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  1. Hasniah AL, Asiah K, Mariana D, Anida AR, Norzila MZ, Sahrir S
    Med J Malaysia, 2006 Dec;61(5):626-9.
    PMID: 17623966 MyJurnal
    Congenital upper airway obstruction is a relatively rare but important cause of major respiratory problems in the neonatal period. Vocal cord paralysis is the second most common cause of congenital airway obstruction presenting with neonatal stridor. It is often the reason for the failure of neonates to wean from the respiratory support. A retrospective analysis of medical record review was conducted. There were seven paediatric patients diagnosed with bilateral vocal fold paralysis in the past three years, of which five were recently diagnosed. All patients underwent flexible with/without rigid bronchoscopes to confirm the diagnosis. This case series highlight our experience in managing the problem of bilateral vocal cord paralysis in the paediatric population, with particular emphasis on their clinical presentations, associated complications and both upper and lower airway abnormalities. The management options and outcome of these patients will also be discussed.
  2. Lee NNA, Long G, Ngai S, Sahrir S, Parker A, Lamont AC
    Med J Malaysia, 2004 Dec;59(5):685-7.
    PMID: 15889576
    A 7-year-old girl with tonsillar infection with antibiotics. Two weeks later, there was a right sided neck lump. Computed tomography scans demonstrated a predominantly hypodense right retropharyngeal area with peripheral enhancement and mass effect. There was intense enhancement within the postero-superior aspect of the lesion which was continuous with the right internal carotid artery. Ultrasound demonstrated tapering of the right internal carotid artery. Magnetic resonance imaging and magnetic resonance arteriography showed a right internal carotid artery pseudoaneurysm. Surgical exploration confirmed the finding. This case highlights an unusual presentation of an internal carotid pseudoaneurysm and how imaging provided the diagnosis.
  3. Fadilah SA, Sahrir S, Raymond AA, Cheong SK, Aziz JA, Sivagengei K
    PMID: 10928365
    Activation of immunoregulatory T lymphocyte subsets has been observed in dengue viral infection, being more evident in dengue hemorrhagic fever (DHF) than in classical dengue fever (DF). There are, however, as yet no well-defined host markers to determine which patients with dengue viral infection will develop severe complications during the acute febrile stage of the disease. A study was performed to compare the cellular immune status in DHF, DF and non-dengue viral infections (NDF) in order to determine the value of these parameters in distinguishing DHF from classic DF and other viral infections during the acute febrile stage of the disease. This study involved 109 febrile patients admitted because of suspected DHF. Fifty patients were serologically confirmed cases of dengue infection, of which 25 had grade 1 or 2 DHF. There was a reduction in total T (CD3), CD4 and CD8 cells in DHF and demonstrated that a low level of CD3, CD4, CD8 and CD5 cells discriminated DHF from DF patients during the febrile stage of the illness. In contrast, B (CD19) cells and natural killer (NK) cells did not appear to be discriminatory in this study. Receiver operating characteristic (ROC) curve analysis showed that a combination of CD3 cell of < or = 45% and CD5 cell of < or = 55% was the best marker to identify DHF patients (sensitivity = 84% and specificity = 52% for CD3 cell of < or = 45%; sensitivity = 92% and specificity = 71% for CD5 cell of < or = 55%). CD4 cell of < or = 25% and CD8 cell < or = 30% were equally good in discriminating DHF from DF patients. On the other hand, the ROC curves indicated no clear difference between the immunoregulatory cell counts in DF from NDF Lymphopenia, atypical lymphocytosis and thrombocytopenia were significantly more evident in dengue compared to non-dengue infection but did not appear to be discriminatory among DHF and DF patients. The reduction in CD3, CD4, CD8, CD5 cells correlated with the degree of thrombocytopenia in DHF (p < 0.05) which suggests that these cells probably participate in a common pathogenetic mechanism.
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