Gastric telangiectasia refers to small dilated blood vessels (vascular malformations) that occur in the mucosal lining of the stomach. These lesions appear as thin, spider-web-like red or dark purple spots that blanch with pressure and can range from 1-2 mm in size.
While they can exist as isolated findings, they are frequently associated with systemic conditions, particularly Hereditary Hemorrhagic Telangiectasia (HHT). These vascular lesions can cause significant gastrointestinal bleeding, leading to iron deficiency anemia and other complications when left untreated.
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Prevalence and Epidemiology
Gastric telangiectasias are most commonly associated with HHT, where studies have shown varied prevalence rates:
- 64% of HHT patients in one study demonstrated gastric telangiectasias when examined with esophagogastroduodenoscopy (EGD)
- Another study reported gastric telangiectasias in 29% of HHT patients, compared to 0% in the general population
- Larger studies have found rates between 46.7% and 77% in HHT patients
The prevalence increases with age, with one study noting that patients found to have small bowel lesions on video capsule endoscopy (VCE) were significantly older (62 vs. 45 years) than those without lesions. In the general population, these lesions are uncommon outside of specific disease contexts.
Distribution Patterns
Gastric telangiectasias can be found throughout the stomach but show certain distribution patterns:
- Often predominant in the gastric fundus
- May occur alongside telangiectasias in other parts of the digestive tract, particularly the duodenum and proximal small bowel
- Patients are typically classified as having few (≤10) or multiple (>10) vascular lesions based on endoscopic findings
Pathophysiology and Etiology
Genetic Basis
In HHT, gastric telangiectasias develop due to mutations in specific genes involved in the transforming growth factor-beta (TGF-β) family signaling cascade:
- ENG (endoglin) gene – causing HHT type 1 (HHT-1)
- ACVRL1/ALK1 (activin receptor-like kinase 1) gene – causing HHT type 2 (HHT-2)
- SMAD4 gene – associated with HHT in combination with juvenile polyposis syndrome[19]
These mutations lead to abnormal formation of blood vessels, creating fragile vascular structures prone to bleeding. Research suggests that HHT-1 may be associated with more extensive gastrointestinal involvement compared to HHT-2.
Structural Characteristics
Histologically, gastric telangiectasias are characterized by:
- Dilated capillaries in the lamina propria (mucosal layer)
- May contain fibrin thrombi
- Tortuous vessels with irregular wall thickness
- Involvement primarily of mucosal and submucosal layers of the stomach
Clinical Presentation
Gastric telangiectasias often present with the following symptoms:
Common Symptoms
- Gastrointestinal bleeding (melena or hematochezia)
- Iron deficiency anemia due to chronic blood loss
- Hematemesis (vomiting blood) in severe cases
- Fatigue and weakness (secondary to anemia)
Many patients may be asymptomatic until significant blood loss occurs. In HHT patients, gastric telangiectasias typically become symptomatic after age 50, with the risk of GI tract bleeding increasing with age.
Associated Conditions
Gastric telangiectasias are strongly associated with:
- Hereditary Hemorrhagic Telangiectasia (HHT) – An autosomal dominant disorder affecting approximately 1 in 5,000-8,000 individuals
- Gastric Antral Vascular Ectasia (GAVE) – Also known as “watermelon stomach,” consists of large dilated veins running linearly along the stomach, creating a striped appearance
- Other conditions associated with vascular ectasias include:
- Portal hypertension
- Chronic kidney failure
- Collagen vascular diseases
- Systemic sclerosis
Diagnosis
Accurate diagnosis of gastric telangiectasias relies primarily on direct visualization through endoscopic procedures:
Endoscopic Evaluation
- Esophagogastroduodenoscopy (EGD) – The gold standard for diagnosis, allowing direct visualization and biopsy if needed
- Video Capsule Endoscopy (VCE) – Particularly useful for identifying lesions in the small intestine that may coexist with gastric telangiectasias
- Push Enteroscopy – Can access the proximal small bowel beyond the reach of standard EGD
During endoscopy, telangiectasias appear as flat or slightly raised, bright red lesions, typically 0.5 to 1.0 cm in diameter.
Imaging Studies
- CT Angiography (CTA) – May help diagnose vascular lesions with a sensitivity of 70% and specificity of 100%
- Mesenteric Angiography – Can be useful for detecting actively bleeding lesions
Differential Diagnosis
Gastric telangiectasias must be distinguished from:
- Portal hypertensive gastropathy
- Dieulafoy lesions
- Arteriovenous malformations (AVMs)
- Hemangiomas
- Gastric antral vascular ectasia (GAVE)
Treatment Approaches
Management of gastric telangiectasias focuses on controlling bleeding and preventing anemia:
Endoscopic Therapies
- Argon Plasma Coagulation (APC) – The most common treatment, using ionized argon gas to deliver electrical current to the lesion
- Laser Therapy – Neodymium-YAG laser can be effective for larger lesions
- Endoscopic Clip Placement – Used for discrete bleeding lesions
- Sclerotherapy – Injection of sclerosing agents around the telangiectasia
In a long-term follow-up study, endoscopic treatment proved effective in 41 of 47 HHT patients, with median hemoglobin levels increasing from 7.0 g/dL to 11.9 g/dL after treatment.
Medical Management
- Iron Supplementation – Oral or intravenous iron to manage chronic anemia
- Blood Transfusions – For severe anemia or acute bleeding episodes
- Hormonal Therapy – Estrogen and progesterone have shown some efficacy
- Antifibrinolytic Therapy – Medications like tranexamic acid may help reduce bleeding
- Experimental Treatments – Antiangiogenic agents like bevacizumab and thalidomide have been reported in case studies
Surgical Approaches
For isolated, problematic gastric telangiectasias that fail to respond to endoscopic therapy:
- Gastric Wedge Resection – Surgical removal of the affected portion of the stomach
- Tattoo-Assisted Laparoscopic Resection – Allows for precise localization of the lesion during surgery
Surgery is generally reserved for cases refractory to endoscopic treatment, as demonstrated in a case report where laparoscopic gastric wedge resection successfully treated recurrent bleeding from gastric telangiectasia after failed endoscopic therapy
Prognosis and Follow-up
The prognosis for patients with gastric telangiectasias varies depending on the underlying cause, extent of involvement, and response to treatment:
- Approximately 50% of gastrointestinal hemorrhage from angiodysplasia ceases without intervention
- First-line endoscopic treatment has a post-treatment bleeding rate of approximately 25%
- Long-term management often requires periodic endoscopic surveillance and repeated treatments
- In one study, repeated endoscopic treatments reduced transfusion requirements from 22.8 to 7.3 red cell units per year
- Patients with multiple lesions (>10) may have a lower chance of response to treatment
Conclusion
Gastric telangiectasia represents an important cause of gastrointestinal bleeding that can significantly impact quality of life through chronic anemia and recurrent hospitalization. While strongly associated with HHT, these vascular lesions can occur in various contexts and require a multidisciplinary approach to management.
Endoscopic therapy remains the cornerstone of treatment, with promising long-term results in controlling bleeding and improving anemia. Ongoing research into the genetic basis of these vascular malformations may provide new therapeutic targets in the future.
For patients with suspected gastric telangiectasias, prompt endoscopic evaluation is essential, particularly in the context of unexplained iron deficiency anemia or occult gastrointestinal bleeding. Regular follow-up and surveillance are crucial components of long-term management, especially in hereditary conditions where new lesions may develop over time.
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