages=363–72 |year=2012 |pmid=21950372 |pmc=3370341 |doi=10.1111/j.1365-2125.2011.04104.x |url=}}</ref>


[Therapy] is recommended among all patients who develop [disease name].
=== 3.Antioxidants: ===
*[[Antioxidant|Antioxidant therapy]] has no established effective role in the management of chronic pancreatitis as various studies have shown conflicting results.<ref name="pmid2103755">{{cite journal |vauthors=Uden S, Bilton D, Nathan L, Hunt LP, Main C, Braganza JM |title=Antioxidant therapy for recurrent pancreatitis: placebo-controlled trial |journal=Aliment. Pharmacol. Ther. |volume=4 |issue=4 |pages=357–71 |year=1990 |pmid=2103755 |doi= |url=}}</ref><ref name="pmid9444547">{{cite journal |vauthors=Banks PA, Hughes M, Ferrante M, Noordhoek EC, Ramagopal V, Slivka A |title=Does allopurinol reduce pain of chronic pancreatitis? |journal=Int. J. Pancreatol. |volume=22 |issue=3 |pages=171–6 |year=1997 |pmid=9444547 |doi=10.1007/BF02788381 |url=}}</ref><ref name="pmid18952082">{{cite journal |vauthors=Bhardwaj P, Garg PK, Maulik SK, Saraya A, Tandon RK, Acharya SK |title=A randomized controlled trial of antioxidant supplementation for pain relief in patients with chronic pancreatitis |journal=Gastroenterology |volume=136 |issue=1 |pages=149–159.e2 |year=2009 |pmid=18952082 |doi=10.1053/j.gastro.2008.09.028 |url=}}</ref><ref name="pmid21083584">{{cite journal |vauthors=Burton F, Alkaade S, Collins D, Muddana V, Slivka A, Brand RE, Gelrud A, Banks PA, Sherman S, Anderson MA, Romagnuolo J, Lawrence C, Baillie J, Gardner TB, Lewis MD, Amann ST, Lieb JG, O'Connell M, Kennard ED, Yadav D, Whitcomb DC, Forsmark CE |title=Use and perceived effectiveness of non-analgesic medical therapies for chronic pancreatitis in the United States |journal=Aliment. Pharmacol. Ther. |volume=33 |issue=1 |pages=149–59 |year=2011 |pmid=21083584 |pmc=3142582 |doi=10.1111/j.1365-2036.2010.04491.x |url=}}</ref><ref name="pmid22683257">{{cite journal |vauthors=Siriwardena AK, Mason JM, Sheen AJ, Makin AJ, Shah NS |title=Antioxidant therapy does not reduce pain in patients with chronic pancreatitis: the ANTICIPATE study |journal=Gastroenterology |volume=143 |issue=3 |pages=655–663.e1 |year=2012 |pmid=22683257 |doi=10.1053/j.gastro.2012.05.046 |url=}}</ref>


OR
=== 4.Specialized approaches: ===


Pharmacologic medical therapy is recommended among patients with [disease subclass 1], [disease subclass 2], and [disease subclass 3].
====== 4.1 Celiac nerve block ======
*Celiac nerve block is not a proven therapy as: <ref name="pmid6640255">{{cite journal |vauthors=Leung JW, Bowen-Wright M, Aveling W, Shorvon PJ, Cotton PB |title=Coeliac plexus block for pain in pancreatic cancer and chronic pancreatitis |journal=Br J Surg |volume=70 |issue=12 |pages=730–2 |year=1983 |pmid=6640255 |doi= |url=}}</ref><ref name="pmid2624751">{{cite journal |vauthors=Busch EH, Atchison SR |title=Steroid celiac plexus block for chronic pancreatitis: results in 16 cases |journal=J Clin Anesth |volume=1 |issue=6 |pages=431–3 |year=1989 |pmid=2624751 |doi= |url=}}</ref><ref name="pmid10201454">{{cite journal |vauthors=Gress F, Schmitt C, Sherman S, Ikenberry S, Lehman G |title=A prospective randomized comparison of endoscopic ultrasound- and computed tomography-guided celiac plexus block for managing chronic pancreatitis pain |journal=Am. J. Gastroenterol. |volume=94 |issue=4 |pages=900–5 |year=1999 |pmid=10201454 |doi=10.1111/j.1572-0241.1999.01042.x |url=}}</ref><ref name="pmid11232683">{{cite journal |vauthors=Gress F, Schmitt C, Sherman S, Ciaccia D, Ikenberry S, Lehman G |title=Endoscopic ultrasound-guided celiac plexus block for managing abdominal pain associated with chronic pancreatitis: a prospective single center experience |journal=Am. J. Gastroenterol. |volume=96 |issue=2 |pages=409–16 |year=2001 |pmid=11232683 |doi=10.1111/j.1572-0241.2001.03551.x |url=}}</ref>
**It may cause serious complications
**Recurrence may occur
**It has limited success in chronic pancreatitis
*It can be achieved by using [[alcohol]] or [[steroid]] via
**[[Percutaneous|Percutaneous approach]] or
**[[Endoscopic]] approach


OR
====== 4.2 Endoscopic therapy ======
*Pain releif can also be acheived by decompression of an obstructed duct via [[endoscopic]] approach.<ref name="pmid10882956">{{cite journal |vauthors=Okolo PI, Pasricha PJ, Kalloo AN |title=What are the long-term results of endoscopic pancreatic sphincterotomy? |journal=Gastrointest. Endosc. |volume=52 |issue=1 |pages=15–9 |year=2000 |pmid=10882956 |doi=10.1067/mge.2000.106669 |url=}}</ref><ref name="pmid2070994">{{cite journal |vauthors=Geenen JE, Rolny P |title=Endoscopic therapy of acute and chronic pancreatitis |journal=Gastrointest. Endosc. |volume=37 |issue=3 |pages=377–82 |year=1991 |pmid=2070994 |doi= |url=}}</ref><ref name="pmid12085037">{{cite journal |vauthors=Choudari CP, Nickl NJ, Fogel E, Lehman GA, Sherman S |title=Hereditary pancreatitis: clinical presentation, ERCP findings, and outcome of endoscopic therapy |journal=Gastrointest. Endosc. |volume=56 |issue=1 |pages=66–71 |year=2002 |pmid=12085037 |doi= |url=}}</ref><ref name="pmid12244496">{{cite journal |vauthors=Rösch T, Daniel S, Scholz M, Huibregtse K, Smits M, Schneider T, Ell C, Haber G, Riemann JF, Jakobs R, Hintze R, Adler A, Neuhaus H, Zavoral M, Zavada F, Schusdziarra V, Soehendra N |title=Endoscopic treatment of chronic pancreatitis: a multicenter study of 1000 patients with long-term follow-up |journal=Endoscopy |volume=34 |issue=10 |pages=765–71 |year=2002 |pmid=12244496 |doi=10.1055/s-2002-34256 |url=}}</ref><ref name="pmid15812411">{{cite journal |vauthors=Gabbrielli A, Pandolfi M, Mutignani M, Spada C, Perri V, Petruzziello L, Costamagna G |title=Efficacy of main pancreatic-duct endoscopic drainage in patients with chronic pancreatitis, continuous pain, and dilated duct |journal=Gastrointest. Endosc. |volume=61 |issue=4 |pages=576–81 |year=2005 |pmid=15812411 |doi= |url=}}</ref><ref name="pmid16733106">{{cite journal |vauthors=Adler DG, Lichtenstein D, Baron TH, Davila R, Egan JV, Gan SL, Qureshi WA, Rajan E, Shen B, Zuckerman MJ, Lee KK, VanGuilder T, Fanelli RD |title=The role of endoscopy in patients with chronic pancreatitis |journal=Gastrointest. Endosc. |volume=63 |issue=7 |pages=933–7 |year=2006 |pmid=16733106 |doi=10.1016/j.gie.2006.02.003 |url=}}</ref>
*Surgery is more effective when compared to [[endoscopic]] therapy.<ref name="pmid17301298">{{cite journal |vauthors=Cahen DL, Gouma DJ, Nio Y, Rauws EA, Boermeester MA, Busch OR, Stoker J, Laméris JS, Dijkgraaf MG, Huibregtse K, Bruno MJ |title=Endoscopic versus surgical drainage of the pancreatic duct in chronic pancreatitis |journal=N. Engl. J. Med. |volume=356 |issue=7 |pages=676–84 |year=2007 |pmid=17301298 |doi=10.1056/NEJMoa060610 |url=}}</ref>


Pharmacologic medical therapies for [disease name] include (either) [therapy 1], [therapy 2], and/or [therapy 3].
====== 4.3 Extracorporeal shock wave lithotripsy (ESWL) ======
*Pain can also be relieved by using ESWL<ref name="pmid19820418">{{cite journal |vauthors=Parsi MA, Stevens T, Lopez R, Vargo JJ |title=Extracorporeal shock wave lithotripsy for prevention of recurrent pancreatitis caused by obstructive pancreatic stones |journal=Pancreas |volume=39 |issue=2 |pages=153–5 |year=2010 |pmid=19820418 |doi=10.1097/MPA.0b013e3181bb1733 |url=}}</ref>
*It causes millimetric fragmentation of pancreatic stones
*Its role in chronic pancreatitis management is still unclear due to the limited studies done in this area


OR
====== 4.4 Radiation ======
*Radiotherapy is also helpful in pain relief due to its anti-inflammatory properties<ref name="pmid19190609">{{cite journal |vauthors=Guarner L, Navalpotro B, Molero X, Giralt J, Malagelada JR |title=Management of painful chronic pancreatitis with single-dose radiotherapy |journal=Am. J. Gastroenterol. |volume=104 |issue=2 |pages=349–55 |year=2009 |pmid=19190609 |doi=10.1038/ajg.2008.128 |url=}}</ref>


Empiric therapy for [disease name] depends on [disease factor 1] and [disease factor 2].
== Management of Steatorrhea: ==
*In chronic pancreatitis, pancreatic enzyme replacement is usually dependent upon
**The size and nature of the meal 
**The residual function of the pancreas
**The goals of therapy (elimination of [[steatorrhea]], reduction in the abdominal symptoms of [[maldigestion]] or achievement of nutritional goals)
====== 1. Dietary modification ======
* The degree of fat intake restriction is usually dependent upon the  severity of [[malabsorption]].
* Medical therapy is considered if [[steatorrhea]] persists after dietary restriction.
* Fat intake of ≤ 20 grams per day is sufficient to prevent steatorrhea.  


OR
====== 2. Lipase supplementation ======
* The pancreas normally responds with between 700,000 and 1,000,000 [[lipase]] units (USP) per meal.<ref name="pmid15951527">{{cite journal |vauthors=Keller J, Layer P |title=Human pancreatic exocrine response to nutrients in health and disease |journal=Gut |volume=54 Suppl 6 |issue= |pages=vi1–28 |year=2005 |pmid=15951527 |pmc=1867805 |doi=10.1136/gut.2005.065946 |url=}}</ref>
*10% of normal pancreatic [[lipase]] replacement (70,000 to 100,000 USP) can manage the symptoms of [[steatorrhea]] even when all of the pancreatic function has been lost.
* Usually 30,000 international units (IU) or 90,000 United States Pharmacopeia units (USP) of lipase per meal (5-10%) are sufficient to correct the malabsorption in chronic pancreatitis.
* 90,000 USP of [[lipase]] per meal (5-10%) is sufficient to abolish steatorrhea in chronic pancreatitis.
* Dosing is usually dependent upon:
** The individual's weight
** The degree of pancreatic insufficiency
** The size and fat content of a meal


Patients with [disease subclass 1] are treated with [therapy 1], whereas patients with [disease subclass 2] are treated with [therapy 2].
* Creon-24,000 lipase, enteric coated formulations, one to two capsules with meals and one capsule with a snack
* Viokace Lipase 20,880, non-enteric coated formthree tablets with meals and one to two tablets with a snack


==Medical Therapy==
====== NOTE: ======
* Non-enteric supplements may require [[H2 antagonist]] or [[Proton pump inhibitor|proton pump inhibitor.]]
* Non-enteric supplements may be more useful in achlorhydric patients or those with dyssynchronous gastric emptying (eg, Billroth II anatomy).


==== 1. Avoidance of alcohol intake: ====
====== 3. Vitamin supplementation ======
* Patients with severe [[steatorrhea]] may require vitamin supplementation.
* [[Calcifediol]], a naturally occurring analogue of [[Vitamin D|vitamin D (25-hydroxylated form)]] is more polar and potent than vitamin D2 or D3.
* It is important to monitor [[Calcium|serum calcium]] levels for the first few week of therapy due to increased risk of developing [[hypercalcemia]].


==== 2. Smoking cessation ====
====== 4. Medium chain triglycerides (MCTs) ======
* [[Medium chain triglycerides]] are preferred over long chain triglycerides as
** MCTs do not need the presence of bile for their degradation
** MCTs may be degraded easily by [[Gastric acid|gastric]] and [[pancreatic lipase]]
** MCTs can be absorbed directly from the [[intestinal mucosa]]
** MCTs have a weak stimulatory affect on pancreatic secretions


==== 3. Antioxidants ====
== Management of glucose intolerance: ==
 
* [[Glucose intolerance]] usually develops in the early course of disease while overt [[diabetes]] may develop in the late course of disease.
==== 4. Analgesics ====
* Patients are usually managed with a trial of [[oral hypoglycemic agent]]<nowiki/>s followed by [[Insulin|insulin therapy]].


==References==
==References==
{{Reflist|2}}
{{Reflist|2}}


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[[Category:Gastroenterology]]
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Latest revision as of 14:55, 31 January 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Iqra Qamar M.D.[2]

Overview

The goals of management for hereditary pancreatitis include pain control, management of pancreatic insufficiency by pancreatic enzyme replacement and management of complications. Pain is managed in a stepwise approach of general recommendations, pancreatic enzyme replacement, analgesics and invasive procedures. General recommendations usually include smoking cessation, cessation of alcohol intake, small meals and hydration. Medical therapy includes pancreatic enzyme supplementation, analgesics and antioxidants. Specialized approaches include celiac nerve block, endoscopic therapy, extracorporeal shock wave lithotripsy (ESWL), and radiation. Steatorrhea can be managed by dietary modification, lipase supplementation, vitamin supplementation, and medium chain triglycerides (MCTs). Diabetes is usually managed with a trial of oral hypoglycemic agents followed by insulin therapy.

Chronic pancreatitis management:

The goals of management are:

Pain management:

Pain is managed in a step-wise approach of:

  • General recommendations
  • Pancreatic enzyme replacement
  • Analgesics
  • Other invasive procedures

General recommendations:

Most of the patients usually improve following the general recommendations with only a few requiring analgesics.

(a) Smoking cessation:
(b) Cessation of alcohol intake:
  • Alcohol cessation may help in symptomatic improvement particularly in alcohol induced chronic pancreatitis.
  • Alcohol intake is associated with increased mortality in pateints with alcohol induced chronic pancreatitis.[3]
(c) Small meals:
  • Dietary preference in chronic pancreatitis should be small meals with low fat content
  • Medium chain triglyceride (MCTs) supplementation is particularly helpful because of:
    • Its antioxidant effects
    • Minimal increase in plasma CCK levels
    • It may prevent weight loss in patients
(d) Hydration:
  • Keeping the patients well hydrated may help in preventing the development of acute flares of pancreatitis.

Medical Therapy:

1.Pancreatic Enzyme Supplementation:

  • Pancreatic enzyme supplementation is associated with pain alleviation and may be used when the general recommendations fail.
  • It decreases the release of CCK and thus reduces the stimulation-induced pancreatic pain but mixed results have been observed from various clinical trials.[4][5][6][7][8][9][10][11]
  • It is particularly beneficial in the management of patients with idiopathic chronic pancreatitis.[12][10]

2.Analgesics:

  • Analgesics are usually required when pancreatic enzyme replacement therapy fails to manage pain in chronic pancreatitis.
  • Pain cycle may be disrupted by:

3.Antioxidants:

4.Specialized approaches:

4.1 Celiac nerve block
4.2 Endoscopic therapy
4.3 Extracorporeal shock wave lithotripsy (ESWL) 
  • Pain can also be relieved by using ESWL[32]
  • It causes millimetric fragmentation of pancreatic stones
  • Its role in chronic pancreatitis management is still unclear due to the limited studies done in this area
4.4 Radiation
  • Radiotherapy is also helpful in pain relief due to its anti-inflammatory properties[33]

Management of Steatorrhea:

  • In chronic pancreatitis, pancreatic enzyme replacement is usually dependent upon
    • The size and nature of the meal 
    • The residual function of the pancreas
    • The goals of therapy (elimination of steatorrhea, reduction in the abdominal symptoms of maldigestion or achievement of nutritional goals)
1. Dietary modification
  • The degree of fat intake restriction is usually dependent upon the severity of malabsorption.
  • Medical therapy is considered if steatorrhea persists after dietary restriction.
  • Fat intake of ≤ 20 grams per day is sufficient to prevent steatorrhea.
2. Lipase supplementation
  • The pancreas normally responds with between 700,000 and 1,000,000 lipase units (USP) per meal.[34]
  • 10% of normal pancreatic lipase replacement (70,000 to 100,000 USP) can manage the symptoms of steatorrhea even when all of the pancreatic function has been lost.
  • Usually 30,000 international units (IU) or 90,000 United States Pharmacopeia units (USP) of lipase per meal (5-10%) are sufficient to correct the malabsorption in chronic pancreatitis.
  • 90,000 USP of lipase per meal (5-10%) is sufficient to abolish steatorrhea in chronic pancreatitis.
  • Dosing is usually dependent upon:
    • The individual's weight
    • The degree of pancreatic insufficiency
    • The size and fat content of a meal
  • Creon-24,000 lipase, enteric coated formulations, one to two capsules with meals and one capsule with a snack
  • Viokace Lipase 20,880, non-enteric coated formthree tablets with meals and one to two tablets with a snack
NOTE:
  • Non-enteric supplements may require H2 antagonist or proton pump inhibitor.
  • Non-enteric supplements may be more useful in achlorhydric patients or those with dyssynchronous gastric emptying (eg, Billroth II anatomy).
3. Vitamin supplementation 
4. Medium chain triglycerides (MCTs)

Management of glucose intolerance:

References

  1. ↑ Callery MP, Freedman SD (2008). "A 21-year-old man with chronic pancreatitis". JAMA. 299 (13): 1588–94. doi:10.1001/jama.299.9.jrr80001. PMID 18319401.
  2. ↑ Maisonneuve P, Lowenfels AB, Müllhaupt B, Cavallini G, Lankisch PG, Andersen JR, Dimagno EP, Andrén-Sandberg A, Domellöf L, Frulloni L, Ammann RW (2005). "Cigarette smoking accelerates progression of alcoholic chronic pancreatitis". Gut. 54 (4): 510–4. doi:10.1136/gut.2004.039263. PMC 1774435. PMID 15753536.
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  10. ↑ 10.0 10.1 10.2 Leung JW, Bowen-Wright M, Aveling W, Shorvon PJ, Cotton PB (1983). "Coeliac plexus block for pain in pancreatic cancer and chronic pancreatitis". Br J Surg. 70 (12): 730–2. PMID 6640255.
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  18. ↑ Banks PA, Hughes M, Ferrante M, Noordhoek EC, Ramagopal V, Slivka A (1997). "Does allopurinol reduce pain of chronic pancreatitis?". Int. J. Pancreatol. 22 (3): 171–6. doi:10.1007/BF02788381. PMID 9444547.
  19. ↑ Bhardwaj P, Garg PK, Maulik SK, Saraya A, Tandon RK, Acharya SK (2009). "A randomized controlled trial of antioxidant supplementation for pain relief in patients with chronic pancreatitis". Gastroenterology. 136 (1): 149–159.e2. doi:10.1053/j.gastro.2008.09.028. PMID 18952082.
  20. ↑ Burton F, Alkaade S, Collins D, Muddana V, Slivka A, Brand RE, Gelrud A, Banks PA, Sherman S, Anderson MA, Romagnuolo J, Lawrence C, Baillie J, Gardner TB, Lewis MD, Amann ST, Lieb JG, O'Connell M, Kennard ED, Yadav D, Whitcomb DC, Forsmark CE (2011). "Use and perceived effectiveness of non-analgesic medical therapies for chronic pancreatitis in the United States". Aliment. Pharmacol. Ther. 33 (1): 149–59. doi:10.1111/j.1365-2036.2010.04491.x. PMC 3142582. PMID 21083584.
  21. ↑ Siriwardena AK, Mason JM, Sheen AJ, Makin AJ, Shah NS (2012). "Antioxidant therapy does not reduce pain in patients with chronic pancreatitis: the ANTICIPATE study". Gastroenterology. 143 (3): 655–663.e1. doi:10.1053/j.gastro.2012.05.046. PMID 22683257.
  22. ↑ Busch EH, Atchison SR (1989). "Steroid celiac plexus block for chronic pancreatitis: results in 16 cases". J Clin Anesth. 1 (6): 431–3. PMID 2624751.
  23. ↑ Gress F, Schmitt C, Sherman S, Ikenberry S, Lehman G (1999). "A prospective randomized comparison of endoscopic ultrasound- and computed tomography-guided celiac plexus block for managing chronic pancreatitis pain". Am. J. Gastroenterol. 94 (4): 900–5. doi:10.1111/j.1572-0241.1999.01042.x. PMID 10201454.
  24. ↑ Gress F, Schmitt C, Sherman S, Ciaccia D, Ikenberry S, Lehman G (2001). "Endoscopic ultrasound-guided celiac plexus block for managing abdominal pain associated with chronic pancreatitis: a prospective single center experience". Am. J. Gastroenterol. 96 (2): 409–16. doi:10.1111/j.1572-0241.2001.03551.x. PMID 11232683.
  25. ↑ Okolo PI, Pasricha PJ, Kalloo AN (2000). "What are the long-term results of endoscopic pancreatic sphincterotomy?". Gastrointest. Endosc. 52 (1): 15–9. doi:10.1067/mge.2000.106669. PMID 10882956.
  26. ↑ Geenen JE, Rolny P (1991). "Endoscopic therapy of acute and chronic pancreatitis". Gastrointest. Endosc. 37 (3): 377–82. PMID 2070994.
  27. ↑ Choudari CP, Nickl NJ, Fogel E, Lehman GA, Sherman S (2002). "Hereditary pancreatitis: clinical presentation, ERCP findings, and outcome of endoscopic therapy". Gastrointest. Endosc. 56 (1): 66–71. PMID 12085037.
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  32. ↑ Parsi MA, Stevens T, Lopez R, Vargo JJ (2010). "Extracorporeal shock wave lithotripsy for prevention of recurrent pancreatitis caused by obstructive pancreatic stones". Pancreas. 39 (2): 153–5. doi:10.1097/MPA.0b013e3181bb1733. PMID 19820418.
  33. ↑ Guarner L, Navalpotro B, Molero X, Giralt J, Malagelada JR (2009). "Management of painful chronic pancreatitis with single-dose radiotherapy". Am. J. Gastroenterol. 104 (2): 349–55. doi:10.1038/ajg.2008.128. PMID 19190609.
  34. ↑ Keller J, Layer P (2005). "Human pancreatic exocrine response to nutrients in health and disease". Gut. 54 Suppl 6: vi1–28. doi:10.1136/gut.2005.065946. PMC 1867805. PMID 15951527.


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