Angiodysplasia risk factors: Difference between revisions
Nikita Singh (talk | contribs) No edit summary |
|||
| Line 1: | Line 1: | ||
__NOTOC__ | __NOTOC__ | ||
{{Angiodysplasia}} | {{Angiodysplasia}} | ||
{{CMG}} {{AE}} | {{CMG}} {{AE}} {{NKS}} | ||
Please help WikiDoc by adding more content here. It's easy! Click [[Help:How_to_Edit_a_Page|here]] to learn about editing. | Please help WikiDoc by adding more content here. It's easy! Click [[Help:How_to_Edit_a_Page|here]] to learn about editing. | ||
Revision as of 23:43, 3 September 2021
|
Angiodysplasia Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Angiodysplasia risk factors On the Web |
|
American Roentgen Ray Society Images of Angiodysplasia risk factors |
|
Risk calculators and risk factors for Angiodysplasia risk factors |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Nikita Singh, M.D.[2]
Please help WikiDoc by adding more content here. It's easy! Click here to learn about editing.
Overview
Risk Factors
The conditions most commonly associated with Angiodysplasia are:
1.Aortic stenosis (AS)
- Heyde et al and then Schwartz et al were the first to report a possible association between AS and bleeding from AD in 1958. This was called ‘Heyde's Syndrome’.
- A retrospective case–control study of 1443 patients found that the incidence of AS in patients with OGIB was much higher (25.5%) compared with controls (4.4).
- Further support for this hypothesis comes from evidence of improvement or cessation of chronic GI bleeding in the vast majority of patients with AS after aortic valve replacement (AVR). This effect was sustained for up to 12 years after surgery in the largest case series of 91 patients.
- This observation has led to the hypothesis that abnormal von Willebrand factors (vWF) could provide the explanation to the increased risk of bleeding in patients with AS or aortic sclerosis and otherwise ‘silent’ AD.
Von Willebrand disease (vWD)
- Patients with certain subtypes of vWD are at an increased risk of GI bleeding from colonic AD. These patients have low levels of the high molecular weight (HMW) multimers of vWF, which is either hereditary (type 2a vWD) or acquired (AS).
Chronic renal failure (CRF)
- AD is more common in patients with CRF . Prevalence is related to the duration and severity of the kidney disease.
- AD accounts for 19–32% of Lower GI bleeding episodes in patients with CRF compared with 5–6% of episodes in the general population.
- Likewise, gastric and small bowel AD are reportedly the most common causes of upper GI bleeding and OGIB in these patients, respectively.
- Patients with CRF are at an increased risk of bleeding due to several mechanisms including uraemic platelet dysfunction75, 76 and use of anti‐coagulants.77 The causes of platelet dysfunction (aggregation and adhesion) are thought to be due to both intrinsic and extrinsic factors.76, 78 Intrinsic factors include reduced levels of agonists like adenosine diphosphate, serotonin, epinephrine, thrombin and collagen leading to impaired platelet function.79 It has also been noted that levels of platelet cyclic adenosine mono‐phosphate –which causes platelet dysfunction by mobilizing calcium – were high in patients with CRF. Extrinsic factors include release of toxins and increased nitric oxide, which inhibits platelet‐to‐platelet interaction and affects platelet to vessel wall interaction.
- AD is therefore an important cause of GI bleeding in patients with CRF. Other factors, which contribute to abnormalities in haemostasis, include reduced production of erythropoietin and effect of drugs.79