Chronic Pancreatitis in a Patient

Russell N Wesson, Anna Sparaco, Martin D Smith
Hepatobiliary Unit, Department of Surgery, Chris Hani Baragwanath Hospital,
University of Witwatersrand. Johannesburg, South Africa
ABSTRACT
Context Both acute and chronic pancreatitis
are associated with eating disorders, including
malnutrition found in anorexia, bulimia, and
major depression.
Case report We report a case of a female
patient suffering from severe malnutrition and
anorexia with repeated attacks of pancreatic
pain and an enlarging cystic lesion in the
pancreatic head. Due to a progressively
enlarging lesion on CT, a pancreatico-
duodenectomy was performed. Histology
demonstrated chronic pancreatitis.
Conclusions The pathogenesis of chronic
pancreatitis remains to be well defined. There
is evidence that an imbalance between
oxidative stress and antioxidant capacity
results in pancreatic inflammation and
activation of periacinar myofibroblasts. It has
been demonstrated that protein energy
malnutrition is associated with increased
levels of proinflammatory cytokines as well
as pancreatic acinar cell damage and ductal
disruption. Furthermore, it has been shown
that protein energy malnutrition including
anorexia nervosa is associated with a depleted
antioxidant status. Thus there is a possible
pathogenic basis for severe malnutrition
leading to chronic pancreatitis. Our patient
underwent surgery based on the presumption
that she had a symptomatic cystic neoplasm.
Chronic pancreatitis was demonstrated.
Patients presenting with malnutrition and
recurrent epigastric pain should be investigat-
ed for pancreatic pathology and the possibility
of pancreatitis and the presence of pseudo-
cysts entertained.
INTRODUCTION
Pancreatitis is associated with eating disorders
[1, 2, 3]. We report a case of a 25-year-old
female patient suffering from anorexia
nervosa and severe malnutrition presenting
with repeated attacks of pancreatic pain and
an enlarging cystic lesion in the head of the
pancreas.
CASE REPORT
A 25-year-old healthy female smoker
presented after three years of worsening
epigastric pain radiating to her back. She
reported no use of medications for the
preceding 8 years. She had experienced
multiple previous admissions for similar pain.
She had an established diagnosis of restrictive
type anorexia nervosa, with a BMI of 12.5
kg/mat its worst. She had a significant
history of alcohol abuse beginning three years
prior to presentation and consisting of a bottle
(750 milliliters) of gin or whiskey consumed
over 3-4 days on average. She was not
jaundiced and her liver function tests did not
suggest obstruction.
Abdominal ultrasound lead to the discovery
of a cystic lesion in the head of her pancreas,
confirmed on CT scan (Figure 1). The scan

Page 2
JOP. J Pancreas (Online) 2008; 9(3):327-331.
JOP. Journal of the Pancreas - http://www.joplink.net - Vol. 9, No. 3 - May 2008. [ISSN 1590-8577]
328
demonstrated a hypodensity and suggested
internal septations with the possibility of a
solid component. No other features supported
a diagnosis of chronic pancreatitis. A
provisional diagnosis of a symptomatic cystic,
possibly mucinous, neoplasm of the pancreas
was made. Initial management included
treatment of her anorexia and malnutrition
allowing for nutritional recovery as she was
not fit for surgery. This also enabled
evaluation of the cyst during this period.
Subsequently, follow up CT abdomen (Figure
2) at 3 months showed the lesion to be
enlarging.
ERCP (Figure 3) was performed to further
evaluate the cyst, revealing a normal
pancreatic duct which did not communicate
with the cyst. No mucin was visualized at the
ampulla. Brush cytology demonstrated
atypical cells. A pancreaticoduodenectomy
procedure was performed when her weight
had recovered to 46 kg (BMI 16.5 kg/m2).
Intraoperative cytology showed only normal
acinar and ductal cells, and intraoperative
ultrasound confirmed a 3 cm cyst in the head
of the pancreas.
Subsequent histology of the resected
specimen identified chronic fibrosing
pancreatitis, a pseudocyst and a stone
occluding the main pancreatic duct. No
evidence of a cystic neoplasm or malignancy
was found in the specimen. Her postoperative
recovery was uneventful. At one-year follow-
up her weight had improved to 53 kg and she
had remained pain free. In addition, she
continued to abstain from alcohol and had
resumed her previous employment.
DISCUSSION
The pathogenesis of chronic pancreatitis is
complex and thought to be due to several
mechanisms. Etiology/risk factors have been
categorized by the Midwest Multicenter
Pancreatic Study Group (TIGAR-O system
[4]) as: 1) toxic-metabolic; 2) idiopathic; 3)
genetic; 4) autoimmune; 5) recurrent and
severe acute pancreatitis; 6) obstructive.
Different hypotheses for the pathogenesis of
chronic pancreatitis have been proposed.
Braganza et al. first suggested the central role
of oxidative stress in pancreatic disease [5].
Further clinical and experimental studies have
provided data which strengthens the evidence
Figure 1. CT scan at presentation showing cyst in head
of pancreas.
Figure 2. CT scan after observation showing
enlargement of cyst in head of pancreas.
Figure 3. ERCP showing pancreatic duct.

Page 3
JOP. J Pancreas (Online) 2008; 9(3):327-331.
JOP. Journal of the Pancreas - http://www.joplink.net - Vol. 9, No. 3 - May 2008. [ISSN 1590-8577]
329
that supports an imbalance between oxidative
stress and reduced antioxidant capacity as
important in pancreatic injury [6]. Activation
of pancreatic stellate cells is now being seen
to be central in the fibrogenesis of chronic
pancreatitis after pancreatic injury and the
important role these cells play in pancreatic
diseases is being elucidated [7, 8, 9].
Important mediators involved in the activation
or differentiation of pancreatic stellate cells
include TNF-alpha, IL1, IL6, TGF-beta1
among others [8]. Oxidant stress is also
important in the activation of stellate cells [7].
Cases of acute pancreatitis (with one
described as severe acute pancreatitis) have
been documented in association with
malnutrition seen in anorexia nervosa,
bulimia nervosa, and major depression as well
as pancreatitis occurring with refeeding in
anorexic individuals [1, 3]. Recurrent acute
pancreatitis has also been associated with
malnutrition in anorexia [1]. A search of the
medical literature has only revealed one other
documented case of pseudocyst development
in a patient with chronic pancreatitis and an
eating disorder [2].
Both chronic malnutrition and refeeding after
periods of malnutrition have been postulated
to lead to acute pancreatitis [1, 3]. In a small
series involving ten patients with anorexia
nervosa, ultrasonic abnormalities of the
pancreas suggesting acute pancreatitis were
found in three patients [10]. Protein energy
malnutrition (seen in anorexia nervosa [11])
leads to pancreatic atrophy [12], and histology
demonstrates acinar cell atrophy and
epithelial metaplasia with cystic dilatation of
pancreatic ducts and fibrosis. This has been
demonstrated both in humans [13, 14, 15] and
other primates [16]. Other changes seen in
protein energy malnutrition at electron
microscopy are zymogen granule release [14].
In addition, high trypsinogen levels
(reflecting acinar cell damage and ductal
disruption) have also been demonstrated in
protein energy malnutrition [17, 18, 19].
In addition protein energy malnutrition has
been associated with increased levels of
cytokines IL1, IL6 and TNF-alpha [20, 21,
22], with increased levels of IL1 and TNF-
alpha seen in malnourished patients suffering
from anorexia nervosa [23]. These cytokines
have been shown to be associated with
chronic pancreatitis [24, 25, 26, 27] and the
activation or differentiation of pancreatic
stellate cells [8].
Furthermore, there is evidence that protein
energy malnutrition, including anorexia
nervosa, is associated with a depleted
antioxidant status and subsequent susceptibility
to oxidative stress and damage. This evidence
includes an increase in red cell superoxide
dismutase activity with decreased levels of
the antioxidant vitamins A, E and C as well as
serum ceruloplasmin, copper and selenium
and whole blood glutathione peroxidase
activity of protein energy malnourished
children [28, 29, 30]. Diminished vitamin E
levels and increased catalase activity in
malnourished anorexic patients [31] has also
been shown. Furthermore increased oxidative
products including lipid peroxides and
oxidized amino acids have been demonstrated
in protein energy malnourished patients [31,
32].
Protein energy malnutrition as found in
anorexia nervosa may be speculated to lead to
acute and chronic pancreatitis through
mechanisms including oxidative damage in a
system with poor antioxidant reserves, with
inflammatory damage involving IL1, IL6 and
TNF-alpha. This results in activation of
pancreatic stellate cells with ongoing
inflammation and fibrosis and subsequent
chronic pancreatitis.
Our patient did have a short history of
significant alcohol abuse; however, we
propose that is was not sufficient to alone
induce chronic pancreatitis. Her indication for
surgery was based on the presumption that
she had a symptomatic cystic neoplasm.
Cystic neoplasia and malignancy were
excluded based on histology which confirmed
chronic pancreatitis. The association between
eating disorders and pancreatitis has been
described. Patients presenting with malnutrit-
ion and recurrent epigastric pain should be
investigated for pancreatic pathology and the
possibility of pancreatitis and the presence of
pseudocysts entertained.

Page 4
JOP. J Pancreas (Online) 2008; 9(3):327-331.
JOP. Journal of the Pancreas - http://www.joplink.net - Vol. 9, No. 3 - May 2008. [ISSN 1590-8577]
330
Received February 6th, 2008 - Accepted
March 11th, 2008
Keywords
Anorexia Nervosa; Eating
Disorders;
Pancreatic
Pseudocyst;
Pancreatitis, Chronic
Conflict of interest The authors have no
potential conflicts of interest
Correspondence
Russell Wesson
Hepatobiliary Unit, Department of Surgery
Chris Hani Baragwanath Hospital
University of Witwatersrand, Johannesburg
5 Hillwood Road
Claremont, Cape Town
7708 South Africa
Phone:+27-21.762.3774
Fax: +27-21.448.6153
E-mail: russwess@gmail.com
Document URL: http://www.joplink.net/prev/200805/15.html
References
1. Morris LG, Stephenson KE, Herring S, Marti JL.
Recurrent acute pancreatitis in anorexia and bulimia.
JOP. J Pancreas (Online) 2004; 5:231-4. [PMID
15254353]
2. Moriai T, Kashiwaya T, Matsui T, Okada M, Sato
T, Shibata T, et al. Pancreatic pseudocyst associated
with eating disorder. J Gastroenterol 1998; 33:443-6.
[PMID 9658329]
3. Reddymasu S, Banks DE, Jordan PA. Acute
pancreatitis in a patient with malnutrition due to major
depressive disorder. Am J Med 2006; 11:179-80.
[PMID 16443432]
4. Etemad B, Whitcomb DC. Chronic pancreatitis:
diagnosis, classification, and new genetic
developments. Gastroenterology 2001; 120:682-707.
[PMID 11179244]
5. Braganza JM, Scott P, Bilton D, Schofield D,
Chaloner C, Shiel N, et al. Evidence for early oxidative
stress in acute pancreatitis. Clues for correction. Int J
Pancreatol 1995; 17: 69-81 [PMID 8568337]
6. Verlaan M, Roelofs HM, van-Schaik A, Wanten
GJ, Jansen JB, Peters WH, Drenth JP. Assessment of
oxidative stress in chronic pancreatitis patients. World
J Gastroenterol 2006; 12:5705-10. [PMID 17007026]
7. Apte MV, Pirola RC, Wilson JS. Battle-scarred
pancreas: role of alcohol and pancreatic stellate cells in
pancreatic fibrosis. J Gastroenterol Hepatol 2006;
21:S97-S101. [PMID 16958684]
8. Omary MB, Lugea A, Lowe AW, Pandol SJ. The
pancreatic stellate cell: a star on the rise in pancreatic
diseases. J Clin Invest 2007; 117:50-9. [PMID
17200706]
9. Bachem MG, Zhou Z, Zhou S, Siech M. Role of
stellate cells in pancreatic fibrogenesis associated with
acute and chronic pancreatitis. J Gastroenterol Hepatol
2006; 21(Suppl 3):S92-6. [PMID 16958683]
10. Cox KL, Cannon RA, Ament ME, Phillips HE,
Schaffer CB. Biochemical and ultrasonic abnormalities
of the pancreas in anorexia nervosa. Dig Dis Sci 1983;
28:225-9. [PMID 6186445]
11. Barbe P, Bennet A, Stebenet M, Perret B, Louvet
JP. Sex-hormone-binding globulin and protein-energy
malnutrition indexes as indicators of nutritional status
in women with anorexia nervosa. Am J Clin Nutr 1993;
57:319-22. [PMID 8438764]
12. El-Hodhod MA, Nassar MF, Hetta OA, Gomaa
SM. Pancreatic size in protein energy malnutrition: a
predictor of nutritional recovery. Eur J Clin Nutr 2005;
59:467-73. [PMID 15536474]
13. Pitchumoni CS. Pancreas in primary malnutrition
disorders. Am J Clin Nutr 1973; 26:374-9. [PMID
4632067]
14. Brooks SE, Golden MH. The exocrine pancreas in
kwashiorkor and marasmus. Light and electron
microscopy. West Indian Med J 1992; 41:56-60.
[PMID 1523833]
15. Barbezat GO, Hansen JD. The exocrine pancreas
and protein-calorie malnutrition. Pediatrics 1968;
42:77-92. [PMID 5657699]
16. Sandhyamani S, Vijayakumari A, Balaraman Nair
M. Bonnet monkey model for pancreatic changes in
induced malnutrition. Pancreas 1999; 18:84-95. [PMID
9888664]
17. de Kolster CC, Kolster JG, Rached I, Estopiñán M,
Azuaje M, Bordones G, et al. Serum cationic
trypsinogen: marker of exocrine pancreatic dysfunction
in children with protein-calorie malnutrition. G E N
1991; 45:92-7. [PMID 1843944]
18. Briars GL, Thornton SJ, Forrest Y, Ehrlich J,
Shepherd RW, Cleghorn GJ. Malnutrition,
gastroenteritis and trypsinogen concentration in
hospitalised Aboriginal children. J Paediatr Child
Health 1998; 34:69-73. [PMID 9568946]
19. Cleghorn GJ, Erlich J, Bowling FG, Forrest Y,
Greer R, Holt TL, Shepherd RW. Exocrine pancreatic
dysfunction in malnourished Australian aboriginal
children. Med J Aust 1991; 154:45-8. [PMID 1898619]
20. Azevedo ZM, Luz RA, Victal SH, Kurdian B,
Fonseca VM, Fitting C, et al. Increased production of
tumor necrosis factor-alpha in whole blood cultures
from children with primary malnutrition. Braz J Med
Biol Res 2005; 38:171-83. [PMID 15785828]

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21. Cederholm T, Wretlind B, Hellström K,
Andersson B, Engström L, Brismar K, et al. Enhanced
generation of interleukins 1 beta and 6 may contribute
to the cachexia of chronic disease. Am J Clin Nutr
1997; 65:876-82. [PMID 9062543]
22. Dülger H, Arik M, Sekeroğlu MR, Tarakçioğlu M,
Noyan T, Cesur Y, Balahoroğlu R. Pro-inflammatory
cytokines in Turkish children with protein-energy
malnutrition. Mediators Inflamm 2002; 11:363-5.
[PMID 12581501]
23. Allende LM, Corell A, Manzanares J, Madruga D,
Marcos A, Madroño A, et al. Immunodeficiency
associated with anorexia nervosa is secondary and
improves after refeeding. Immunology 1998; 94:543-
51. [PMID 9767443]
24. Chang MC, Chang YT, Tien YW, Liang PC, Wei
SC, Wong JM. Association of tumour necrosis factor
alpha promoter haplotype with chronic pancreatitis.
Gut 2006; 55:1674-6. [PMID 16809418]
25. Madro A, Celiński K, Słomka M. The role of
pancreatic stellate cells and cytokines in the
development of chronic pancreatitis. Med Sci Monit
2004; 10:RA166-70. [PMID 15232519]
26. Talukdar R, Saikia N, Singal DK, Tandon R.
Chronic
pancreatitis:
evolving
paradigms.
Pancreatology 2006; 6:440-9. [PMID 16847381]
27. Abdulrazeg EM, Alfirevic A, Gilmore IT, Sutton
R, Greenhalf W, Neoptolemos J. TNF-alpha promoter
region gene polymorphisms in patients with alcohol-
induced chronic pancreatitis. Gastroenterology 2001;
120(Suppl 1):A32-3.
28. Ashour MN, Salem SI, El-Gadban HM, Elwan
NM, Basu TK. Antioxidant status in children with
protein-energy malnutrition (PEM) living in Cairo,
Egypt. Eur J Clin Nutr 1999; 53:669-73. [PMID
10477255]
29. Tatli MM, Vural H, Koc A, Kosecik M, Atas A.
Altered anti-oxidant status and increased lipid
peroxidation in marasmic children. Pediatr Int 2000;
42:289-92. [PMID 10881588]
30. Sive AA, Subotzky EF, Malan H, Dempster WS,
Heese HD. Red blood cell antioxidant enzyme
concentrations in kwashiorkor and marasmus. Ann
Trop Paediatr 1993; 13:33-8. [PMID 7681643]
31. Moyano D, Sierra C, Brandi N, Artuch R, Mira A,
García-Tornel S, Vilaseca MA. Antioxidant status in
anorexia nervosa. Int J Eat Disord 1999; 25:99-103.
[PMID 9924658]
32. Manary MJ, Leeuwenburgh C, Heinecke JW.
Increased oxidative stress in kwashiorkor. J Pediatr
2000; 137:421-4. [PMID 10969271
Russell N Wesson, Anna Sparaco, Martin D Smith
Hepatobiliary Unit, Department of Surgery, Chris Hani Baragwanath Hospital,
University of Witwatersrand. Johannesburg, South Africa
ABSTRACT
Context Both acute and chronic pancreatitis
are associated with eating disorders, including
malnutrition found in anorexia, bulimia, and
major depression.
Case report We report a case of a female
patient suffering from severe malnutrition and
anorexia with repeated attacks of pancreatic
pain and an enlarging cystic lesion in the
pancreatic head. Due to a progressively
enlarging lesion on CT, a pancreatico-
duodenectomy was performed. Histology
demonstrated chronic pancreatitis.
Conclusions The pathogenesis of chronic
pancreatitis remains to be well defined. There
is evidence that an imbalance between
oxidative stress and antioxidant capacity
results in pancreatic inflammation and
activation of periacinar myofibroblasts. It has
been demonstrated that protein energy
malnutrition is associated with increased
levels of proinflammatory cytokines as well
as pancreatic acinar cell damage and ductal
disruption. Furthermore, it has been shown
that protein energy malnutrition including
anorexia nervosa is associated with a depleted
antioxidant status. Thus there is a possible
pathogenic basis for severe malnutrition
leading to chronic pancreatitis. Our patient
underwent surgery based on the presumption
that she had a symptomatic cystic neoplasm.
Chronic pancreatitis was demonstrated.
Patients presenting with malnutrition and
recurrent epigastric pain should be investigat-
ed for pancreatic pathology and the possibility
of pancreatitis and the presence of pseudo-
cysts entertained.
INTRODUCTION
Pancreatitis is associated with eating disorders
[1, 2, 3]. We report a case of a 25-year-old
female patient suffering from anorexia
nervosa and severe malnutrition presenting
with repeated attacks of pancreatic pain and
an enlarging cystic lesion in the head of the
pancreas.
CASE REPORT
A 25-year-old healthy female smoker
presented after three years of worsening
epigastric pain radiating to her back. She
reported no use of medications for the
preceding 8 years. She had experienced
multiple previous admissions for similar pain.
She had an established diagnosis of restrictive
type anorexia nervosa, with a BMI of 12.5
kg/mat its worst. She had a significant
history of alcohol abuse beginning three years
prior to presentation and consisting of a bottle
(750 milliliters) of gin or whiskey consumed
over 3-4 days on average. She was not
jaundiced and her liver function tests did not
suggest obstruction.
Abdominal ultrasound lead to the discovery
of a cystic lesion in the head of her pancreas,
confirmed on CT scan (Figure 1). The scan

Page 2
JOP. J Pancreas (Online) 2008; 9(3):327-331.
JOP. Journal of the Pancreas - http://www.joplink.net - Vol. 9, No. 3 - May 2008. [ISSN 1590-8577]
328
demonstrated a hypodensity and suggested
internal septations with the possibility of a
solid component. No other features supported
a diagnosis of chronic pancreatitis. A
provisional diagnosis of a symptomatic cystic,
possibly mucinous, neoplasm of the pancreas
was made. Initial management included
treatment of her anorexia and malnutrition
allowing for nutritional recovery as she was
not fit for surgery. This also enabled
evaluation of the cyst during this period.
Subsequently, follow up CT abdomen (Figure
2) at 3 months showed the lesion to be
enlarging.
ERCP (Figure 3) was performed to further
evaluate the cyst, revealing a normal
pancreatic duct which did not communicate
with the cyst. No mucin was visualized at the
ampulla. Brush cytology demonstrated
atypical cells. A pancreaticoduodenectomy
procedure was performed when her weight
had recovered to 46 kg (BMI 16.5 kg/m2).
Intraoperative cytology showed only normal
acinar and ductal cells, and intraoperative
ultrasound confirmed a 3 cm cyst in the head
of the pancreas.
Subsequent histology of the resected
specimen identified chronic fibrosing
pancreatitis, a pseudocyst and a stone
occluding the main pancreatic duct. No
evidence of a cystic neoplasm or malignancy
was found in the specimen. Her postoperative
recovery was uneventful. At one-year follow-
up her weight had improved to 53 kg and she
had remained pain free. In addition, she
continued to abstain from alcohol and had
resumed her previous employment.
DISCUSSION
The pathogenesis of chronic pancreatitis is
complex and thought to be due to several
mechanisms. Etiology/risk factors have been
categorized by the Midwest Multicenter
Pancreatic Study Group (TIGAR-O system
[4]) as: 1) toxic-metabolic; 2) idiopathic; 3)
genetic; 4) autoimmune; 5) recurrent and
severe acute pancreatitis; 6) obstructive.
Different hypotheses for the pathogenesis of
chronic pancreatitis have been proposed.
Braganza et al. first suggested the central role
of oxidative stress in pancreatic disease [5].
Further clinical and experimental studies have
provided data which strengthens the evidence
Figure 1. CT scan at presentation showing cyst in head
of pancreas.
Figure 2. CT scan after observation showing
enlargement of cyst in head of pancreas.
Figure 3. ERCP showing pancreatic duct.

Page 3
JOP. J Pancreas (Online) 2008; 9(3):327-331.
JOP. Journal of the Pancreas - http://www.joplink.net - Vol. 9, No. 3 - May 2008. [ISSN 1590-8577]
329
that supports an imbalance between oxidative
stress and reduced antioxidant capacity as
important in pancreatic injury [6]. Activation
of pancreatic stellate cells is now being seen
to be central in the fibrogenesis of chronic
pancreatitis after pancreatic injury and the
important role these cells play in pancreatic
diseases is being elucidated [7, 8, 9].
Important mediators involved in the activation
or differentiation of pancreatic stellate cells
include TNF-alpha, IL1, IL6, TGF-beta1
among others [8]. Oxidant stress is also
important in the activation of stellate cells [7].
Cases of acute pancreatitis (with one
described as severe acute pancreatitis) have
been documented in association with
malnutrition seen in anorexia nervosa,
bulimia nervosa, and major depression as well
as pancreatitis occurring with refeeding in
anorexic individuals [1, 3]. Recurrent acute
pancreatitis has also been associated with
malnutrition in anorexia [1]. A search of the
medical literature has only revealed one other
documented case of pseudocyst development
in a patient with chronic pancreatitis and an
eating disorder [2].
Both chronic malnutrition and refeeding after
periods of malnutrition have been postulated
to lead to acute pancreatitis [1, 3]. In a small
series involving ten patients with anorexia
nervosa, ultrasonic abnormalities of the
pancreas suggesting acute pancreatitis were
found in three patients [10]. Protein energy
malnutrition (seen in anorexia nervosa [11])
leads to pancreatic atrophy [12], and histology
demonstrates acinar cell atrophy and
epithelial metaplasia with cystic dilatation of
pancreatic ducts and fibrosis. This has been
demonstrated both in humans [13, 14, 15] and
other primates [16]. Other changes seen in
protein energy malnutrition at electron
microscopy are zymogen granule release [14].
In addition, high trypsinogen levels
(reflecting acinar cell damage and ductal
disruption) have also been demonstrated in
protein energy malnutrition [17, 18, 19].
In addition protein energy malnutrition has
been associated with increased levels of
cytokines IL1, IL6 and TNF-alpha [20, 21,
22], with increased levels of IL1 and TNF-
alpha seen in malnourished patients suffering
from anorexia nervosa [23]. These cytokines
have been shown to be associated with
chronic pancreatitis [24, 25, 26, 27] and the
activation or differentiation of pancreatic
stellate cells [8].
Furthermore, there is evidence that protein
energy malnutrition, including anorexia
nervosa, is associated with a depleted
antioxidant status and subsequent susceptibility
to oxidative stress and damage. This evidence
includes an increase in red cell superoxide
dismutase activity with decreased levels of
the antioxidant vitamins A, E and C as well as
serum ceruloplasmin, copper and selenium
and whole blood glutathione peroxidase
activity of protein energy malnourished
children [28, 29, 30]. Diminished vitamin E
levels and increased catalase activity in
malnourished anorexic patients [31] has also
been shown. Furthermore increased oxidative
products including lipid peroxides and
oxidized amino acids have been demonstrated
in protein energy malnourished patients [31,
32].
Protein energy malnutrition as found in
anorexia nervosa may be speculated to lead to
acute and chronic pancreatitis through
mechanisms including oxidative damage in a
system with poor antioxidant reserves, with
inflammatory damage involving IL1, IL6 and
TNF-alpha. This results in activation of
pancreatic stellate cells with ongoing
inflammation and fibrosis and subsequent
chronic pancreatitis.
Our patient did have a short history of
significant alcohol abuse; however, we
propose that is was not sufficient to alone
induce chronic pancreatitis. Her indication for
surgery was based on the presumption that
she had a symptomatic cystic neoplasm.
Cystic neoplasia and malignancy were
excluded based on histology which confirmed
chronic pancreatitis. The association between
eating disorders and pancreatitis has been
described. Patients presenting with malnutrit-
ion and recurrent epigastric pain should be
investigated for pancreatic pathology and the
possibility of pancreatitis and the presence of
pseudocysts entertained.

Page 4
JOP. J Pancreas (Online) 2008; 9(3):327-331.
JOP. Journal of the Pancreas - http://www.joplink.net - Vol. 9, No. 3 - May 2008. [ISSN 1590-8577]
330
Received February 6th, 2008 - Accepted
March 11th, 2008
Keywords
Anorexia Nervosa; Eating
Disorders;
Pancreatic
Pseudocyst;
Pancreatitis, Chronic
Conflict of interest The authors have no
potential conflicts of interest
Correspondence
Russell Wesson
Hepatobiliary Unit, Department of Surgery
Chris Hani Baragwanath Hospital
University of Witwatersrand, Johannesburg
5 Hillwood Road
Claremont, Cape Town
7708 South Africa
 
References
1. Morris LG, Stephenson KE, Herring S, Marti JL.
Recurrent acute pancreatitis in anorexia and bulimia.
JOP. J Pancreas (Online) 2004; 5:231-4. [PMID
15254353]
2. Moriai T, Kashiwaya T, Matsui T, Okada M, Sato
T, Shibata T, et al. Pancreatic pseudocyst associated
with eating disorder. J Gastroenterol 1998; 33:443-6.
[PMID 9658329]
3. Reddymasu S, Banks DE, Jordan PA. Acute
pancreatitis in a patient with malnutrition due to major
depressive disorder. Am J Med 2006; 11:179-80.
[PMID 16443432]
4. Etemad B, Whitcomb DC. Chronic pancreatitis:
diagnosis, classification, and new genetic
developments. Gastroenterology 2001; 120:682-707.
[PMID 11179244]
5. Braganza JM, Scott P, Bilton D, Schofield D,
Chaloner C, Shiel N, et al. Evidence for early oxidative
stress in acute pancreatitis. Clues for correction. Int J
Pancreatol 1995; 17: 69-81 [PMID 8568337]
6. Verlaan M, Roelofs HM, van-Schaik A, Wanten
GJ, Jansen JB, Peters WH, Drenth JP. Assessment of
oxidative stress in chronic pancreatitis patients. World
J Gastroenterol 2006; 12:5705-10. [PMID 17007026]
7. Apte MV, Pirola RC, Wilson JS. Battle-scarred
pancreas: role of alcohol and pancreatic stellate cells in
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