Le syndrome de Sneddon (notice n° 996838)
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| fixed length control field | 04167cam a2200277 4500500 |
| 005 - DATE AND TIME OF LATEST TRANSACTION | |
| control field | 20250125132848.0 |
| 041 ## - LANGUAGE CODE | |
| Language code of text/sound track or separate title | fre |
| 042 ## - AUTHENTICATION CODE | |
| Authentication code | dc |
| 100 10 - MAIN ENTRY--PERSONAL NAME | |
| Personal name | Hamri, Laïla |
| Relator term | author |
| 245 00 - TITLE STATEMENT | |
| Title | Le syndrome de Sneddon |
| 260 ## - PUBLICATION, DISTRIBUTION, ETC. | |
| Date of publication, distribution, etc. | 2023.<br/> |
| 500 ## - GENERAL NOTE | |
| General note | 46 |
| 520 ## - SUMMARY, ETC. | |
| Summary, etc. | RésuméIntroduction. Le syndrome de Sneddon est défini par l’association de deux atteintes cardinales : l’une est la présence d’un livedo racemosa et l’autre est la survenue d’accidents vasculaires cérébraux, souvent multiples et progressifs. Ce syndrome présente un lien étroit avec le syndrome des anti-phospholipides (SAPL), avec lequel les limites nosologiques ne sont pas encore bien claires. Une auto-immunité et/ou une thrombophilie peuvent accompagner ce syndrome, expliquant en partie sa physiopathologie.Observation. Nous rapportons le cas d’une patiente âgée de 46 ans, sans antécédent pathologique notable, présentant une longue histoire de symptômes neurologiques à type de céphalées et vertiges. Elle se plaint de troubles mnésiques progressifs, apparus plus récemment, ainsi que de paresthésies. Elle décrit également un phénomène de Raynaud. L’examen clinique objective un livedo racemosa et une hypertension artérielle. Le bilan biologique, notamment immunologique (anticorps anti-nucléaires et anticorps antiphospholipides), revient négatif. L’imagerie par résonance magnétique (IRM) cérébrale, réalisée à deux reprises et à cinq ans d’intervalle, met en évidence des lésions ischémiques cérébrales, progressives, intéressant les territoires frontaux, pariétaux et occipitaux en bilatéral. Un syndrome de Sneddon est retenu sur des éléments de présomption cliniques, biologiques et radiologiques. Un traitement anti-agrégant plaquettaire et anti-hypertenseur est instauré. L’évolution est marquée par une stabilité de la maladie.Conclusion. Depuis sa première description en 1965, le syndrome de Sneddon suscite toujours des questions étiopathogéniques et nosologiques. D’autres études s’avèrent nécessaires pour mieux comprendre cette maladie. |
| 520 ## - SUMMARY, ETC. | |
| Summary, etc. | Introduction. Sneddon syndrome is defined by the association of two cardinal disorders: one is the presence of livedo racemosa, and the other is the occurrence of strokes, often multiple and progressive. This syndrome is closely related to the anti-phospholipid syndrome (APS), with which the nosological limits are not yet clear. Autoimmunity and/or thrombophilia may accompany this syndrome, explaining in part its pathophysiology.Observation. We report the case of a 46-year-old female patient, without any notable pathological history, who presented with a long history of neurological symptoms such as headaches and dizziness. She complained of progressive memory problems, which appeared more recently, as well as paresthesia. She also described a Raynaud’s phenomenon. The clinical examination showed livedo racemosa and arterial hypertension. The biological workup, notably immunological (anti-nuclear and anti-phospholipid antibodies), was negative. Cerebral MRI, performed twice, five years apart, revealed progressive cerebral ischemic lesions involving the frontal, parietal and occipital territories bilaterally. Sneddon syndrome was retained on the basis of clinical, biological and radiological presumptions. Anti-platelet aggregation and anti-hypertensive treatment was instituted. The evolution is marked by a stability of the disease.Conclusion. Since its first description in 1965, Sneddon syndrome still raises etio-pathogenic and nosological questions. Further studies are needed to better understand this disease. |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | accident vasculaire cérébral. |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | Sneddon |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | livedo |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | Sneddon |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | livedo |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | ischemic stroke. |
| 700 10 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Zaidi, Kamal |
| Relator term | author |
| 700 10 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Boujraf, Said |
| Relator term | author |
| 700 10 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Rahbi, Samira |
| Relator term | author |
| 786 0# - DATA SOURCE ENTRY | |
| Note | Sang Thrombose Vaisseaux | Volume 35 | 3 | 2023-05-01 | p. 118-124 | 0999-7385 |
| 856 41 - ELECTRONIC LOCATION AND ACCESS | |
| Uniform Resource Identifier | <a href="https://shs.cairn.info/revue-sang-thrombose-vaisseaux-2023-3-page-118?lang=fr&redirect-ssocas=7080">https://shs.cairn.info/revue-sang-thrombose-vaisseaux-2023-3-page-118?lang=fr&redirect-ssocas=7080</a> |
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