Introduction There is limited data on the effects of low carbohydrate diets on renal outcomes particularly in patients with underlying diabetic kidney disease. Therefore, this study determined the safety and effects of very low carbohydrate (VLCBD) in addition to low protein diet (LPD) on renal outcomes, anthropometric, metabolic and inflammatory parameters in patients with T2DM and underlying mild to moderate kidney disease (DKD). Materials and methods This was an investigator-initiated, single-center, randomized, controlled, clinical trial in patients with T2DM and DKD, comparing 12-weeks of low carbohydrate diet (<20g daily intake) versus standard low protein (0.8g/kg/day) and low salt diet. Patients in the VLCBD group underwent 2-weekly monitoring including their 3-day food diaries. In addition, Dual-energy x-ray absorptiometry (DEXA) was performed to estimate body fat percentages. Results The study population (n = 30) had a median age of 57 years old and a BMI of 30.68kg/m2. Both groups showed similar total calorie intake, i.e. 739.33 (IQR288.48) vs 789.92 (IQR522.4) kcal, by the end of the study. The VLCBD group showed significantly lower daily carbohydrate intake 27 (IQR25) g vs 89.33 (IQR77.4) g, p<0.001, significantly higher protein intake per day 44.08 (IQR21.98) g vs 29.63 (IQR16.35) g, p<0.05 and no difference in in daily fat intake. Both groups showed no worsening of serum creatinine at study end, with consistent declines in HbA1c (1.3(1.1) vs 0.7(1.25) %) and fasting blood glucose (1.5(3.37) vs 1.3(5.7) mmol/L). The VLCBD group showed significant reductions in total daily insulin dose (39(22) vs 0 IU, p<0.001), increased LDL-C and HDL-C, decline in IL-6 levels; with contrasting results in the control group. This was associated with significant weight reduction (-4.0(3.9) vs 0.2(4.2) kg, p = <0.001) and improvements in body fat percentages. WC was significantly reduced in the VLCBD group, even after adjustments to age, HbA1c, weight and creatinine changes. Both dietary interventions were well received with no reported adverse events. Conclusion This study demonstrated that dietary intervention of very low carbohydrate diet in patients with underlying diabetic kidney disease was safe and associated with significant improvements in glycemic control, anthropometric measurements including weight, abdominal adiposity and IL-6. Renal outcomes remained unchanged. These findings would strengthen the importance of this dietary intervention as part of the management of patients with diabetic kidney disease.

Introduction Insulinoma is a functioning pancreatic neuroendocrine tumor primarily leading due to hypoglycemia due to hypersecretion of insulin. This case illustrates the real challenges faced in the detection of an occult insulinoma, which resulted in a protracted course of the disease. Case presentation A 33-year-old female presented with recurrent hypoglycemia. Endogenous hyperinsulinemia was confirmed by a prolonged fast, however serial imaging was negative. Incidental finding of an ovarian mass gave rise to the suspicion of an insulin-producing ovarian tumor. Subsequent multimodality pancreatic imaging remained negative, requiring more invasive investigations. The tumor was localized by specialized arteriography using calcium stimulation to support the diagnosis of an insulinoma. However, repeated negative imaging led to further delays in definitive management, with worsening hypoglycemia. The surgery was finally performed three years after the initial presentation with successful removal of the tumor using intra-operative ultrasound. Clinical discussion It is important to emphasize that preoperative radiological imaging is useful to localize pancreatic lesions. However, most insulinomas could only be detected intraoperatively. The absence of suggestive radiological evidence should not deter surgeons from proceeding with definitive surgical intervention. Conclusion The case highlights the importance of a multidisciplinary approach in the management of a complicated case.

Objectives: Although the risk of diabetes mellitus has been recognised in rheumatoid arthritis, undiagnosed dysglycaemia remained under-reported. The study aimed to determine the prevalence and associated factors of dysglycaemia among patients with rheumatoid arthritis, utilising the oral glucose tolerance test. Methods: This cross-sectional study involved patients with rheumatoid arthritis, aged ⩾30 years. Following an oral glucose tolerance test, they were divided into two: dysglycaemia and normoglycaemia. Demographic and laboratory parameters were compared using logistic regression analyses. Results: There were 35.5% (55/155) patients with dysglycaemia (including 25.8% impaired glucose tolerance, 7.1% diabetes mellitus and 1.9% with both impaired fasting glucose and impaired glucose tolerance). Patients with dysglycaemia were heavier (65.5 ± 12.3 versus 60.7 ± 10.6 kg, p = 0.01), had wider waist (89.0 ± 12.5 versus 83.1 ± 9.6 cm, p < 0.01), lower high-density lipoprotein cholesterol (1.4 ± 0.3 versus 1.5 ± 0.4 mmol/L, p = 0.02), higher triglyceride (1.3 (0.9–1.8) versus 0.9 (0.8–1.2) mmol/L, p < 0.01) and intercellular adhesion molecule-1 (361.79 (290.38–481.84) versus 315.92 (251.45–407.93) ng/mL, p = 0.01). History of smoking (odds ratio: 5.70, confidence interval: 1.27–25.7), elevated triglyceride (odds ratio: 2.87, confidence interval: 1.33–6.22) and intercellular adhesion molecule-1 (odds ratio: 1.003, confidence interval: 1.001–1.006) were significantly associated with dysglycaemia. Conclusions: Prevalence of undiagnosed dysglycaemia, particularly impaired glucose tolerance, was high in these patients with rheumatoid arthritis, using a 75-g oral glucose tolerance test, which was not associated with disease activity or corticosteroid use. Those with high triglyceride, history of smoking and elevated intercellular adhesion molecule-1 were the two significant predictors for dysglycaemia in our patients with rheumatoid arthritis. Oral glucose tolerance test could be an important laboratory investigation for dysglycaemia in these high-risk patients.

BackgroundRheumatoid arthritis (RA) is a chronic inflammatory disease with an increased risk of diabetes and insulin resistance.1, 2 The prevalence of type 2 diabetes mellitus (T2DM) were demonstrated to be 10.4% as compared to only 7.6% in 1:4 controls matched for age, sex and geographical region, with an odds ratio of 1.4.3ObjectivesTo determine the prevalence of dysglycaemia (T2DM, impaired fasting glucose (IFG) and impaired glucose tolerance (IGT)) and the factors associated with dysglycaemia in patients with established RA.MethodsThis is a cross-sectional study conducted in a rheumatology centre in Malaysia. Patients with established RA aged 30 years or more were included. Exclusion criteria were overlap syndrome, pre-existing diabetes or pre-diabetes, pregnant and within 6 weeks of post-partum period. An oral glucose tolerance test (OGTT) was performed for all patients. Comparison of various factors between dysglycaemia and normoglycaemia were analysed. Multivariate analysis was performed using logistic regression analysis to ascertain the true effects of significant factors found on univariate analysis.ResultsThe mean age of patients was 57.2 ± 8.1 years and 87.7% were female. Of 155 patients included in this study, 55 (35.5%) were found to have dysglycaemia; 40 (72.7%) had IGT, 11 (20%) had T2DM, 3 had IFG and IGT (5.5%) and 1 had IFG (1.8%). Significant factors between dysglycaemia and normoglycaemia is tabulated in Table 1. The predictors of dysglycaemia were previous or current smoker (OR 4.28, 95% CI 1.02 – 17.90) and raised triglycerides (OR 3.29, 95% CI 1.29 – 8.37).ConclusionOne third of 155 patients had dysglycaemia and majority had IGT. The predictors of dysglycaemia in patients with established RA aged 30 years and more, were previous or current smoker and raised triglycerides.Table 1 Factors investigated for differences between dysglycaemia and normoglycaemia.Risk factorsDysglycaemia n=55Normoglycaemia n=100p-valuePrevious or current smoker, n (%)7 (13.0)3 (3.0)0.02Waist circumference (cm), mean ± SD89.0 ± 12.583.1± 9.6<0.01Weight (kg), mean ± SD65.5 ± 12.360.7 ± 10.60.01Systolic blood pressure (mmHg), mean ± SD134.5 ± 17.5128.2 ± 18.10.04Diastolic blood pressure (mmHg), mean ± SD79.7 ± 8.776.3 ± 10.50.04High density lipoprotein (mmol/L), mean ± SD1.4 ± 0.31.5 ± 0.40.02Triglycerides (mmol/L), mean ± SD1.3 ± 0.51.1 ± 0.5<0.01References[1] Su C-C, Chen I-C, Young F-N, Lian I-B. Risk of diabetes in patients with rheumatoid arthritis: a 12-year retrospective cohort study. The Journal of rheumatology. 2013;40(9):1513-8.[2] Ursini F, Russo E, D’Angelo S, Arturi F, Hribal ML, D’Antona L, et al. Prevalence of undiagnosed diabetes in rheumatoid arthritis: an OGTT study. Medicine. 2016;95(7):e2552[3] Han C, Robinson DW, Hackett MV, Paramore LC, Fraeman KH, Bala MV. Cardiovascular disease and risk factors in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. The Journal of rheumatology. 2006;33(11):2167-72.AcknowledgementWe would like to thank the Rheumatology team in Hosp...