Osler-Weber-Rendu Disease (Hereditary Hemorrhagic Telangiectasia, HHT)


Article Author:
Angela Macri
Allecia Wilson
Omid Shafaat


Article Editor:
Sandeep Sharma


Editors In Chief:
Dustin Constant
Donald Kushner


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Trevor Nezwek
Radia Jamil
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes


Updated:
6/19/2019 12:29:14 PM

Introduction

Hereditary hemorrhagic telangiectasia (HHT) is also known as Osler–Weber–Rendu disease. It is an autosomal dominant disorder characterized by multiple mucocutaneous telangiectasias. These telangiectasias represent small arterio-venous malformations that frequently tend to bleeds causing the patient a significant amount of distress in their daily lives. Patients typically present with nose bleeds, gastrointestinal (GI) bleeds, and iron deficiency anemia. This disease puts patients at risk for life-threatening complications from having arteriovenous malformations in several organ systems. It is critical for these patients to get the appropriate diagnostic screening they need to prevent internal bleeding or even death.

Etiology

There are 2 main types of HHT that are both caused by heterozygous mutations. HHT1 involves a mutation in endoglin (ENG). With this type, patients, especially women, are at a higher risk of getting pulmonary and cerebral AVMs. HHT2 involves a mutation in activin A receptor-like type 1 (ACVRL1), also known as ALK1. Patients with HHT2 have a higher risk of getting liver AVMs. ENG comprises about 61%, and ACVRL1 comprises about 37% of the mutations known to cause HHT. Mutations in growth differentiation factor 2 (GDF2) have been found. These encode the protein that binds to endoglin and ACVRL1. Lastly, there are mutations in SMAD4 which encodes a protein that transmits signals from the transforming growth factor-beta (TGF-beta) receptor. This mutation only comprises about 2% of cases. Patients with this gene mutation get juvenile GI polyposis and HHT.[1][2]

Epidemiology

The prevalence of HHT is 1.5 to 2 persons/10,000; although, some sources say that it is higher due to variable penetrance and because symptoms do not present until later in adult life. HHT has a higher prevalence in certain populations, such as the Afro-Caribbean residents of Curacao and Bonaire.[3]

Pathophysiology

The mutations found in HHT disrupt TGF-beta-mediated pathways in vascular endothelial cells. Disruption in this pathway results in aberrant blood vessel development leading to extreme fragility and arteriovenous malformations.

Histopathology

The histopathology description of telangiectasias is characterized as having dilated capillaries lined with flat endothelial cells. AVMs are characterized as having a mixture of thick and thin-walled vessels in the dermis.

History and Physical

The primary and most common manifestation of HHT is usually epistaxis that begins during childhood or adolescence at a mean age of 12 years. Telangiectasias do not usually appear until after puberty but may not occur until adulthood. They typically occur on the face, lips, tongue, palms, and fingers including the periungual area and the nail bed. Telangiectasias are dilated blood vessels that appear as thin spiderweb-like red and dark purple lesions that blanch with pressure.  AVMs are abnormal connections between arteries and veins that bypass the capillary system. Patients with HHT have multiple AVMs throughout the body. However, the most important AVMs for which clinicians should screen are in the brain, lungs, GI tract, and liver. AVMs in the lung and brain can be asymptomatic.[4]

Pulmonary AVMs can cause hypoxemia, hemorrhage, and cerebral abscesses or strokes due to paradoxical emboli. They can lead to the right to left shunting in approximately 15% to 50% of HHT patients.

Cerebral AVMs can lead to lethal intracranial hemorrhage starting from infancy. They occur in 25% of HHT patients.

Spinal AVMs can occur in children and can cause acute paraplegia.

GI bleeding can occur from AVMs and typically occurs in adults in their 40s. Patients often present with iron deficiency anemia.

Liver AVMs can lead to high-output heart failure, portal hypertension, and biliary disease. They present in 30% to 80%, but they are symptomatic in less than 10% of patients.[1]

Evaluation

If 3 or more clinical criteria are met, then the individual has definite HHT. If they only meet 1 or 2 criteria, then HHT is suspected. The clinical criteria are spontaneous recurrent epistaxis, characteristic mucocutaneous telangiectasias, visceral telangiectasias/AVMs, and HHT in a first-degree relative. More than 90% of patients with HHT will meet these criteria by 40 years of age.

Because of the life-threatening complications that can occur in a patient who has visceral AVMs, it is important to order the appropriate diagnostic tests.

  • Pulmonary AVMs: Transthoracic contrast echocardiography should be ordered. If negative, repeat screening should be considered after puberty, within the 5 years preceding a planned pregnancy, after pregnancy, and otherwise every 5 to 10 years. This test is indicated for either suspected or confirmed HHT. If positive, confirmation with high-resolution thoracic CT should be performed.
  • Brain AVMs: Brain MRI with and without gadolinium should be ordered for suspected and confirmed HHT.
  • Liver AVMs: Screening via doppler ultrasound or triphasic helical CT is recommended in all patients with HHT and abnormal liver enzyme tests or clinical evidence of complications from liver AVMs, including high-output heart failure, portal hypertension, and cholestasis.
  • Anemia: Annual blood tests to look at hemoglobin and hematocrit levels should be completed in HHT patients over 35 years old.
  • Genetic analysis: A screen for ENG and ACVRL1 ± SMAD4 and/or GDF2 should be done in those that are at risk because of an affected first-degree relative or are clinically suspected to have HHT.[1][5]

Treatment / Management

Transcatheter embolotherapy is recommended for all adults and symptomatic children with pulmonary AVMs, and on a case-by-case basis for asymptomatic children. Treatment strategies for AVMs of the central nervous system (CNS) include embolization, microsurgery, and stereotactic radiation. If brain AVMs are found the patient, he or she should be referred to a neurovascular surgeon for management as treatment for these is highly controversial. Acute GI bleeds should be managed according to hospital protocol. GI AVMs can be managed with endoscopic cauterization. Hormonal or antifibrinolytic therapy may be used as adjunct therapy to prevent ongoing bleeding. In patients that have liver AVMs, embolization is not recommended given the risk post-embolization necrosis and death. Surgical intervention should only be considered if they become symptomatic or develop complications. For those with significant hepatic AVM involvement, partial liver resection is a safe treatment option. If a patient’s hemoglobin and hematocrit are low, an upper endoscopy should be completed if the anemia is disproportionate to epistaxis. Iron supplementation should be initiated, either oral or intravenous (IV) and endoscopic cauterization can be considered. It is recommended that acute epistaxis be managed with low-pressure, less-traumatic packing techniques. In some studies, a mild benefit was shown for the use of humidifiers to prevent chronic epistaxis, and there have been no controlled trials comparing more definitive surgical techniques such as nasal artery embolization or coagulation techniques.[1]

Differential Diagnosis

Some differential diagnoses are CREST syndrome, spider angiomas, Ataxia-Telangiectasia, Bloom syndrome, Rothmund syndrome.

Prognosis

Most HHT patients who have adequate access to healthcare will have normal life expectancies. There is a bimodal distribution of mortality, with peaks at age 50 and then from 60 to 79. Most of the mortality of HHT is the result of complications of AVMs, particularly in the brain, lungs, and GI system.

Enhancing Healthcare Team Outcomes

Hereditary hemorrhagic telangiectasia (HHT) result in a significant amount of distress in the daily lives of patients and their families. This disease puts patients at risk for life-threatening complications. It is critical for these patients to get the appropriate diagnostic screening they need to prevent internal bleeding or even death and have an interdisciplinary team of clinicians and specialty trained nurses assisting in the coordination of follow-up care. This will result in the best patient outcome. [Level V]


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Osler-Weber-Rendu Disease (Hereditary Hemorrhagic Telangiectasia, HHT) - Questions

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A 16-year-old- boy presents to the emergency room for a massive nosebleed. He says that the bleeding began about two hours ago and occurred spontaneously. He denies any trauma or inhaling any medication or illicit drugs through his nose. He reports multiple similar episodes of epistaxis requiring admission to the emergency room, and he has been received several episodes of blood transfusion due to massive blood loss. Physical examination of his oral mucosa is presented in the below picture. Laboratory findings are as follows: Hemoglobin: 9.6 g/dl Mean corpuscular volume: 75 µm3 Platelets: 430,000/mm3 Leukocytes: 4,8000/mm3 Ferritin, serum: 9 ng/ml Iron studies: Iron, serum: 25 µg/dl Iron-binding capacity: 476 µg/dl (normal: 251-406 µg/dl). Which of the following complication associated with this disease can lead to the death of the patient?

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    Contributed by Robert E. Sumpter, The Centers for Disease Control and Prevention (CDC)
Attributed To: Contributed by Robert E. Sumpter, The Centers for Disease Control and Prevention (CDC)



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A 24-year-old male presents to the office with complaints of numerous red spots on his skin, lips, and gums. He denies any trauma and denies any medication or illicit drug use. He says that his brother had the same disorder. He reports recurrent nosebleed that may need medical intervention to control. Examination reveals numerous petechiae and telangiectasia on the skin and the lips. Auscultation reveals continuous bruit over his anterior chest. Which complication is he at risk for developing in the future as a result of his lung findings?



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What is the MOST common clinical presentation of a patient with Osler Weber Rendu syndrome?



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A 16-year-old male presents to the office with a 5-month history of progressive shortness of breath with exertion. He works as a manager in a construction company and is concerned that he will not be able to continue working due to this shortness of breath. His past medical history is significant for asthma from his childhood but has not experienced any symptoms for years before presentation. He reports frequent nosebleed that was not due to coagulation disorders based on his previous workup. Physical examination reveals numerous blanching lesions on the lips, tongue, and palms, and finding on his fingers, which are shown in the picture below. Administration of inhaled short-acting beta-2 agonist does not improve the patient’s shortness of breath. Which of the following is most likely responsible for this patient’s current symptoms?

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The doctor identifies numerous petechiae and telangiectasia on the skin, lips, and gums during an exam of a middle aged male. His brother has similar lesions. Recently he had massive lower GI bleeding and is booked for a colonoscopy today. During this procedure, what feature is usually seen in these patients?



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A young patient presents with her 6th severe episode of epistaxis. She has a family of nose bleeds and telangiectasias on her face. Despite tamponade with a balloon catheter, the nosebleed appears to be ongoing. What hormonal treatment has been used to manage severe nose bleeds in these patients?



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What is the MOST common neurological manifestation of Osler Weber Rendu syndrome?



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What is the most common skin manifestation of Osler-Weber-Rendu syndrome?

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    Contributed by Wikimedia Commons, Herbert L. Fred, MD and Hendrik A. van Dijk (CC by 2.0) https://creativecommons.org/licenses/by/2.0/
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In a patient with Osler Weber Rendu syndrome with recurrent epistaxis, what is the ideal treatment?



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A 46-year-old man presents to the emergency room after developing acute left-sided weakness and slurred speech. Past medical history is significant for diabetes, hypertension, multiple episodes of epistaxis, and gastrointestinal bleeding. Laboratory findings are as follow: Leukocytes: 7,500/mm3 Hemoglobin: 10.5 g/dl Mean corpuscular volume: 72 microm3 Platelets: 290,000/mm3 On physical examination, the patient has marked left-sided weakness, slurred speech, and hemineglect. He also has multiple small reds and pinks spots on his lips, face, and oral mucosa. A non-contrast head CT demonstrates a right-sided hemorrhagic stroke. Which of the following is the most likely underlying diagnosis of this patient?



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What is the inheritance pattern of hereditary hemorrhagic telangiectasia?



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A 24-year-old African-Caribbean male presents with recurrent nosebleeds. Detailed history reveals his father died in his 40's after massive gastrointestinal bleeding and two of his father's five siblings have also had frequent nosebleeds. On physical examination, he has multiple small dark red, blanchable papules and macules over his lips and skin. Which of the following explains the pathogenesis of his condition?



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An 18-year-old male presents with a long history of easy bruising and recurrent nosebleeds, for which he has required multiple admissions. He has a family history of nosebleeds. Now he has been complaining of a headache, gait difficulty with weakness, paresthesias, confusion and nausea. Examination reveals that he numerous telangiectasias over his face and lips. MRI reveals that he has a ring-enhancing lesion in the brain. The reason for this brain lesion is because?



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What is the primary mechanism leading to cerebral infarction in patients with hereditary hemorrhagic telangiectasia?



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Which of the following statements is not true about hereditary hemorrhagic telangiectasia?



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A 16-year-old girl is transferred from a rural hospital for hemiplegia and focal neurological disorder. Earlier this morning, she was admitted to that hospital with headache followed by a tonic-clonic seizure. Imaging of the brain reveals arteriovenous malformation. The patient otherwise has no significant medical history except for massive recurrent nosebleed. Her family report history of bleeding in her older brother and father who died at a young age in a car accident. On physical examination, there are multiple mucocutaneous telangiectasias on her oral cavity, lips, fingers, and nose. Diagnosis of a hereditary disorder is confirmed. Which of the following diseases has the same mode of inheritance as this condition?



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A patient with a family history of telangiectasis and nose bleeds is found to be dyspneic and has a continuous chest bruit over his chest. At the point where the bruit is heard best, a chest film demonstrates a rounded mass. He is at risk for developing?



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A 36-year-old man presented to the emergency room after having an episode of nose bleeding. The bleeding started about an hour ago, and the patient's attempt to stop the bleeding was not successful. The patient reports multiple similar episodes in the past, which needed medical attention to stop and required blood transfusions in the past two episodes. The patient does not smoke and never used illicit drugs. Physical examination reveals numerous blanching lesions on the lips, tongue, and palms. The patient's laboratory studies reveal: Complete blood count: Leukocytes: 8,000/mm3 Hemoglobin: 9 g/dl Mean corpuscular volume: 74 microm3 Platelets: 310,000/mm3 The patient had an older sibling with similar episodes of nose bleeding who had died in a car accident ten years ago. The patient is at highest risk for which of the following condition?



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Which gene mutation has not been found in hereditary hemorrhagic telangiectasia syndrome?



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A 16-year-old female presents to the emergency department accompanied by her mother with a nosebleed that has failed to stop after 30 minutes of pressure. She denies any inciting trauma. Her mother reports the patient has had numerous unprovoked nosebleeds in the last year. Family history is significant for a father who died at the age of 52 from a “brain bleed.” The mother is unable to provide any further information. Vital signs are within normal limits. Physical examination reveals mild bright-red bleeding from the external nares and blood in the posterior oropharynx. Modest dried blood is present over the upper lip. Multiple small, dark red, blanching papules and macules are scattered on the patient’s upper and lower lips. This patient is at greatest risk for which of the following condition?



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Osler-Weber-Rendu Disease (Hereditary Hemorrhagic Telangiectasia, HHT) - References

References

Gastrointestinal Manifestations of Hereditary Hemorrhagic Telangiectasia (HHT): A Systematic Review of the Literature., Jackson SB,Villano NP,Benhammou JN,Lewis M,Pisegna JR,Padua D,, Digestive diseases and sciences, 2017 Oct     [PubMed]
The prevalence and manifestations of hereditary hemorrhagic telangiectasia in the Afro-Caribbean population of the Netherlands Antilles: a family screening., Westermann CJ,Rosina AF,De Vries V,de Coteau PA,, American journal of medical genetics. Part A, 2003 Feb 1     [PubMed]
International guidelines for the diagnosis and management of hereditary haemorrhagic telangiectasia., Faughnan ME,Palda VA,Garcia-Tsao G,Geisthoff UW,McDonald J,Proctor DD,Spears J,Brown DH,Buscarini E,Chesnutt MS,Cottin V,Ganguly A,Gossage JR,Guttmacher AE,Hyland RH,Kennedy SJ,Korzenik J,Mager JJ,Ozanne AP,Piccirillo JF,Picus D,Plauchu H,Porteous ME,Pyeritz RE,Ross DA,Sabba C,Swanson K,Terry P,Wallace MC,Westermann CJ,White RI,Young LH,Zarrabeitia R,, Journal of medical genetics, 2011 Feb     [PubMed]
Hereditary hemorrhagic telangiectasia., Guttmacher AE,Marchuk DA,White RI Jr,, The New England journal of medicine, 1995 Oct 5     [PubMed]
Intracranial hemorrhage in infants and children with hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)., Morgan T,McDonald J,Anderson C,Ismail M,Miller F,Mao R,Madan A,Barnes P,Hudgins L,Manning M,, Pediatrics, 2002 Jan     [PubMed]

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