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WJIM
A rare cause of upper GI bleed
1
*Waseem Raja Dar, 2
Najeeb Ullah Sofi, 3
Imtiyaz Ahmad Dar, 4
Basharat Ahmad Kasana,
5
Moomin Hussain and 6
Muzamil Latief
1*,2,3,4,5
Department of Medicine, Gastroenterology Division. Shere Kashmir Institute of Medical Sciences,
Soura.Srinagar, J& K, India
Upper GI bleed is a common, scary and life threatening medical condition usually caused by
peptic ulcer disease or oesophageal varices. Uncommon causes include neoplasms,
aortoenteric fistulas, vascular lesions, Dieulafoy's lesion etc. Patients usually present with
hematemesis or melena. GIST is the third most common tumor of stomach and also the
most common mesenchymal tumor. GIST may be asymptomatic and discovered incidentally
or they may cause nonspecific symptoms like early satiety and fullness. Although major
presentation of GIST is upper GI bleed, GIST as a cause of upper GI bleed is very rare. We
here present a patient admitted to us with massive upper GI bleed due to gastrointestinal
stromal tumor.
Keywords: GIST, upper GI bleed, carney complex, imatinib, regorafenib.
INTRODUCTION
Upper gastrointestinal bleeding (UGIB) refers to blood
loss of recent onset originating from a site proximal to
the ligament of Treitz. It is a common clinical problem
seen in the practice of Gastroenterology and Internal
Medicine. Patients may present either with
hematemesisor melena. Common causes include
ulcers, varices, Mallory Weiss tears, erosions and
erosive esophagitis. Rare causes include neoplasms,
aortoenteric fistulas, vascular lesions, Dieulafoy's
lesion, prolapse gastropathy and hemobilia or
hemosuccus pancreaticus. We here present a patient
admitted with upper GI bleed due to a very rare cause
i.e. Gastrointestinal Stromal Tumor (GIST). A brief
review of literature follows.
CASE REPORT
A 55 year old male was admitted to our
Gastroenterology Department with complaints of
passage of multiple black tarry foul smelling stools of
two days duration. There was no history of
hematemesis, abdominal pain, jaundice or bleeding
from any other orifice. Patient was non-alcoholic and
did not report intake of any NSAIDS. There was no
previous history of hypertension, diabetes mellitus or
travel outside the state. On clinical examination, patient
was conscious and oriented. There was tachycardia
and postural drop in blood pressure. No signs of
chronic liver disease were present. Respiratory,
Cardiovascular and Abdominal examinations were
normal. An initial diagnosis of Peptic Ulcer Disease was
made and patient resuscitated with intravenous fluids,
blood transfusions and pantoprazole infusions.
Baseline investigations revealed microcytic anemia
(Table 1). Meanwhile patient was taken to endoscopy
room for urgent procedure. Endoscopy revealed a 4-5
cm sub mucosal bulge with central depression in
stomach (Fig 1) with a differential diagnosis of
leiomyoma or GIST. CECT abdomen showed an
exoluminal homogenous enhancing mass (5 x 4.5cm)
in fundus with indentation of fundic wall (Fig 2).
Patient however continued to lose blood and hence it
was decided to operate patient for diagnostic and
therapeutic reasons. Intraoperative findings included a
6×6 cm mass in anterior wall of stomach at junction of
body and fundus and small enlarged lymph node at the
root of left gastric vessels (Fig 3, 4).
*Corresponding Author: Waseem Raja Dar,
Department of Medicine, Gastroenterology Division.
Shere Kashmir Institute of Medical Sciences, Soura.
Srinagar, J&K, India. Email: drwaseem.mw@gmail.com
World Journal of Internal Medicine
Vol. 2(1), pp. 003-006. May, 2015. © www.premierpublishers.org,ISSN: XXXX-XXXXx
Case Report
Dar et al. 003
Parameter Result Parameter Result ECG:- Sinus Tachycardia
X-rayChest: - Normal.
Coagulogram : Normal
USG abdomen: normal
Urine exam: normal
HIV /HBV /HCV/HAV serology:
negative
Hb 5.7 g% Urea 28 mg/dl
TLC 8200/mm
3
Creatinine 0.5 mg/dl
DLC Neutros=83%
Lymphos=12%
Bilirubin 0.4 mg/dl
PLT 117 lacs/mm
3
ALT 15U/L
MCV 71 fL ALP 77 U/L
MCH 23 pg Total Protein 6.76 g/dl
Albumin 3.8 g/dl
Table 1.Baseline Investigations.
Figure 1. UGI endoscopy: 4 -5 cm sub mucosal
bulgewith central depression in stomach.
Figure 2. CECT Abdomen: Homogenous, enhancing
mass (5 x 4.5cm) in fundus.
No omental and liver metastasis were seen. Wide local
excision of the tumour was carried out. Microscopic
examination of the tumor was suggestive of GIST (Fig
5) while as lymph node showed reactive hyperplasia
only. Tumour cells were positive for C kit, CD34 and
DOG1. SMA was focally positive. Our complete
diagnosis was Gastro Intestinal Stromal Tumor Stage
III A (TNM Staging) presenting as massive upper GI
bleed.
Patient was referred to medical oncology department
where he was put on Imatinib 400mg/day. Presently
patient is on their follow up and has completed three
months of treatment.
DISCUSSION
Previously classified as leiomyomas, leiomyosarcomas
and leiomyoblastomas, GIST is a term introduced by
Mazur and Clark for a group of gastrointestinal tumors
that lack the immune histochemical features of
Schwann cells and did not have the ultrastructural
World J. Int. Med. 004
Figure 3. Intraop: 6×6 cm mass in anterior wall Figure 4. Operative Specimen of stomach
Figure 5. High Power Microscopy: Spindle cell tumour with
areas of hyalinization.
characteristics of smooth muscle cells (Mazur et al
1983). Although stomach is the most common site, they
may occur anywhere along the GI tract. They usually
occur in middle age but may occur rarely in children as
a part of Carney's triad (gastric stromal tumor, extra
adrenal paraganglioma and pulmonary chordoma).
Most common mutation in GISTs is gain-of-function
mutations in the KIT (c-kit) proto-oncogene, which
almost occurs in all GISTs (Hirota et al 1998). These
mutations lead to constitutive over expression and
autophosphorylation of c-Kit, provoking a cascade of
intracellular signalling that propels cells toward
proliferation or away from apoptotic pathways. A small
subset of patients (5%) may be KIT-negative (Corless
et al 2005).In such cases, mutations of platelet-derived
growth factor receptor-alpha (PDGFA), protein kinase
C, and DOG1have been detected.
GISTs may be asymptomatic and discovered
incidentally. More often, they are associated with
nonspecific symptoms i.e., early satiety and bloating
unless they ulcerate, bleed, or grow large enough to
cause pain or obstruction. Three major presentations
include overt GI bleeding (40%), abdominal mass
(40%) and abdominal pain (20%) (Miettinen et al 2005).
Although the most common presentation of GIST is
bleeding, GIST as a cause of upper UGI bleeding is
very rare and only case reports exist (Tomoko et al
2008, Tarun et al 2010). A small minority of GISTs are
associated with hereditary syndromes like Type 1
Neurofibromatosis and Carney Complex. GISTs have
uncertain malignant potential. Between 10% and 25%
Dar et al. 005
of patients present with metastatic disease (Tran et al
2005).
GISTs arise from pleuripotential mesenchymal stem
cell programmed to differentiate into the interstitial cell
of Cajal (Pacemaker cells of GIT).Microscopically, GIST
cell morphology is usually spindle-shaped (70%), but
some GISTs consist of rounded cells (epithelioid type,
20%) or a mixture, but they can also be pleomorphic.
GISTs have a fragile pseudo capsule, which may
rupture during surgery which could increase the risk of
peritoneal dissemination (Fletcher et al 2002).
Treatment of GISTs is medical as well as surgical.
Surgery remains the treatment of choice for low risk
patients’ i.e. non-metastatic local disease (Wu et al
2003). Low risk patients include those with size of
tumor < 3 cm, mitotic index < 5/50 hpf and location of
tumour in stomach. Lymph node metastasis is rare and
routine removal of lymph nodes is typically not
necessary. GIST lesions exhibit a fragile pseudo
capsule, so the intraop-procedure must be optimized to
minimize the risk of tumour rupture which could
increase the risk of peritoneal dissemination.
Laparoscopic resection has recently come as an
important modality of surgical treatment (Chen et al
2012).Medical treatment is reserved for patients with
advanced metastatic disease or as an adjuvant
treatment in intermediate cases (Eisenbergh et al
2012). Imatinib (a tyrosine kinase inhibitor, TKI) is the
drug of choice in such cases particularly in patients with
mutation in Exon 11 of KIT gene (most common
molecular sub type) and is started at a dose of 400mg
/day, higher dose of 800 mg daily reserved for patients
with KIT Exon 9 mutation. Around 15% patients may
develop resistance to Imatininb manifesting as rapid
progression of disease, despite Imatinib dosing that
may be primary or secondary to emergence of new
secondary mutation within a separate portion of KIT
kinase coding sequence. Such cases may respond to
other TKIs like Sunitinib (Demetri et al 2006, George et
al 2009).In January 2006, the FDA approved Sunitinib
as a second-line agent for patients with advanced
GIST. Regorafenib received FDA approval for locally
advanced, unresectable GISTs that no longer respond
to Imatinib or Sunitinib. The pivotal phase III GRID trial
of 199 patients with metastatic or unresectable GIST
showed that Regorafenib plus best supportive care
(BSC) significantly improved progression-free survival
(PFS) compared to placebo plus BSC(Demetri et al
2013, Chustecka et al 2015). Conventional cytotoxic
therapy is usually not used in management of GISTs.
CONCLUSION
GISTs are an uncommon form of gastric neoplasia and
a very rare cause of upper GI bleed. Patients usually
rebleed and need emergency care commonly in the
form of surgery. Malignant potential is uncertain.
Surgery is the treatment of choice for local disease.
Advanced disease may be treated conservatively only.
REFERENCES
Mazur MT, Clark HB (1983). Gastric stromal tumors:
Reappraisal of histogenesis. Am J Surg Pathol; 7:
507–519.
Hirota S, Isozaki K, Moriyama Y (1998). Gain-of-
function mutations of c-kit inhuman gastrointestinal
stromal tumors. Science; 279: 577–580.
Corless CL, Schroeder A, Griffith D (2005). PDGFRA
Mutations in Gastrointestinal Stromal Tumors:
Frequency, Spectrum and In Vitro Sensitivity to
Imatinib. J ClinOncol; 23: 5357–5364.
Miettinen M, Sobin LH, Lasota J (2005).
Gastrointestinal stromal tumors of the stomach:
aclinicopathologic, immunohistochemical, and
molecular genetic study of 1765 cases with long-term
follow-up. Am J Surg Pathol; 29: 52–68.
Seya T, Tanaka N, Yokoi K, Shinji S, Oaki Y, Tajiri T
(2008). Life-threatening Bleeding from
Gastrointestinal Stromal Tumor of the
Stomach.Journal of Nippon Medical School. 75(5):
306-311.
Singhal T, Doddi S, Leake T, Parsi S, Hussain A,
Chandra A, Smedley F, Ellul J (2010). Upper
gastrointestinal bleeding due to gastric stromal
tumour: a case report. Cases Journal, 3:58
doi:10.1186/1757-1626-3-58.
Tran T, Davila JA, El-Serag HB (2005). The
epidemiology of malignant gastrointestinalstromal
tumors: an analysis of 1458 cases from 1992 to 2000.
Am JGastroenterol; 100: 162–168.
Fletcher CD, Berman JJ, Corless C (2005). Diagnosis
of gastrointestinal stromaltumors: A consensus
approach. Hum Pathol; 33: 459–465.
Wu PC, Langerman A, Ryan CW, Hart J, Swiger S,
Posner MC (2003). Surgical treatment of
gastrointestinal stromal tumors in the imatinib (STI-
571) era. Surgery. Oct; 134(4): 656-65; discussion
665-6.
Chen YH, Liu KH, Yeh CN (2012). Laparoscopic
resection of gastrointestinal stromal tumors: safe,
efficient, and comparable oncologic outcomes. J
Laparoendosc AdvSurg Tech A. 22(8):758-63.
Eisenberg BL, Judson I (2004). Surgery and Imatinib in
management of GIST.Emerging approach to adjuvant
and neoadjuvanct therapy. Ann of Surg Onco.,
11:465–475.
Demetri GD, van Oosterom AT, Garrett CR (2006).
Efficacy and safety of sunitinib in patients with
advanced gastrointestinal stromal tumour after failure
of imatinib: a randomised controlled trial. Lancet.,
368(9544):1329-38.
George S, Blay JY, Casali PG, Le Cesne A,
Stephenson P, Deprimo SE (2009). Clinical
evaluation of continuous daily dosing of sunitinib
malate in patients with advanced gastrointestinal
stromal tumour after imatinib failure. Eur J Cancer.
45(11):1959-68.
Demetri GD, Reichardt P, Kang YK, Blay JY, Rutkowski
P, Gelderblom H (2013). Efficacy and safety of
regorafenib for advanced gastrointestinal stromal
World J. Int. Med. 006
tumours after failure of imatinib and sunitinib (GRID):
an international, multicentre, randomised, placebo-
controlled, phase 3 trial. Lancet., 381(9863):295-302.
Chustecka Z. Regorafenib Approved for
Gastrointestinal Stromal Tumors. Available
athttp://www.medscape.com/viewarticle/779854.
Accepted 28 April, 2015.
Citation: Dar WJ, Sofi N, Dar IA, Kasana BA, Hussain
M, Latief M (2015). A rare cause of upper GI bleed.
World Journal of Internal Medicine, 2(1): 003-006.
Copyright: © 2014. Dar et al. This is an open-access
article distributed under the terms of the Creative
Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any
medium, provided the original author and source are
cited.

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A rare cause of upper GI bleed

  • 1. WJIM A rare cause of upper GI bleed 1 *Waseem Raja Dar, 2 Najeeb Ullah Sofi, 3 Imtiyaz Ahmad Dar, 4 Basharat Ahmad Kasana, 5 Moomin Hussain and 6 Muzamil Latief 1*,2,3,4,5 Department of Medicine, Gastroenterology Division. Shere Kashmir Institute of Medical Sciences, Soura.Srinagar, J& K, India Upper GI bleed is a common, scary and life threatening medical condition usually caused by peptic ulcer disease or oesophageal varices. Uncommon causes include neoplasms, aortoenteric fistulas, vascular lesions, Dieulafoy's lesion etc. Patients usually present with hematemesis or melena. GIST is the third most common tumor of stomach and also the most common mesenchymal tumor. GIST may be asymptomatic and discovered incidentally or they may cause nonspecific symptoms like early satiety and fullness. Although major presentation of GIST is upper GI bleed, GIST as a cause of upper GI bleed is very rare. We here present a patient admitted to us with massive upper GI bleed due to gastrointestinal stromal tumor. Keywords: GIST, upper GI bleed, carney complex, imatinib, regorafenib. INTRODUCTION Upper gastrointestinal bleeding (UGIB) refers to blood loss of recent onset originating from a site proximal to the ligament of Treitz. It is a common clinical problem seen in the practice of Gastroenterology and Internal Medicine. Patients may present either with hematemesisor melena. Common causes include ulcers, varices, Mallory Weiss tears, erosions and erosive esophagitis. Rare causes include neoplasms, aortoenteric fistulas, vascular lesions, Dieulafoy's lesion, prolapse gastropathy and hemobilia or hemosuccus pancreaticus. We here present a patient admitted with upper GI bleed due to a very rare cause i.e. Gastrointestinal Stromal Tumor (GIST). A brief review of literature follows. CASE REPORT A 55 year old male was admitted to our Gastroenterology Department with complaints of passage of multiple black tarry foul smelling stools of two days duration. There was no history of hematemesis, abdominal pain, jaundice or bleeding from any other orifice. Patient was non-alcoholic and did not report intake of any NSAIDS. There was no previous history of hypertension, diabetes mellitus or travel outside the state. On clinical examination, patient was conscious and oriented. There was tachycardia and postural drop in blood pressure. No signs of chronic liver disease were present. Respiratory, Cardiovascular and Abdominal examinations were normal. An initial diagnosis of Peptic Ulcer Disease was made and patient resuscitated with intravenous fluids, blood transfusions and pantoprazole infusions. Baseline investigations revealed microcytic anemia (Table 1). Meanwhile patient was taken to endoscopy room for urgent procedure. Endoscopy revealed a 4-5 cm sub mucosal bulge with central depression in stomach (Fig 1) with a differential diagnosis of leiomyoma or GIST. CECT abdomen showed an exoluminal homogenous enhancing mass (5 x 4.5cm) in fundus with indentation of fundic wall (Fig 2). Patient however continued to lose blood and hence it was decided to operate patient for diagnostic and therapeutic reasons. Intraoperative findings included a 6×6 cm mass in anterior wall of stomach at junction of body and fundus and small enlarged lymph node at the root of left gastric vessels (Fig 3, 4). *Corresponding Author: Waseem Raja Dar, Department of Medicine, Gastroenterology Division. Shere Kashmir Institute of Medical Sciences, Soura. Srinagar, J&K, India. Email: drwaseem.mw@gmail.com World Journal of Internal Medicine Vol. 2(1), pp. 003-006. May, 2015. © www.premierpublishers.org,ISSN: XXXX-XXXXx Case Report
  • 2. Dar et al. 003 Parameter Result Parameter Result ECG:- Sinus Tachycardia X-rayChest: - Normal. Coagulogram : Normal USG abdomen: normal Urine exam: normal HIV /HBV /HCV/HAV serology: negative Hb 5.7 g% Urea 28 mg/dl TLC 8200/mm 3 Creatinine 0.5 mg/dl DLC Neutros=83% Lymphos=12% Bilirubin 0.4 mg/dl PLT 117 lacs/mm 3 ALT 15U/L MCV 71 fL ALP 77 U/L MCH 23 pg Total Protein 6.76 g/dl Albumin 3.8 g/dl Table 1.Baseline Investigations. Figure 1. UGI endoscopy: 4 -5 cm sub mucosal bulgewith central depression in stomach. Figure 2. CECT Abdomen: Homogenous, enhancing mass (5 x 4.5cm) in fundus. No omental and liver metastasis were seen. Wide local excision of the tumour was carried out. Microscopic examination of the tumor was suggestive of GIST (Fig 5) while as lymph node showed reactive hyperplasia only. Tumour cells were positive for C kit, CD34 and DOG1. SMA was focally positive. Our complete diagnosis was Gastro Intestinal Stromal Tumor Stage III A (TNM Staging) presenting as massive upper GI bleed. Patient was referred to medical oncology department where he was put on Imatinib 400mg/day. Presently patient is on their follow up and has completed three months of treatment. DISCUSSION Previously classified as leiomyomas, leiomyosarcomas and leiomyoblastomas, GIST is a term introduced by Mazur and Clark for a group of gastrointestinal tumors that lack the immune histochemical features of Schwann cells and did not have the ultrastructural
  • 3. World J. Int. Med. 004 Figure 3. Intraop: 6×6 cm mass in anterior wall Figure 4. Operative Specimen of stomach Figure 5. High Power Microscopy: Spindle cell tumour with areas of hyalinization. characteristics of smooth muscle cells (Mazur et al 1983). Although stomach is the most common site, they may occur anywhere along the GI tract. They usually occur in middle age but may occur rarely in children as a part of Carney's triad (gastric stromal tumor, extra adrenal paraganglioma and pulmonary chordoma). Most common mutation in GISTs is gain-of-function mutations in the KIT (c-kit) proto-oncogene, which almost occurs in all GISTs (Hirota et al 1998). These mutations lead to constitutive over expression and autophosphorylation of c-Kit, provoking a cascade of intracellular signalling that propels cells toward proliferation or away from apoptotic pathways. A small subset of patients (5%) may be KIT-negative (Corless et al 2005).In such cases, mutations of platelet-derived growth factor receptor-alpha (PDGFA), protein kinase C, and DOG1have been detected. GISTs may be asymptomatic and discovered incidentally. More often, they are associated with nonspecific symptoms i.e., early satiety and bloating unless they ulcerate, bleed, or grow large enough to cause pain or obstruction. Three major presentations include overt GI bleeding (40%), abdominal mass (40%) and abdominal pain (20%) (Miettinen et al 2005). Although the most common presentation of GIST is bleeding, GIST as a cause of upper UGI bleeding is very rare and only case reports exist (Tomoko et al 2008, Tarun et al 2010). A small minority of GISTs are associated with hereditary syndromes like Type 1 Neurofibromatosis and Carney Complex. GISTs have uncertain malignant potential. Between 10% and 25%
  • 4. Dar et al. 005 of patients present with metastatic disease (Tran et al 2005). GISTs arise from pleuripotential mesenchymal stem cell programmed to differentiate into the interstitial cell of Cajal (Pacemaker cells of GIT).Microscopically, GIST cell morphology is usually spindle-shaped (70%), but some GISTs consist of rounded cells (epithelioid type, 20%) or a mixture, but they can also be pleomorphic. GISTs have a fragile pseudo capsule, which may rupture during surgery which could increase the risk of peritoneal dissemination (Fletcher et al 2002). Treatment of GISTs is medical as well as surgical. Surgery remains the treatment of choice for low risk patients’ i.e. non-metastatic local disease (Wu et al 2003). Low risk patients include those with size of tumor < 3 cm, mitotic index < 5/50 hpf and location of tumour in stomach. Lymph node metastasis is rare and routine removal of lymph nodes is typically not necessary. GIST lesions exhibit a fragile pseudo capsule, so the intraop-procedure must be optimized to minimize the risk of tumour rupture which could increase the risk of peritoneal dissemination. Laparoscopic resection has recently come as an important modality of surgical treatment (Chen et al 2012).Medical treatment is reserved for patients with advanced metastatic disease or as an adjuvant treatment in intermediate cases (Eisenbergh et al 2012). Imatinib (a tyrosine kinase inhibitor, TKI) is the drug of choice in such cases particularly in patients with mutation in Exon 11 of KIT gene (most common molecular sub type) and is started at a dose of 400mg /day, higher dose of 800 mg daily reserved for patients with KIT Exon 9 mutation. Around 15% patients may develop resistance to Imatininb manifesting as rapid progression of disease, despite Imatinib dosing that may be primary or secondary to emergence of new secondary mutation within a separate portion of KIT kinase coding sequence. Such cases may respond to other TKIs like Sunitinib (Demetri et al 2006, George et al 2009).In January 2006, the FDA approved Sunitinib as a second-line agent for patients with advanced GIST. Regorafenib received FDA approval for locally advanced, unresectable GISTs that no longer respond to Imatinib or Sunitinib. The pivotal phase III GRID trial of 199 patients with metastatic or unresectable GIST showed that Regorafenib plus best supportive care (BSC) significantly improved progression-free survival (PFS) compared to placebo plus BSC(Demetri et al 2013, Chustecka et al 2015). Conventional cytotoxic therapy is usually not used in management of GISTs. CONCLUSION GISTs are an uncommon form of gastric neoplasia and a very rare cause of upper GI bleed. Patients usually rebleed and need emergency care commonly in the form of surgery. Malignant potential is uncertain. Surgery is the treatment of choice for local disease. Advanced disease may be treated conservatively only. 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Upper gastrointestinal bleeding due to gastric stromal tumour: a case report. Cases Journal, 3:58 doi:10.1186/1757-1626-3-58. Tran T, Davila JA, El-Serag HB (2005). The epidemiology of malignant gastrointestinalstromal tumors: an analysis of 1458 cases from 1992 to 2000. Am JGastroenterol; 100: 162–168. Fletcher CD, Berman JJ, Corless C (2005). Diagnosis of gastrointestinal stromaltumors: A consensus approach. Hum Pathol; 33: 459–465. Wu PC, Langerman A, Ryan CW, Hart J, Swiger S, Posner MC (2003). Surgical treatment of gastrointestinal stromal tumors in the imatinib (STI- 571) era. Surgery. Oct; 134(4): 656-65; discussion 665-6. Chen YH, Liu KH, Yeh CN (2012). Laparoscopic resection of gastrointestinal stromal tumors: safe, efficient, and comparable oncologic outcomes. J Laparoendosc AdvSurg Tech A. 22(8):758-63. Eisenberg BL, Judson I (2004). Surgery and Imatinib in management of GIST.Emerging approach to adjuvant and neoadjuvanct therapy. Ann of Surg Onco., 11:465–475. Demetri GD, van Oosterom AT, Garrett CR (2006). Efficacy and safety of sunitinib in patients with advanced gastrointestinal stromal tumour after failure of imatinib: a randomised controlled trial. Lancet., 368(9544):1329-38. George S, Blay JY, Casali PG, Le Cesne A, Stephenson P, Deprimo SE (2009). Clinical evaluation of continuous daily dosing of sunitinib malate in patients with advanced gastrointestinal stromal tumour after imatinib failure. Eur J Cancer. 45(11):1959-68. Demetri GD, Reichardt P, Kang YK, Blay JY, Rutkowski P, Gelderblom H (2013). Efficacy and safety of regorafenib for advanced gastrointestinal stromal
  • 5. World J. Int. Med. 006 tumours after failure of imatinib and sunitinib (GRID): an international, multicentre, randomised, placebo- controlled, phase 3 trial. Lancet., 381(9863):295-302. Chustecka Z. Regorafenib Approved for Gastrointestinal Stromal Tumors. Available athttp://www.medscape.com/viewarticle/779854. Accepted 28 April, 2015. Citation: Dar WJ, Sofi N, Dar IA, Kasana BA, Hussain M, Latief M (2015). A rare cause of upper GI bleed. World Journal of Internal Medicine, 2(1): 003-006. Copyright: © 2014. Dar et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are cited.