Systemic features of retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations: a monogenic small vessel disease.


Journal

Journal of internal medicine
ISSN: 1365-2796
Titre abrégé: J Intern Med
Pays: England
ID NLM: 8904841

Informations de publication

Date de publication:
03 2019
Historique:
pubmed: 10 11 2018
medline: 17 3 2020
entrez: 10 11 2018
Statut: ppublish

Résumé

Retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations (RVCL-S) is a small vessel disease caused by C-terminal truncating TREX1 mutations. The disease is typically characterized by vascular retinopathy and focal and global brain dysfunction. Systemic manifestations have also been reported but not yet systematically investigated. In a cross-sectional study, we compared the clinical characteristics of 33 TREX1 mutation carriers (MC+) from three Dutch RVCL-S families with those of 37 family members without TREX1 mutation (MC-). All participants were investigated using personal interviews, questionnaires, physical, neurological and neuropsychological examinations, blood and urine tests, and brain MRI. In MC+, vascular retinopathy and Raynaud's phenomenon were the earliest symptoms presenting from age 20 onwards. Kidney disease became manifest from around age 35, followed by liver disease, anaemia, markers of inflammation and, in some MC+, migraine and subclinical hypothyroidism, all from age 40. Cerebral deficits usually started mildly around age 50, associated with white matter and intracerebral mass lesions, and becoming severe around age 60-65. Retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations is a rare, but likely underdiagnosed, systemic small vessel disease typically starting with vascular retinopathy, followed by multiple internal organ disease, progressive brain dysfunction, and ultimately premature death.

Sections du résumé

BACKGROUND
Retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations (RVCL-S) is a small vessel disease caused by C-terminal truncating TREX1 mutations. The disease is typically characterized by vascular retinopathy and focal and global brain dysfunction. Systemic manifestations have also been reported but not yet systematically investigated.
METHODS
In a cross-sectional study, we compared the clinical characteristics of 33 TREX1 mutation carriers (MC+) from three Dutch RVCL-S families with those of 37 family members without TREX1 mutation (MC-). All participants were investigated using personal interviews, questionnaires, physical, neurological and neuropsychological examinations, blood and urine tests, and brain MRI.
RESULTS
In MC+, vascular retinopathy and Raynaud's phenomenon were the earliest symptoms presenting from age 20 onwards. Kidney disease became manifest from around age 35, followed by liver disease, anaemia, markers of inflammation and, in some MC+, migraine and subclinical hypothyroidism, all from age 40. Cerebral deficits usually started mildly around age 50, associated with white matter and intracerebral mass lesions, and becoming severe around age 60-65.
CONCLUSIONS
Retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations is a rare, but likely underdiagnosed, systemic small vessel disease typically starting with vascular retinopathy, followed by multiple internal organ disease, progressive brain dysfunction, and ultimately premature death.

Identifiants

pubmed: 30411414
doi: 10.1111/joim.12848
doi:

Substances chimiques

Phosphoproteins 0
Exodeoxyribonucleases EC 3.1.-
three prime repair exonuclease 1 EC 3.1.16.-

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

317-332

Informations de copyright

© 2018 The Association for the Publication of the Journal of Internal Medicine.

Auteurs

N Pelzer (N)

Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands.

E S Hoogeveen (ES)

Department of Radiology, Leiden University Medical Centre, Leiden, The Netherlands.

J Haan (J)

Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands.
Department of Neurology, Alrijne Hospital, Leiderdorp, The Netherlands.

R Bunnik (R)

Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands.

C C Poot (CC)

Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands.

E W van Zwet (EW)

Department of Biomedical Data Sciences, Leiden University Medical Centre, Leiden, The Netherlands.

A Inderson (A)

Department of Gastroenterology-Hepatology, Leiden University Medical Centre, Leiden, The Netherlands.

A J Fogteloo (AJ)

Department of Internal Medicine (Acute Care), Leiden University Medical Centre, Leiden, The Netherlands.

M E J Reinders (MEJ)

Department of Internal Medicine (Nephrology), Leiden University Medical Centre, Leiden, The Netherlands.

H A M Middelkoop (HAM)

Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands.
Institute of Psychology, Health, Medical and Neuropsychology Unit, Leiden University, Leiden, The Netherlands.

M C Kruit (MC)

Department of Radiology, Leiden University Medical Centre, Leiden, The Netherlands.

A M J M van den Maagdenberg (AMJM)

Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands.
Department of Human Genetics, Leiden University Medical Centre, Leiden, The Netherlands.

M D Ferrari (MD)

Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands.

G M Terwindt (GM)

Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands.

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