LETTER TO EDITOR
|Year : 2014 | Volume
| Issue : 6 | Page : 689--690
Systemic lupus erythematosus and subarachnoid hemorrhage
Hasan Hüseyin Kozak, Muazzez Betigül Yürüten Çorbacioglu, Süleyman Ömer Anliacik
Department of Neurology, Meram Faculty of Medicine, Necmettin Erbakan University, Meram, Konya, Turkey
Hasan Hüseyin Kozak
Department of Neurology, Meram Faculty of Medicine, Necmettin Erbakan University, Meram, Konya
|How to cite this article:|
Kozak HH, Çorbacioglu MB, Anliacik SÖ. Systemic lupus erythematosus and subarachnoid hemorrhage.Neurol India 2014;62:689-690
|How to cite this URL:|
Kozak HH, Çorbacioglu MB, Anliacik SÖ. Systemic lupus erythematosus and subarachnoid hemorrhage. Neurol India [serial online] 2014 [cited 2021 Jan 21 ];62:689-690
Available from: https://www.neurologyindia.com/text.asp?2014/62/6/689/149412
Systemic lupus erythematosus (SLE) is an autoimmune disorder characterized by exacerbation and remission periods, triggered in genetically susceptible subjects by a set of hormonal and environmental factors. It is an inflammatory disorder that prominently affects the kidneys; although, any organ systems, including the skin, joints, or central nervous system, can be involved. We report a patient of SLE with subarachnoid hemorrhage (SAH).
A 43-year-old woman with no history of diabetes mellitus, hyperlipidemia, headaches, and smoking admitted to emergency department for sudden onset of severe headache and pre-syncope. She has been under follow-up for SLE since 10 years and on low-dose steroids. Physical examination revealed normal vital signs. Neurologic examination revealed patient in somnolent state with mild nucal rigidity and no fical deficit. Cranial computed tomography (CT) revealed SAH in quadrigeminal system. Magnetic resonance angiography and four vessel angiography studies were normal. Laboratory work-up was normal except for elevated urea (61,8 mg/dL), and creatinine (2,48 mg/dL) levels. A year before this admission, she was detected to have high blood pressure was secondary to renal involvement of SLE for which she was started on amlodipine and cyclophosphamide. However, drug compliance was poor and she had missed her routine follow-up visits. The working diagnosis was SAH probably due hypertension due to SLE kidney. Her general condition and neurological findings progressively got better, and control CT showed a total resorption.
The reported frequency of cerebral vascular events during the course of the disease in patients with SLE varied between 3% and 15%, a frequency higher than that in the general population, especially in young women.  The reported rates of SAH in patients with SLE varied from 1% to 3.9%.  The pathogenic mechanisms underlying SAH in SLE remain poorly understood. In SLE patients, SAH may be related to the primary disease, complications related to SLE, and treatment. Histopathologic studies in patients with SLE and SAH showed inflammatory response in the cerebral arterial and arteriolar walls, features that can go with vasculitis.  These patients were thought to have high disease activity. However, there have also been reports of SAH in patients with little or no disease activity. In these cases with low disease activity, other possible contributors to SAH include hemodynamic changes, coagulopathy, angiopathy due to premature atherosclerosis, and anticoagulant therapy in addition to other recognized factors. ,,
In a series of 57 patients with SLE and SAH, 24 (42%) patients had variable degree of renal involvement.  In the study by Baizabal et al., nine patients had hypertension on medication at the time of SAH.  The importance of the kidneys in the long-term control of blood pressure and the pathogenesis of hypertension is well-documented.  Therefore, it is not surprising that impaired renal function is a primary culprit in the progression of SLE hypertension.
Our patient suggests that early diagnosis and treatment of SLE exacerbations, as well as monitorization of severity of renal involvement, hypertension, and thrombotic and hemorrhagic events are critical for the optimal management of SLE patients. Otherwise, the sequels and death due to complications will bring about irreversible consequences and costs.
|1||Jennekenns FG, Kater L. The central nervous system in systemic lupus erythematosus. Part 2. Pathogenetic mechanisms of clinical syndromes: A literature investigation. Rheumatology 2002;41:619-30.|
|2||Baizabal Carvallo JF, Cantú Brito C, Estañol B, García Ramos GS. Subarachnoid hemorrhage as a complication of systemic lupus erythematosus. Cerebrovasc Dis 2007;24:301-4.|
|3||Kawamata T, Kagawa M, Kubo O, Takeshita M, Ujiie H, Sato K, et al. Clinicopathological studies of three cases of cerebral aneurysms associated with systemic lupus erythematosus. No Shinkei Geka 1991;19:633-9.|
|4||Oshiro S, Motomura K, Fukushima T. Systemic lupus erythematosus manifesting as subarachnoid hemorrhage induced by cortical venous thrombosis and followed by medial medullary infarction. No To Shinkei 2003;55:791-5.|
|5||van Gijn J, Rinkel GJ. Subarachnoid haemorrhage: Diagnosis, causes and management. Brain 2001;124:249-78.|
|6||Owada T, Takahashi K, Kita Y. Subarachnoid hemorrhage in systemic lupus erythematosus in Japan: Two case reports and a review of the literature. Mod Rheumatol 2009;19:573-80.|
|7||Guyton AC, Manning RD Jr, Hall JE, Norman RA Jr, Young DB, Pan YJ, et al. The pathogenic role of the kidney. J Cardiovasc Pharmacol 1984;6(Suppl 1):151-61.|