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trying to answer this question. However, it has certainly been found to be effective
in the metastatic setting. In Lynch syndrome, the use of checkpoint blockade alone
as a single agent results in high response rates.
Do you agree that for the same stage of colon cancer, patients with microsat-
ellite unstable colon cancers have a better prognosis than patients with spo-
radic colon cancer?
It is very important to emphasize that mismatch repair deciency/microsatellite
instability can be germline (Lynch syndrome) or acquired. The percentage of
patients with microsatellite instability incidence is about 15% in patients with local-
ized colon cancer, but in the metastatic setting, that percentage is much lower, about
5%. This is because microsatellite unstable tumors do not metastasize as much. In
addition, these patients are very often part of a screening program, and things get
picked up sooner, but, regardless, they tend to have better disease biology, and better
prognosis, stage for stage than sporadic colon cancer.
Case 3 A 68-year-old woman with alcoholic cirrhosis (abstinent for 5 years) was
having routine surveillance USA and AFP every 6 months but then missed follow-
up for 18 months. She is found to have two hepatomas, one 4 cm in size and
another one is 5cm. AFP is 600. TACE is performed, and both lesions decrease
in size to 3cm. However, the AFP rose to 700. The patient’s functional status
is good.
Can you discuss the use of systemic chemotherapy in this setting?
An important question here is whether this woman could potentially be a trans-
plant candidate. With tumor downsizing after TACE, the patient meets Milan crite-
ria—a set of criteria that determines transplant eligibility.
So, let’s think about it in two different ways. First, let’s say the patient is deemed
not to be a transplant candidate after medical evaluation by the transplant team. If
she is not a transplant candidate, the best systemic therapy options for this patient
are either a combination of bevacizumab+ atezolizumab or tremelimumab (anti-
cytotoxic T lymphocyte-associated antigen 4) plus durvalumab (anti-programmed
cell death ligand-1).
Prior to receiving bevacizumab + atezolizumab, patients need to undergo an
EGD to assess for varices and undergo variceal banding.
The other frontline systemic therapy options include lenvatinib and sorafenib,
but certainly the preference would be either bevacizumab+atezolizumab or treme-
limumab plus durvalumab on account of their efcacy and toxicity prole.
If the patient is a transplant candidate, immunotherapy should be avoided in
the pre-transplant setting. The optimal systemic therapy options would be lenva-
tinib or sorafenib but preferably lenvatinib due to the higher objective
response rates.
Has lenvatinib largely supplanted sorafenib in patients who have contrain-
dications to immunotherapy and get tyrosine kinase inhibitor therapy?
Yes, lenvatinib has for the most part supplanted sorafenib, because of improved
efcacy. That said, the side effect prole is not necessarily more favorable than
sorafenib, it’s just different.
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Are checkpoint inhibitors felt to be less effective in HCC associated with
alcohol? associated with NASH?
We don’t have prospective data addressing that specic question. However, the
available data certainly seem to indicate that checkpoint inhibitors are more effec-
tive in viral-induced (hepatitis B and hepatitis C) HCC compared to sorafenib. The
magnitude of benet with checkpoint inhibitors appears to be less compared to
sorafenib in patients with hepatocellular carcinoma due to non-viral etiologies.
Right now, we are not prioritizing treatment based on etiology of HCC, but this
may become part of routine clinical practice in the future as more data emerge.
Case 4 A 67-year-old man presenting with dysphagia is found to have adenocarci-
noma of the esophagogastric junction (EGJ). EUS shows positive lymph nodes.
Tumor markers are sent off and the tumor has HER-2 overexpression.
Do you manage adenocarcinoma of the esophagus the same as adenocarci-
noma of the stomach?
Yes and no. For all intents and purposes, the chemotherapy agents that are active
in adenocarcinomas of the stomach and the esophagus/EG junction are very similar.
However, there are some key differences between tumors of the distal esophagus/
EG junction, and tumors in the stomach, particularly as it pertains to treatment for
localized disease. From a staging perspective, a diagnostic laparoscopy to look for
peritoneal carcinomatosis is mandated for T2 or higher tumors in the stomach while
that is not done routinely for tumors of the distal esophagus/GE junction (dictated
by patterns of spread). In terms of neoadjuvant/peri-operative treatment, radiother-
apy is more commonly utilized in tumors of the distal esophagus/EG junction than
tumors of the stomach. Surgical approaches are different for these entities as well.
There are some biological differences between these entities as well. We know
that tumors in the EG junction are more likely to overexpress HER2/neu than tumors
in the stomach. Similarly, tumors that originate in the EG junction are more likely
to respond to immunotherapy than tumors that originate in the stomach based on
available data (this has not been prospectively validated).
At a molecular level, tumors in the distal esophagus/EG junction and stomach
are classied into four distinct subgroups: (a) chromosomally unstable (CIN), (b)
genomically stable, (c) microsatellite unstable, and (d) the EBV-positive.
The EG junction tumors tend to belong to the chromosomally unstable subtype
(characterized by alterations in the signal transduction pathway) and the EBV-
positive subtype (characterized by alterations in thePI3 kinase pathway and greater
likelihood of response to immunotherapy).
Microsatellite unstable tumors tend to be present throughout the stomach, with a
preponderance in the distal stomach while the genomically stable subtype correlates
very closely with linitis plastica or diffuse gastric cancer.
Why might trastuzumab be useful in the above patient, with HER-2
overexpression?
Trastuzumab is a monoclonal antibody that binds to ERBB2 (Her-2) preventing
the dimerization with ERBB3 and inhibiting downstream signaling that contributes
to cancer progression. So essentially, it’s a targeted agent that improves treatment
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response and prolongs survival in patients with metastatic EG junction/gastric can-
cers with a very favorable toxicity prole.
Can you discuss the general approach to treatment of localized adenocarci-
noma of the esophagus (and stomach)?
For localized tumors of the esophagus and EG junction, we typically use neoad-
juvant chemotherapy and radiation, followed by surgery for curative intent treat-
ment. For tumors of the stomach, we use neoadjuvant or perioperative chemotherapy
and surgery for curative intent therapy. The role of radiation in tumors of the stom-
ach is controversial and it’s not routinely used.
Is there a role for checkpoint inhibitors?
Yes, there is a role for utilizing a checkpoint inhibitor in the treatment of meta-
static disease regardless of the PD-L1 expression. Typically, the frontline systemic
therapy program for tumors of the stomach and distal esophagus/EG junction
includes a uoropyrimidine, a platinum, and a checkpoint inhibitor, if the tumor
does not over express HER2/neu. If HER2/neu overexpression is present, we utilize
a combination of uoropyrimidine, platinum, trastuzumab, and a checkpoint
inhibitor.
Case 5 A 71-year-old woman presents with abdominal pain, weight loss, and new-
onset diabetes. A CAT scan reveals probable cancer of the body of the pancreas.
EUS shows malignant appearing lymph nodes and FNA is positive for adenocarci-
noma. Genetic testing is performed that includes MSI testing and homologous
recombination deciency (HRD) testing.
Is it true that when we talk about HRD testing we are checking for muta-
tions in all of these genes: BRCA1/2, PALB2, ATM, BAP1, BARD1, BLM,
BRIP1, CHEK2, FAM175A, FANCA, FANCC, NBN, RAD50, RAD51, RAD51C,
and RTEL1?
We are interested in assessing the HRD status of pancreas cancers to help make
treatment decisions. Assays that determine the HRD status of tumors use different
methods, and the parameters tested vary based on the assay that is utilized. It is true
that many of the above genes play a key role in DNA damage repair.
Is it true that if a pancreas cancer is found to have HRD you will turn to a
platinum-based therapy like FOLFOX or FOLFIRINOX?
Yes, we will utilize platinum-based chemotherapy if a pancreatic adenocarci-
noma harbors HRD.
Are all patients with pancreatic cancer getting this genetic testing done?
We offer germline testing to all patients with pancreatic cancer, and it has been
incorporated in national guidelines.
Is gemcitabine commonly used anymore-alone or with nabpaclitaxil?
Yes, gemcitabine is used quite a bit both in the treatment of metastatic and local-
ized pancreatic adenocarcinomas. Gemcitabine can be used as a single agent or in
combination (with Nab-paclitaxel or Nab-paclitaxel and cisplatin). Gemcitabine is
also utilized as a single agent for purposes of radio-sensitization in patients who
undergo concurrent chemoradiotherapy.
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When do you use a PARP inhibitor and how does it work?
PARP inhibitors are used currently in patients with pancreatic adenocarcinoma
who have germline pathogenic alterations in BRCA1 and BRCA2. It is utilized for
maintenance therapy in patients with metastatic pancreas cancer who are platinum-
responsive. Olaparib is the PARP inhibitor approved for use in pancreatic adenocar-
cinoma., The idea behind treatment with the PARP inhibitors is that they cause
synthetic lethality in the cancer cells of patients who have BRCA1 or BRCA2 germ-
line alterations. Normally, PARP helps in the repair of single-stranded DNA breaks
and PARP inhibitors prevent that. So, DNA in cancer cells that are exposed to DNA-
damaging drugs undergo single- and double-stranded DNA breaks, and PARP
inhibitors prevent the cancer cells from repairing them, causing increased cancer
cell death.
Are you using checkpoint inhibitors in pancreatic cancer?
There are a lot of clinical trials in this space. Currently, there is no proven role
for checkpoint inhibitors in pancreas cancer other than in the 1% of tumors that have
a decient mismatch repair gene status. There is also a very small percentage of
pancreatic adenocarcinomas with an elevated tumor mutational burden that may
respond to checkpoint inhibitors as well.
Are there any other points about pancreatic cancer management that you
would like to emphasize for the community gastroenterologist?
One point I’d like to stress is the importance of a metallic common bile duct stent
(as opposed to a plastic stent)—once tissue diagnosis is established—in patients
with pancreatic head adenocarcinomas that cause biliary compromise. This helps
decrease the incidence of stent occlusion and cholangitis in patients with pancreatic
adenocarcinoma while on treatment.
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159© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
W. H. Sobin et al. (eds.), Managing Complex Cases in Gastroenterology,
https://doi.org/10.1007/978-3-031-48949-5_23
Chapter 23
Issues inTherapeutic Endoscopy
KulwinderDua
Management ofRefractory Benign Esophageal Stricture
(RBES) Including Placement ofEsophageal Stents
Case 1 A 70-year-old man has prolonged NG tube insertion after a complicated
colon resection for diverticulitis. Following that, he develops dysphagia. An EGD
shows a tight stricture in the mid-to-distal esophagus from 27 to 37 cm, and biopsies
are benign. He has received several endoscopic dilations but continues to re-
stricture and is referred to you.
How do you manage a patient with a refractory benign esophageal stricture?
The denition of RBES is that one cannot achieve an esophageal luminal diam-
eter of ≥14mm despite one dilation done every 2 weeks×5 or if the patient requires
one dilation every 4 weeks to maintain a diameter of ≥14mm. In this patient, the
stricture is due to prolonged trauma from the NG tube and damage from acid reux-
ing alongside the tube (like capillary action) for prolonged periods. Some of the
other causes of RBES include corrosive ingestion, pill injury, radiation-related,
post-endoscopic mucosal resections and ablations, and surgery.
In patients with RBES, besides etiology, it is important to know the diameter to
which the patient was dilated previously, the frequency of dilations, and how soon
the patient developed recurrent dysphagia. Based on this, one can decide on a treat-
ment plan. Let’s say you are dilating every 4 weeks and you can only achieve a
diameter of 12 mm, then you need to dilate every 2 weeks. If you are going two
steps forward and then two steps backward every 2 weeks, then you need to dilate
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GI and Hepatology Division, Dept. of Medicine, Medical College of Wisconsin,
Milwaukee, WI, USA
e-mail: kdua@mcw.edu
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every week. One can also consider injecting steroids (triamcinolone) into the stric-
ture to delay brosis and recurrence. There is no limit to how many times you inject
triamcinolone. If the stricture keeps closing up after each dilation, I would inject at
every dilation.
At each dilation session, assess how much the stricture has regressed and then
decide whether you need to increase or decrease the frequency of dilations (two
steps forward and one step backward), but even though you are making progress
you never want to leave the patient for more than 2 weeks without repeat dilation
until you have achieved your goal. Once a diameter of 14–18mm is achieved and
maintained at weekly or every 2-week dilations, lengthen the interval between dila-
tions. If the stricture continues to regress, one can consider other interventions, such
as stent insertion, electrocautery incision, or both.
What sort of stents do you place?
The self-expanding stent has to be a fully covered stent so that it can be removed
at a later date. If the stent is uncovered or partly covered, it will get embedded in the
esophageal wall and may not be easy to remove. The only fully covered stent that is
FDA approved and available in the USA for benign esophageal stricture is a plastic
expandable stent (Polyex
®
stent). This stent is difcult to load, has a high migra-
tion rate, and tends to cause chest pain. As a result, most gastroenterologists are
using fully covered metal expandable stents, off-label.
For precise placement such as when the strictures are near (<2cm) the UES, as
we sometimes see in head and neck cancers after radiation therapy, non-
foreshortening stents (laser-cut) are preferred. More often, we tend to use electro-
cautery and avoid placing stents in this location if the stricture is short and like
a shelf.
When the stricture is in the lower esophagus and failed dilations, we will use
stents, even if they need to bridge the LES.However, patients are predisposed to
having signicant gastroesophageal reux that can create a considerable aspiration
risk. Therefore, we have to use strict anti-reux measures in these cases.
Stents for RBES are usually left in for 2–4 weeks. After removing the stent, rein-
stitute regular esophageal dilations. For those who fail the above approach, we offer
them surgery (in many cases, this may not be possible) or train them to do
self-dilation.
How do you teach self-dilation?
All patients get apprehensive when told about self-dilation. Good discussion
with the patient and showing them videos of those who have successfully adopted
this approach help. Patient is initially dilated to a diameter of 16–18mm endoscopi-
cally. A week or so later, the patient is taught to self-dilate holding a non-wire-
guided weighted dilator (such as the Maloney
®
dilator) of around 15mm diameter,
sitting on a chair, and watching the dilator go down under uoroscopy (biofeed-
back), and immediately repeat without uoroscopy. After that, the patient takes the
dilator home and dilates himself once or twice a day. Initially, patients like to use
some viscous lidocaine, but after a week or two it’s no longer necessary. If, after a
while, the patient nds it is once again becoming more difcult to pass the dilator
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because the stricture is tightening, we bring the patient back and dilate them endo-
scopically to 16–18mm and after that they nd the 15-mm self-dilation go eas-
ily again.
How do you decide what type of dilator to use in treating a benign esopha-
geal stricture?
In talking about the type of dilator used, there are balloon dilators that have good
radial force and there are bougies that have both radial and longitudinal force. In
expert hands, the safety prole is equivalent. It is a good idea to use a bougie in
cases where the stricture is long, or multifocal as bougies cause pan-esophageal
dilation. These kinds of strictures are usually encountered with corrosives, radia-
tion, and prolonged NG tube use. Balloon dilators are certainly acceptable for short
strictures, such as anastomotic strictures, or short peptic strictures.
Case 2 A 72-year-old smoker presents with dysphagia and is found to have a tight
stricture of the mid-esophagus caused by esophageal squamous cell cancer.
Chemoradiation is planned.
Is there a role for a stent in this malignant esophageal stricture?
Generally, no; the initial enthusiasm for stents as a bridge to surgery for those
receiving neoadjuvant therapy or even for those receiving palliative chemotherapy
has been dampened by the high rate of adverse events and side effects from stents
that may interrupt chemo-/chemoradiation treatments. With the tumor regressing
and becoming “softer” with chemo-/chemoradiation treatments, stents can migrate,
cause ulcers and bleeding, and perforate the esophagus.
Stents, however, are very effective in immediately relieving dysphagia. Therefore,
if we have a patient with severe dysphagia (barely able to swallow liquids or total
dysphagia), we will communicate with the oncologist and nd out how long a delay
they anticipate before chemoradiation will be started and how long a lag period
between initiation of therapy and when tumor response is anticipated. If therapy is
being delayed for a month and response will probably take 2 weeks, we may decide
to place a temporary stent if the patient is suffering from severe dysphagia. In this
instance, we will consider placement of a fully covered metal stent as a temporary
bridge so that the patient can swallow and plan on removing it around the time
chemo-/chemoradiation therapy is being initiated to avoid delayed stent-related
adverse events. If the dysphagia is just for solids, I would not place a stent because
I am ne with the patient simply swallowing a soft diet or liquids, such as Ensure
and milkshakes.
Covered stents are the treatment of choice for those who have esophageal-airway
stulae or perforations. In these patients, available options, including stenting,
should be discussed in a tumor-board or multidisciplinary meeting.
What about using an esophageal stent for a malignant stricture where the
patient refuses chemoradiation?
It is important to discuss the expectations the patient may have about stents. The
best one can eat with a stent is a soft-liquid diet, not a normal diet. So, do not place
stents in those who are eating a soft diet at baseline.
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In patients receiving a stent for palliation, it is important to counterbalance the
benets of the stent vs the side effects/adverse events. If the patient does not want
any palliative chemoradiation, then optimally one can place a partially covered stent
where the upper and lower ends of the stent are uncovered. This will allow tissue
ingrowth and embed the stent, which will prevent migration, but if the patient
changes his/her mind and decides to go for chemoradiation, removing the stent will
be difcult (if not impossible). Therefore, one should have a frank discussion about
this with the patient before placing the stent. Alternatively, fully covered stents with
xing devices to prevent migration can also be used in these patients for potential
removal in the future if needed.
The other problem with the partly covered stent, along with the fact that it is not
easily removed, is that you tend to get tumor ingrowth, which may eventually lead
to secondary dysphagia.
In most cases of malignant stricture, we are reserving stents for patients who can
barely handle liquids. We are placing stents in patients with severe, grade 3 or 4
dysphagia, but will not consider them with mild (grade 1 or 2) dysphagia.
Case 3 A 67-year-old man receiving radiation therapy for metastatic lung cancer
with enlarged mediastinal lymph nodes has a tight extrinsic compression of his mid-
esophagus. The esophageal mucosa itself appears normal.
What is the role of an esophageal stent in a case of extrinsic, malignant
obstruction?
The best approach for extrinsic compression will be to treat the underlying cause,
which may not always be easy or possible. However, if there is hope that planned
chemoradiation or surgery will resolve the extrinsic pressure, one can consider plac-
ing a removable stent for the patient with grade 3 or 4 dysphagia.
A concern about stenting an extrinsic compression is that the mass may be press-
ing on the left or right main stem bronchus or trachea, and the moment the stent
expands, it may cause occlusion of the airways. With upper esophageal cancers or
obstruction from a mediastinal mass, it is very important to get and review a good
quality CT scan of the chest to ensure that there is no impending airway
compression.
If you have a patient who will be getting treatment and is not at risk of airway
obstruction, one can place a fully covered stent and x it in place, or place a partially
uncovered stent based on long-term outcomes as discussed above.
Nutrition Needs
Although stents relieve dysphagia and allow feeding, often patients don’t eat enough
secondary to either chest discomfort or anorexia from chemotherapy. In these
patients, one can consider alternatives such as placing a G- or a J-tube to supple-
ment nutrition, while the stent improves quality of life, allowing the patient to take
oral feeding.
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Pancreatic Cancer
Case 4 A 68-year-old man comes in with painless jaundice. He has no history of
alcohol use, diabetes, or gallbladder disease. On examination, he is jaundiced;
examination is otherwise unremarkable. His laboratory ndings include: Bili 5.6,
Alk phos 320, ALT 70, AST 55, and lipase 300.
An ultrasound shows a dilated common bile duct, a normal gallbladder and liver,
and a questionable mass in the head of the pancreas.
In a case of painless jaundice, what imaging studies do you like to start with?
If the patient has no contraindication (renal insufciency or dye allergy), the
preferred study will be a pancreas protocol CT scan with IV contrast. This provides
accurate staging of the disease and must be done before other procedures such as
EUS-FNA/B or ERCP, as these other procedures can result in pancreatitis, and then,
CT staging can get clouded. If CT with contrast cannot be done, then MRI can be
considered. One would also like to order a CA 19-9 on the patient.
The community gastroenterologist plans on doing an ERCP on this patient
to decompress the bile duct with a plastic stent and do diagnostic brushing of
the bile duct for tissue diagnosis. What do you think of this approach?
No, this is the wrong approach. This decision is based on two faulty premises.
The rst is the fear that if a patient is jaundiced from presumed pancreatic cancer,
the patient is at a high risk of getting cholangitis. Patients with malignant obstruc-
tion of the bile duct rarely develop cholangitis. The second is that doing an ERCP
and cytology brushing is an efcient way of making a tissue diagnosis, but it is not.
An EUS-FNA is far superior. Moreover, EUS-FNA-ERCP-metal stent (“one-stop
shop”) all can be done in one setting with rapid on-site rapid cytology (ROSE)
evaluation by a cytopathologist. Hence, if one does not have EUS-FNA and ROSE
available, one should not do ERCP and, instead, refer the patient to a tertiary care
center. Moreover, placing plastic biliary stents (because metal stents for durable
biliary drainage should not be placed without tissue diagnosis) carries an increased
risk of recurrent cholangitis. In addition, the patient will have to have another ERCP
to exchange for a metal stent if the brushing came back positive for cancer, hence,
all the more reason to refer these patients to centers with expertise.
Even in those with resectable pancreatic cancer, this approach of “one-stop shop”
is being widely used, as more and more patients with resectable pancreatic cancer
are getting neoadjuvant therapy rather than early surgery. Tissue diagnosis and dura-
ble biliary drainage are essential prerequisites for neoadjuvant therapy, and if,
indeed, the patient is being considered for early surgery, biliary drainage before
surgery is not required and can be detrimental. Hence, in this patient, ERCP should
not be done.
Case 5 A 65-year-old man presents with an episode of acute pancreatitis. There is
no history of diabetes. He does not drink much alcohol. An ultrasound shows a
normal gallbladder. A pancreas protocol CT shows pancreatitis but no mass or no
stone. A CA 19-9 is sent off and returns 50 (normal is up to 35).
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What do you do when you suspect a patient may have pancreatic cancer but
there is no mass on US or CT?
Not every case of obscure pancreatitis is pancreatic cancer. Some patients may
have microlithiasis, etc., but when we see a patient who comes in out of the blue
with pancreatitis we worry about pancreatic cancer, while keeping the rest of the
differential in mind. Also, there can be a nonspecic rise in CA 19-9 with
pancreatitis.
In the face of active pancreatitis, an EUS is less helpful as pancreatitis will show
up as diffuse or focal hypoechogenicity of the pancreas, and a cancer can be missed.
So, in a number of these cases, where one is concerned about possible pancreatic
cancer, it is best to wait and let the inammation settle down in 4–6 weeks and then
repeat the pancreas protocol CT scan and CA 19-9. Then, one could consider EUS.
We recently saw a patient referred by one of our pancreatic surgeons because the
patient had a dilated upstream pancreatic duct that stopped abruptly at the neck of
the pancreas. This patient did not have pancreatitis and had undergone two MRIs
and three CT scans in the last 5 months, and no mass was identied. On EUS, there
was a half-cm hypoechogenic mass at the site of pancreatic duct obstruction that on
FNA turned out to be a mucinous adenocarcinoma.
Here’s another scenario. A patient with elevated liver enzymes is seen who
doesn’t have pancreatitis, but does have a bile duct that is mildly dilated. A CA 19-9
can be elevated in patients with bile duct obstruction. There is no mass in the pan-
creas in this patient. Could the dilation be due to stones? Could this be a cholangio-
carcinoma along the wall of the bile duct? In these situations, we do an EUS, even
if there is no mass identied on imaging studies.
Are there any red ags that make you worry that someone with some subtle
ndings could have pancreatic cancer when others aren’t suspecting it?
I worry about this in an elderly person with unexplained weight loss or an unex-
plained attack of pancreatitis. I also worry if I see someone with an elevated CA
19-9. If normal is around 35 but I see a patient who is smoldering around 110, but
nothing is showing up on the pancreas protocol CT scan, I still worry. Then, there
are cases where someone has a family history with two members who had pancre-
atic cancer or a family member who had breast or ovarian cancer and was BRCA
positive. In all these cases if pancreatic protocol CT is negative, we still do an
EUS.In families with a worrisome history, we may do EUS and MRI in alternate
years as part of our screening process.
Similarly, patients with pancreatic cysts/dilated main pancreatic duct with worri-
some or high-risk features do merit an EUS (at times, these patients get operated
upon based on these worrisome features).
Sometimes, we have the opposite problem, where the CT scan and EUS de-
nitely show a lesion that looks like cancer but repeated FNA is negative for cancer.
A recent patient presented with jaundice and a mass on CT scan; CA 19-9 was 900,
and EUS with FNA/B was repeatedly negative. Everyone thought this was pancre-
atic cancer, but the oncologist would not give neoadjuvant therapy without a
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