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Indian Pediatr 2009;46: 1099-1101 |
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Acute Pancreatitis Associated with
Rotavirus Infection |
Hideki Kumagai, Shizuko Matsumoto, Masahiro Ebashi
and Takashi Ohsone*
From the Department of Pediatrics,
Hitachiomiya Saiseikai Hospital, and *Ohsone
Internal Medicine and Pediatrics,
Ibaraki, Japan
Correspondence to: Hideki Kumagai,
3033-3 Tagouchi, Hitachiomiya, Ibaraki 319-2256,
Japan.
Email:
[email protected]
Received: June 6, 2009;
Initial review: June 6, 2009;
Accepted: June 12, 2009. |
Abstract
We report the first documented
case of pancreatitis associated with rotavirus
infection in an infant. Estimation of amylase
level is important in infants with severe
rotavirus gastroenteritis, hyperamylasemia should
alert one to the presence of overt pancreatitis
which should be investigated by lipase estimation
and/or imaging.
Keywords: Amylase, Computed tomography,
Infant, Pancreatitis, Rotavirus.
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H yperamylasemia
during gastroenteritis is relatively frequent, but
overt pancreatitis is rare(1). Association of
pancreatitis is rare with rotavirus infection(2,3)
and no case is reported below 1 year of age.
Case report
The infant was referred from a
community clinic with diarrhea and severe
dehydration. There were no previous medical
problems. On arrival, the infant had tachycardia and
his activity was poor, with fever (temperature,
38.6°C). He had lost more than 10% of his original
body weight. His fontanel and orbits were sunken and
his skin turgor was decreased. The abdomen was flat
and soft, without hepato-splenomegaly. The
laboratory data (Table I) were
consistent with severe dehydration, and also showed
elevated levels of both transaminase and amylase.
Stool was positive for rotavirus antigen and
negative for adenovirus antigen using the RapidTesta®
ROTA-ADENO (Immuno-chromatography kit, Sekisui
Medical Co., Ltd., Tokyo, Japan). Abdominal X-ray
demonstrated mild nonspecific bowel dilation without
free air or portal venous air, whereas chest X-ray
findings were normal.
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Reference range |
2 days before |
On admission |
Following day |
The 4th day |
9 days |
later |
Hemoglobin |
10.5-13.5 |
g/dL |
11.7 |
15.1 |
10.4 |
11.4 |
11.6 |
Hematocrit |
33-39 |
% |
35.3 |
43.9 |
31.2 |
33.8 |
34.3 |
TP |
6.7-8.3 |
g/dL |
7.1 |
8.5 |
5.3 |
5.8 |
6.9 |
AST |
10-40 |
U/L |
61 |
61 |
135 |
62 |
47 |
ALT |
5-40 |
U/L |
58 |
80 |
154 |
108 |
43 |
TB |
0.2-1.0 |
mg/dL |
0.2 |
0.2 |
0.3 |
ND |
< 0.1 |
GGTP |
0-47 |
U/L |
11 |
14 |
12 |
ND |
12 |
Amylase |
37-125 |
U/L |
32 |
291 |
322 |
60 |
74 |
P-PLA2 |
130-400 |
ng/dL |
ND |
2,740 |
358 |
ND |
164 |
Lipase |
13.6-22.8 |
U/L |
ND |
41 |
35 |
ND |
ND |
BUN |
4.0-15 |
mg/dL |
14.2 |
80.3 |
5.1 |
1.8 |
5.3 |
Cr |
0.3-0.6 |
mg/dL |
0.21 |
1.20 |
0.17 |
0.15 |
0.16 |
Sodium |
136-147 |
mEq/L |
129 |
152 |
147 |
144 |
139 |
Potassium |
3.6-5.0 |
mEq/L |
3.8 |
5.5 |
3.2 |
4.8 |
4.7 |
Triglyceride |
25-135 |
mg/dL |
38 |
ND |
181 |
ND |
ND |
Blood glucose |
60-100 |
mg/dL |
98 |
155 |
88 |
ND |
98 |
CRP |
0.0-0.3 |
mg/dL |
0.51 |
0.40 |
0.05 |
0.09 |
0.05 |
WBC = white blood cells, TP = total protein, AST = aspartate aminotransferase, ALT = alanine aminotransferase,
TB = total bilirubin, GGTP = gamma-glutamyltranspeptidase, P-PLA2 = pancreatic phospholipase A2,
BUN = blood urea nitrogen, Cr = creatinine, CRP = C-reactive protein, ND = not done.
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Aggressive fluid-resuscitation
was started. The hyperamylasemia was considered to
be related to severe gastroenteritis. Investigations
on the following day revealed evidence of recovery
from dehydration, but the ALT and AST levels, and
hyperamylasemia had increased. Since pancreatitis
could not be ruled out, abdominal computed
tomography (CT) was performed. CT demonstrated a
mildly enlarged edematous pancreas and a small
amount of accumulated fluid, but ultrasonography one
month later showed that this had normalized for age:
pancreatic body 0.75 cm (normal dimension 0.6±0.2
cm). The diagnosis of acute pancreatitis was made on
the basis of the elevated pancreatic enzyme values
and CT findings.
The patient’s condition improved
over several days, with gradual normalization of the
amylase, lipase, and pancreatic phospholipase A2
levels within 10 days.
Discussion
Acute pancreatitis is less common
in children than in adults, and clinical diagnosis
in pediatric patients is often challenging(4). In
particular, children may not only present with
nonspecific symptoms, but hyperamylasemia during
gastroenteritis is also relatively frequent(1).
Generally, the values of serum amylase, pancreatic
phospholipase A2, and lipase are elevated in renal
failure. In our patient, the transient renal
dysfunction due to severe dehydration would have
contributed to the elevation of these values on
admission. However, on the second hospital day, the
level of serum amylase was higher than on the day of
admission, and the level of lipase was still high
despite correction of dehydration. Pancreatic
imaging by contrast-enhanced CT provides good
evidence for the presence or absence of pancreatitis
in adults(5). Since there are no CT standards of
pancreatic size for children, measurement for this
patient was based on standards established in the
sonographic literature(6). CT revealed relative
pancreatic enlargement for age: pancreatic body 1.3
cm (normal dimension 0.6±0.2 cm), tail 1.3 cm
(normal 1.0±0.4 cm), and a small amount of
accumulated fluid. Accordingly, this case met the
stringent diagnostic criteria for acute pancreatitis
in infants(7).
It has been demonstrated
experimentally that reoviruses, which belong to the
same family as rotaviruses, can produce inflammatory
edema with infiltrates of neutrophils and
mononuclear round cells, degranulation of acinar
cells, and dissociation of lobules and acini with
necrosis(7). In the same way, it was thought that
the damage to the pancreatic tissue in this case
could have been caused directly by rotavirus
infection. However, it is unknown whether
rotaviruses reach the pancreas by ascending
infection through the pancreatobiliary tree or via a
hematogenous route(3, 8). Another hypothesis is that
obstruction of pancreatic fluid outflow through an
edematous ampulla of Vater might have induced
pancreatitis(3), but in this case the laboratory
data and CT imaging revealed no evidence of bile
flow obstruction or dilatation of the pancreatic
duct, respectively.
References
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Furlan F, Franzetti M, Stecca C, et al.
Pancreatic hyperamylasemia during acute
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hypoglycemia-associated convulsions following
rotavirus gastroenteritis. J Pediatr Gastroenterol
Nutr 1991; 12: 280-282.
3. De La Rubia L, Herrera MI,
Cebrero M, De Jong JC. Acute pancreatitis associated
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unguiculatus)—lesions in pancreas and brain. J
Basic Microbiol 1993; 33: 147-152.
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V, Warfield KL, Ciarlet M, Estes MK, et al.
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