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235© 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_45
Chapter 45
Nonspecic Ileal Ulcers
AmirPatel
A 35-year-old nonsmoking male is referred with chronic diarrhea. All stool cultures
are negative. Diarrhea is watery and non-bloody. Stool calprotectin is 250. You
decide to do a colonoscopy. The colon appears normal, but you enter the terminal
ileum and nd three or four small ulcers that are fairly nondescript. Biopsies of the
colon are negative, and biopsies of the ulcers are nondiagnostic, with no granulo-
mas present. You think these ndings are not convincing for IBD.The patient does
not routinely take NSAIDS but did take some one weekend, a month earlier, after a
basketball injury.
What is the level of calprotectin that you will pursue?
It depends on the range at the institution, but at our institution, anything greater
than 50 can be considered elevated. Now that being said, I think the range between
50 and 80 is a gray area. So, if it's in that low range, right below a hundred, I might
consider repeating the fecal calprotectin in a few weeks just to see if it's still ele-
vated. Some of the literature suggests that we'll see higher fecal calprotectin when
there’s signicant colitis versus ileitis.
The value generally does not correlate with disease severity; however, if I see
numbers in the thousands, that’s when I get really concerned, and that result is prob-
ably more sensitive for inammatory bowel disease.
A. Patel (*)
Dept. of Medicine, Division of Gastroenterology and Hepatology, Medical College of
Wisconsin, Milwaukee, WI, USA
e-mail: ampatel@mcw.edu
https://t.me/medicina_free
236
When you see a patient with ulcers in the terminal ileum that you think are
probably not Crohn’s, how do you approach them? Will you do further small
bowel imaging (capsule, SBFT, or CTE)? Will you give a trial of budesonide?
Just follow them?
Although we’ve always been taught to look for granulomas, the actual nding of
granulomas is pretty low, they’re only found in a minority, perhaps 30% of patients
with Crohn’s disease. When you think about the different causes of ileal ulcers, it
could be NSAIDs, or it could be Crohn’s disease, and you always think about your
bacterial infections, like yersinia and tuberculosis, but we’re not seeing those in
developed countries.
But when I see ulcers in the small bowel, I do want to consider further testing,
just to make sure that we’re not missing anything. So, your options include capsule
endoscopy, CT, MRE, or the old-school, small bowel follow-through. We do know
that capsule endoscopy is the most sensitive test because it can actually get direct
visualization.
In Crohn’s disease, we use scoring systems, like the Lewis scoring system, where
we look at the villous appearance on a capsule, look for ulcers, and look for stric-
tures. Capsule endoscopy has a pretty high negative predictive value; when you’re
looking at Crohn’s disease, it’s almost a hundred percent; I think it’s around 95%.
So, in this case, if the patient has never had bowel obstructions or any abdominal
surgeries, I’d probably go with a capsule endoscopy to evaluate the remainder of the
small bowel.
Now, if capsule endoscopy is not available, CTE and MREs have become more
popular. And there have been studies looking at our ability to diagnose or dene
Crohn’s disease using enterography studies. What you’re looking for, on CTE, is
mucosal enhancement, fat stranding, and hyper-enhancement as well.
Dynamic MRIs have also been used in our institution. When they’re looking at
the contrast in the ileum, they can actually see how well the ileum is moving. So, not
only can they determine if there’s an inammatory component of the Crohn’s, but
they can actually see if there’s any brotic appearance. So that’s some exciting, new
technology we can apply to our patients with Crohn’s disease. But typically, I would
do a capsule endoscopy in this case, but I think a CT or MR would be acceptable
as well.
The patient has a capsule endoscopy, which is otherwise negative.
Would you do any further testing, do any treatment, or simply follow the
patient at this point?
If I’m not concerned about Crohn’s disease, I would simply tell the patient to
avoid NSAIDs. NSAID damage can happen pretty quickly, within 10 days, accord-
ing to the Crohn’s disease literature. If I’m not concerned about Crohn’s disease, I
will not treat them. Some practitioners will give a course of Entocort, 9mg a day,
and try it for a couple of months. But I would only do this if I think the patient might
have mild Crohn’s disease and has ongoing symptoms.
A. Patel
https://t.me/medicina_free
237© 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_46
Chapter 46
Concern About Pneumocystis jirovecii
PoonamBeniwal-Patel
A 32-year-old female presents with acute ulcerative colitis, requiring admission and
a course of IV steroids. She improves markedly within a couple of days, and she is
able to be discharged on prednisone 40mg a day. You begin therapy with iniximab
after sending off hepatitis serology, a QuantiFERON assay, and TPMT.A few days
after the TPMT returns normal, azathioprine is added. The patient’s dose of predni-
sone has been dropped to 20mg.
Would you agree with adding azathioprine in a patient still receiving pred-
nisone along with iniximab? Would you wait until prednisone is tapered off?
If you do start azathioprine, along with iniximab and prednisone, would you
start prophylaxis for pneumocystis (in the face of triple immunosuppressive
therapy?)
The SONIC trial showed that starting patients on azathioprine when beginning
iniximab led to higher steroid-free remission. Additional data has shown that the
use of an immunomodulator with antitumor necrosis factor therapy decreases the
risk of drug antibody formation [1]. Therefore, in a patient with aggressive disease
who is starting iniximab, I would start azathioprine as an outpatient without wait-
ing for prednisone to be completely tapered off.
However, over the last year or two, there have been studies that show that if you
treat someone with iniximab monotherapy and then they develop antibodies, it is
possible to add azathioprine at that time and usually be able to recapture them by
eliminating their antibodies [1, 2].
That’s really interesting data, because the question arises whether you really
have to start azathioprine at the outset. Certainly, I will say that for patients with
severe ulcerative colitis who are at high risk for a colectomy, I will denitely start
P. Beniwal-Patel (*)
Medicine, Gastroenterology/Hepatology Division, Medical College of Wisconsin,
Milwaukee, WI, USA
e-mail: pbeniwal@mcw.edu
https://t.me/medicina_free
238
azathioprine at the same time as iniximab. These patients, especially if they’ve
been hospitalized, have proven that they have aggressive disease. We don’t have
time for them to develop antibodies and then reverse them.
So, in this patient, I would start azathioprine, start it at the same time that she
receives iniximab, and not wait until prednisone is tapered off. With the long half-
life of azathioprine, it actually takes about 8 weeks for it to reach its steady state. So,
even though we’re starting the azathioprine at the same time as the other two, it
really doesn’t kick in full effect until the prednisone dose is leveling off.
As to whether you need prophylaxis for PJP, there have been some small cohort
studies, looking at the rate of PJP in patients who have IBD but do not have
HIV.There was one study, about 10 years ago, that found the absolute risk to be
only about 0.07% of developing PJP in non-HIV IBD patients [3].
In general, it is high-dose, long-duration prednisone scenarios in older patients
where you want to prophylax against PJP.But in our patients, we really start taper-
ing them after the rst week. So, if it’s a patient in whom I’m tapering off steroids,
I do not prophylax them. On the other hand, if I have a patient who’s older than 55
who I’m meeting for the rst time and they’ve been on steroids for 3–4 months, then
that’s someone who I may consider doing a PJP prophylaxis, especially if they have
underlying lung disease. So, it’s really on a case-by-case basis. But most of the time,
I do not prophylax. them.
References
1. Villareal EM, Yarur AJ. Better late than never: adding thiopurines after loss of response
to iniximab monotherapy. Dig Dis Sci. 2021;66(9):2851–2. https://doi.org/10.1007/
s10620- 020- 06681- w. Epub 2020 Oct 31.
2. Zeze K, Hirano A, Torisu T, Esaki M, Moriyama T, Umeno J, Kawasaki K, Fujioka S,
Fuyuno Y, Matsuno Y, Kitazono T. Adding thiopurine after loss of response to iniximab
versus early combination in treating Crohn’s disease: a retrospective study. Dig Dis Sci.
2021;66(9):3124–31. https://doi.org/10.1007/s10620- 020- 06600- z. Epub 2020 Sep 13.
3. Sierra CM, Daiya KC.Prophylaxis for Pneumocystis jirovecii pneumonia in patients with inam-
matory bowel disease: a systematic review. Pharmacotherapy. 2022;42(11):858–67. https://doi.
org/10.1002/phar.2733. Epub 2022 Oct 25. PMID: 36222368; PMCID: PMC9828113.
P. Beniwal-Patel
https://t.me/medicina_free
239© 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_47
Chapter 47
Bloating inCrohn’s
PoonamBeniwal-Patel
A 42-year-old female with a history of Crohn’s disease well-controlled on iniximab
and azathioprine comes in for complaints of diarrhea and bloating. She had a prior
terminal ileal resection (20 cm) for her Crohn’s. Her CRP and fecal calprotectin are
normal. A colonoscopy to the neoileum is normal.
Is there any treatment you would consider?
First, if there’s signicant diarrhea or bloating, and this is relatively new, I would
do cross-sectional imaging, like a CTE or MRE, to make sure there’s no upstream
disease activity that we’re not capturing on a colonoscopy.
If that comes back negative, then I’d be interested in knowing what kind of anas-
tomosis they have, because patients who have a side-to-side anastomosis do have a
higher rate of SIBO compared to those with an end-to-end anastomosis.
If there’s no active disease on cross-sectional imaging, you could try cholestyr-
amine. But be judicious with it; I would just give it once a day. Also, you could try
treating with rifaximin, just empirically for SIBO, given that they have had an
abdominal intestinal surgery, which is a risk factor for SIBO.
The patient is started on cholestyramine, 4 g, once daily, and diarrhea improves
but bloating gets worse. A CTE shows some areas of small bowel dilation without
signicant stricture.
Would you consider doing a capsule in someone like this?
I think it would be reasonable to do, but I certainly would do a patency capsule
before that. The interesting thing is that to have dilation, there’s one of three things
that could cause that. There might be a mechanical stricture, there could be
P. Beniwal-Patel (*)
Medicine, Gastroenterology/Hepatology Division, Medical College of Wisconsin,
Milwaukee, WI, USA
e-mail: pbeniwal@mcw.edu
https://t.me/medicina_free
240
aperistalsis at that point, or it could be that we’re viewing the x-ray in the middle of
a peristaltic wave and it’s not truly a dilation. I would also consider a small bowel
follow-through in order to get a functional assessment of the area.
Would you bother doing a breath test looking for SIBO or would you just
treat with rifaximin?
In this case, because rifaximin is relatively low risk, I’d treat it empirically. If this
occurs again, then I’d perform testing for SIBO before retreating.
P. Beniwal-Patel
https://t.me/medicina_free
241© 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_48
Chapter 48
Severe Diarrhea inaPatient
onChemotherapy
AmirPatel
A 57-year-old male is admitted to the oncology service with severe diarrhea. He has
been having diarrhea for weeks. The patient is on chemotherapy for metastatic lung
cancer but is not receiving a checkpoint inhibitor. You look up the drugs he is receiv-
ing and see that they may cause diarrhea but do not tend to cause colitis. His chemo
has been on hold since his diarrhea started, but his oncologists are anxious to
restart it. His stool cultures are negative. He had his last screening colonoscopy 4
years ago, just before his lung cancer was rst diagnosed, and it was
unremarkable.
Obviously if you’re consulted on a patient receiving checkpoint inhibitors
and having bad diarrhea, you’re going to do a colonoscopy, looking for the
inammatory bowel disease-type phenotype. Do you ever do that with patients
who are on other chemotherapy?
We've been seeing a lot of checkpoint inhibitor therapy causing colitis in the last
decade, but we have also found that some other chemotherapy medications that are
not checkpoint inhibitors can cause an immune-mediated colitis as well.
So, a lot of times the oncologists will send these patients to us, and we will do a
colonoscopy just to make sure that there's no immune-mediated colitis occurring. If
that does happen, we treat it like checkpoint inhibitor colitis. The oncologists are
pretty vigilant about this, and a lot of times when we see these patients, they’re
already on steroids. If they have a response to prednisone, that tells you that this is
likely some type of autoimmune-mediated colitis, even if the biopsies are not
specic.
A. Patel (*)
Dept. of Medicine, Division of Gastroenterology and Hepatology, Medical College of
Wisconsin, Milwaukee, WI, USA
e-mail: ampatel@mcw.edu
https://t.me/medicina_free
242
Together, the oncologists and gastroenterologists have generated some guide-
lines and have good data on the use of anti-TNFs as well as anti-integrins. We tend
to see a robust response to anti-TNFs and Entyvio for treatment of these medication-
induced autoimmune immune-mediated colitis cases.
To treat checkpoint inhibitor colitis, usually it takes one or two doses of an anti-
TNF, at the standard 5mg per kg dosing of iniximab, 2 weeks apart. Sometimes,
one dose alone is enough to knock out the colitis; sometimes you need two. And for
vedolizumab, 300mg IV, one to two doses can be quite effective.
I think the oncologists are actually looking at what they can do preventatively.
There are no good studies on this, but they’re studying this particular question: if
someone is going to be put on a checkpoint inhibitor, should they be started on an
anti-TNF or anti-integrin therapy prophylactically?
You decide to do a colonoscopy to evaluate the diarrhea, and you nd mild dif-
fuse erythema and some minimal friability involving portions of the colon. The
appearance is nonspecic. Although it might be a milder IBD, the appearance is
consistent with infection or possibly a drug-induced colitis. Biopsies are not diag-
nostic for IBD and are rather nonspecic.
Would you treat for IBD?
With these ndings, I would not give therapy for IBD if the patient was not on a
checkpoint inhibitor. We’ll give them antidiarrheals, but a lot of times, if the diar-
rhea is really debilitating, the oncologist will be changing the choice of
chemotherapy.
A. Patel
https://t.me/medicina_free
243© 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_49
Chapter 49
Microscopic Colitis
PoonamBeniwal-Patel
A 67-year-old female presents with diarrhea. She had a screening colonoscopy 2
years earlier that was negative. Her only medical problem is hyperlipidemia. Her
meds include simvastatin and baby ASA.A repeat colonoscopy is performed, which
is grossly normal, but biopsies are positive for lymphocytic colitis. She is started on
budesonide 9mg a day, and her diarrhea resolves. After a month, her gastroenter-
ologist tapers her dose to 6 mg, and she does well. But every time she tries to drop
the dose further, the diarrhea worsens. She is referred to you for a second opinion.
What would be your initial approach upon seeing her, and would you stop
her statin, since statins have been associated with microscopic colitis?
The rst thing I think about, even though it sounds like she responded to
budesonide initially, is to check a celiac panel, because patients with microscopic
colitis are at increased risk of developing celiac disease.
Her celiac panel returns negative. Her IgA level is normal.
I would not stop her statin, because even though there is an association between
statins and microscopic colitis, the statin clearly has cardiovascular benets that are
more important.
Would you keep a patient on budesonide 3mg or even 6mg long term?
Yes, sometimes I do; if we need to, then we need to. With lymphocytic colitis,
sometimes they’re aring, and I’ll keep them on 6 mg for 6 months, bring them
back, and then try to drop them to 3mg. So, it’s denitely not a rapid taper. And I’ve
actually had pretty good success with that. I nd that keeping them on the higher
dose for longer periods, not just a month, makes it much more likely they will stay
in remission and are not as likely to rebound.
P. Beniwal-Patel (*)
Medicine, Gastroenterology/Hepatology Division, Medical College of Wisconsin,
Milwaukee, WI, USA
e-mail: pbeniwal@mcw.edu
https://t.me/medicina_free
244
The other thing I will sometimes do in these scenarios is drop the budesonide
dose and use loperamide for breakthrough diarrhea. And then, if this works, I’ll wait
6 months before trying to bring the dose down further. I've had pretty good success
with this strategy. However, there are some patients who develop bad diarrhea and
electrolyte abnormalities, because their diarrhea is so severe. Those patients I’ll just
leave on higher-dose budesonide.
The good news is that there have been studies looking at metabolic bone disease
with budesonide, and thankfully, budesonide really does not impact bone health
signicantly [1]. In patients with concurrent osteoporosis, I’ll loop in an endocri-
nologist, and generally I’ve never had pushback regarding budesonide use.
Have you ever had cases where you’ve had to go to stronger medications?
Not for purely lymphocytic colitis. I can only think of one patient who had a
family history of ulcerative colitis and was initially diagnosed with lymphocytic
colitis. But then years later, things evolved. We repeated the scope, and now, it
looked like it was ulcerative colitis. So, we ended up putting that person on a bio-
logic. Rarely, there are indications for placing patients on a biologic, such as
vedolizumab.
Reference
1. Reilev M, Hallas J, Thomsen Ernst M, Nielsen GL, Bonderup OK.Long-term oral budesonide
treatment and risk of osteoporotic fractures in patients with microscopic colitis. Aliment
Pharmacol Ther. 2020;51(6):644–51. https://doi.org/10.1111/apt.15648. Epub 2020 Jan 30.
P. Beniwal-Patel
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