
Efficacy of octreotide and somatostatin in acute pancreatitis 199
Vol. 67(2): 189 - 204, 2026
ogy, a variety of new drugs have appeared in
clinical practice, and their application has,
to a certain extent, reduced morbidity and
mortality in patients with severe acute pan-
creatitis, but some patients still die. The
occurrence of acute pancreatitis is mainly
due to the continuous release of pancreatic
enzymes in the body, influenced by a series
of intertwined factors, resulting in the acti-
vation of phospholipase A2, etc. Under the
influence of the inflammatory response, the
pancreas undergoes microcirculation abnor-
malities, accelerating pancreatic digestion,
destroying the normal blood supply, and
ultimately leading to pancreatic necrosis.
Niu et al.22 proposed that phospholipase D2
(PLD2) plays a crucial regulatory role. In the
medical management of patients with severe
acute pancreatitis, comprehensive therapeu-
tic approaches are typically used to reduce
pancreatic secretion, inhibit pancreatic en-
zyme synthesis, improve clinical signs, and
promote recovery.
AMY and LPS are two important labo-
ratory tests for acute pancreatitis 23; the
former is mainly due to the activation of
pancreatic amylase by trypsinogen in the
pancreas, which subsequently causes the
elevation of AMY, and the latter is due to
the activation of pancreatic lipase by lipas-
eogen in the pancreas; therefore, AMY and
LPS are the characteristic indicators for
the diagnosis of acute pancreatitis. Sun et
al.24, in a multicenter retrospective study,
suggested that both somatostatin and oc-
treotide could normalize serum AMY and
LPS in patients with acute pancreatitis, and
this article’s research showed that octreo-
tide could normalize pancreatic function
more quickly than somatostatin. CRP, an
acute-phase reactant synthesized by IL-
6-stimulated hepatocytes, is one of the pro-
teins mediating the inflammatory response
in acute pancreatitis. The inflammatory re-
sponse in acute pancreatitis and its concen-
tration can reflect the presence or absence
of inflammation and the intensity of the
response in the organism 25. TNF-α, mainly
produced by monocytes and macrophages,
can regulate immune function and enhance
anti-infection capacity, and the multiple-
organ damage caused by inflammation is
closely associated with TNF-α 26.
IL-6 plays an important role in the
proliferation and activation of lympho-
cytes, and can promote the synthesis of
CRP and the development of blood cells,
but its concentration is too high, which
can stimulate the granulocytes to release
a large number of oxygen-free radicals and
proteases, thus destroying the vascular en-
dothelium and the endothelial cells. How-
ever, its high concentration can stimulate
granulocytes to release large quantities of
oxygen-free radicals and proteases, there-
by destroying the vascular endothelium
and aggravating organ damage. During
inflammatory reactions, macrophages and
monocytes in the liver, lymphocytes and
endocrine cells in the lungs and intesti-
nal tissues can synthesize and secrete PCT
in response to bacterial endotoxin, TNF-α,
and IL-6; these substances work together,
leading to an apparent increase in the lev-
el of PCT in the blood circulation 27. The
present study suggests that, in patients
with acute pancreatitis, CRP, IL-6, TNF-α,
and PCT levels in the blood were reduced
more significantly in those treated with
octreotide than in those treated with so-
matostatin, indicating that octreotide can
normalize inflammatory responses and
immune functions. Mao et al. 28, in a mul-
ticenter retrospective study, validated so-
matostatin and octreotide as widely used
medications for acute pancreatitis and re-
ported octreotide’s superior therapeutic
effect, which is more attuned to the re-
sults of this study. When germs invade the
human body, leukocytes can pass through
the capillary wall by deformation, con-
centrate at the site of germ invasion, sur-
round and engulf the germs, and produce
an inflammatory reaction, resulting in a
higher leukocyte count than normal. ALB
unequivocally expands blood volume and