Differential Diagnosis of Gastrointestinal Polyps Based on a

Transkript

Differential Diagnosis of Gastrointestinal Polyps Based on a
CASE REPORT / OLGU SUNUMU
2013
Differential Diagnosis of Gastrointestinal Polyps Based on a
Dyspeptic Patient
Dispeptik Bir Olgu Üzerinden Gastrointestinal Poliplerin Ayırıcı Tanısı
AUTHORS /
YAZARLAR
Fatih Borlu
Internal Medicine
Clinics, Sisli Etfal
Training and Research
Hospital, Istanbul,
Turkey
Binnur Tagtekin
Sezer
Family Medicine Clinics,
Sisli Etfal Training and
Research Hospital,
Istanbul, Turkey
Önder Sezer
Bagcilar Community
Health Care Center,
Istanbul, Turkey
CASE
A 35-year-old caucasian man who has dyspeptic symptoms for over two
years in spite of using several gastroprotective agents. He had an epileptic attack
15 years ago. There was not any particular disease in his family. The patient was
taking carbamazepine epokside, topiramate, escitalopram and several
proton-pump inhibitors. He was smoking for 16 years and rarely drinking
alcohol. In his physical examination, he had epigastric pain with palpation. He
was nibbling and after that he had dyspeptic symtoms with vomiting.
Esophago-gastroduedonoscopy was performed to see if there was a patologic
lesion causing this symptoms. A diminutive polypoidal lesion was determined at
duodenal bulb and diagnostic biopsy was performed.
Based on the patient’s physical examination and findings, which one of the
following is the most likely diagnosis?
A. Gastrointestinal Stromal Tumour
B. Primary Gastric Lymphoma
C. Familial Adenomatous Poliposis
D. Brunner Gland Hyperplasia
E. Gastric Cancer
OLGU
Dispeptik yakınmaları olan 35 yaşında erkek hastanın birkaç gastroprotektif
ajan kullanımına rağmen iki yıldır devam eden şikayetleri mevcuttu. 15 yıl önce
bir epileptik nöbet geçirmişti. Aile öyküsünde belirgin bir özellik yoktu. Hasta
karbamazepin epoksit, topiramat, essitalopram ve bazı proton pompa inhibitörü
kullanıyordu. 16 yıldır sigara içiyor ve nadiren alkol alıyordu. Fizik
muayenesinde palpasyon ile epigastrik ağrı mevcuttu. Azar azar yiyor ve
sonrasında kusma ile birlikte dispeptik yakınmaları oluyordu. Bu bulguları
oluşturacak olası bir patolojik lezyon için özofagogastroduodenoskopi yapıldı.
Duodenum bulbusunda minik bir polipoid lezyon saptandı ve diagnostik biyopsi
yapıldı.
Hastanın fizik muayene ve bulgularına göre, en olası tanı aşağıdakilerden
hangisidir?
A. Gastrointestinal Stromal Tümör
B. Primer Gastrik Lenfoma
C. Familiyal Adenomatöz Polipozis
D. Brunner Gland Hiperplazisi
E. Gastrik Kanser
48 Euras J Fam Med 2013; 2(1):48-50
Discussion
The answer is “D”. Brunner glands are localized
in the submucosa layer of the first part of duodenum
(bulbi) and descendent duodenum. These structures
are making mucous and serous secretions draining
from Lieberkühn crypts (1). Small mucosal folds in
the proximal duodenum are usually associated with
Brunner Gland Hyperplasia (BGH) and gastric
metaplasia (2). Brunner Gland Hyperplasia is not
well known. It is thought that gastric hyperacidity
stimulates gland hyperplasia (1). But despite the fact
that 45% of patients have hyperacidity, 20% of
patients have hypoacidity. Other mechanisms put
forth are local irritation, increased parasempatical
activity, helicobacter pylori infestations and chronic
pancreatitis (3,4). Feyrter (5) classified the abnormal
glandular proliferation in three types. Type 1; diffuse
nodulary hyperplasia with multiple sessile
projections. Type 2; nodulary hyperplasia which is
limitted to duodenal bulb. Type 3; glandular adenoma
appeared with polypoidal lesions. But this
classification is controversial. There is no concensus
to classify the benign pathologies of brunner glands
(3).
BGH seems in middle-aged men and women. In a
study with 27 patients the most common localizations
of BGH are the back of the first and second parts of
duodenum (3). These lesions can cause pancreatic
and biliary obstructions and pancreatitis (6). Fourty
five percent of them can couse bleeding and 51%
seems with enteric obstruction (7). Most lesions are
Table 1. Selected differential diagnosis of dyspeptic symptoms
Condition
Characteristics
Primary Gastric Lym- Seen in sixties, patients come with stomach pain, ulcers or other localized symptoms,
phoma
fever or fatigue
Gastrointestinal
Stromal Tumour
Usually asymptomatic, can bleed, ulcerate and mostly seen between 55-65
Familial Adenomatous Poliposis
Autosomal dominant disorder. Extraintestinal lesions are osteomas, epidermoid cysts,
desmoid tumours, congenital hypertrophy of the retinal pigment epithelyum. Seems
with thyroid cancer, pancreatic cancer and hepatoblastomas
Gastric Cancer
Epigastric pain which may be relieved by food or antiacids, nausea, weight loss, vomiting, dysphagia, anaemia
Brunner Gland Hyperplasia
Usually asymptomatic, epigastric pain, vomitting after food intake, gastrointestinal
bleeding
49
Borlu F ve ark. Differential Diagnosis of Gastrointestinal Polyps Based on a Dyspeptic Patient
benign, but there are patients observed with
malignansy. In Sakuri’s study only 2 percent of
patients had dysplasia and invasive carcinoma. It is
hard to exclude malignancy; so patients with big
lesions needed surgical resection (8).
Primary Gastric Lymphoma: Mucosa-associated
lymphatic tissue lymphomas constitute about 10% of
all types of non-Hodgkin’s lymphoma. It has seen in
sixties with stage 1 or stage 2 disease outside the
lymph nodes. Patients come with stomach pain,
ulcers or other localized symptoms. Rarely they come
with fever or fatigue (9).
Gastrointestinal Stromal Tumour (GIST): GISTs
are a group of gastrointestinal mesenkimal tumours.
They are usually asymptomatic and found by chance.
They can bleed, ulcerate and mostly seem between
55-65. GISTs generally grow slowly but may be
malignant. Treatment is surgical as far as possible (9).
Familial Adenomatous Poliposis (FAP): FAP is
an autosomal dominant disorder. It is characterized
by the presence of hundreds to thousands of
cholorectal adenomas and duedonal adenomas. Cystic
gland polyps, predominantly in the procsimal
stomach, and duodenal adenomas are foun in FAP.
Other extraintestinal lesions are osteomas,
epidermoid cysts, desmoid tumours, congenital
hypertrophy of the retinal pigment epithelyum. Other
cancers in FAP include thyroid, pancreatic and
hepatoblastomas (9).
Gastric Cancer: There is a strong link between
H.pylori infection and distal gastric cancer.The other
epidemiologic factors are dietary, smoking tobacco
and genetic abnormality. Weight loss is the dominant
feature.Other symptoms are epigastric pain which
may be relieved by food or antiacids, nausea, weight
loss, vomiting, dysphagia, anaemia (9).
Kaynaklar
1. De Angelis G, Villanacci V,
Lovotti D, Gianni E, Mazzi
A, Buonocore M et al.
Hamartomatous polyps of
Brunner’s gland. Presentation
of 2 cases. Review of the
literature. Minerva Chir
1989; 44: 1761-6.
2. Cotton P, Williams C.
Practical Gastrointestinal
Endoscopy. 4th ed. Oxford,
Blackwell Science Ltd, 1997;
38-47.
3. Levine JA, Burgart LJ, Batts
KP, Wang KK, Brunner’s
gland hamartomas: clinical
presentation and patological
features of 27 cases. Am J
Gastroentorol 1995; 90(2):
290-4.
4. Kovacevic I, Ljubicic N,
Cubic H, Doko M, Zovak M,
Troskot B, et al. Helicobacter
pylori infection in patients
with Brunner’s gland
adenoma. Acta Med Croatica
50 2001;55(4-5):157-60.
5. Feyrter F. Uber wucherunger
der Brunnerschen Drusen.
Wirchows Arch 1938; 293:
509-26.
6. Stermer E, Elias N, Keren D,
Rainis T, Goldsteim O, Lavy
A. Acute pancreatitis and
upper gastrointestinal
bleeding as precenting
symptoms of duedonal
Brunner’s gland hamartoma.
Can J Gastroentorol 2006;
20(8): 541-2.
7. Walden DT, Marcon NE.
Endoscopic injection and
polypectomy for bleeding
Brunner’s gland hamartoma;
case report and expanded
literature review. Gastrointest
endosc 1998; 47(5):403-7.
8. Sakurai T, Sakashita H,
Honjo G, Kasyu I, Manabe T.
Gastric foveolar metaplasia
withdysplastic changes in
Brunner gland hyperplasia:
possible precursor lesions for
Brunner gland
adenocarsinoma. Am j Surg
Pathol 2005; 29(11):1442-8.
9. Fairclough PD, Silk DBA.
Gastrointestinal disease. In:
Kumar P, Clark M, ed.
Textbook of Clinical
Medicine. 7th ed. Spain:
Elsevier; 2009. p. 264-301.
Corresponding Author / İletişim için
Dr. Binnur Tagtekin Sezer, MD
Family Medicine Clinics,
Sisli Etfal Training and Research Hospital
Istanbul, Turkey
E-mail: [email protected]

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