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Corresponding author: Carmen Salvador Coloma; Department of Medical Oncology, Hospital Universitari i Politècnic La Fe, Valencia, Spain.
Cite this article as: Salvador-Coloma C, Bennis M, Díez-Langhetée L, Niño-Gómez O, Reche-Santos E, Juan-Vidal O. Intestinal pseudo-obstruction: An im-
portant diagnostic challenge. Int J Cancer Ther Oncol 2015; 3(3):339. DOI: 10.14319/ijcto.33.9

[A part of this research was presented at Desafío Oncológico-2014, which was held From March 12- April 12, 2014 in Valencia, Spain]

© Salvador-Coloma et al. ISSN 2330-4049

Intestinal pseudo-obstruction: An important diagnostic challenge
Carmen Salvador Coloma1, Mohamed Hassan Bennis2, Lydia Díez Langhetée3, Óscar Niño Gómez1,

Encarnación Reche Santos1, Óscar Juan Vidal1

1Department of Medical Oncology, Hospital Universitari i Politècnic La Fe, Valencia, Spain
2Department of Medical Oncology, Hospital de Xativa, Valencia, Spain

3Department of Internal Medicine, Hospital Universitari i Politècnic La Fe, Valencia, Spain

Received April 12, 2015; Revised May 12, 2015; Accepted May 17, 2015; Published Online June 09, 2015

Case Report

Abstract
We present the case of a 72-year-old patient admitted on various occasions with symptoms of intestinal pseudo-obstruction.
Extensive diagnostic tests eventually found that the patient had small-cell lung cancer associated with high anti-HU antibody
titres, which pointed to a probable paraneoplastic intestinal obstruction syndrome associated with small-cell lung cancer. A
paraneoplastic syndrome causing abnormal changes in gastrointestinal motility can be the first signs of small cell lung cancer.
These syndromes improve with treatment of the underlying disease, as seen in our patient, who stopped having episodes of i n-
testinal pseudo-obstruction after administration of chemotherapy.

Keywords: Lung Cancer; Small-Cell Lung Cancer; Anti-HU; Paraneoplastic Syndrome; Intestinal Obstruction

Introduction
A 72-year-old patient with a number of cardiovascular risk
factors (hypertension, diabetes, dyslipidaemia, obesity and
smoking, with a history of 120 pack-years) and chronic ob-
structive pulmonary disease on treatment with insulin, anti-
hypertensive drugs, lipid-lowering drugs and bronchodila-
tors.

He came to Accident and Emergency Department with a
three-day history of nausea, vomiting, intolerance of oral
diet and generalised abdominal pain associated with not
having passed wind or moved his bowels for eight days.

The patient’s general condition was fair. Haemodynamically
was stable. Heart and lung sounds were normal. Abdomen
was distended. Tympanic percussion was observed. No bowel
sounds were detected. Diffuse pain on abdominal palpation
was observed. No relevant findings on rectal examination
and the rest of examination were found.

Additional tests were done: normal blood test results except
creatinine 1.53 mg/dl; Urea 71 mg/dl; CRP 89 mg/l; trans-
aminases and bilirubin within normal limits; haemoglobin
11.2 g/dl; MCV 74 fl; MCH 22.9 pg; Leucocytes 10.2×103 per
ul (differential normal); Quick’s Test 72%. The X-ray Abdo-
men showed small bowel loops greatly dilated and no gas
observed in colon, even distally. Erect, there areair-fluid

levels and more than three levels. Images suggestive of small
bowel obstruction (Figure 1). The CT Abdomen-Pelvis scan
manifested a distension of stomach and jejunum as far as
right iliac fossa, where change in lumen visible although
with no evidence of obstructive cause. No other relevant
findings (Figure 2).

FIG. 1: Image suggestive of small bowel obstruction.

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FIG. 2: Distension of stomach and jejunum as far as right iliac fossa, where change in lumen visible although with no evidence of obstructive
cause.

TABLE 1: Intestinal pseudo-obstruction causes.
Auto-
immune
diseases

Infectious
diseases

Endocrine diseases Neurological
diseases

Oncological
disease

Myopathy
Granuloma-
tous diseases

Drugs Other causes

LESa HIVc Hypo- parathy-
roidism

D.Ng Pheo-chromo
cytoma

MMj Tuberculosis Anti- depres-
sants

Ehlers-Danlos

Crohn
disease

CMVd Hypo- thyroidism Stroke Multiple
Myeloma

Duchenne Sarcoidosis Anti-
parkisonian

Radiation enteritis

Celiac
disease

VZVe Hyper- thyroidism M.Sh M.Dk Wegener Vincristine eosinophilic gas-
troenteritis

Sclero-
derma

VEBf Parane-
oplastic

DOFl Churg
Strauss

Diltiazem lymphoid infiltra-
tion

DMb Kawasaki SC injuryi Nifedipine sickle-cell anemia
Chagas Amyloidosis Narcotics Diverticulosis

Parkinson

Abbreviations: aLES: Systemic lupus erythematosus, bDM: Diabetes mellitus, cHIV: Human immunodeficiency virus, dCMV: Cytomegalovirus,
eVZV: Varicella zoster, fVEB: Epstein barr virus, g D.N: Diabetic neuropathy, hM.S: Multiple sclerosis, ispinal cord injury, jMM: Mitochondrial
myopathy, kM.D: Myotonic dystrophy, loculopharyngeal dystrophy.

In view of the above, an exploratory laparotomy was per-
formed, but no obstructive component was found, only a
dilation of small bowel loops from the ligament of Treitz to
the terminal ileum with dilation of the caecum without signs
of obstructive cause. Following the intervention, the patient
was transferred to the Recovery Unit and once he had suffi-
ciently recovered, a CT scan of the chest/abdomen/pelvis was
ordered which showed lymphadenopathy-type mediastinal
masses in virtually all the node spaces, in addition to ischae-
mia with pneumatosis intestinalis in the caecum and part of
the ascending colon, along with pneumoperitoneum, which
was possibly secondary to microperforation. The patient was
eventually discharged once normal bowel function was re-
stored, with conservative treatment and follow-up at Respir-
atory Medicine Outpatients.

Two weeks after being discharged, the patient had a further
episode of abdominal pain, vomiting and diarrhoea lasting a
week, with deterioration in his general condition, and had to
be re-admitted. Suspecting dysentery, tests were ordered for
rotavirus and adenovirus antigens, clostridium toxin, para-
sites in faeces, stool cultures and human immunodeficiency
virus (HIV) serology, all of which were negative. A

drug-related cause was ruled out. The symptoms were not
suggestive of either food poisoning or food allergy. Thyroid
hormones and transglutaminase antibodies were normal. A
colonoscopy was performed showing ulceration of the right
colon/caecum; biopsies were taken but results came back as
normal. Having made good progress, the patient was dis-
charged with the diagnosis of suspected ischemic colitis and
an appointment for follow-up at Gastrointestinal Medicine
Outpatients.

Over the following four weeks, he was admitted on two
more occasions for partial obstruction which, like the previ-
ous episodes, simulated intestinal obstruction but in the ab-
sence of any anatomical obstruction. The main causes of
intestinal pseudo-obstruction were ruled out (Table 1): au-
toimmune (for not meeting criteria; ANAs, ENAs, ANCAs
negative; absence of skin manifestations and normal colon-
oscopy), endocrine-metabolic (hormones negative), myopa-
thy (biopsy negative), infectious causes (serology negative).

At the end of this process, the differential diagnosis was be-
tween granulomatous, neurological and oncological diseases.
We then ordered a positron-emission tomography (PET)



Volume 3 • Number 3 • 2015 International Journal of Cancer Therapy and Oncology 3
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© Salvador-Coloma et al. ISSN 2330-4049

scan, endobronchial ultrasound (EBUS) with bronchoalveo-
lar lavage, electromyogram (EMG), anti-HU antibodies,
Mantoux test and tumour markers. The PET showed abnor-
mal uptake in a number of different lymph node regions
with SUV (standardized uptake value) ranging from 4.8 to
11.3. The Mantoux test was negative and tumour markers
and angiotensin-converting enzyme (ECA) were normal.

The pathology results were compatible with small cell lung
cancer. At the same time, the lymph node samples were sub-
jected to flow cytometry analysis, ruling out lymph node cell
proliferation.

With the diagnosis of small cell lung cancer with disease
limited to the thorax, the patient was started on cispla-
tin/etoposide-based chemotherapy with concomitant radio-
therapy. We received the positive anti-HU anti-neuronal
antibody results after starting the treatment.

After five cycles of chemotherapy, the patient’s general con-
dition is good and he has had no further admissions for new
episodes of partial bowel obstruction.

Discussion
A paraneoplastic syndrome causing abnormal changes in
gastrointestinal motility can be the first signs of small cell
lung cancer.2, 3

Paraneoplastic syndromes can affect any organ or tissue,
including both the central nervous system (CNS) and the
peripheral nervous system. The latter type occurs in less than
1% of all cancer patients. The cause of the majority of para-
neoplastic neurological syndromes is unknown, but it is
thought that the pathogenesis is immune-mediated due to
fact that the expression of neuronal antigens by the tumour
triggers an immune response against it and the immune re-
sponse, in turn, affects the nervous system.3, 4

Paraneoplastic autonomic neuropathy normally occurs as a
component of other disorders, but it is very rare for it to be
the predominant sign.1 These patients may develop
life-threatening complications such as gastrointestinal pare-
sis, cardiac arrhythmias and postural hypotension. They are
frequently associated with small cell lung cancer (SCLC),
cancer of the pancreas, carcinoid tumours and lymphoma.

Anti-HU antibodies are seen in single or multiple (combined
forms) paraneoplastic syndromes, such as sensory-motor
neuropathy, neuropathy, cerebellar degeneration and gas-
trointestinal pseudo-obstruction.5-6

The production of HU antigens by SCLC is not fully under-
stood. In normal tissues, HU antigen production is restricted
to the tissues of the nervous system. This antigen is found in
the majority of SCLC cases. Although the neuroendocrine

origin of SCLC is widely accepted, only 50% of neuroblasto-
mas and very few neuroendocrine tumours express the HU
antigen.7

We have presented the case of a patient with chronic intes-
tinal pseudo-obstruction as the first sign of his cancer. Pseu-
do-obstruction is defined as recurrent or persistent episodes
of obstructed bowel symptoms in the absence of any me-
chanical obstruction. In the majority of reported cases, this
complication is associated with SCLC and thymoma.

Nguyen-tat et al. detected in 1 patient, four months earlier of
the diagnosis of SCLC, a symptomatic paraneoplastic gastro-
paresis with high anti-HU antibody titres.3

Our patient was anti-HU antibody positive and the finding
of high anti-HU antibody titres suggests a clear influence of
these antibodies on the development of our patient’s disease.
However, low titres have been detected in 16% of patients
with SCLC without paraneoplastic syndrome.8 These anti-
bodies exhibit reactivity against mesenteric plexus neurons
producing inflammatory changes at these levels.9

The average time between the development of neurological
paraneoplastic syndromes and diagnosis of cancer is four
months;1-3 in our case, there was a gap of four and a half
months between the onset of symptoms and the histological
diagnosis.

Based on the assumption that paraneoplastic neuropathies
are autoimmune disorders, several studies have been carried
out with steroids, immuno-suppressants and even plasma-
pheresis, but with no clinical benefit being found.3-10-11 These
syndromes improve with treatment of the underlying dis-
ease, as seen in our patient, who stopped having episodes of
intestinal pseudo-obstruction after administration of chem-
otherapy.

Clinicians should consider paraneoplastic neuropathies, as
chronic intestinal pseudo-obstruction, as a differential diag-
nosis for gastrointestinal dysmotility. Identification of para-
neoplastic gastroparesis can lead to earlier diagnosis of a ma-
lignancy, and, in some cases, better prognosis.

Conflict of interest
The authors declare that they have no conflicts of interest.
The authors alone are responsible for the content and writ-
ing of the paper.

References
1. Dalmau J, Graus F, Rosenblum MK, Posner JB. An-

ti-Hu--associated paraneoplastic encephalomyeli-

http://dx.doi.org/10.1097/00005792-199203000-00001


4 Salvador-Coloma et al.: Paraneoplastic syndrome International Journal of Cancer Therapy and Oncology
www.ijcto.org

© Salvador-Coloma et al. ISSN 2330-4049

tis/sensory neuronopathy. A clinical study of 71
patients. Medicine (Baltimore). 1992;71:59-72.

2. Jun S, Dimyan M, Jones KD, Ladabaum U. Obstipa-
tion as a paraneoplastic of small cell lung cancer:
case report and literature review. Neurogastroen-
terology Motil. 2005;17:16-22.

3. Nguyen-tat M, Pohl J, Günter E, et al. Severe para-
neoplastic gastroparesis associated with anti-Hu
antibodies preceding the manifestation of
small-cell lung cancer. Z Gastroenterol.
2008;46:274-8.

4. Abeloff M, Armitage J, Niederhuber J, et al. Sín-
dromes Neurológicos paraneoplásicos. Oncología
Clínica. 2005; 1:993.

5. Heidenreich F, Schober R, Brinck U, Hartung HP.
Multiple paraneoplastic syndromes in a patient
with antibodies to neuronal nucleoproteins (an-
ti-Hu). J Neurol. 1995;242:210-6.

6. Cuillerier E, Coffin B, Potet F, et al. Paraneoplastic
intestinal pseudo-obstruction revealing small cell
lung carcinoma: "the anti-Hu syndrome". Gastro-
enterol Clin Biol. 1998; 22: 346-8.

7. Dalmau J, Furneaux HM, Cordon-Cardo C, Posner
JB. The expression of the Hu (paraneoplastic en-
cephalomyelitis/sensory neuronopathy) antigen in
human normal and tumor tissues. Am J Pathol.
1992;141:881-6.

8. Lennon VA, Sas DF, Busk MF, Scheithauer B. En-
teric neuronal antibodies in pseudoobstruction
with small-cell lung carcinoma. Gastroenterology.
1991;100:137-42.

9. Altermatt HJ, Rodriguez M, Scheithauer B, Lennon
VA. Paraneoplastic anti-Purkinje and type 1 an-
ti-neuronal autoantibodies bind selectively to cen-
tral peripheral and autonomic nervous system cells.
Lab Invest. 1991; 65:412-20.

10. Thirkill CE, FitzGerald P, Sergutt RC. Can-
cer-associated retinopathy (CAR syndrome) with
antibodies reacting with retinal, optic nerve and
cancer cells. N England Journal of Medicine. 1989;
321: 1589-94.

11. Bell CE, Seetharam S. Expression of endodermally
derived and neural crest-derived differentiation
antigens by human lung and colon tumors. Cancer.
1979; 44:13-8.

http://dx.doi.org/10.1097/00005792-199203000-00001
http://dx.doi.org/10.1111/j.1365-2982.2004.00608.x
http://dx.doi.org/10.1055/s-2007-963429
http://dx.doi.org/10.1007/BF00919593
http://www.ncbi.nlm.nih.gov/pubmed/97622211415481
http://www.ncbi.nlm.nih.gov/pubmed/97622211845756
http://dx.doi.org/10.1056/NEJM198912073212307
http://dx.doi.org/10.1002/1097-0142(197907)44:1<13::AID-CNCR2820440103>3.0.CO;2-B
http://www.ncbi.nlm.nih.gov/pubmed/9762221
http://www.ncbi.nlm.nih.gov/pubmed/97622211921331

