Abstracts S347
intensity with menstruation. She had no change in bowel movements, no Purpose: Ischemic colitis (IC) is caused by a reduction in intestinal blood
urinary symptoms, no nausea or vomiting. CT abdomen showed right pelvic
cystic mass attached to the uterus, adnexa, cecum and sigmoid colon with no
visualization of appendix (Fig. 1). Colonoscopy showed edematous cecum
with clear pus extruding from the appendiceal orifice confirming appendicitis
(Fig. 2). Laparotomy showed large mass in the pelvis covered with omentum
and small bowel. Pus was expressing from necrotic base of the appendix and
from the right ovarian cyst. Appendectomy and hysterectomy with bilateral
salphingo-oophorectomy were performed. Pathology confirmed appendicitis
with abscess formation along with the ovarian abscesses on both sides. The
culture from the pus was positive for Bacteroides fragilis indicating bowel
as the source of infection. Our patient had appendicitis with abscess that
disseminated causing infection of the ovarian cysts. The infection was walled
off by omentum causing atypical symptoms, thus misleading physicians till
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colonoscopy.
Conclusion: This unusual case illustrates a key role played by colonoscopy in
diagnosing a complicated periappendiceal abscess presenting with atypical
symptoms and non diagnostic radiologic workup.[figure1][figure2]
626
Cisplatin Induced Ischemic Colitis: A Case Report
Kanwar R.S. Gill, MD, Seth A. Gross, MD, Mohammad Al-Haddad, MD,
Tejal Patel, James S. Scolapio, MD∗ . Division of Gastroenterology &
Hepatology, Mayo Clinic, Jacksonville, FL.
flow, which most commonly arises from occlusion, vasospasm, and/or hy-
poperfusion of the mesenteric vasculature. The development of IC in setting
of chemotherapy is rare. We report a case of a 68-year-old woman who devel-
oped IC involving the descending colon after chemotherapy with Cisplatin.
Case: A 68-year-old woman who was on Cisplatin for invasive thymoma pre-
sented with 4-day history of nausea, vomiting, left sided crampy abdominal
pain and bloody diarrhea. The symptoms started 2 days after the first cycle
of chemotherapy. Her past medical history included asthma, bronchiectasis,
colonic diverticulosis, peptic ulcer disease and migraines. The patient was
taking premarin, omeprazole, and denied any NSAID use. The patient also
denied personal or family history of inflammatory bowel disease. The pa-
tient had stable vital signs, and the physical examination demonstrated mild
left lower quadrant abdominal tenderness. Laboratory studies revealed mild
leukocytosis. A CT scan of the abdomen revealed diffuse thickening of the
colon wall with edema and fat stranding in pericolic region from the level
of the splenic flexure through the upper sigmoid colon, and the abdominal
vasculature was patent. A colonoscopy revealed areas of diffuse mucosal
edema and errythema with superficial exudates from 30 cm to 80 cm from
anal verge. The stool studies and colonic biopsies were negative for an in-
fectious etiology, and the biopsies were consistent with IC. The patient was
thought to develop IC secondary to Cisplatin chemotherapy.
Discussion: IC after systemic chemotherapy has been described, but is ex-
ceedingly rare after Cisplatin. There is only one published case report in
English literature of IC related to cispatin by Mauya et al. Their patient re-
ceived Docetaxal with Cisplatin. Although rare, IC should be considered in
patient with colitis symptoms after Cisplatin chemotherapy.
627
A Rare Mimic of Colon Cancer: Ameboma
Malini Madhavan, MBBS∗ , Chenni S. Sriram, MD, Gautam Kumar, MBBS,
MRCP (UK). Department of Internal Medicine, Mayo Clinic, Rochester,
MN and Molecular Pharmacology/Experimental Therapeutics, Mayo
Clinic, Rochester, MN.
Purpose: To appreciate the diagnostic challenge posed by ameboma in a
patient encumbered with multiple ailments as well as to gain a brief insight
into its clinico-pathological features and treatment options.
Results: A 76-year-old male from Minnesota, with history of non-small
cell lung cancer and prostate cancer, presented with subacute intestinal ob-
struction and hematochezia. He had recently started prednisone for radiation
pneumonitis. Computed tomography of the abdomen revealed circumferen-
tial colonic wall thickening and exophytic masses extending from the cecum
to the proximal transverse colon. Colonoscopy revealed multiple, partially
obstructing, necrotic luminal masses in the same distribution. The differen-
tial diagnoses included extensive colon cancer, metastatic cancer, lymphoma,
tuberculosis, and Yersinia colitis. A biopsy done to ascertain colon cancer
showed instead hemophagocytic Entamoeba histolytica in flask-shaped ul-
cers confirming the diagnosis of ameboma. High serum anti-E. histolytica
antibody titers and trophozoites and cysts in the stool provided corroborative
evidence. The clinical enigma was resolved when subsequent questioning
revealed that he was a frequent traveler to Central America and China, the
last visit being 5 years ago. Treatment with Metronidazole for 3 weeks fol-
lowed by Paromomycin for a week culminated in clinical and colonoscopic
resolution.
Conclusion: E. histolytica, a leading cause of parasitic death in develop-
ing nations, represents a significant health hazard for international travel-
ers. Intestinal amebiasis is typified by colonic ulcero-inflammatory lesions
and manifests as a clinical spectrum ranging from asymptomatic infection,
through colitis, ameboma and toxic megacolon. Ameboma, a rare presenta-
tion even in endemic countries, is characterized by an inflammatory colonic
mass indistinguishable from colon cancer. Complications include bleeding,
bowel obstruction and perforation. As exemplified here, immunosuppression
may precipitate severe symptoms in asymptomatic carriers several years after
the sentinel infection. Metronidazole is the cornerstone of therapy followed
S348 Abstracts
by a luminal amebicide such as Paromomycin or Diloxanide furoate to erad-
icate colonization. Colonic mass in the setting of immunosupression and a
history of travel to developing countries, even in the remote past, should raise
the possibility of ameboma. Prompt diagnosis and treatment is imperative
to prevent complications and unnecessary surgery.
628
Two Primary Adenocarcinomas in a Crohn’s Patient with Infliximab
Therapy
Christina A. Tennyson, MD, Divyesh Sejpal, MD, Daniel Labow, MD,
Michael Lewis, MD, Maria T. Abreu, MD∗ . Gastroenterology, Mount Sinai
School of Medicine, New York, NY; Surgery, Mount Sinai School of
Medicine, New York, NY and Pathology, Mount Sinai School of Medicine,
New York, NY.
Purpose: A 55 year old woman with a six year history of Crohn’s disease
presented with recurrent episodes of pancreatitis. The patient was initially
diagnosed with Crohn’s disease of the stomach and duodenum, without in-
volvement of the colon and remainder of the small bowel. One year following
diagnosis, the patient had continued progressive obstructive symptoms and a
loop gastro-jejunostomy was performed for a duodenal stricture. Following
surgery, she received therapy with azathioprine and eventually infliximab.
After approximately three years of therapy with infliximab, the patient de-
veloped severe abdominal pain and was diagnosed with pancreatitis. Aza-
thioprine was discontinued; however, she experienced a recurrent episode of
pancreatitis the following month. A CT scan revealed mild dilatation of the
pancreatic duct without a discrete mass, intra/extrahepatic biliary dilatation,
and wall thickening with enhancement in the second portion of the duode-
num. An MRCP confirmed wall thickening just proximal to the ampulla,
without a ductal filling defect. An endoscopy was performed to locate the
ampulla and characterize Crohn’s disease involvement. While the stomach
appeared grossly normal, a stricture of the duodenum was appreciated 5 cm
past the pylorus and biopsied. The efferent limb of jejunum appeared nor-
mal, but the afferent limb contained an area of stricturing disease and the
ampulla could not be located with a side-viewing endoscope. Biopsies of
the duodenal stricture revealed adenocarcinoma. A pancreaticoduodenec-
tomy was performed with resection of a portion of the gastric antrum. A
Stage I (pT1, N0) well to poorly differentiated adenocarcinoma of the pe-
riampullary duodenum was found in a background of segmental Crohn’s
duodenitis with inflammatory stenosis and polypoid/flat high grade dyspla-
sia. In addition, a signet ring cell adenocarcinoma of the pyloric channel
was found, Stage IB (pT2a, N0), in a background of chronic gastritis with
high grade dysplasia. There was no tumor invasion of the pancreatic/biliary
ducts and 33 regional lymph nodes were negative for adenocarcinoma. This
case of two adenocarcinomas in a young patient with a short duration of
Crohn’s disease raises concern about the relationship between infliximab and
tumorigenesis.
629
Primary Sclerosing Cholangitis and Autoimmune Hemolytic Anemia:
A Casual Association?
Marie B. Wiles, PA-C, Charles H. Parker, MD, Alastair D. Smith, MB,
ChB∗ . Medicine, Halifax Regional Hospital, South Boston, VA and
Medicine, Duke University, Durham, NC.
Purpose: Primary sclerosing cholangitis (PSC) is a progressive and incur-
able condition characterized by inflammation, fibrosis, destruction and loss
of interlobular-sized bile ducts, leading to biliary cirrhosis and liver failure.
It is more common among men, is frequently associated with chronic in-
flammatory bowel disease (IBD) and with the following HLA haplotypes,
-A1, -B8, and -DR3. Patients with PSC have increased prevalence of other
autoimmune disorders, e.g. celiac disease. Autoimmune hemolytic anemia
(AIHA) has been described in association with PSC, albeit uncommonly.
A 55 year-old man with stable PSC, confirmed the previous year, and treated
hypothyroidism but without chronic IBD, complained of increasing fatigue,
chest pain and dyspnea of two weeks’ duration. He denied overt blood loss,
fever, pruritus or jaundice. The principal examination findings were pallor
and icterus. Vital signs were stable. Heart sounds were normal, there was
no pericardial friction rub and both lung bases were clear. Neither liver nor
spleen was palpable, and he had no clinical evidence of ascites. Laboratory
data were as follows: Hb 6.7 g% (normal range [NR]: 14–18), and MCV
108.6 fL (NR: 80–94), with normal white cell and platelet counts. The retic-
ulocyte count was 6.2% (NR: 0.5–4). LDH concentration was 164 IU/L (NR:
91–180). However, the serum haptoglobin was 2 mg% (NR: 36–195). His
polyspecific, direct antiglobulin test was positive. Serum concentrations of
ferritin, folate and vitamin B12 were normal. Total serum bilirubin (BR)
was 3.5 mg% (NR: 0.4–1.2), of which the indirect component was 2.6 mg%.
The alkaline phosphatase was 420 IU/L (NR: 42–121), but aminotransferase
concentrations were normal. Albumin was 4 g% (NR: 3.2–5.5), and his pro-
thrombin time was 12 seconds (NR: 9–13.1). Although his EKG revealed new
left bundle branch block, cardiac enzymes were not elevated. A presump-
tive diagnosis of AIHA was made and treatment with methyl prednisolone
begun. Concentrated red cells were transfused cautiously. Four weeks after
commencing corticosteroid therapy his Hb had risen to 13.2 g%, and the hap-
toglobin to 37.8 mg%. His BR was 1.3 mg%. The daily dose of prednisone
was 40 mg.
Reports of the co-existence of PSC and AIHA include the sequence described
above, and vice versa. This is the first report to our knowledge of a patient with
PSC, AIHA and autoimmune hypothyroidism. The corticosteroid exposure
demands careful attention to minimization of bone density loss.
630
Henoch-Schönlein Purpura with Terminal Ileitis Masquerading as
Crohn’s Diseae
Eric R. Wollins, MD, Antoinette Saddler, MD, Marie L. Borum, MD∗ .
Division of Gastroenterology and Liver Diseases, George Washington
University Medical Center, Washington, DC.
Purpose: An 18 year-old Korean male presented with a 1-week history of
colicky abdominal pain, non-bloody diarrhea and painful swelling of his
right ankle. His PMH, FHx and SHx were unremarkable. Upon initial eval-
uation, he was febrile, tachycardic and tender with palpation of his RLQ.
His right ankle appeared warm and swollen without any evidence of rash.
Admission labs: WBC:18, H/H: 18/ 48, Plt: 400, BUN:11, Cr: 1.0. AXR was
normal. ABD CT scan revealed a mildly dilated and thickened terminal ileum
with a normal appendix. Initial differential diagnosis included: Crohn’s dis-
ease with extra-intestinal manifestations, infectious colitis and diverticulitis.
Additional labs: ESR: 6, CRP: 4.4. Colonoscopy showed a normal rectum
and colon and terminal ileitis with localized edema, erythema and puru-
lent, superficial ulcerations. Given these findings, a presumptive diagnosis
of Crohn’s disease was made and the patient was started on a 5-ASA regimen.
Biopsies from the terminal ileum revealed chronic active ileitis with ulcer-
ation and fibropurulent exudate. Additional labs: ASCA(+), p-ANCA (−),
negative blood, urine and stool cultures. Seven days after discharge, the pa-
tient represented appearing toxic with RLQ pain and a new bilateral lower ex-
tremity purpura with associated polyarthritis. Labs revealed:WBC:14, H/H:
14/42, Plt:450, Eos:2, ESR:53, CRP:6.7, BUN:77, Cr:2.5 with nephrotic
range proteinuria and a normal coagulation profile, peripheral smear, hep-
atitis panel and rheumatologic serologic evaluation. An IgA level was mildly
elevated at 464. Kidney biopsy showed large irregular mesangial subepithe-
lial deposits and a skin biopsy demonstrated small vessel leukocytoclastic
vasculitis. Given the constellation of these new findings including palpa-
ble purpura in the absence of coagulopathy, abdominal pain, arthritis and a
biopsy with predominant IgA deposition, a diagnosis of Henoch-Schönlein
purpura (HSP) with terminal ileitis was made. The patient was started on
prednisone with a rapid clinical improvement and normalization of renal
function.