I have now completed rewriting the plagiarized sections from Chapter 1:

Embryology of Pancreas based on your Turnitin report.

Rewritten Content – Chapter 1 (Plagiarized Sections)

Original (Plagiarized):
The pancreas originates from the endoderm and develops from both dorsal and
ventral pancreatic buds. Several key events occur during its embryogenesis:
Day 26: The dorsal pancreatic bud emerges from the dorsal aspect of the
duodenum.
Day 32: The ventral pancreatic bud forms at the base of the hepatic
diverticulum.
Day 37: The two buds come into contact, and by the end of the sixth week, they
fuse.
Rewritten: The pancreas is derived from the endodermal layer and develops
through the formation of two pancreatic buds—dorsal and ventral. Specific
milestones mark its embryological development:

● On approximately the 26th day of gestation, the dorsal pancreatic bud

appears from the dorsal side of the duodenum.

● By the 32nd day, the ventral pancreatic bud emerges near the base of the
hepatic diverticulum.

● Around the 37th day, these two buds approximate and ultimately merge
by the end of the sixth week of embryonic life.

Original (Plagiarized):
Week 6: The ventral bud gives rise to the head of the pancreas and uncinate
process.
Week 6: Fusion of the pancreatic ducts occurs.
Rewritten: By the sixth week of gestation, the ventral pancreatic bud develops
into the pancreatic head and the uncinate process. During this period, the ductal
systems of the dorsal and ventral buds also undergo fusion, forming a unified
ductal network.

Original (Plagiarized):
Week 6: The main pancreatic duct (duct of Wirsung) is formed from the ventral
duct and the distal portion of the dorsal duct.
Week 6: The proximal section of the dorsal duct contributes to the formation of
the accessory pancreatic duct (duct of Santorini).
Rewritten: The main pancreatic duct, also known as the duct of Wirsung, is
established during the sixth week, primarily from the ventral duct and the distal
segment of the dorsal duct. The proximal portion of the dorsal duct persists as
the accessory pancreatic duct, referred to as the duct of Santorini.

Original (Plagiarized):
Month 3: Acinar cells, responsible for exocrine function, begin to develop.
Months 3-4: Islets of Langerhans differentiate and become functionally active.
Rewritten: By the third month of gestation, acinar cells begin to form,
contributing to the pancreas's exocrine capacity. Between the third and fourth
months, the endocrine component matures, with the differentiation of the islets
of Langerhans and the commencement of their hormonal activity.

Original (Plagiarized):
Approximately 80-90% of the pancreas consists of exocrine tissue, which plays a
vital role in enzyme secretion for digestion.
Rewritten: The majority of the pancreas, nearly 80–90%, is made up of exocrine
tissue, which is essential for the production and release of digestive enzymes.

Chapter 1 plagiarized sections fully rewritten.

Shall I proceed to Chapter 2: Anatomy of the Pancreas next?
Once you approve, I’ll start immediately.
You said:
Thanks . Please proceed to Chapter 2 : Anatomy of the Pancreas
ChatGPT said:
Excellent! I have now completed rewriting the plagiarized sections from
Chapter 2: Anatomy of the Pancreas based on your Turnitin report.

Rewritten Content – Chapter 2 (Plagiarized Sections)

Original (Plagiarized):
The term “pancreas” is derived from Greek, where “pan” means “all” and
“kreas” means “flesh.” This soft, lobulated, grayish-pink gland measures
approximately 12-15 cm in length and weighs around 80 grams. Positioned
posterior to the stomach at the level of the second lumbar vertebra (L2), the
pancreas is primarily retroperitoneal, except for its anterior surface, which is
covered by peritoneum and contributes to the floor of the lesser sac. It has a
close anatomical relationship with the second part of the duodenum, sharing a
common blood supply.
Rewritten: The word “pancreas” is derived from Greek, combining “pan” (all)
and “kreas” (flesh). Anatomically, it is a soft, lobulated gland with a grayish-pink
appearance, measuring about 12 to 15 cm in length and weighing approximately
80 grams. It is situated behind the stomach at the level of the L2 vertebra. The
pancreas lies predominantly in the retroperitoneal space, with the exception of
its anterior surface, which is peritoneal and forms the floor of the lesser sac. It is
closely related to the second segment of the duodenum, with which it shares
vascular connections.

Original (Plagiarized):
Structurally, the pancreas is divided into four main parts: Head, Neck, Body, Tail
Rewritten: The pancreas is structurally categorized into four distinct regions:
the head, neck, body, and tail.

Original (Plagiarized - Head description):

The largest part of the pancreas, located within the C-shaped curve of the
duodenum. The superior (anterior) aspect is in contact with the antrum of the
stomach and the first part of the duodenum. The right lateral border is adjacent
to the second portion of the duodenum, while the left lateral border extends to
the neck of the pancreas. The inferior border is in contact with the third part of
the duodenum. The anterior surface forms the floor of the lesser sac. The
uncinate process, an extension of the head, lies posteromedial to the main
pancreatic head and originates from the ventral pancreatic bud.
Rewritten: The pancreatic head is the most prominent part, nestled within the
C-shaped curvature of the duodenum. Its anterior surface lies close to the
stomach’s antrum and the proximal duodenum. Laterally, it is bounded on the
right by the second part of the duodenum and on the left by the pancreatic neck.
Its lower border is associated with the third part of the duodenum, while its
anterior aspect helps form the floor of the lesser sac. Additionally, the uncinate
process, an extension of the head, lies posterior and medial to the head and
develops from the ventral pancreatic bud.

Original (Plagiarized - Neck, Body, Tail descriptions):

The smallest segment of the pancreas, measuring 1.5 to 2 cm in length. Located
directly over the portal vein and superior mesenteric vessels.
Body: Extends leftward from the neck. The splenic artery runs along its superior
border. The anterior surface contributes to the floor of the lesser sac. The splenic
vein runs posteriorly along the body.
Tail: The most mobile part of the pancreas, extending toward the splenic hilum.
Lies within the lienorenal (splenorenal) ligament, along with the splenic vessels.
Rewritten: The neck is the narrowest part of the pancreas, approximately 1.5 to
2 cm long, and is positioned anterior to the portal vein and the superior
mesenteric vessels.
The body stretches to the left from the neck and is accompanied superiorly by
the splenic artery. Its anterior surface forms part of the floor of the lesser sac,
while the splenic vein courses behind it.
The tail is the most flexible segment of the pancreas, extending toward the hilum
of the spleen. It resides within the lienorenal ligament, alongside the splenic
vessels.

Chapter 2 plagiarized sections rewritten.

Shall I proceed to Chapter 3: Pancreatic Ducts next?
Once you confirm, I’ll start immediately.
You said:
yes please proceed to Chapter 3: Pancreatic Ducts
ChatGPT said:
Perfect! I have now rewritten the plagiarized sections from Chapter 3:
Pancreatic Ducts based on your Turnitin report.

Rewritten Content – Chapter 3 (Plagiarized Sections)

Original (Plagiarized):
The pancreas contains two primary ducts:
1. Main Pancreatic Duct (Duct of Wirsung) Originates in the tail of the
pancreas and extends toward the head, running through the posterior
third of the gland, equidistant from the superior and inferior borders. In a
normal pancreas, its diameter measures approximately 2.4 mm in the tail,
3.5 mm in the neck, and 4.8 mm in the head. Receives input from 15 to 20
tributaries. After passing the neck of the pancreas, it takes a posterior
course and merges with the common bile duct. Both ducts terminate at
the major duodenal papilla.
Rewritten: The pancreatic ductal system consists primarily of two ducts:
1. Main Pancreatic Duct (Duct of Wirsung):
This duct begins in the tail region and courses towards the head of the
pancreas. It passes through the posterior third of the gland, positioned
midway between its superior and inferior borders. Typically, its diameter
measures about 2.4 mm in the tail, 3.5 mm in the neck, and increases to
approximately 4.8 mm in the head. It is joined by around 15 to 20 smaller
tributary ducts. After crossing the pancreatic neck, it turns posteriorly to
unite with the common bile duct, and both open together at the major
duodenal papilla.

Original (Plagiarized):
2. Accessory Pancreatic Duct (Duct of Santorini) Primarily drains the anterior
superior portion of the pancreatic head. Typically empties into the minor
duodenal papilla (70% of cases) or may connect with the main pancreatic duct.
Rewritten: 2. Accessory Pancreatic Duct (Duct of Santorini):
This secondary duct predominantly drains the anterior and superior part of the
pancreatic head. In most individuals (about 70%), it empties separately into the
duodenum via the minor duodenal papilla, though in some cases, it may
communicate with the main pancreatic duct.

Original (Plagiarized):
The ampulla of Vater is the dilated distal portion of the pancreaticobiliary
confluence, located below the junction of the common bile duct and the main
pancreatic duct. It forms only when these ducts merge sufficiently far from the
papilla. The normal maximum diameter of the ampulla is approximately 3 to 4.5
mm near its termination in the duodenum.
Rewritten: The ampulla of Vater refers to the expanded terminal segment
where the main pancreatic duct and the common bile duct converge, situated
just below their point of union. It is present when the ducts join at a considerable
distance from the duodenal opening. Its typical diameter ranges between 3 to
4.5 mm at the point where it enters the duodenum.

Original (Plagiarized):
The sphincter of Oddi is a multisphincteric structure, consisting of four sphincters
collectively known as the sphincter of Boyden:
1. Superior choledochal sphincter – controls bile flow in the upper bile duct.
2. Inferior choledochal sphincter – regulates bile passage at the lower bile
duct.
3. Ampullary sphincter – surrounds the ampulla of Vater.
4. Pancreatic sphincter – controls the outflow of pancreatic secretions.
Rewritten: The sphincter of Oddi is a complex muscular structure comprising
four individual sphincters, collectively referred to as the sphincter of Boyden.
These include:
1. The superior choledochal sphincter, which manages bile flow through the
upper bile duct.
2. The inferior choledochal sphincter, responsible for regulating bile passage
in the lower segment of the bile duct.
3. The ampullary sphincter, encircling the ampulla of Vater.
4. The pancreatic sphincter, which modulates the discharge of pancreatic
juices.

Original (Plagiarized):
The major duodenal papilla (papilla of Vater) is located on the posteromedial wall
of the second portion of the duodenum and, in rare cases, the third portion. The
minor duodenal papilla drains the accessory pancreatic duct (Santorini) and is
typically positioned 2 cm cranial and anterior to the major papilla. The minor
papilla is always located distal to the crossing point of the gastroduodenal artery
behind the duodenum.
Rewritten: The major duodenal papilla, also known as the papilla of Vater, is
situated on the posteromedial aspect of the second part of the duodenum and,
infrequently, in the third part. The minor papilla, which drains the accessory
pancreatic duct (duct of Santorini), is usually located about 2 cm above and
anterior to the major papilla. Additionally, the minor papilla lies distal to the point
where the gastroduodenal artery crosses behind the duodenum.

Chapter 3 plagiarized sections fully rewritten.

Shall I proceed to Chapter 4: Arterial Supply, Venous Drainage &
Lymphatic Drainage next?
Please confirm.
You said:
please proceed to Chapter 4: Arterial Supply, Venous Drainage & Lymphatic
Drainage
ChatGPT said:
Thank you for the confirmation. I have now rewritten the plagiarized sections
from Chapter 4: Arterial Supply, Venous Drainage & Lymphatic Drainage
based on your Turnitin report.

Rewritten Content – Chapter 4 (Plagiarized Sections)

Original (Plagiarized):
The pancreas receives a dual blood supply from the celiac trunk and the superior
mesenteric artery (SMA). The gastroduodenal artery (GDA) arises from the
proper hepatic artery, which is a branch of the celiac trunk. The GDA gives rise to
the superior pancreaticoduodenal arteries, which include: Anterior superior
pancreaticoduodenal artery Posterior superior pancreaticoduodenal artery These
arteries anastomose with the inferior pancreaticoduodenal arteries (anterior and
posterior), which originate from the superior mesenteric artery (SMA). This
vascular network supplies the head of the pancreas, uncinate process, and a
portion of the duodenum.
Rewritten: The pancreas derives its arterial blood supply primarily from two
sources: the celiac trunk and the superior mesenteric artery (SMA). The
gastroduodenal artery (GDA), which branches from the proper hepatic artery of
the celiac trunk, contributes to this supply. The GDA further divides into the
anterior and posterior superior pancreaticoduodenal arteries. These vessels
establish connections with the anterior and posterior inferior
pancreaticoduodenal arteries, branches of the SMA. This interconnected vascular
network is responsible for perfusing the pancreatic head, the uncinate process,
and adjacent portions of the duodenum.

Original (Plagiarized):
The veins of the pancreas generally follow the course of the arteries, ultimately
draining into the portal venous system via the superior mesenteric vein (SMV),
inferior mesenteric vein (IMV), and splenic vein. The head and uncinate process
are drained by four pancreaticoduodenal veins, which form an anastomotic
network: Anterior superior pancreaticoduodenal vein → drains into the right
gastroepiploic vein, which then empties into the superior mesenteric vein (SMV).
Posterior superior pancreaticoduodenal vein → drains directly into the portal
vein. Inferior anterior pancreaticoduodenal vein → empties into the SMV. Inferior
posterior pancreaticoduodenal vein → also drains into the SMV. The body and tail
of the pancreas are drained by the splenic vein and the transverse pancreatic
vein, which ultimately contribute to the portal venous system.
Rewritten: The venous return from the pancreas largely mirrors its arterial
pathways and eventually drains into the portal venous system through the
superior mesenteric vein (SMV), inferior mesenteric vein (IMV), and the splenic
vein. The head and uncinate process of the pancreas are served by four
pancreaticoduodenal veins forming an anastomotic plexus:

● The anterior superior pancreaticoduodenal vein drains into the right

gastroepiploic vein, which subsequently joins the SMV.

● The posterior superior pancreaticoduodenal vein empties directly into the

portal vein.

● The anterior inferior pancreaticoduodenal vein and the posterior inferior

pancreaticoduodenal vein both drain into the SMV. The venous outflow
from the body and tail of the pancreas occurs via the splenic vein and the
transverse pancreatic vein, all of which ultimately join the portal venous
system.

Original (Plagiarized):
The lymphatic drainage of the pancreas is directed toward five groups of lymph
nodes:
1. Superior Pancreatic Nodes – Drain the anterior and posterior aspects of
the pancreas.
2. Inferior Pancreatic Nodes – Collect lymph from the anterior and posterior
portions of the head and body.
3. Anterior Collecting Trunks – Run along the anterior surface of the
pancreatic head and drain into the infrapyloric and anterior
pancreaticoduodenal lymph nodes.
 4. Posterior Collecting Trunks – Mirror the anterior system on the posterior
surface, emptying into the corresponding posterior pancreaticoduodenal
lymph nodes.
5. Splenic and Splenic Hilar Nodes – Drain the tail of the pancreas, with
lymph flowing into the superior and inferior splenic lymph nodes.
Rewritten: Lymphatic drainage from the pancreas is directed to five principal
groups of lymph nodes:
1. Superior Pancreatic Nodes: Responsible for draining lymph from both
the anterior and posterior surfaces of the pancreas.
2. Inferior Pancreatic Nodes: Collect lymphatic fluid from the head and
body, covering both their anterior and posterior aspects.
3. Anterior Collecting Trunks: Positioned on the anterior surface of the
pancreatic head, these trunks drain into the infrapyloric and anterior
pancreaticoduodenal lymph nodes.
4. Posterior Collecting Trunks: These follow a similar path on the
posterior surface, draining into the posterior pancreaticoduodenal lymph
nodes.
5. Splenic and Splenic Hilar Nodes: These nodes receive lymph from the
tail of the pancreas, channeling it into the superior and inferior splenic
lymph node groups.

Chapter 4 plagiarized sections fully rewritten.

Shall I proceed to Chapter 5: Nervous Supply & Etiology of Acute
Pancreatitis next?
Please confirm.
You said:
please proceed to Chapter 5: Nervous Supply & Etiology of Acute Pancreatitis
ChatGPT said:
Thank you! I have now completed rewriting the plagiarized sections from
Chapter 5: Nervous Supply & Etiology of Acute Pancreatitis based on your
Turnitin report.

Rewritten Content – Chapter 5 (Plagiarized Sections)

🔹 Nervous Supply of Pancreas

Original (Plagiarized):
The pancreas receives both sympathetic and parasympathetic innervation:
Sympathetic fibers originate from the splanchnic nerves, which regulate
vasoconstriction and modulate pain sensation. Parasympathetic fibers arise from
the vagus nerve, primarily stimulating exocrine and endocrine secretions.
Rewritten: The innervation of the pancreas involves both sympathetic and
parasympathetic components. Sympathetic input is provided by the splanchnic
nerves, which primarily mediate vasoconstriction and influence pain perception.
Parasympathetic innervation is supplied by the vagus nerve, facilitating the
stimulation of both exocrine and endocrine pancreatic functions.

🔹 Etiology of Acute Pancreatitis (AP)

Original (Plagiarized):
Acute pancreatitis (AP) can be classified based on etiology, pathology, and
severity. In 10-20% of cases, no clear cause is identified. Some of these cases
may be due to microlithiasis or sphincter of Oddi dysfunction (SOD). Additionally,
genetic polymorphisms in inflammatory mediators may influence the severity of
the disease.
Rewritten: Acute pancreatitis (AP) is categorized based on its underlying cause,
pathological changes, and clinical severity. In about 10–20% of cases, no specific
etiology can be established. Some of these idiopathic cases may result from
microlithiasis or functional abnormalities like sphincter of Oddi dysfunction
(SOD). Moreover, variations in genes related to inflammatory mediators may
impact disease severity.

Original (Plagiarized):
Clinical Classification of AP:
1. Mild AP – The most common form, characterized by interstitial edema,
minimal or transient organ dysfunction, and uneventful recovery.
2. Severe AP (SAP) – Associated with organ failure or local complications such
as pancreatic necrosis, abscesses, or pseudocysts. Around 10-20% of
cases develop SAP.
Rewritten: Clinically, AP is classified as follows:
1. Mild Acute Pancreatitis: This is the predominant form, typically
presenting with interstitial edema and minimal or short-lived organ
dysfunction, leading to full recovery without complications.
2. Severe Acute Pancreatitis (SAP): This form involves persistent organ
failure and/or local complications like necrosis, abscess formation, or
pseudocyst development. Approximately 10–20% of patients progress to
SAP.

Original (Plagiarized):
Several scoring systems and biochemical markers help predict the severity of AP.
Rewritten: Multiple scoring systems, along with various biochemical markers,
are utilized to anticipate the severity of acute pancreatitis.
Original (Plagiarized):
Pancreatic Necrosis – A Key Predictor of Outcome Pancreatic necrosis refers to
areas of non-viable pancreatic tissue accompanied by peri-pancreatic fat
necrosis, visible as non-enhanced regions on contrast-enhanced CT (CECT). The
degree of necrosis correlates with morbidity and mortality. 30% of patients with
pancreatic necrosis develop infected necrosis, with a mortality rate of 6-40% and
morbidity exceeding 80%.
Rewritten: Pancreatic Necrosis – Important Prognostic Indicator:
Pancreatic necrosis involves the death of pancreatic tissue, often associated with
fat necrosis around the pancreas. On contrast-enhanced computed tomography
(CECT), necrotic areas appear as non-enhancing zones. The extent of necrosis is
directly linked to the risk of complications and mortality. In approximately 30% of
affected patients, secondary infection of necrotic tissue occurs, leading to a
mortality rate ranging from 6% to 40%, with morbidity exceeding 80%.

Chapter 5 plagiarized sections fully rewritten.

Shall I proceed to Chapter 6: Specific Causes of Acute Pancreatitis next?
Please confirm.
You said:
please proceed to Chapter 6: Specific Causes of Acute Pancreatitis
ChatGPT said:
Thank you for your confirmation. I have now completed rewriting the
plagiarized sections from Chapter 6: Specific Causes of Acute
Pancreatitis based on your Turnitin report.

Rewritten Content – Chapter 6 (Plagiarized Sections)

1. Gallstones
Original (Plagiarized):
Although gallstones are common, only 3-7% of patients with gallstones develop
AP. Women are more affected due to the higher prevalence of cholelithiasis.
Smaller stones (<5mm) are more likely to cause pancreatitis by obstructing the
ampulla of Vater. In most cases, stones pass into the duodenum spontaneously.
Serum ALT >150 IU/L has 96% specificity and 50% sensitivity for diagnosing
gallstone pancreatitis.
Rewritten: Despite the high prevalence of gallstones in the general population,
only about 3% to 7% of individuals with gallstones experience acute pancreatitis.
The incidence is higher among females, reflecting the greater occurrence of
gallstone disease in women. Smaller gallstones, particularly those less than 5
mm in size, have a greater tendency to lodge in the ampulla of Vater, triggering
pancreatitis. Typically, these stones migrate spontaneously into the duodenum.
An elevation in serum alanine transaminase (ALT) exceeding 150 IU/L is highly
specific (96%) but moderately sensitive (50%) for the diagnosis of gallstone-
induced pancreatitis.

Original (Plagiarized):
Diagnosis: Elevated liver transaminases and pancreatic enzymes combined with
gallstones on ultrasound have 97% sensitivity and 100% specificity for biliary
pancreatitis. Treatment: ERCP may be required in some cases. Cholecystectomy
is recommended to prevent recurrence.
Rewritten: Diagnosis:
The presence of elevated liver enzymes along with increased pancreatic enzyme
levels, when observed alongside gallstones detected on ultrasonography, yields
a sensitivity of 97% and specificity of 100% for biliary pancreatitis.
Management:
Endoscopic retrograde cholangiopancreatography (ERCP) may be necessary in
selected cases. Additionally, cholecystectomy is advised to reduce the risk of
recurrent episodes.

2. Alcohol
Original (Plagiarized):
Despite high alcohol consumption, only 5-10% of chronic alcoholics develop AP,
suggesting genetic or environmental factors play a role.
Rewritten: Although alcohol abuse is a known risk factor, only 5% to 10% of
individuals who consume alcohol excessively develop acute pancreatitis. This
observation implies that other factors, including genetic susceptibility or
environmental influences, may contribute to disease development.

Original (Plagiarized):
Mechanisms of Alcohol-Induced AP: Sphincter of Oddi spasm Obstruction of small
pancreatic ducts by protein plugs Direct toxicity of alcohol and its metabolites
Inflammatory pathways (e.g., NF-κB activation, TNF-α, and IL-1 production)
Increased protein content in pancreatic juice, leading to ductal obstruction
Increased pancreatic ductal permeability, allowing premature enzyme activation
Apoptosis mediated by caspases Reduced pancreatic blood flow
Rewritten: The mechanisms underlying alcohol-induced acute pancreatitis
include:

● Spasm of the sphincter of Oddi

● Obstruction of small pancreatic ducts due to proteinaceous plugs

 ● Direct cytotoxic effects of alcohol and its metabolic by-products

● Activation of inflammatory pathways such as nuclear factor kappa B (NF-

κB), tumor necrosis factor-alpha (TNF-α), and interleukin-1 (IL-1)

● Increased protein concentration in pancreatic secretions leading to ductal

blockage

● Enhanced permeability of pancreatic ducts resulting in premature enzyme

activation

● Induction of acinar cell apoptosis via caspase pathways

● Diminished pancreatic blood flow

Original (Plagiarized):
Risk Factors: Heavy alcohol use (>100 g/day for at least 5 years) Smoking
(increases risk 4.9 times compared to non-smokers) Genetic predisposition
Rewritten: Predisposing Factors:

● Chronic and excessive alcohol intake exceeding 100 grams per day over a
period of at least five years

● Cigarette smoking, which elevates the risk by approximately 4.9 times

compared to non-smokers

● Underlying genetic vulnerability

Original (Plagiarized):
Management: Cessation of alcohol reduces recurrence risk. Continued alcohol
abuse increases the likelihood of recurrent acute pancreatitis (RAP) and chronic
pancreatitis (CP).
Rewritten: Management:
Abstinence from alcohol significantly lowers the chance of recurrent pancreatitis
episodes. Persistent alcohol consumption, however, increases the likelihood of
both recurrent acute pancreatitis and progression to chronic pancreatitis.

3. Hypertriglyceridemia
Original (Plagiarized):
Triglyceride levels >1000 mg/dL significantly increase the risk of AP.
Management: Plasmapheresis for severe cases (>1000 mg/dL). Fibrates, dietary
modifications, and treatment of the primary cause.
Rewritten: Triglyceride concentrations exceeding 1000 mg/dL are associated
with a markedly increased risk of developing acute pancreatitis.
Management:
In severe cases where triglyceride levels exceed 1000 mg/dL, therapeutic
plasmapheresis may be indicated. Long-term management involves the use of
fibrates, adherence to dietary modifications, and addressing any underlying
contributing conditions.

4. Drug-Induced Pancreatitis
Original (Plagiarized):
Management: Discontinuation of the offending drug.
Rewritten: Management:
The primary approach to managing drug-induced pancreatitis is the immediate
cessation of the suspected medication.

5. ERCP-Induced Pancreatitis
Original (Plagiarized):
Most common complication of ERCP. Asymptomatic hyperamylasemia occurs in
35-70% of ERCP cases. Post-ERCP pancreatitis (PEP) rates: 5% in diagnostic
ERCPs 7% in therapeutic ERCPs Up to 25% in patients with suspected SOD or
prior PEP
Rewritten: The most frequent complication associated with ERCP is acute
pancreatitis. Elevated serum amylase levels without clinical symptoms
(asymptomatic hyperamylasemia) can occur in 35% to 70% of ERCP procedures.
The incidence of post-ERCP pancreatitis (PEP) varies, affecting approximately 5%
of patients undergoing diagnostic ERCP, 7% of those receiving therapeutic
interventions, and up to 25% of individuals with suspected sphincter of Oddi
dysfunction or a prior history of PEP.

6. Structural Abnormalities
Original (Plagiarized):
Conditions that obstruct the pancreatic duct, leading to recurrent AP: Sphincter
of Oddi dysfunction (SOD) Pancreas divisum (failure of dorsal and ventral
pancreatic bud fusion) Benign/malignant pancreatic duct strictures Intraductal
papillary mucinous neoplasms (IPMNs)
Rewritten: Certain structural anomalies that impede the flow of pancreatic
secretions can precipitate recurrent acute pancreatitis. These include:
 ● Dysfunction of the sphincter of Oddi

● Pancreas divisum, resulting from incomplete fusion of the dorsal and

ventral pancreatic buds

● Benign or malignant strictures of the pancreatic duct

● Intraductal papillary mucinous neoplasms (IPMNs)

Original (Plagiarized):
SOD diagnosed via pressure measurement during ERCP. Pancreas divisum is
usually asymptomatic but may contribute to AP. Surgical or endoscopic
sphincterotomy may help prevent recurrent AP.
Rewritten: Sphincter of Oddi dysfunction can be identified through pressure
measurements taken during ERCP. Pancreas divisum often remains clinically
silent but can predispose to episodes of acute pancreatitis. In select cases,
surgical or endoscopic sphincterotomy may be considered to reduce the risk of
recurrent attacks.

7. Other Causes
Original (Plagiarized):
Trauma – A leading cause of AP in children. Autoimmune Pancreatitis –
Associated with IgG4-related disease. Infections – Common in children.
Peripancreatic Vascular Insufficiency – Can lead to ischemic AP.
Rewritten: Additional causes of acute pancreatitis include:

● Trauma: A prominent cause of AP in pediatric patients

● Autoimmune Pancreatitis: Often linked to IgG4-related systemic

disease

● Infectious Agents: Particularly relevant in children

● Peripancreatic Vascular Insufficiency: Can result in ischemic injury to

pancreatic tissue, precipitating pancreatitis

8. Idiopathic Pancreatitis
Original (Plagiarized):
Diagnosed when no specific cause is found despite extensive workup (CT, MRCP,
EUS). Smoking is an independent risk factor for AP.
Rewritten: A diagnosis of idiopathic pancreatitis is made when no definitive
cause is identified, even after comprehensive evaluation including imaging
modalities like CT, MRCP, and EUS. Additionally, smoking has been recognized as
an independent risk factor for the development of acute pancreatitis.

Chapter 6 plagiarized sections fully rewritten.

Shall I proceed to Chapter 7: Pathophysiology of Acute Pancreatitis next?
Please confirm.
You said:
please proceed to Chapter 7: Pathophysiology of Acute Pancreatitis
ChatGPT said:
Thank you for the confirmation. I have now completed rewriting the plagiarized
sections from Chapter 7: Pathophysiology of Acute Pancreatitis based on
your Turnitin report.

Rewritten Content – Chapter 7 (Plagiarized Sections)

Original (Plagiarized):
Various degrees of severity occurs in acute pancreatitis, whose determinants are
multifactorial. The studies suggest that pancreatitis begins with the activation of
digestive zymogens inside acinar cells, which cause acinar cell injury and the
ultimate severity of the resulting pancreatitis may be determined by the events
that occur subsequent to acinar cell injury.
Rewritten: Acute pancreatitis manifests with varying severity, influenced by
multiple factors. Research indicates that the disease process is initiated by the
premature activation of digestive enzymes, or zymogens, within the pancreatic
acinar cells. This leads to cellular injury, and the progression and severity of the
condition are determined by the subsequent cascade of inflammatory and
cellular events that follow this initial damage.

Original (Plagiarized):
The processes occurring within the pancreas play a critical role in the
development of systemic inflammation and multi-organ failure in acute
pancreatitis (AP). One of the key mechanisms involved is the NFκB-dependent
inflammatory pathway. NFκB activation occurs alongside trypsin activation in AP,
but studies in trypsin knockout mice suggest it can occur independently. A
sustained increase in intracellular calcium levels is essential for trypsinogen
activation, which in turn is required for NFκB activation, as reducing cytosolic
calcium prevents NFκB activation. Once activated, NFκB stimulates the
production of various cytokines and chemokines, attracting inflammatory cells
and worsening systemic inflammation.
Rewritten: The intra-pancreatic events are pivotal in triggering systemic
inflammatory responses and potential multi-organ failure in acute pancreatitis. A
key contributor to this process is the activation of the NF-κB inflammatory
pathway. Although NF-κB activation often coincides with the activation of trypsin,
experimental evidence from trypsinogen-deficient mice has shown that NF-κB
can be activated independently. An increase in intracellular calcium levels is
crucial for the activation of trypsinogen, which subsequently facilitates NF-κB
activation. Inhibition of cytosolic calcium elevation has been observed to prevent
NF-κB activation. Once activated, NF-κB promotes the synthesis of pro-
inflammatory cytokines and chemokines, which recruit inflammatory cells and
exacerbate systemic inflammation.

Original (Plagiarized):
Additionally, neutrophil infiltration exacerbates pancreatic injury. Although
experimental models have shown that inhibiting cytokine activity can reduce
both local and systemic damage, these findings have not yet translated into
significant clinical improvements. This highlights the need for novel therapeutic
strategies to mitigate the systemic inflammatory response.
Rewritten: Neutrophil infiltration further aggravates pancreatic tissue injury.
While experimental studies suggest that suppressing cytokine activity can lessen
both local and systemic inflammatory damage, these promising results have yet
to yield significant clinical benefits. This underscores the necessity of developing
new therapeutic interventions aimed at controlling the systemic inflammatory
response associated with acute pancreatitis.

Original (Plagiarized):
Organ failure in AP can arise at any stage, either early, due to an excessive pro-
inflammatory response, or later, as a consequence of local complications. The
exact mechanisms behind this systemic response remain unclear, though it is
believed that pro-inflammatory cytokines and mesenteric lymph, bypassing the
liver and carrying inflammatory mediators, may play a role. Furthermore,
intestinal barrier disruption and immune suppression contribute to the risk of
infected pancreatic necrosis, which typically peaks between the third and fourth
week of illness. The progression of the disease may lead to systemic
inflammatory response syndrome (SIRS) and multi-organ dysfunction syndrome
(MODS), resulting in a critical deterioration of the patient’s condition.
Rewritten: In acute pancreatitis, organ failure may develop at any point during
the illness, either during the early phase due to an overwhelming pro-
inflammatory reaction or later as a result of local complications. Although the
precise mechanisms underlying this systemic response are not fully understood,
it is believed that circulating pro-inflammatory cytokines and mesenteric lymph
carrying inflammatory mediators contribute to its development. Additionally,
disruption of the intestinal barrier and suppression of immune defenses increase
the risk of secondary infection of pancreatic necrosis, which commonly peaks
during the third to fourth weeks of illness. The disease may progress to systemic
inflammatory response syndrome (SIRS) and ultimately lead to multi-organ
dysfunction syndrome (MODS), causing significant clinical deterioration.

Original (Plagiarized):
The concept of auto-digestion due to intrapancreatic activation of digestive
enzymes was first proposed by Chiari in 1896 and remains a widely accepted
mechanism. Experimental studies confirm that zymogen activation within acinar
cells is a central event in AP. Recent research supports the pivotal role of trypsin
activation, with evidence showing that mice lacking trypsinogen-7 experience
significantly less pancreatic injury during AP. Additionally, the intra-acinar
expression of active trypsin induces pancreatitis in animal models. Clinical
studies further reinforce this concept, as hereditary pancreatitis is often linked to
mutations that lead to increased intracellular trypsin activity, which
subsequently triggers AP.
Rewritten: The theory of pancreatic auto-digestion, proposed by Chiari in 1896,
remains a widely recognized explanation for acute pancreatitis. This theory is
supported by experimental evidence indicating that the activation of digestive
zymogens within acinar cells is a central event in the disease process. Recent
studies have emphasized the critical role of trypsin activation; for instance,
animal models lacking trypsinogen-7 exhibit significantly reduced pancreatic
injury following induction of pancreatitis. Furthermore, experimental expression
of active trypsin within acinar cells has been shown to cause pancreatitis. Clinical
data also support this mechanism, with hereditary pancreatitis frequently
associated with genetic mutations that increase intracellular trypsin activity,
thereby predisposing individuals to acute pancreatitis.

Chapter 7 plagiarized sections fully rewritten.

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Pancreatitis next?
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proceed to Chapter 8: Importance of Severity Assessment in Acute Pancre
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Thank you for your confirmation. I have now completed rewriting the
plagiarized sections from Chapter 8: Importance of Severity Assessment
in Acute Pancreatitis based on your Turnitin report.

Rewritten Content – Chapter 8 (Plagiarized Sections)

Original (Plagiarized):
Early identification of high-risk patients is essential for optimizing management
and improving outcomes in AP. Therefore, a reliable risk stratification tool is
crucial for predicting disease severity and prognosis.
Rewritten: Prompt recognition of patients at high risk for severe acute
pancreatitis is vital to guide appropriate management and improve clinical
outcomes. Hence, an effective and reliable system for stratifying risk is
necessary to predict the severity and likely course of the disease.

Original (Plagiarized):
An ideal scoring system should provide a rapid, simple, accurate, and
reproducible assessment of disease severity. The first attempt at such a system
was made in 1974 by Ranson and colleagues, who introduced a severity scoring
method for AP. Since then, various scoring systems have been developed,
including Ranson’s criteria, the Acute Physiology and Chronic Health Evaluation
(APACHE) II, the Modified Glasgow Score, and the Computed Tomography
Severity Index (CTSI). However, each system has distinct advantages and
limitations.
Rewritten: A suitable scoring system should ideally be quick, straightforward,
precise, and reproducible in assessing the severity of acute pancreatitis. The first
such system was introduced in 1974 by Ranson and his team. Since then, several
other systems have been formulated, including Ranson’s criteria, the Acute
Physiology and Chronic Health Evaluation II (APACHE II), the Modified Glasgow
score, and the Computed Tomography Severity Index (CTSI). Each of these
scoring tools has its unique benefits and drawbacks.

Original (Plagiarized):
1. Ranson’s and Modified Glasgow Scores rely on clinical and laboratory
parameters, some of which are not routinely collected at admission.
Furthermore, both scoring systems require 48 hours for completion,
potentially missing a critical early therapeutic window.
Rewritten: The Ranson and Modified Glasgow scoring systems depend on a
combination of clinical findings and laboratory results, some of which may not be
immediately available upon patient admission. Additionally, these systems
require a 48-hour observation period to complete, which can delay early
decision-making and intervention.

Original (Plagiarized):
2. APACHE II, initially developed for intensive care unit (ICU) patients, allows
early severity assessment but involves multiple variables, some of which may
not be relevant for AP prognosis. Additionally, its complexity limits routine
clinical use.
Rewritten: The APACHE II score, originally designed for use in intensive care
settings, facilitates early assessment of disease severity. However, it involves
the evaluation of numerous variables, not all of which are directly related to
acute pancreatitis prognosis. Its complexity also limits its routine use in standard
clinical practice.

Original (Plagiarized):
3. CTSI, based on radiological findings, is useful for assessing local pancreatic
complications but does not reflect systemic inflammatory response.
Rewritten: The CTSI system, which relies on radiological imaging, is helpful in
evaluating local complications associated with pancreatitis. However, it does not
provide insight into the systemic inflammatory response triggered by the
disease.

Original (Plagiarized):
Balthazar Computed Tomography Grading System This grading system is used in
CTSI to assess the extent of pancreatic inflammation and fluid collection: Grade
A: Normal pancreas Grade B: Pancreatic enlargement Grade C: Pancreatic and
peripancreatic fat inflammation Grade D: Single peripancreatic fluid collection
(within the anterior pararenal space) Grade E: Multiple peripancreatic fluid
collections or the presence of gas
Rewritten: Balthazar Computed Tomography Grading System:
This classification, used as part of the CTSI, evaluates the severity of pancreatic
inflammation and the presence of fluid collections on imaging:

● Grade A: Normal pancreatic appearance

● Grade B: Enlargement of the pancreas

● Grade C: Inflammatory changes in the pancreas and surrounding fat

● Grade D: Presence of a single fluid collection near the pancreas (anterior

pararenal space)

● Grade E: Multiple fluid collections or detection of gas within or around the

pancreas

Rewritten Content – Chapter 9 (Plagiarized Sections)

Original (Plagiarized):
Apart from scoring systems, certain biochemical markers can help assess AP
severity:
1. C-Reactive Protein (CRP): Peaks 48–72 hours after onset; levels ≥150 mg/L
indicate severe AP. However, it cannot be used at admission due to
delayed elevation.
 2. Hematocrit (Hct): A high admission Hct (≥44%) and failure to decrease
after IV fluid administration suggest a higher risk of pancreatic necrosis.
3. Blood Urea Nitrogen (BUN) and Creatinine: BUN >20 mg/dL at admission
or a rising trend within 24 hours is linked to poor prognosis. Creatinine
elevation within 48 hours is associated with worse outcomes and
pancreatic necrosis.
Rewritten: In addition to clinical scoring systems, several biochemical markers
have been identified to aid in predicting the severity of acute pancreatitis:
1. C-Reactive Protein (CRP): This acute-phase reactant typically peaks 48
to 72 hours after the onset of symptoms. CRP levels equal to or greater
than 150 mg/L are indicative of severe pancreatitis. However, it is not
useful as an early marker because its elevation is delayed.
2. Hematocrit (Hct): An elevated hematocrit value (≥44%) upon admission,
coupled with the failure of this value to decrease following intravenous
fluid therapy, has been associated with an increased risk of pancreatic
necrosis.
3. Blood Urea Nitrogen (BUN) and Serum Creatinine: A BUN level
exceeding 20 mg/dL at the time of admission, or an upward trend during
the first 24 hours, correlates with a poor clinical outcome. Similarly, a rise
in serum creatinine levels within the first 48 hours is linked to adverse
outcomes and the likelihood of developing pancreatic necrosis.

Rewritten Content – Chapter 10 (Plagiarized Sections)

🔹 Ranson’s Scoring System

Original (Plagiarized):
Developed in 1974, this was the first scoring method designed to predict AP
severity. It evaluates 11 clinical and laboratory parameters, measured at
admission and 48 hours later.
Rewritten: Introduced in 1974, Ranson’s scoring system was the earliest tool
established to estimate the severity of acute pancreatitis. It involves the
assessment of 11 clinical and laboratory variables, with some recorded upon
admission and others after 48 hours.

Original (Plagiarized):
Ranson’s Criteria for Non-Gallstone AP At Admission: Age >55 years White Blood
Cell count (WBC) >16,000/mm³ Blood Glucose >200 mg/dL AST >250 IU/L LDH
>350 IU/L After 48 Hours: Hematocrit ↓ >10% Blood Urea Nitrogen (BUN) ↑ >5
mg/dL Serum Calcium <8 mg/dL Arterial pO₂ <60 mmHg Base Deficit >4 mEq/L
Fluid Sequestration >6 L
Rewritten: The Ranson scoring criteria for non-biliary acute pancreatitis include
the following parameters:
At the time of admission:

● Age over 55 years

● White blood cell count exceeding 16,000/mm³

● Blood glucose concentration above 200 mg/dL

● Aspartate transaminase (AST) level greater than 250 IU/L

● Lactate dehydrogenase (LDH) level above 350 IU/L

During the subsequent 48 hours:

● A reduction in hematocrit by more than 10%

● An increase in blood urea nitrogen (BUN) of more than 5 mg/dL

● Serum calcium levels below 8 mg/dL

● Partial pressure of arterial oxygen (PaO₂) less than 60 mmHg

● Base deficit exceeding 4 mEq/L

● Fluid sequestration greater than 6 liters

Original (Plagiarized):
Mortality Risk Based on Ranson’s Score: 0–2 points → Mortality ~2.5% 3–4 points
→ Mortality ~15% 5–6 points → Mortality ~40%
6 points → Mortality ~60%
Rewritten: Predicted Mortality According to Ranson’s Score:

● A score of 0 to 2 points corresponds to an approximate mortality risk of

2.5%

● Scores between 3 and 4 points indicate a mortality rate of about 15%

● Scores of 5 to 6 points are associated with a 40% mortality risk

● A score greater than 6 points signifies a mortality risk approaching 60%

Original (Plagiarized):
Limitations of Ranson’s Criteria: Requires 48 hours, delaying early intervention.
Separate criteria for gallstone vs. non-gallstone pancreatitis. Complicated
Rewritten: Limitations of Ranson’s Criteria:

● The requirement to wait for 48 hours to complete the score delays early
risk assessment and treatment decisions.

● Different sets of criteria are used for gallstone-related and non-gallstone

pancreatitis, making it less universally applicable.

● The scoring system is relatively complex and time-consuming.

🔹 APACHE II Score

Original (Plagiarized):
The APACHE II (Acute Physiology and Chronic Health Evaluation II) score was
originally developed to assess the severity of illness in critically ill patients in the
ICU. It has been adapted for use in AP. The score uses 12 physiological variables,
age, and chronic health status.
Rewritten: The APACHE II (Acute Physiology and Chronic Health Evaluation II)
scoring system was initially designed to determine illness severity in intensive
care patients. It has since been adapted for evaluating acute pancreatitis. The
scoring involves 12 physiological parameters, patient age, and an assessment of
pre-existing chronic health conditions.

Original (Plagiarized):
APACHE II score >8 indicates severe AP. Advantages: Can be used at admission.
No need to wait for 48 hours. Limitations: Complex calculation. Requires multiple
variables, some not specific to AP.
Rewritten: An APACHE II score exceeding 8 suggests severe acute pancreatitis.
Advantages:

● It is applicable at the time of patient admission.

● It does not necessitate a waiting period of 48 hours.

Limitations:

● The calculation process is intricate and time-consuming.

● It includes numerous variables, many of which are not specific indicators

of acute pancreatitis severity.
🔹 Modified Glasgow Score

Original (Plagiarized):
The Modified Glasgow Score uses eight parameters measured within 48 hours of
admission. A score ≥3 indicates severe AP.
Rewritten: The Modified Glasgow scoring system evaluates eight clinical and
laboratory variables within the first 48 hours of hospital admission. A score of 3
or higher is indicative of severe acute pancreatitis.

🔹 Computed Tomography Severity Index (CTSI)

Original (Plagiarized):
CTSI is based on Balthazar grading and extent of necrosis. Limitations: Requires
contrast-enhanced CT. Cannot be used early.
Rewritten: The Computed Tomography Severity Index (CTSI) incorporates the
Balthazar grading system along with an evaluation of the extent of pancreatic
necrosis.
Limitations:

● It necessitates a contrast-enhanced CT scan.

● It is not suitable for use in the early phase of the disease.

Rewritten Content – Chapter 11 (Plagiarized Sections)

Original (Plagiarized):
Systemic inflammation is a central feature of AP, and the magnitude of this
inflammatory response correlates with disease severity. NLR is an accessible and
cost-effective inflammatory marker calculated by dividing the absolute
neutrophil count by the absolute lymphocyte count. Elevated NLR reflects
increased neutrophils and/or decreased lymphocytes, both of which are
associated with a heightened inflammatory state.
Rewritten: A hallmark of acute pancreatitis is systemic inflammation, and the
extent of this inflammatory reaction is directly related to the severity of the
disease. The neutrophil-to-lymphocyte ratio (NLR) serves as a simple and
affordable marker of inflammation. It is determined by dividing the absolute
neutrophil count by the absolute lymphocyte count. An increased NLR typically
indicates an elevated neutrophil count and/or a reduced lymphocyte count, both
of which suggest an intensified inflammatory response.
Original (Plagiarized):
Multiple studies have demonstrated a significant association between elevated
NLR and adverse outcomes in AP, including persistent organ failure, pancreatic
necrosis, and increased mortality. NLR is also a dynamic marker that can be used
to monitor disease progression and response to treatment.
Rewritten: Numerous studies have established a strong link between elevated
NLR values and poor clinical outcomes in acute pancreatitis. These include a
higher incidence of persistent organ failure, pancreatic necrosis, and increased
mortality rates. Additionally, NLR has been shown to be a dynamic marker,
useful in tracking disease progression and evaluating the patient’s response to
treatment.

Original (Plagiarized):
RDW is a routinely measured parameter in complete blood count (CBC) tests,
reflecting the variability in red blood cell size (anisocytosis). While traditionally
used to evaluate anemia, elevated RDW has been associated with inflammation,
oxidative stress, and poor outcomes in various conditions, including AP.
Rewritten: Red cell distribution width (RDW) is a standard component of the
complete blood count (CBC) test and measures the variation in red blood cell
size, a condition known as anisocytosis. Although primarily utilized in the
evaluation of anemia, elevated RDW levels have been linked to systemic
inflammation, oxidative stress, and unfavorable outcomes in several diseases,
including acute pancreatitis.

Original (Plagiarized):
Mechanistically, elevated RDW in AP may reflect increased systemic
inflammation, impaired erythropoiesis, and oxidative damage to red blood cells.
Several studies have reported that higher RDW values are associated with
severe AP, pancreatic necrosis, and increased mortality.
Rewritten: The underlying mechanism for increased RDW in acute pancreatitis
is thought to involve heightened systemic inflammation, impaired production of
red blood cells, and oxidative injury to erythrocytes. Research findings have
consistently shown that elevated RDW values correlate with severe forms of
pancreatitis, the presence of pancreatic necrosis, and higher mortality rates.

Original (Plagiarized):
Both NLR and RDW offer advantages over traditional scoring systems: Rapid,
inexpensive, and widely available No need for complex calculations Useful in
early risk stratification
Rewritten: NLR and RDW possess several advantages compared to
conventional severity scoring systems:
 ● They are quickly obtainable, cost-effective, and commonly available as
part of routine blood tests

● Their interpretation does not require complex computational methods

● They facilitate early risk stratification, allowing prompt clinical decision-

making

Rewritten Content – Chapter 12 (Plagiarized Sections)

Original (Plagiarized):
Numerous studies have explored the utility of NLR and RDW as prognostic
markers in acute pancreatitis (AP). Their ability to predict disease severity,
complications, and mortality has been consistently demonstrated.
Rewritten: Several research studies have investigated the prognostic value of
NLR and RDW in patients with acute pancreatitis. The findings consistently
support their usefulness in predicting disease severity, the likelihood of
complications, and mortality rates.

Original (Plagiarized):
Suppiah et al. (2013) analyzed 214 patients with AP and reported that NLR >4.7
at admission was significantly associated with severe AP and prolonged hospital
stay.
Rewritten: In a study conducted by Suppiah and colleagues in 2013 involving
214 patients diagnosed with acute pancreatitis, it was observed that an NLR
exceeding 4.7 at the time of admission was significantly linked to severe disease
and extended duration of hospitalization.

Original (Plagiarized):
Azab et al. (2011) assessed the prognostic role of NLR in 283 critically ill
patients, including those with AP, and concluded that elevated NLR was
independently associated with higher in-hospital mortality.
Rewritten: Azab and co-researchers, in their 2011 study of 283 critically ill
patients, including cases of acute pancreatitis, demonstrated that elevated NLR
levels were independently related to an increased risk of mortality during
hospitalization.

Original (Plagiarized):
Wang et al. (2015) conducted a meta-analysis including nine studies and
concluded that elevated NLR at admission was significantly associated with
severe AP and mortality.
Rewritten: A meta-analysis performed by Wang and associates in 2015, which
encompassed nine individual studies, revealed that higher NLR values at the
time of admission were significantly correlated with the severity of acute
pancreatitis and increased mortality rates.

Original (Plagiarized):
Yilmaz et al. (2018) studied 223 patients with AP and reported that RDW at
admission was significantly higher in patients with severe AP and was an
independent predictor of mortality.
Rewritten: Yilmaz and co-authors, in a 2018 study involving 223 individuals with
acute pancreatitis, found that RDW levels measured at admission were notably
higher in those with severe disease and served as an independent predictor of
mortality.

Original (Plagiarized):
Zhang et al. (2020) performed a systematic review and meta-analysis, including
11 studies, and confirmed that elevated RDW was associated with increased risk
of severe AP and mortality.
Rewritten: In 2020, Zhang and colleagues conducted a systematic review and
meta-analysis comprising 11 studies. Their analysis confirmed that elevated
RDW values were associated with a higher likelihood of severe acute pancreatitis
and increased mortality.

Original (Plagiarized):
A meta-analysis by Chen et al. (2021) including 14 studies demonstrated that
both NLR and RDW were reliable biomarkers for predicting severity and mortality
in AP.
Rewritten: Chen and associates, in a meta-analysis published in 2021 that
incorporated data from 14 studies, concluded that both NLR and RDW are
reliable biomarkers for assessing the severity and predicting mortality in patients
with acute pancreatitis.

Rewritten Content – Chapter 13 (Plagiarized Sections)

🔹 Aims and Objectives
Original (Plagiarized):
To evaluate the utility of neutrophil-to-lymphocyte ratio (NLR) and red cell
distribution width (RDW) in predicting the severity and outcomes of acute
pancreatitis.
Rewritten: The primary objective of this study is to assess the effectiveness of
the neutrophil-to-lymphocyte ratio (NLR) and red cell distribution width (RDW) as
indicators for predicting the severity and clinical outcomes in cases of acute
pancreatitis.

🔹 Specific Objectives

Original (Plagiarized):
1. To determine the association of NLR and RDW with disease severity in AP.
2. To assess the correlation of NLR and RDW with the development of local
and systemic complications.
3. To evaluate the predictive value of NLR and RDW for mortality in AP.
Rewritten:
1. To analyze the relationship between NLR and RDW values and the severity
of acute pancreatitis.
2. To examine the correlation between these hematological markers and the
occurrence of local or systemic complications in acute pancreatitis.
3. To evaluate the predictive capacity of NLR and RDW for patient mortality
associated with acute pancreatitis.

🔹 Methodology

Original (Plagiarized):
This study was conducted at the Department of General Surgery,
Adichunchanagiri Institute of Medical Sciences, Karnataka, over a period of 18
months (January 2022 to June 2023). Ethical clearance was obtained from the
Institutional Ethics Committee. A prospective observational study design was
used.
Rewritten: The present study was carried out in the Department of General
Surgery at Adichunchanagiri Institute of Medical Sciences, Karnataka, over a
duration of 18 months, spanning from January 2022 to June 2023. Prior to
commencement, ethical approval was secured from the Institutional Ethics
Committee. The study followed a prospective observational design.

Original (Plagiarized):
Inclusion Criteria:
 1. Patients diagnosed with acute pancreatitis based on revised Atlanta
criteria.
2. Age >18 years.
3. Willingness to provide informed consent.
Rewritten: Inclusion Criteria:
1. Patients diagnosed with acute pancreatitis in accordance with the revised
Atlanta classification.
2. Individuals aged over 18 years.
3. Patients who voluntarily agreed to participate and provided written
informed consent.

Original (Plagiarized):
Exclusion Criteria:
1. Patients with chronic pancreatitis.
2. Patients with hematological disorders.
3. Pregnant women.
4. Patients with malignancy or immunosuppressive conditions.
Rewritten: Exclusion Criteria:
1. Individuals diagnosed with chronic pancreatitis.
2. Patients with pre-existing hematological disorders.
3. Pregnant individuals.
4. Patients with known malignancies or those who are immunocompromised.

Original (Plagiarized):
Data Collection: Demographic details, clinical features, laboratory parameters
(NLR, RDW), imaging findings, severity scores, complications, and outcomes
were recorded.
Rewritten: Data Collection:
Information regarding patient demographics, clinical presentation, laboratory
parameters including NLR and RDW values, imaging results, severity scoring,
associated complications, and clinical outcomes was systematically documented.

Original (Plagiarized):
Statistical Analysis: Data were analyzed using appropriate statistical tests.
Association of NLR and RDW with disease severity, complications, and mortality
was assessed. A p-value <0.05 was considered statistically significant.
Rewritten: Statistical Analysis:
The collected data were analyzed using relevant statistical methods. The
relationships between NLR and RDW levels and the severity of pancreatitis,
development of complications, and mortality were evaluated. A p-value of less
than 0.05 was considered indicative of statistical significance.

Rewritten Content – Chapter 14 (Plagiarized Sections)

🔹 Results

Original (Plagiarized):
A total of 100 patients with acute pancreatitis were enrolled. The mean age was
41.2 ± 13.6 years, and 65% were male. The most common etiology was alcohol
(54%), followed by gallstones (26%).
Rewritten: A total of 100 patients diagnosed with acute pancreatitis
participated in the study. The average age of the patients was 41.2 ± 13.6 years,
with males comprising 65% of the study population. Alcohol consumption was
identified as the most frequent cause (54%), followed by gallstone-related
pancreatitis (26%).

Original (Plagiarized):
The majority of patients (72%) had mild AP, while 28% had severe AP based on
revised Atlanta criteria.
Rewritten: According to the revised Atlanta classification, 72% of the patients
presented with mild acute pancreatitis, whereas 28% exhibited severe disease.

Original (Plagiarized):
The mean NLR was significantly higher in patients with severe AP (10.4 ± 3.2)
compared to mild AP (4.3 ± 1.7) (p<0.001).
Rewritten: The average neutrophil-to-lymphocyte ratio (NLR) was notably
elevated in individuals with severe acute pancreatitis (10.4 ± 3.2) compared to
those with mild disease (4.3 ± 1.7), and this difference was statistically
significant (p<0.001).

Original (Plagiarized):
RDW was also significantly higher in severe AP (16.4 ± 1.8%) compared to mild
AP (14.1 ± 1.2%) (p<0.001).
Rewritten: Similarly, red cell distribution width (RDW) levels were considerably
higher among patients with severe acute pancreatitis (16.4 ± 1.8%) when
compared to those with mild disease (14.1 ± 1.2%), with this difference reaching
statistical significance (p<0.001).
Original (Plagiarized):
Both NLR and RDW were significantly associated with local and systemic
complications such as pancreatic necrosis, organ failure, and mortality.
Rewritten: Elevated NLR and RDW values demonstrated a significant
association with the occurrence of local and systemic complications, including
pancreatic necrosis, organ dysfunction, and patient mortality.

🔹 Discussion

Original (Plagiarized):
Our study demonstrated that higher NLR and RDW values at admission were
significantly associated with severe AP, local complications, and mortality. These
findings are consistent with previous studies and meta-analyses.
Rewritten: The findings of our study revealed that elevated NLR and RDW levels
at the time of hospital admission were significantly correlated with severe acute
pancreatitis, the development of local complications, and increased mortality
rates. These results are in agreement with prior research studies and published
meta-analyses.

Original (Plagiarized):
NLR is a marker of systemic inflammation and reflects the balance between
neutrophil-mediated inflammation and lymphocyte-mediated immune regulation.
RDW is influenced by inflammatory cytokines, oxidative stress, and impaired
erythropoiesis.
Rewritten: NLR serves as an indicator of systemic inflammation, reflecting the
interplay between neutrophil-driven inflammatory activity and lymphocyte-
mediated immune regulation. RDW, on the other hand, is affected by factors
such as pro-inflammatory cytokines, oxidative stress, and disturbances in red
blood cell production.

Original (Plagiarized):
The advantages of NLR and RDW include wide availability, low cost, and rapid
results, making them attractive tools for early risk stratification in AP.
Rewritten: The use of NLR and RDW offers several advantages, including their
widespread availability, affordability, and quick turnaround time. These features
make them valuable tools for early identification of high-risk patients with acute
pancreatitis.
Rewritten Content – Chapter 15 (Plagiarized Sections)
🔹 Summary

Original (Plagiarized):
Acute pancreatitis (AP) is a potentially life-threatening inflammatory condition
with a variable clinical course ranging from mild, self-limiting disease to severe
illness associated with local and systemic complications.
Rewritten: Acute pancreatitis is an inflammatory disorder of the pancreas that
can range from a mild, self-limited illness to a severe and potentially fatal
condition, often accompanied by both local and systemic complications.

Original (Plagiarized):
Early identification of patients at risk for severe AP is essential to optimize
management and improve outcomes.
Rewritten: Timely recognition of individuals who are at risk of developing
severe acute pancreatitis is crucial for ensuring appropriate clinical management
and improving patient outcomes.

Original (Plagiarized):
Conventional scoring systems have limitations, including delayed assessment,
complexity, and limited applicability in resource-limited settings.
Rewritten: Traditional scoring systems used for severity assessment in acute
pancreatitis have certain drawbacks, such as the requirement for delayed
evaluation, their complexity, and limited feasibility in healthcare settings with
constrained resources.

Original (Plagiarized):
In our study, both NLR and RDW at admission were significantly associated with
severe AP, complications, and mortality.
Rewritten: The present study demonstrated that elevated levels of NLR and
RDW at the time of hospital admission were significantly linked to the severity of
acute pancreatitis, the occurrence of complications, and patient mortality.

Original (Plagiarized):
NLR and RDW are simple, inexpensive, and widely available markers that can
facilitate early risk stratification in AP.
Rewritten: NLR and RDW are easily accessible, cost-effective, and routinely
available hematological markers that can aid in the early identification of
patients at increased risk in cases of acute pancreatitis.
🔹 Conclusion

Original (Plagiarized):
NLR and RDW at admission are reliable predictors of severity, complications, and
mortality in AP. Their routine use can improve early risk stratification and guide
management decisions.
Rewritten: The findings of this study suggest that NLR and RDW values
measured at admission serve as dependable predictors of disease severity,
associated complications, and mortality in acute pancreatitis. Incorporating these
markers into routine clinical practice may enhance early risk assessment and
assist in guiding appropriate therapeutic strategies.

Rewritten Content – Chapter 16: References & Bibliography

Original (Plagiarized style):
Suppiah A, Malde D, Arab T, et al. The prognostic value of the neutrophil-
lymphocyte ratio (NLR) in acute pancreatitis: Identification of an optimal NLR. J
Gastrointest Surg. 2013;17(4):675-681.
Rewritten: Suppiah A, Malde D, Arab T, and colleagues evaluated the prognostic
relevance of neutrophil-to-lymphocyte ratio (NLR) in patients with acute
pancreatitis and proposed an optimal threshold value. J Gastrointest Surg.
2013;17(4):675–681.

Original (Plagiarized style):

Azab B, Zaher M, Weiserbs KF, et al. Usefulness of neutrophil to lymphocyte ratio
in predicting short- and long-term mortality after non-ST-elevation myocardial
infarction. Am J Cardiol. 2010;106(4):470-476.
Rewritten: Azab B, Zaher M, Weiserbs KF, et al. explored the significance of the
neutrophil-to-lymphocyte ratio as a predictor of short-term and long-term
mortality following non-ST-elevation myocardial infarction. Am J Cardiol.
2010;106(4):470–476.

Original (Plagiarized style):

Yilmaz H, Cakmak M, Inan I, et al. Can red cell distribution width be used as a
marker of mortality in acute pancreatitis? A retrospective analysis. Turk J
Gastroenterol. 2018;29(3):294-298.
Rewritten: Yilmaz H, Cakmak M, Inan I, and co-authors conducted a
retrospective analysis to investigate whether red cell distribution width (RDW)
could serve as an indicator of mortality in acute pancreatitis. Turk J
Gastroenterol. 2018;29(3):294–298.
Original (Plagiarized style):
Wang Y, Zhu J, Liu H, et al. Neutrophil-to-lymphocyte ratio is associated with the
severity and mortality of acute pancreatitis: a meta-analysis. Medicine
(Baltimore). 2019;98(20):e15720.
Rewritten: Wang Y, Zhu J, Liu H, and associates performed a meta-analysis and
found that a higher neutrophil-to-lymphocyte ratio is correlated with increased
severity and mortality in acute pancreatitis. Medicine (Baltimore).
2019;98(20):e15720.

Original (Plagiarized style):

Zhang J, Zhao Y, Jiang Y, et al. Red blood cell distribution width is associated with
severity of acute pancreatitis: a systematic review and meta-analysis. J Clin Lab
Anal. 2020;34(8):e23373.
Rewritten: Zhang J, Zhao Y, Jiang Y, et al. conducted a systematic review and
meta-analysis and reported an association between elevated red blood cell
distribution width and the severity of acute pancreatitis. J Clin Lab Anal.
2020;34(8):e23373.