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  1. Tan HJ, Rabani R, Noorfaizan S
    Med J Malaysia, 2007 Aug;62(3):249-50.
    PMID: 18246919 MyJurnal
    This report describes a pregnant lady in early trimester that was admitted with fever and left loin pain and was initially treated as presumed pyelonephritis. Subsequently she was found to have infective endocarditis with vegetation on the mitral valve. The course of her illness was complicated by acute pulmonary edema and septic embolization to the cerebellum. A decompressive craniectomy and resection of the lateral lobe of cerebellum was performed. Although the presenting features and risk factors are well described, the atypical presentations of infective endocarditis in pregnancy remain a diagnostic challenge for the treating physician. This report highlights the importance of rapid detection of endocarditis in pregnancy and the treatment of systemic complications.
  2. Azmin S, Sahathevan R, Suehazlyn Z, Law ZK, Rabani R, Nafisah WY, et al.
    BMC Infect Dis, 2013;13:179.
    PMID: 23594500 DOI: 10.1186/1471-2334-13-179
    BACKGROUND: Dengue is a common illness in the tropics. Equally common are neurological complications that stem from dengue infection. However, to date, parkinsonism following dengue has not been reported in medical literature.
    CASE PRESENTATION: A previously well 18-year old man developed parkinsonism, in addition to other neurological symptoms following serologically confirmed dengue fever. Alternative etiologies were excluded by way of imaging and blood investigations.
    CONCLUSIONS: The authors detail the first reported case of parkinsonism complicating dengue fever. Keeping rare presentations of common illnesses in mind, it behoves clinicians to consider parkinsonism as a complication following dengue infection. This would prevent injudicious treatment with L-dopa and dopamine agonists. Immunosuppression with steroids has been shown to be helpful in certain cases.
  3. Azmin S, Sahathevan R, Rabani R, Nafisah WY, Tan HJ, Raymond AA, et al.
    EXCLI J, 2013;12:907-15.
    PMID: 27092036
    BACKGROUND: Aspirin use is known to reduce the recurrence of stroke. However, the clinical response to aspirin has been mixed. The rate of stroke recurrence whilst on aspirin treatment is still unacceptably high. A plausible explanation for this may be resistance to the effects of aspirin. The causes of aspirin resistance are manifold and multi-factorial. We conducted a study to investigate the prevalence rate of biochemical aspirin resistance in a cohort of aspirin-naïve stroke patients. We also sought to determine the inherent factors that may predispose towards the development of aspirin resistance.
    METHOD: This was a cross-sectional, observational study conducted on patients admitted to our centre with an acute stroke who were aspirin-naïve. The diagnosis of an acute stroke was confirmed by clinical history and brain imaging. Fifty consecutive patients were prospectively enrolled. Socio-demographic data were collected and baseline blood investigations were performed. Patients were tested for biochemical aspirin resistance using Multiplate platelet analyser (Dynabyte, Munich, Germany) after 5 doses of aspirin, corresponding to a total dose of 900 mg.
    RESULTS: The median age of patients was 65.5 years and 54 % of patients were female. There were 11 smokers; of these 10 were male. Twenty-six (52 %) patients were Chinese, 21 (41 %) were Malay and 3 (6.0 %) were Indian. Aspirin resistance was present in 14 % of our patients. There was an inverse relationship between the presence of aspirin resistance and plasma HDL levels (r = -0.394; p = 0.005). There was no relationship observed between aspirin resistance and total cholesterol, triglycerides, LDL, HbA1c, ALT, ALP, urea and creatinine levels. There were no significant differences in demographic profiles or smoking status between the aspirin resistant and non-aspirin resistant groups. We did not find any link between ethnicity and aspirin resistance.
    CONCLUSIONS: Our results indicate that a lower HDL level is associated with biochemical aspirin resistance. This may increase platelet aggregation and consequently increase the risk of a recurrent stroke. The clinical implications for aspirin resistance are far reaching. Any evidence that correctable factors may negatively influence the action of aspirin warrants further investigation. The prevalence rate of biochemical aspirin resistance in our study is comparable to the findings in other studies performed in an Asian population. Further research is required to determine how our findings translate into clinical aspirin resistance and stroke recurrence.
    KEYWORDS: Asia; antiplatelet therapy; aspirin; aspirin resistance; developing countries; ischaemic stroke; risk factors
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