Clinical relevance of trace element measurement in patients on initiation of parenteral nutrition.

Background and Aims Serum zinc, copper and selenium are measured in patients prior to commencing on parenteral nutrition; however, their interpretation can be difficult due to acute phase reactions. We assessed (i) the relationship of raised C-reactive protein with trace elements and albumin (ii) benefits of measuring trace elements when C-reactive protein is raised in patients requiring short-term parenteral nutrition. Methods Samples were collected for zinc, copper, selenium and albumin at baseline and then every two weeks and correlated with C-reactive protein results in patients on parenteral nutrition. Results were categorized into four groups based on the C-reactive protein concentrations: (i) <20 mg/L, (ii) 20-39 mg/L, (iii) 40-79 mg/L and (iv) ≥80 mg/L. Results In 166 patients, zinc, selenium and albumin correlated (Spearman's) negatively with C-reactive protein; r = -0.26, P < 0.001 (95% CI -0.40 to -0.11), r = -0.44, P < 0.001 (-0.56 to -0.29) and r = -0.22 P = 0.005 (-0.36 to -0.07), respectively. Copper did not correlate with C-reactive protein (r = 0.09, P = 0.25 [-0.07 to 0.25]). Comparison of trace elements between the four groups showed no difference in zinc and copper (both P > 0.05), whereas selenium and albumin were lower in the group with C-reactive protein > 40 mg/L ( P < 0.05). Conclusion In patients on short-term parenteral nutrition, measurement of C-reactive protein is essential when interpreting zinc and selenium but not copper results. Routine measurement of trace elements prior to commencing parenteral nutrition has to be considered on an individual basis in patients with inflammation.

Urine bile acids relate to glucose control in patients with type 2 diabetes mellitus and a body mass index below 30 kg/m2.

Bile acids are important endocrine signalling molecules, modulating glucose homeostasis through activation of cell surface and nuclear receptors. Bile acid metabolism is altered in type 2 diabetes mellitus; however, whether this is of pathogenic consequence is not fully established. In this study urinary bile acid excretion in individuals with type 2 diabetes and matched healthy volunteers was assessed. Urinary bile acid excretion in type 2 diabetes patients was considered in the context of prevailing glycaemia and the patient body mass index. Urine bile acids were measured by liquid chromatography-tandem mass spectrometry, allowing individual quantification of 15 bile acid species. Urinary bile acid excretion in patients with type 2 diabetes who were normal weight (BMI 18.5-24.9 kg/m2) and overweight (BMI 25-29.9 kg/m2) were elevated compared to healthy normal weight volunteers, both p<0.0001. In obese (BMI ≥ 30 kg/m2) type 2 diabetes patients, urinary bile acid excretion was significantly lower than in the normal and overweight type 2 diabetes groups (both p<0.01). Total bile acid excretion positively correlated with HbA1c in normal (rs=0.85, p=<0.001) and overweight (rs=0.61, p=0.02) but not obese type 2 diabetes patients (rs=-0.08, p=0.73). The glycaemia-associated increases in urine bile acid excretion in normal weight and overweight type 2 diabetes seen in this study may represent compensatory increases in bile acid signalling to maintain glucose homeostasis. As such alterations appear blunted by obesity; further investigation of weight-dependent effects of bile acid signalling on type 2 diabetes pathogenesis is warranted.

Higher circulating bile acid concentrations in obese patients with type 2 diabetes.

BACKGROUND: Bile acids (BAs) play an important role in releasing incretin hormones via the enteroendocrine L-cell surface TGR5 receptors. The aim of this study was to investigate the difference in BA concentration at baseline and in response to a meal stimulus between type 2 diabetes mellitus (T2DM) and a matched normoglycaemic group. MATERIALS AND METHODS: A cross-sectional study of 12 patients with known T2DM and 12 matched normoglycaemic controls compared BA fractions after an overnight fast and following a standard meal. RESULTS: The T2DM group had higher baseline glucose (P < 0.001), but baseline total BA, total glycine conjugated BAs (GCBA) and total taurine conjugated BA (TCBA) were similar between both groups. The T2DM group compared to the normoglycaemic group had a higher post-prandial peak change in total BAs 4.28 (3.51-5.38) µmol/L vs. 0.88 (0.60-1.57) µmol/L (P < 0.001) and peak total GCBA 2.77 (1.07-4.19) µmol/L vs. 0.94 (0.34-1.15) µmol/L (P < 0.0001), but similar peak total TCBA 0.36 (0.02-0.76) µmol/L vs. 0.08 (0.04-0.22) µmol/L (P=0.91). CONCLUSION: The post-prandial bile acid response is elevated in obese patients with T2DM compared to matched normoglycaemic individuals.

Adherence to the National Institute of Clinical Excellence guidance on parenteral nutrition screening is not enough to improve outcomes.

BACKGROUND & AIM: Majority of the National Institute of Clinical Excellence (NICE) nutrition guidance recommendations were based on Grade D evidence due to absence of randomised controlled trials. The aim was to assess outcomes of parenteral nutrition (PN) administration when the guidance was adhered to. METHODS: The prospective study included patients referred for PN. Patients were divided into two groups: guidance compliant and guidance non-compliant. Primary outcome measures were duration of PN treatment, number of PN bags used per patient, length of hospital stay and mortality. RESULTS: There were 262 patients, aged 54(42-67) [median (IQR)] years. The guidance compliant and the non-compliant groups consisted of 143 and 119 patients respectively. In the guidance compliant group all patients were screened on admission compared to 40% in the non-compliant group (p < 0.001). Among those malnourished/at risk of malnutrition all were referred for early dietetic assessment in the compliant group but only 14% in the non-compliant group (p < 0.001). There was no difference in any of the outcome measures between the groups. CONCLUSION: Compliance with the nutritional guidance in the UK was not enough to improve outcomes in patients requiring PN in our cohort. Evidence based changes to PN practice are required to optimise care.