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  1. Soo CI, Abdul Wahab S, Abdul Hamid F
    Respir Med Case Rep, 2015;16:54-6.
    PMID: 26744655 DOI: 10.1016/j.rmcr.2015.07.005
    Melioidosis is a serious infection, which can involve multiple systems. We report a case of pulmonary melioidosis with the initial presentation mimicking a partially treated pneumonia complicated by right-sided pleural effusion. The patient is a 49-year old man who did not respond to parenteral ceftriaxone and tazobactam/piperacillin therapy. However, upon culture and sensitivity results from blood and pleural samples isolated Burkholderia pseudomallei; antimicrobial therapy was de-escalated to parenteral ceftazidime. Within 72 h duration, his fever subsided and other respiratory symptoms improved tremendously. This case highlights the importance of early recognition of B. pseudomallei in pulmonary infection in order for prompt institution of appropriate antibiotics treatment; thus reducing morbidity and mortality.
  2. Sivasothy Y, Liew SY, Othman MA, Abdul Wahab SM, Hariono M, Mohd Nawi MS, et al.
    Trop Biomed, 2021 Jun 01;38(2):79-84.
    PMID: 33973577 DOI: 10.47665/tb.38.2.044
    The NS2B/NS3 protease is crucial for the pathogenesis of the DENV. Therefore, the inhibition of this protease is considered to be the key strategy for the development of new antiviral drugs. In the present study, malabaricones C (3) and E (4), acylphenols from the fruits of Myristica cinnamomea King, have been respectively identified as moderate (27.33 ± 5.45 μM) and potent (7.55 ± 1.64 μM) DENV-2 NS2B/NS3 protease inhibitors, thus making this the first report on the DENV-2 NS2B/NS3 protease inhibitory activity of acylphenols. Based on the molecular docking studies, compounds 3 and 4 both have π-π interactions with Tyr161. While compound 3 has hydrogen bonding interactions with Gly151, Gly153 and Tyr161, compound 4 however, forms hydrogen bonds with Ser135, Asp129, Phe130 and Ile86 instead. The results from the present study suggests that malabaricones C (3) and E (4) could be employed as lead compounds for the development of new dengue antivirals from natural origin.
  3. Mohamed S, Mei Fong C, Jie Ming Y, Naila Kori A, Abdul Wahab S, Mohd Ali Z
    J Pharm Technol, 2021 Dec;37(6):286-292.
    PMID: 34790965 DOI: 10.1177/87551225211034175
    Background: he number of patients on warfarin therapy is rising steadily. Although warfarin is beneficial, it carries a high risk of bleeding, especially if the international normalized ratio (INR) values exceed 3.0. Currently, no warfarin initiation regimens have been developed for the Asian population, especially for Malaysians. Objective: This article describes the efficacy and safety of a new initiation regimen for warfarin among warfarin-naive patients. Method: Data were retrospectively collected from the ambulatory and inpatient settings. Results: A total of 165 patients who each had a target INR of 2.0 to 3.0 were included in the study. The mean age was 57.2 years and 94 patients were male. A total of 108 patients used Regimen 1 (5 mg/5 mg/3mg) and the rest of the patients used Regimen 2 (5 mg/3 mg/3 mg). Most patients used warfarin either for atrial fibrillation (52.1%) or for venous thromboembolism (29.7%). Overall, 88 of the patients had INR values above 50% from the baseline on Day 4. Additionally, 13 patients had INR values of >3.2, which required withholding and lower dose of warfarin. The predicted weekly maintenance warfarin dose (23 ± 0.5 mg/week) was found to have correlated closely with the actual maintenance dose (22.8 ± 0.5 mg/week; r 2 = 0.75). Nearly two thirds (70.3%) of the patients achieved the target INR on Day 11. Conclusion: The warfarin initiation regimens in this study was simple, safe, and suitable to be used in both ambulatory and inpatient settings for managing warfarin therapy.
  4. Abdul Wahab S, Hassan A, Latif MT, Vadiveel Y, Jeyabalan T, Soo CI, et al.
    Asian Pac J Cancer Prev, 2019 07 01;20(7):1959-1965.
    PMID: 31350951 DOI: 10.31557/APJCP.2019.20.7.1959
    Objective: Epidemiological studies have reported the close relationship between risk for lung cancers and air pollution
    in particular, for non-smoking related lung cancers. However, most studies used residential address as proxies which may
    not estimate accurately an individual’s air pollution exposure. Therefore, the aim of this study was to identify risk factors
    such as occupation and mode of transportation associated with lung cancer diagnosis and death. Methods: Subjects
    with lung cancer (n=514) were evaluated both by chart reviews for clinical data and interviews to determine residential
    address for ten years, main occupation and main mode of transportation. Annual particulate matter with diameter size
    less than 2.5 micrometre (PM2.5) concentration were calculated based on particulate matter with diameter size less than
    10 micrometre (PM10) data recorded by Malaysian Department of Environment. Logistic regression analysis, cluster
    analysis and the Cox regression analysis were performed to the studied variables. Results: This study concurred with
    previous studies that lung adenocarcinoma were diagnosed in predominantly younger, female non-smokers compared
    to the other types of lung cancers. Lung adenocarcinoma subjects had annual PM2.5 that was almost twice higher than
    squamous cell carcinoma, small cell carcinoma and other histological subtypes (p=0.024). Independent of smoking,
    the κ -means cluster analysis revealed two clusters in which the high risk cluster involves occupation risk with air
    pollution of more than four hours per day, main transportation involving motorcycle and trucks and mean annual PM2.5
    concentration of more than 30 based on residential address for more than ten years. The increased risk for the high-risk
    cluster was more than five times for the diagnosis of lung adenocarcinoma (OR=5.69, 95% CI=3.14-7.21, p<0.001).
    The hazard ratio for the high-risk cluster was 3.89 (95% CI=2.12-4.56, p=0.02) for lung adenocarcinoma mortality at
    1 year. Conclusion: High-risk cluster including PM2.5, occupation risk and mode of transportation as surrogates for
    air-pollution exposure was identified and highly associated with lung adenocarcinoma diagnosis and 1-year mortality.
  5. Chuah CH, Chow TS, Hor CP, Cheng JT, Ker HB, Lee HG, et al.
    Clin Infect Dis, 2021 Nov 19.
    PMID: 34849615 DOI: 10.1093/cid/ciab962
    BACKGROUND: Role of favipiravir in preventing disease progression in COVID-19 remains uncertain. We aimed to determine its effect in preventing disease progression from non-hypoxia to hypoxia among high risk COVID-19 patients.

    STUDY DESIGN: This was an open-label, randomized clinical trial conducted at 14 public hospitals across Malaysia from February to June 2021 among 500 symptomatic, RT-PCR confirmed COVID-19 patients, aged ≥50 years with ≥1 co-morbidity, and hospitalized within first 7 days of illness. Patients were randomized on 1:1 ratio to favipiravir plus standard care or standard care alone. Favipiravir was administered at 1800mg twice-daily on day 1 followed by 800mg twice-daily until day 5. The primary endpoint was rate of clinical progression from non-hypoxia to hypoxia. Secondary outcomes included rates of mechanical ventilation, intensive care unit (ICU) admission, and in-hospital mortality.

    RESULTS: Among 500 patients were randomized (mean age, 62.5 [SD 8.0] years; 258 women [51.6%]; and 251 [50.2%] had COVID-19 pneumonia), 487 (97.4%) patients completed the trial. Clinical progression to hypoxia occurred in 46 (18.4%) patients on favipiravir plus standard care and 37 (14.8%) on standard care alone (OR 1.30; 95%CI, 0.81-2.09; P=.28). All three pre-specified secondary end points were similar between both groups. Mechanical ventilation occurred in 6 (2.4%) vs 5 (2.0%) (OR 1.20; 95%CI, 0.36-4.23; P=.76), ICU admission in 13 (5.2%) vs 12 (4.8%) (OR 1.09; 95%CI, 0.48-2.47; P=.84), and in-hospital mortality in 5 (2.0%) vs 0 (OR 12.54; 95%CI, 0.76- 207.84; P=.08).

    CONCLUSIONS: Among COVID-19 patients at high risk of disease progression, early treatment with oral favipiravir did not prevent their disease progression from non-hypoxia to hypoxia.

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