Displaying publications 1 - 20 of 477 in total

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  1. Kok Leng Tan, Seng Loong Ng, Soon Eu Chong1, W Yus Haniff W Isa, Hady, Jun Jie Tan, et al.
    MyJurnal
    Introduction: Iron deficiency (ID) has recently been identified as a threat to patients with heart failure with reduced ejection fraction (HFrEF). This study was conducted to determine the occurrence of ID among HFrEF patients in a Malaysian tertiary hospital and its correlation between left ventricular ejection fraction (LVEF). Methods: Stable patients with LVEF less than 45% were included. Demographic data, LVEF (Simpsons) and cardiac functional status were studied, along with full blood count and iron profile. Results: 81 patients with a mean LVEF of 33.6% were recruited. 43.2% of them were NYHA class II patients, followed by 38.3% class III, 13.6% class I and 4.9% class IV patients. About 2/5 of the study population were anaemic, and of those, 48.5% were iron deficient. Majority of these anaemic patients (87.5%) had an absolute iron deficiency. Pearson’s statistical analysis showed positive correlation between ejection fraction and serum ferritin (r=0.624, p< 0.001), serum iron (r= 0.302, p
    Matched MeSH terms: Anemia, Iron-Deficiency
  2. Chin KY, Soelaiman IN, Naina Mohamed I, Shahar S, Teng NI, Suhana Mohd Ramli E, et al.
    Aging Male, 2012 Dec;15(4):240-5.
    PMID: 23098182 DOI: 10.3109/13685538.2012.724740
    OBJECTIVE: Variations in testosterone levels are associated with several outcomes of aging. The present study aimed to examine the relationship between age-related decline of testosterone levels and changes in bone health status, handgrip strength, body fat percentage and fat-free mass.
    MATERIALS AND METHODS: A total of 335 Malaysian Chinese and Malay men aged 40 years and above were recruited for this study. Their body compositions, calcaneal speed of sound and handgrip strength were measured and their blood was collected. Linear regression analysis was done to examine the relationship among age, testosterone levels and outcomes of aging.
    RESULTS: The results indicated significant changes in all testosterone measurements, sex hormone binding globulin level, calcaneal speed of sound, handgrip strength, body fat percentage and fat-free mass with age (p < 0.05). Age-dependent decline in bioavailable and free testosterone levels were significantly associated with reduction in calcaneal speed of sound, fat-free mass and handgrip strength (p < 0.05). Age-dependent decline in the total testosterone level was significantly associated with an increase in body fat percentage among the elderly men (p < 0.05).
    CONCLUSION: Testosterone levels are associated with changes in outcome of aging such as bone health status, muscle strength and body composition, and the relationships are age-dependent.
    Matched MeSH terms: Testosterone/deficiency
  3. Zulkifli A
    Med J Malaysia, 1979 Jun;33(4):360-1.
    PMID: 522751
    Matched MeSH terms: Factor VII Deficiency/complications*
  4. Hess SY, Zimmermann MB
    Eur. J. Endocrinol., 2000 Jun;142(6):599-603.
    PMID: 10822222
    The determination of goiter prevalence in children by thyroid ultrasound is an important tool for assessing iodine deficiency disorders. The current World Health Organization/International Council for the Control of Iodine Deficiency Disorders (WHO/ICCIDD) normative values, based on thyroid volume in iodine-sufficient European children, have recently been questioned, as thyroid volumes in iodine-sufficient children from the USA and Malaysia are smaller than the WHO/ICCIDD reference data. Our objective was to describe ultrasonographic thyroid volumes in a representative national sample of iodine-sufficient Swiss school children, and to compare these with the current reference data for thyroid volume.
    Matched MeSH terms: Iodine/deficiency*
  5. Amini F, Ismail E, Zilfalil BA
    Intern Med J, 2011 Apr;41(4):351-3.
    PMID: 21507164 DOI: 10.1111/j.1445-5994.2011.02456.x
    This study aims to define the prevalence and the molecular basis of G6PD deficiency in the Negrito tribe of the Malaysian Orang Asli. Four hundred and eighty seven consenting Negrito volunteers were screened for G6PD deficiency through the use of a fluorescent spot test. DNA from deficient individuals underwent PCR-RFLP analysis using thirteen recognized G6PD mutations. In the instances when the mutation could not be identified by PCR-RFLP, the entire coding region of the G6PD gene was subjected to DNA sequencing. In total, 9% (44/486) of the sample were found to be G6PD-deficient. However, only 25 samples were subjected to PCR-RFLP and DNA sequencing. Of these, three were found to carry Viangchan, one Coimbra and 16, a combination of C1311T in exon 11 and IVS11 T93C. Mutation(s) for the five remaining samples are unknown. The mean G6PD enzyme activity ranged 5.7 IU/gHb in deficient individuals. Our results demonstrate that the frequency of G6PD deficiency is higher among the Negrito Orang Asli than other Malaysian races. The dual presence of C1311T and IVS11 T93C in 64% of the deficient individuals (16/44) could well be a result of genetic drift within this isolated group.
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/ethnology*; Glucosephosphate Dehydrogenase Deficiency/genetics*; Glucosephosphate Dehydrogenase Deficiency/epidemiology
  6. Azira N MS, Zeehaida M
    Trop Biomed, 2012 Dec;29(4):626-31.
    PMID: 23202608
    Trichuris dysentery syndrome is caused by Trichuris trichiura which contributes to one of the most common helminthic infections in the world. It is associated with heavy colonic infection that manifests as mucoid diarrhoea, rectal bleeding, rectal prolapse, iron deficiency anaemia, and finger clubbing. Here, we report a case of trichuris dysentery syndrome complicated with severe chronic iron deficiency anaemia in a 4-year-old girl who required blood transfusion. The nematode was visualized on stool microscopic and colonoscopic examination. A longer duration of anti-helminthic treatment is required to achieve effective and better outcome.
    Matched MeSH terms: Anemia, Iron-Deficiency/diagnosis*; Anemia, Iron-Deficiency/parasitology; Anemia, Iron-Deficiency/pathology*
  7. Zakiah I, Zaini AR, Jamilah B, Zawiah A
    Malays J Pathol, 1992 Dec;14(2):91-4.
    PMID: 1304630
    Over a three-year-period, 310 babies with prolonged jaundice admitted to GHKL were studied, to determine the incidence of alpha-1-antitrypsin deficiency as a cause of the problem. Ninety-two babies (29.7%) were found to be alpha-1-antitrypsin deficient. The percentage incidence was found to be highest in Indians (33.3%), followed by Malays (31.9%) and Chinese (26.7%). There was a male preponderance with a M:F ratio of 1.6:1. Most of these babies presented at the hospital at the age of more than two weeks but less than one month. Apart from the problem of prolonged jaundice and alpha-1-antitrypsin deficiency, 2 had associated bleeding problems, 11 associated infections and 3 respiratory problems. Two babies had clinical features of Down's syndrome, 2 had G6PD deficiency and 1 had congenital hypothyroidism. AST, ALT and ALPO4 were high in 20, 26 and 3 babies respectively.
    Matched MeSH terms: alpha 1-Antitrypsin Deficiency*
  8. Ainoon O, Alawiyah A, Yu YH, Cheong SK, Hamidah NH, Boo NY, et al.
    PMID: 12971572
    Neonatal screening for G6PD deficiency has long been established in many countries. The aim of the study was to determine whether the routine semiquantitative fluorescent spot test could detect all cases of G6PD deficiency, including those cases with partial deficiency (residual red cell G6PD activity between 20-60% of normal). We compared the results of G6PD screening by the semiquantitative fluorescent spot test and quantitative G6PD activity assay on a group of 976 neonates and 67 known female heterozygotes. The values for mean G6PD activity of G6PD-normal neonates and 293 healthy adult females were determined. There was no significant difference in the mean normal G6PD activity between the two racial groups in the neonates (669 Malays, 307 Chinese) and in the 293 healthy adult females (150 Malays, 143 Chinese) group. The values for the upper limits of total deficiency (20% of normal residual activity) for neonates and adult females were 2.92 U/gHb and 1.54 U/gHb, respectively. The upper limits of partial deficiency (60% of normal residual activity) were 8.7 U/gHb and 4.6 U/gHb respectively. The prevalence of G6PD deficiency among the male neonates was 5.1% (26) by both the fluorescent spot test and the enzyme assay method. The G6PD activity levels of all 26 cases of G6PD-deficient male neonates were < 20% normal (severe enzyme deficiency). In the female neonate group, the frequency of G6PD deficiency was 1.3% (6 of 472) by the fluorescent spot test and 9.35% (44 of 472) by enzyme assay. The 6 cases diagnosed as deficient by the fluorescent spot test showed severe enzyme deficiency (< 2.92 U/gHb). The remaining 38 female neonates had partial enzyme deficiency and all were misdiagnosed as normal by the fluorescent spot test. In the female heterozygote group, G6PD deficiency was diagnosed in 53% (35 of 67) by enzyme assay and in 7.5% (4 of 67) of cases by the fluorescent spot test. The 4 cases detected by fluorescent spot test had severe enzyme deficiency (<1.6 U/gHb). The remaining 31 (46.3%) cases, diagnosed as normal by fluorescent spot test, showed partial G6PD deficiency. In conclusion, we found that the semiquantitative fluorescent spot test could only diagnose cases of total G6PD deficiency and misclassified the partially-deficient cases as normal. In this study, the overall prevalence of G6PD deficiency was 3.28% by the semiquantitative fluorescent spot test and 7.17% by enzyme assay. This means that 3.9% of G6PD-deficient neonates were missed by the routine fluorescent spot test and they were found to be exclusively females. This study demonstrates a need to use a method that can correctly classify female heterozygotes with partial G6PD deficiency. The clinical implication is that these individuals may be at risk of the hemolytic complication of G6PD deficiency.
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/blood*; Glucosephosphate Dehydrogenase Deficiency/genetics; Glucosephosphate Dehydrogenase Deficiency/epidemiology
  9. Ngu LH, Afroze B, Chen BC, Affandi O, Zabedah MY
    Singapore Med J, 2009 Oct;50(10):e365-7.
    PMID: 19907877
    Molybdenum cofactor deficiency is a rare autosomal recessive disorder with devastating neurological manifestations, characterised by neonatal-onset encephalopathy mimicking hypoxic-ischaemic insult, intractable seizure, and feeding and respiratory difficulties. It is often fatal in the early life. We report an affected 8-year-old boy, who presented with severe neurological manifestations since birth, but without clinically-significant seizure. Molybdenum cofactor deficiency must be included in the differential diagnosis of patients presenting with unexplained encephalopathy in the newborn period, and whose neuroimaging findings are consistent with hypoxic ischaemic encephalopathy. The classic laboratory hallmark of this disorder is low serum uric acid, positive urine sulphite dipstick test, and elevated urinary S-sulphocysteine, hypoxanthine and xanthine.
    Matched MeSH terms: Coenzymes/deficiency*; Metalloproteins/deficiency*
  10. Al-Alimi AA, Kanakiri N, Kamil M, Al-Rimawi HS, Zaki AH, Yusoff NM
    J Coll Physicians Surg Pak, 2010 Dec;20(12):794-7.
    PMID: 21205543 DOI: 12.2010/JCPSP.794797
    OBJECTIVE:
    To evaluate the G6PD(C563T) Mediterranean mutation among Jordanian females who were admitted to Princess Rahma Teaching Hospital (PRTH) with/or previous history of favism.
    STUDY DESIGN:
    A descriptive study.
    PLACE AND DURATION OF STUDY:
    Jordanian University of Science and Technology and PRTH, from October 2003 to October 2004.
    METHODOLOGY:
    After obtaining approval from the Ethics Committee of Jordanian University of Science and Technology, a total of 32 females were included in this study. Samples from 15 healthy individual females were used as a negative control. Blood samples from these patients were collected and analyzed by allele-specific polymerase chain reaction (AS-PCR) to determine the G6PD(C563T) mutation.
    RESULTS:
    Twenty one out of 32 patients were found to be G6PD(C563T) Mediterranean mutation (65.6%) positive. Three out of 21 patients were homozygous and remaining 18 were heterozygous for G6PD(C563T) Mediterranean mutation. Eleven (34.4%) out of 32 patients were found to be negative for G6PD(C563T) mutation indicating the presence of other G6PD mutations in the study sample.
    CONCLUSION:
    G6PD(C563T) Mediterranean mutation accounted for 65.6% of the study sample with favism in the North of Jordan. There is likely to be another G6PD deficiency variant implicated in acute hemolytic crisis (favism).
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/complications; Glucosephosphate Dehydrogenase Deficiency/genetics*
  11. Molouki A, Yusoff K
    Virol J, 2012;9:179.
    PMID: 22935147 DOI: 10.1186/1743-422X-9-179
    Recently it was shown that following infection of HeLa cells with Newcastle disease virus (NDV), the matrix (M) protein binds to Bax and subsequently the intrinsic pathway of apoptosis is activated. Moreover, there was very little alteration on mRNA and protein levels of Bax and Bcl-2 after infection with NDV.
    Matched MeSH terms: bcl-2-Associated X Protein/deficiency*
  12. Toh VK, Yung CH
    Med J Malaysia, 2009 Sep;64(3):242-3.
    PMID: 20527279 MyJurnal
    We report a case of a 16 years old girl who presented sequentially with primary amenorrhoea, hypertension and hypokalaemia. Eight years later, she was finally diagnosed with 17alpha-hydroxylase deficiency congenital adrenal hyperplasia. Previous antihypertensive medications were stopped. Hydrocortisone alone successfully maintained normotension and normokalaemia.
    Matched MeSH terms: Steroid Hydroxylases/deficiency*
  13. Bukhary NBI, Isa ZM, Shamsuddin K, Lin KG, Mahdy ZA, Hassan H, et al.
    BMC Pregnancy Childbirth, 2016 07 13;16(1):156.
    PMID: 27411716 DOI: 10.1186/s12884-016-0939-3
    BACKGROUND: Pregnant women form one of the high risk groups facing hypovitaminosis D. Low level of vitamin D will affect directly or indirectly both mother and fetus. Screening vitamin D in the first trimester of pregnancy is important to determine the necessary preventive action. Therefore, this study was aimed to determine the prevalence of hypovitaminosis D and its risk factors among pregnant women in the first trimester.

    METHODS: A cross sectional study was carried out among first trimester pregnant women during their first antenatal visit. Samples were taken from different ethnicities in an urban district in Malaysia. A total of 396 respondents (99 % response rate) aged 18-40 years completed self-administered and guided questionnaire (characteristics and risk factors), validated semi-quantitative food frequency questionnaire for vitamin D in Malaysia (FFQ vitamin D/My), anthropometric measures (weight and height), blood test for serum 25(OH)D, skin measurement using Mexameter (MX 18) and Fitzpatrick Skin Type Chart Measurement (FSTCM). Data were analyzed to determine the association between risk factors and hypovitaminosis D.

    RESULTS: The prevalence of hypovitaminosis D (serum 25(OH)D 

    Matched MeSH terms: Vitamin D Deficiency/ethnology; Vitamin D Deficiency/etiology*; Vitamin D Deficiency/epidemiology
  14. Yeo TC
    Med J Malaysia, 1987 Dec;42(4):276-83.
    PMID: 3454400
    Thirteen cases of late haemorrhagic disease of infancy due to vitamin K deficiency presenting with intracranial haemorrhage were seen over a three - year period from 1984 to 1986. The clinical picture was fairly typical; a short history of being unwell (poor feeding, vomiting, irritability, high pitched cry, fits) and physical findings of pallor, a normal body temperature, impairment of consciousness, abnormal respiration and a very tense anterior fontanelle. Vitamin K deficiency was implicated by the prolonged prothrombin time which rapidly returned to normal with vitamin K injection. The outcome was poor. Possible factors giving rise to vitamin K deficiency are discussed. The author suggests the introduction of the giving of vitamin K to all new-borns.
    Matched MeSH terms: Vitamin K Deficiency Bleeding/complications*; Vitamin K Deficiency/complications
  15. Tripathi M, Zhang CW, Singh BK, Sinha RA, Moe KT, DeSilva DA, et al.
    Cell Death Dis, 2016 12 08;7(12):e2513.
    PMID: 27929536 DOI: 10.1038/cddis.2016.374
    Hyperhomocysteinemia (HHcy) is a well-known risk factor for stroke; however, its underlying molecular mechanism remains unclear. Using both mouse and cell culture models, we have provided evidence that impairment of autophagy has a central role in HHcy-induced cellular injury in the mouse brain. We observed accumulation of LC3B-II and p62 that was associated with increased MTOR signaling in human and mouse primary astrocyte cell cultures as well as a diet-induced mouse model of HHcy, HHcy decreased lysosomal membrane protein LAMP2, vacuolar ATPase (ATP6V0A2), and protease cathepsin D, suggesting that lysosomal dysfunction also contributed to the autophagic defect. Moreover, HHcy increased unfolded protein response. Interestingly, Vitamin B supplementation restored autophagic flux, alleviated ER stress, and reversed lysosomal dysfunction due to HHCy. Furthermore, the autophagy inducer, rapamycin was able to relieve ER stress and reverse lysosomal dysfunction caused by HHcy in vitro. Inhibition of autophagy by HHcy exacerbated cellular injury during oxygen and glucose deprivation and reperfusion (OGD/R), and oxidative stress. These effects were prevented by Vitamin B co-treatment, suggesting that it may be helpful in relieving detrimental effects of HHcy in ischemia/reperfusion or oxidative stress. Collectively, these findings show that Vitamin B therapy can reverse defects in cellular autophagy and ER stress due to HHcy; and thus may be a potential treatment to reduce ischemic damage caused by stroke in patients with HHcy.
    Matched MeSH terms: Glucose/deficiency
  16. Ambayya A, Su AT, Osman NH, Nik-Samsudin NR, Khalid K, Chang KM, et al.
    PLoS One, 2014;9(3):e91968.
    PMID: 24642526 DOI: 10.1371/journal.pone.0091968
    INTRODUCTION: Similar to other populations, full blood count reference (FBC) intervals in Malaysia are generally derived from non-Malaysian subjects. However, numerous studies have shown significant differences between and within populations supporting the need for population specific intervals.

    METHODS: Two thousand seven hundred twenty five apparently healthy adults comprising all ages, both genders and three principal races were recruited through voluntary participation. FBC was performed on two analysers, Sysmex XE-5000 and Unicel DxH 800, in addition to blood smears and haemoglobin analysis. Serum ferritin, soluble transferrin receptor and C-reactive protein assays were performed in selected subjects. All parameters of qualified subjects were tested for normality followed by determination of reference intervals, measures of central tendency and dispersion along with point estimates for each subgroup.

    RESULTS: Complete data was available in 2440 subjects of whom 56% (907 women and 469 men) were included in reference interval calculation. Compared to other populations there were significant differences for haemoglobin, red blood cell count, platelet count and haematocrit in Malaysians. There were differences between men and women, and between younger and older men; unlike in other populations, haemoglobin was similar in younger and older women. However ethnicity and smoking had little impact. 70% of anemia in premenopausal women, 24% in postmenopausal women and 20% of males is attributable to iron deficiency. There was excellent correlation between Sysmex XE-5000 and Unicel DxH 800.

    CONCLUSION: Our data confirms the importance of population specific haematological parameters and supports the need for local guidelines rather than adoption of generalised reference intervals and cut-offs.

    Matched MeSH terms: Anemia, Iron-Deficiency/blood*; Anemia, Iron-Deficiency/ethnology
  17. Kong SL, Abdullah SNA, Ho CL, Musa MHB, Yeap WC
    BMC Genom Data, 2021 02 05;22(1):6.
    PMID: 33568046 DOI: 10.1186/s12863-021-00962-7
    BACKGROUND: Phosphorus (P), in its orthophosphate form (Pi) is an essential macronutrient for oil palm early growth development in which Pi deficiency could later on be reflected in lower biomass production. Application of phosphate rock, a non-renewable resource has been the common practice to increase Pi accessibility and maintain crop productivity in Malaysia. However, high fixation rate of Pi in the native acidic tropical soils has led to excessive utilization of P fertilizers. This has caused serious environmental pollutions and cost increment. Even so, the Pi deficiency response mechanism in oil palm as one of the basic prerequisites for crop improvement remains largely unknown.

    RESULTS: Using total RNA extracted from young roots as template, we performed a comparative transcriptome analysis on oil palm responding to 14d and 28d of Pi deprivation treatment and under adequate Pi supply. By using Illumina HiSeq4000 platform, RNA-Seq analysis was successfully conducted on 12 paired-end RNA-Seq libraries and generated more than 1.2 billion of clean reads in total. Transcript abundance estimated by fragments per kilobase per million fragments (FPKM) and differential expression analysis revealed 36 and 252 genes that are differentially regulated in Pi-starved roots at 14d and 28d, respectively. Genes possibly involved in regulating Pi homeostasis, nutrient uptake and transport, hormonal signaling and gene transcription were found among the differentially expressed genes.

    CONCLUSIONS: Our results showed that the molecular response mechanism underlying Pi starvation in oil palm is complexed and involved multilevel regulation of various sensing and signaling components. This contribution would generate valuable genomic resources in the effort to develop oil palm planting materials that possess Pi-use efficient trait through molecular manipulation and breeding programs.

    Matched MeSH terms: Phosphorus/deficiency*
  18. Ohba K, Ichiyama K, Yajima M, Gemma N, Nikaido M, Wu Q, et al.
    PLoS One, 2014;9(5):e97787.
    PMID: 24858917 DOI: 10.1371/journal.pone.0097787
    High prevalence of infection with high-risk human papilloma virus (HPV) ranging from 25 to 100% (average 31%) was observed in breast cancer (BC) patients in Singapore using novel DNA chip technology. Early stage of BC demonstrated higher HPV positivity, and BC positive for estrogen receptor (ER) showed significantly higher HPV infection rate. This unique association of HPV with BC in vivo prompted us to investigate a possible involvement of HPV in early stages of breast carcinogenesis. Using normal breast epithelial cells stably transfected with HPV-18, we showed apparent upregulation of mRNA for the cytidine deaminase, APOBEC3B (A3B) which is reported to be a source of mutations in BC. HPV-induced A3B overexpression caused significant γH2AX focus formation, and DNA breaks which were cancelled by shRNA to HPV18 E6, E7 and A3B. These results strongly suggest an active involvement of HPV in the early stage of BC carcinogenesis via A3B induction.
    Matched MeSH terms: Cytidine Deaminase/deficiency
  19. Mustapa Kamal Basha MA, Majid HA, Razali N, Yahya A
    PLoS One, 2020;15(6):e0233890.
    PMID: 32542014 DOI: 10.1371/journal.pone.0233890
    BACKGROUND: Allergic conditions and respiratory tract infections (RTIs) are common causes of morbidity and mortality in childhood. The relationship between vitamin D status in pregnancy (mothers), early life (infants) and health outcomes such as allergies and RTIs in infancy is unclear. To date, studies have shown conflicting results.

    OBJECTIVE: This systematic review aims to gather and appraise existing evidence on the associations between serum vitamin D concentrations during pregnancy and at birth and the development of eczema, wheezing, and RTIs in infants.

    DATA SOURCES: PubMed, MEDLINE, ProQuest, Scopus, CINAHL, Cochrane Library and Academic Search Premier databases were searched systematically using specified search terms and keywords.

    STUDY SELECTION: Articles on the associations between serum vitamin D concentrations during pregnancy and at birth and eczema, wheezing, and RTIs among infants (1-year-old and younger) published up to 31 March 2019 were identified, screened and retrieved.

    RESULTS: From the initial 2678 articles screened, ten met the inclusion criteria and were included in the final analysis. There were mixed and conflicting results with regards to the relationship between maternal and cord blood vitamin D concentrations and the three health outcomes-eczema, wheezing and RTIs-in infants.

    CONCLUSION: Current findings revealed no robust and consistent associations between vitamin D status in early life and the risk of developing eczema, wheezing and RTIs in infants. PROSPERO registration no. CRD42018093039.

    Matched MeSH terms: Vitamin D Deficiency/blood; Vitamin D Deficiency/epidemiology*
  20. Krishnan GD, Zakaria MH, Yahaya N
    J ASEAN Fed Endocr Soc, 2020;35(2):163-168.
    PMID: 33442187 DOI: 10.15605/jafes.035.02.03
    Introduction: Vitamin B12 deficiency is more common among metformin-treated subjects although the prevalence is variable. Many factors have been associated with this. The aim of this study is to determine the prevalence of vitamin B12 deficiency and its associated factors among patients with type 2 diabetes mellitus (DM) who are on metformin.

    Methodology: A total of 205 patients who fit eligibility criteria were included in the study. A questionnaire was completed, and blood was drawn to study vitamin B12 levels. Vitamin B12 deficiency was defined as serum B12 level of ≤300 pg/mL (221 pmol/L).

    Results: The prevalence of vitamin B12 deficiency among metformin-treated patients with type 2 DM patients was 28.3% (n=58). The median vitamin B12 level was 419 (±257) pg/mL. The non-Malay population was at a higher risk for metformin-associated vitamin B12 deficiency [adjusted odds ratio (OR) 3.86, 95% CI: 1.836 to 8.104, p<0.001]. Duration of metformin use of more than five years showed increased risk for metformin-associated vitamin B12 deficiency (adjusted OR 2.06, 95% CI: 1.003 to 4.227, p=0.049).

    Conclusion: Our study suggests that the prevalence of vitamin B12 deficiency among patients with type 2 diabetes mellitus on metformin in our population is substantial. This is more frequent among the non-Malay population and those who have been on metformin for more than five years.

    Matched MeSH terms: Vitamin B 12 Deficiency
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