|
|
| (15 intermediate revisions by the same user not shown) |
| Line 15: |
Line 15: |
| MeshNumber = C06.405.748.280 | | | MeshNumber = C06.405.748.280 | |
| }} | | }} |
| {{SI}} | | {{Gastric antral vascular ectasia}} |
| | |
| {{CMG}} | | {{CMG}} |
|
| |
|
| {{SK}} Watermelon stomach; GAVE | | {{SK}} Watermelon stomach; GAVE |
|
| |
|
| ==Overview== | | ==[[Gastric antral vascular ectasia overview|Overview]]== |
| Gastric antral vascular ectasia is an uncommon cause of chronic [[gastrointestinal bleeding]] or [[iron deficiency anemia]]. The condition is associated with dilated small blood vessels in the [[antrum]], or the last part of the [[stomach]]. It is also called watermelon stomach because streaky long red areas that are present in the stomach may resemble the markings on [[watermelon]]<ref>{{cite journal | author = Suit P, Petras R, Bauer T, Petrini J | title = Gastric antral vascular ectasia. A histologic and morphometric study of "the watermelon stomach". | journal = Am J Surg Pathol | volume = 11 | issue = 10 | pages = 750-7 | year = 1987 | id = PMID 3499091}}</ref>.
| |
| | |
| ==Historical Perspective==
| |
| The condition was first discovered in 1952, and reported in the literature in 1953.<ref name=Rider>{{cite journal |last1=Rider |first1=JA |last2=Klotz |first2=AP |last3=Kirsner |first3=JB |title=Gastritis with veno-capillary ectasia as a source of massive gastric hemorrhage |journal=Gastroenterology |volume=24 |issue=1 |pages=118–23 |year=1953 |pmid=13052170}}</ref> Watermelon disease was first diagnosed by Wheeler ''et al.'' in 1979, and definitively described in four living patients by Jabbari ''et al''. only in 1984. As of 2011, the etiology and pathogenesis are still not known.<ref name=Unusual>{{cite journal |last1=Tuveri |first1=Massimiliano |last2=Borsezio |first2=Valentina |last3=Gabbas |first3=Antonio |last4=Mura |first4=Guendalina |title=Gastric antral vascular ectasia—an unusual cause of gastric outlet obstruction: report of a case |journal=Surgery today |volume=37 |issue=6 |pages=503–5 |year=2007 |pmid=17522771 |doi=10.1007/s00595-006-3430-3}}</ref> However, there are several competing hypotheses as to various etiologies.
| |
| | |
| ==Pathophysiology==
| |
| GAVE is characterized by dilated capillaries in the lamina propria with fibrin thrombi.
| |
| | |
| ===Microscopic Pathology===
| |
| [[Image:Gastric_antral_vascular_ectasia.jpg|thumb|left|Micrograph showing gastric antral vascular ectasia. A large spherical, eosinophilic (i.e. pink) fibrin thrombus is seen off-center right. Stomach biopsy. H&E stain.]]
| |
| <br clear="left"/>
| |
| | |
| ===Asociated Conditions===
| |
| GAVE is associated with a number of conditions, including
| |
| * [[Portal hypertension]]
| |
| * [[Chronic renal failure]]
| |
| * [[Collagen vascular disease]]s, particularly [[scleroderma]]
| |
| * [[Pernicious anemia]]
| |
| * [[Liver cirrhosis]]
| |
| * [[Chronic renal failure]]
| |
| * [[Bone marrow transplantation]]
| |
| | |
| ==Causes==
| |
| 65% of patients with both cirrhosis and GAVE are male, but a total of 30% have both conditions. The causal connection between cirrhosis and GAVE has not been proven.
| |
|
| |
|
| A [[connective tissue]] disease has been suspected in some cases.
| | ==[[Gastric antral vascular ectasia historical perspective|Historical Perspective]]== |
|
| |
|
| Autoimmunity may have something to do with it,<ref name=RNA>{{cite journal |doi=10.1093/nar/24.7.1220 |last1=Valdez |first1=BC |last2=Henning |first2=D |last3=Busch |first3=RK |last4=Woods |first4=K |last5=Flores-Rozas |first5=H |last6=Hurwitz |first6=J |last7=Perlaky |first7=L |last8=Busch |first8=H |title=A nucleolar RNA helicase recognized by autoimmune antibodies from a patient with watermelon stomach disease |journal=Nucleic Acids Research |volume=24 |issue=7 |pages=1220–4 |year=1996 |pmid=8614622 |pmc=145780}}</ref> as 25% of all sclerosis patients who had a certain anti-RNA marker have GAVE. RNA autoimmunity has been suspected as a cause or marker since at least 1996.
| | ==[[Gastric antral vascular ectasia pathophysiology|Pathophysiology]]== |
|
| |
|
| One theory current since the 1990s focuses on a history of [[prolapse]] of the stomach into the [[small intestine]].
| | ==[[Gastric antral vascular ectasia causes|Causes]]== |
|
| |
|
| [[Gastrin]] levels may indicate a hormonal connection. This may be due to vasoactive intestinal peptide and 5-hydroxy-tryptamine. | | ==[[Gastric antral vascular ectasia differential diagnosis|Differentiating Gastric antral vascular ectasia from other Diseases]]== |
|
| |
|
| It is also possible that infection by ''[[H. pylori]]'' can cause it.
| | ==[[Gastric antral vascular ectasia epidemiology and demographics|Epidemiology and Demographics]]== |
|
| |
|
| ==Differentiating Gastric antral vascular ectasia from other Diseases== | | ==[[Gastric antral vascular ectasia natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
| GAVE should be differentiated from other causes of intestinal bleeding such as
| |
| * [[Duodenal ulcer]]
| |
| * [[Portal hypertension]]<ref name=Portal>{{cite journal |last1=Spahr |first1=L |last2=Villeneuve |first2=J-P |last3=Dufresne |first3=M-P |last4=Tasse |first4=D |last5=Bui |first5=B |last6=Willems |first6=B |last7=Fenyves |first7=D |last8=Pomier-Layrargues |first8=G |title=Gastric antral vascular ectasia in cirrhotic patients: absence of relation with portal hypertension |journal=Gut |volume=44 |issue=5 |pages=739 |year=1999 |pmid=10205216 |pmc=1727493 |doi=10.1136/gut.44.5.739}}</ref>
| |
| | |
| The differential diagnosis is important because treatments are different.
| |
| | |
| ==Epidemiology and Demographics==
| |
| ===Age===
| |
| The average age of diagnosis for GAVE is 73 years of age for females, and 68 for males. Patients in their thirties have been found to have GAVE. It becomes more common in women in their eighties, rising to 4% of all such gastrointestinal conditions.
| |
| | |
| ===Gender===
| |
| Women are about twice as often diagnosed with gastric antral vascular ectasia than men. 71% of all cases of GAVE are diagnosed in females.
| |
|
| |
|
| ==Diagnosis== | | ==Diagnosis== |
| ===Symptoms===
| |
| * [[Fatigue]], [[tiredness]], [[palpitations]] - [[Anemia]]
| |
| * [[Blood loss]]
| |
| * [[GI bleeding]] - [[melena]] or [[hematochezia]]
| |
|
| |
|
| ===Endoscopy===
| | [[Gastric antral vascular ectasia history and symptoms|History and Symptoms ]] | [[ Gastric antral vascular ectasia physical examination|Physical Examination]] | [[Gastric antral vascular ectasia laboratory findings|Laboratory Findings]] | [[Gastric antral vascular ectasia ultrasound|Ultrasound]] | [[Gastric antral vascular ectasia endoscopy|Endoscopy]] | [[Gastric antral vascular ectasia other imaging findings|Other Imaging Findings]] | [[Gastric antral vascular ectasia other diagnostic studies|Other Diagnostic Studies]] |
| The endoscopic appearance of GAVE is similar to [[portal hypertensive gastropathy]]. Dilated capillaries are seen in the endoscopy which resemble the tell-tale watermelon stripes.
| |
|
| |
|
| ==Treatment== | | ==Treatment== |
| GAVE is treated with treatment through the endoscope, including [[argon plasma coagulation]] and electrocautery. Other medical treatments have been tried and include [[estrogen]] and [[progesterone]] therapy and anti-fibrinolytic drugs such as [[tranexamic acid]].
| | [[Gastric antral vascular ectasia medical therapy|Medical Therapy]] | [[Gastric antral vascular ectasia surgery |Surgery]] | [[Gastric antral vascular ectasia primary prevention|Primary Prevention]] | [[Gastric antral vascular ectasia secondary prevention|Secondary Prevention]] | [[Gastric antral vascular ectasia cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Gastric antral vascular ectasia future or investigational therapies|Future or Investigational Therapies]] |
| | |
| | ==Case Studies== |
|
| |
|
| ==References==
| | [[Gastric antral vascular ectasia case study one|Case #1]] |
| {{Reflist|2}}
| |
|
| |
|
| {{WikiDoc Help Menu}} | | {{WikiDoc Help Menu}} |
