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Neuropsychiatic systematic lupus erythematosus (NPSLE) is a form of SLE involves the inflammation and/or thrombotic event in the nervous system. Patients with NPSLE are likely to have a positive antiphospholipid antibody (aPL), therefore are at higher risk of recurrent ischemic stroke. The management of NPSLE with aPLrelated stroke is rather different from the traditional ischemic stroke. One must treat it with anticoagulation and immunosuppressive therapy. The present case is a 47-yearold Taiwanese female with NPSLE and positive aPL, presented with a recurrent MCA ischemic stroke. Initial laboratory results showed significantly elevated levels of anti-ANA, anti-dsDNA, anti-cardiolipin, and decreased complement levels. Due to multiple contraindications for tPA, she was treated with antiplatelet, anticoagulation, steroid pulse therapy, and plasmapheresis during the hospitalization. Despite treatments, her stroke progressed to multi-focal lesions, involving the ACA, MCA, and basal ganglion. On follow up of her brain CT scan showed tissue edema and suspicious for subfalcine herniation. Responding to this clinical deterioration, we stopped warfarin and started mannitol. Eventually, her condition improved and was transferred to the rehabilitation program. Currently, there is no unified guideline regarding the secondary prevention of ischemic stroke in NPSLE with aPL patients. Additionally, previously reported use of steroid pulse therapy and plasmapheresis can potentially harm the patient. Clinicians must be cautious when treating such patient.

Abstract:The ACE (angiotensin converting enzyme) inhibitors are not only drugs widely prescribed drugs in cardiovascular diseases, but also potentially therapeutic agents in dementia. Based on the findings that the ACE inhibitors could activate the c-Jun N-terminal kinase signal to increase the ACE gene expression and that the Alu element of the human ACE gene involved in regulating ACE promoter activity, we aimed to investigate whether there are different pharmacogenetic responses of ACE I/D polymorphism to the ACE inhibitors in neurons. The three reporter vectors, pACEpro(f)-SEAP, p-I-ACEpro-SEAP, and p-D-ACEpro-SEAP were used to examine the transcriptional activity of the vectors responding to the lisinopril treatment using a transient-transfection method in SH-SY5Y cells. Our results showed that lisinopril increased the promoter activity of an ACE gene by 16.7%. Additionally, we found the lisinopril enhanced the ACE promoter activity of the I-form vector by 17.2%, but adversely reduced that of the D-form vector by 16.8%, as compared with the respective control without the lisinopril treatment. Firstly, our findings had proved that the I/D polymorphism of ACE gene contrarily responds to the ACE inhibitors in regulating the ACE expression in neurons, which provide a novel insight suggesting genetic testing to tailor the treatment regimens in AD (Alzheimer's disease) patients.

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