CASE PRESENTATION: We report an Indian boy diagnosed as variant of Klinefelter syndrome with 47 XXY/46 XX mosaicism at age 12 years. He was noted to have right cryptorchidism and chordae at birth, but did not have surgery for these until age 3 years. During surgery, the right gonad was atrophic and removed. Histology revealed atrophic ovarian tissue. Pelvic ultrasound showed no Mullerian structures. There was however no clinical follow up and he was raised as a boy. At 12 years old he was re-evaluated because of parental concern about his 'female' body habitus. He was slightly overweight, had eunuchoid body habitus with mild gynaecomastia. The right scrotal sac was empty and a 2mls testis was present in the left scrotum. Penile length was 5.2 cm and width 2.0 cm. There was absent pubic or axillary hair. Pronation and supination of his upper limbs were reduced and x-ray of both elbow joints revealed bilateral radioulnar synostosis. The baseline laboratory data were LH
DISCUSSION: The MyBFF@home (Phase II) was a quasi-experimental study and it was conducted among overweight and obese housewives living in the urban areas in Malaysia. In this phase, the study involved a weight loss intervention phase (6 months) and a weight loss maintenance phase (6 months). The intervention group received a standard weight loss intervention package and the control group received group seminars related to women's health. Measurements of weight, height, waist circumference, body composition, fasting blood lipids, dietary intake, physical activity, health literacy, body pain and quality of life were conducted during the study. Overweight and obese housewives from 14 People's Housing/Home Project (PHP) in Federal Territory of Kuala Lumpur (Klang Valley) were selected as control and intervention group (N = 328). Majority of the participants (76.1%) were from the low socioeconomic group. Data were analysed and presented according to the specific objectives and the needs for the particular topic in the present supplement report.
CONCLUSION: MyBFF@home is the first and the largest community-based weight loss intervention study which was conducted among overweight and obese housewives in Malaysia. Findings of the study could be used by the policy makers and the researchers to enhance the obesity intervention programme among female adults in Malaysia.
OBJECTIVE: (i) To examine the triglyceride glucose (TyG) index (Ln[fasting triglycerides (mg/dL) × fasting glucose (mg/dL)/2]) and its relationship to in vivo insulin sensitivity in obese adolescents (OB) along the spectrum of glucose tolerance and (ii) to compare TyG index with triglyceride/high-density lipoprotein TG/HDL and 1/fasting insulin (1/IF ), other surrogates of insulin sensitivity.
PATIENTS AND DESIGN: Cross-sectional data in 225 OB with normal glucose tolerance (NGT), prediabetes (preDM), and type 2 diabetes (T2DM) who had a 3-h hyperinsulinemic-euglycemic clamp and fasting lipid measurement.
RESULTS: Insulin-stimulated glucose disposal (Rd) declined significantly across the glycemic groups from OB-NGT to OB-preDM to OB-T2DM with a corresponding increase in TyG index (8.3 ± 0.5, 8.6 ± 0.5, 8.9 ± 0.6, p
METHODS: The recruitment of participants' was carried out at Selayang Hospital, Selangor, Malaysia. Vaginal swabs were prospectively taken from 104 patients of PPROM and 111 with spontaneous onset of labour at term. Swabs were also taken from the axillae and ears of their babies. These swabs were cultured to isolate A. baumannii. Maternal and neonatal adverse outcomes were documented.
RESULTS: Sixteen mothers were A. baumannii positive, eight from each group respectively. None of the cases developed chorioamnionitis or sepsis. Those positive were four cases of PPROM and two babies of term labour. None of the babies developed sepsis.
CONCLUSIONS: This study does not support the suggestion that A. baumannii colonisation during pregnancy is associated with adverse maternal and neonatal outcomes.
CASE PRESENTATION: This is a rare case of a pair of 8-year-old monochorionic diamniotic identical twin, who on family cascade screening were diagnosed as definite FH, according to the Dutch Lipid Clinic Criteria (DLCC) with a score of 10. There were no lipid stigmata noted. Baseline lipid profiles revealed severe hypercholesterolaemia, (TC = 10.5 mmol/L, 10.6 mmol/L; LDL-c = 8.8 mmol/L, 8.6 mmol/L respectively). Their father is the index case who initially presented with premature CAD, and subsequently diagnosed as FH. Family cascade screening identified clinical FH in other family members including their paternal grandfather who also had premature CAD, and another elder brother, aged 10 years. Genetic analysis by targeted next-generation sequencing using MiSeq platform (Illumina) was performed to detect mutations in LDLR, APOB100, PCSK9, ABCG5, ABCG8, APOE and LDLRAP1 genes. Results revealed that the twin, their elder brother, father and grandfather are heterozygous for a missense mutation (c.530C > T) in LDLR that was previously reported as a pathogenic mutation. In addition, the twin has heterozygous ABCG8 gene mutation (c.55G > C). Their eldest brother aged 12 years and their mother both had normal lipid profiles with absence of LDLR gene mutation.
CONCLUSION: A rare case of Asian monochorionic diamniotic identical twin, with clinically diagnosed and molecularly confirmed heterozygous FH, due to LDLR and ABCG8 gene mutations have been reported. Childhood FH may not present with the classical physical manifestations including the pathognomonic lipid stigmata as in adults. Therefore, childhood FH can be diagnosed early using a combination of clinical criteria and molecular analyses.
Methods: Analyses were performed on 243 women (mean body mass index 31.27 ± 4.14 kg/m2) who completed a 12-month lifestyle intervention in low socioeconomic communities in Klang Valley, Malaysia. Analysis of covariance (ANCOVA) was used to compare changes of cardiometabolic risk factors across weight change categories (2% gain, ±2% maintain, >2 to <5% loss, and 5 to 20% loss) within intervention and control group.
Results: A graded association for changes in waist circumference, fasting insulin, and total cholesterol (p=0.002, for all variables) across the weight change categories were observed within the intervention group at six months postintervention. Participants who lost 5 to 20% of weight had the greatest improvements in those risk markers (-5.67 cm CI: -7.98 to -3.36, -4.27 μU/mL CI: -7.35, -1.19, and -0.59 mmol/L CI: -.99, -0.19, respectively) compared to those who did not. Those who lost >2% to <5% weight reduced more waist circumference (-4.24 cm CI: -5.44 to -3.04) and fasting insulin (-0.36 μU/mL CI: -1.95 to 1.24) than those who maintained or gained weight. No significant association was detected in changes of risk markers across the weight change categories within the control group except for waist circumference and adiponectin.
Conclusion: Weight loss of >2 to <5% obtained through lifestyle intervention may represent a reasonable initial weight loss target for women in the low socioeconomic community as it led to improvements in selected risk markers, particularly of diabetes risk.
Methods: A cross-sectional study involving 503 drug naive subjects (163 males, aged 30-65 years old (mean age ± SD = 47.4 ± 8.3 years)) divided into MS, COB and NC groups. COB was defined as central obesity (waist circumference (WC) males ≥90 cm, females ≥80 cm) in the absence of MS according to the International Diabetes Federation 2006. Fasting blood levels of tPA and PAI-1were analyzed.
Results: MS and COB had significantly higher concentration of all biomarkers compared to NC. The MS group had significantly higher concentration of tPA and PAI-1 compared to COB. WC and HDL-c had significant correlation with all biomarkers (tPA p < 0.001, PAI-1 p < 0.001). Fasting plasma glucose and diastolic blood pressure were independent predictors after correcting for confounding factors.
Conclusion: Central obesity with or without MS both demonstrated enhanced prothrombogenesis. This suggests that simple obesity possibly increases the risk of coronary artery disease in part, via increased susceptibility to thrombogenesis.
METHODS: This is a follow-up study among 84 obese housewives without co-morbidities aged 18 to 59 years old who previously participated as a control group (delayed intervention, G1) in the My Body is Fit and Fabulous at Home (MyBFF@home) Phase II. Baseline data were obtained from 12 month data collection for this group. A new group of 42 obese housewives with co-morbidities (G2) were also recruited. Both groups received a 6 month intervention (July-December 2015) consisting of dietary counselling, physical activity (PA) and self-monitoring tools (PA diary, food diary and pedometer). Study parameters included weight, height, waist circumference, blood pressure and body compositions. Body compositions were measured using a bioelectrical impedance analysis device, Inbody 720. Descriptive and repeated measures ANOVA analyses were performed using SPSS 21.
RESULTS: There were reductions in mean body fat, fat mass and visceral fat area, particularly among obese women without co-morbidities. There were also decreases fat and skeletal muscle from baseline to month six with mean difference - 0.12 (95% CI: -0.38, 0.14) and visceral fat area from month three to month six with mean difference - 9.22 (- 17.87, - 0.56) for G1. G2 showed a decreasing pattern of skeletal muscle from baseline to month six with mean difference - 0.01(95% CI: -0.38, 0.37). There was a significant difference for group effect of visceral fat area (p
METHODS: A total of 322 participants from the MyBFF@home study completed the Newest Vital Sign (NVS) test at baseline. However, only data from 209 participants who completed the NVS test from baseline to WL intervention were used to determine the HL groups. Change of the NVS scores from baseline to WL intervention phase was categorized into two groups: those with HL improvement (increased 0.1 score and above) and those without HL improvement (no change or decreased 0.1 score and more). Independent variables in this study were change of energy intake, nutrient intake, physical activity, anthropometry measurements, and body composition measurements between baseline and WL intervention as well as between WL intervention and WL maintenance. An Independent sample t-test was used in the statistical analysis.
RESULTS: In general, both intervention and control participants have low HL. The study revealed that the intervention group increased the NVS mean score from baseline (1.19 scores) to the end of the WL maintenance phase (1.51 scores) compared to the control group. There was no significant difference in sociodemographic characteristics between the group with HL improvement and the group without HL improvement at baseline. Most of the dietary intake measurements at WL intervention were significantly different between the two HL groups among intervention participants. Physical activity and body composition did not differ significantly between the two HL groups among both intervention and control groups.
CONCLUSION: There was an improvement of HL during the WL intervention and WL maintenance phase in intervention participants compared to control participants. HL shows positive impacts on dietary intake behavior among intervention participants. New research is suggested to explore the relationship between HL and weight loss behaviors in future obesity intervention studies.
CASE REPORT: Primary and secondary causes of hyperlipidaemia were investigated. Her blood was sent for fasting lipid profile, thyroid function test (TFT), fasting plasma glucose (FPG), liver function test (LFT), renal profile (RP) and HIV screening. Lipaemic interference was removed by high-speed centrifugation. She is a product of non-consanguineous marriage. She is staying together with her stepfather who is HIV positive. Her mother's infective status was negative with no dyslipidaemic features and a normal lipid profile. Lipid profile of her biological father was not known. No other lipid stigmata such as eruptive xanthoma or lipaemia retinalis was seen in the patient. Haemoglobin analysis showed Hb E-Beta thalassaemia major. Her triglycerides was 9.05 mmol/L with normal total cholesterol, 2.85 mmol/L and high-density lipoprotein cholesterol (HDL-c), 0.26 mmol/L. Calculated low-density lipoprotein cholesterol (LDL-c) was invalid as triglycerides was >4.5 mmol/L. TFT, RP, FPG, LFT were normal and HIV status was negative. She was transfused with 10 ml/kg packed cell and her blood post transfusion appeared non lipaemic.
CONCLUSION: Primary hypertriglyceridaemia was excluded based on insignificant family history of dyslipidaemia. Secondary causes of hypertriglyceridaemia were ruled out based on unremarkable laboratory investigations. Thus, we conclude that this patient is having hypertriglyceridaemia thalassaemia syndrome (HTS) which is a rare disorder with unknown pathogenesis. Further research may be required to explore this unknown association.