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Dietary intake and hospitalisation due to diabetic ketoacidosis and hypoglycaemia in individuals with type 1 diabetes.

ABSTRACT: We investigated the association between diet and risk of hospitalisation for diabetic ketoacidosis (DKA) or hypoglycaemia in type 1 diabetes. Food records were used to assess dietary intake. Data on DKA and hypoglycaemia hospitalisations, within two years of dietary assessments, were obtained from registries. Analyses were conducted with and without macronutrient substitution. Data were available from 1391 participants, 28 (2.0%) and 55 (4.0%) of whom were hospitalised due to DKA or hypoglycaemia, respectively. In the adjusted model, self-reported alcohol intake was associated with increased (per 10 g: B?=?1.463, 95% CI?=?1.114-1.922, p?=?0.006; per E%: B?=?1.113, 95% CI?=?1.027-1.206, p?=?0.009), and fibre intake with reduced (per g/MJ: B?=?0.934, 95% CI?=?0.878-0.995, p?=?0.034) risk of DKA hospitalisation. Substituting carbohydrates for fats was associated with increased risk for hypoglycaemia hospitalisation (B?=?1.361, 95% CI?=?1.031-1.795, p?=?0.029), while substituting alcohol for carbohydrates (B?=?1.644, 95% CI?=?1.006-2.685, p?=?0.047) or proteins (B?=?2.278, 95% CI?=?1.038-4.999, p?=?0.040) increased the risk for DKA hospitalisation. In conclusion, refraining from alcohol intake is a preventable risk factor for DKA, while higher fibre intake seems rather protective. Increasing carbohydrate intake while decreasing that of fats, is associated with higher hypoglycaemia risk. Whether this is a cause or effect of hypoglycaemia remains to be established.

SUBMITTER: Ahola AJ

PROVIDER: S-EPMC7810746 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature

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Dietary intake and hospitalisation due to diabetic ketoacidosis and hypoglycaemia in individuals with type 1 diabetes.

Ahola Aila J AJ Harjutsalo Valma V Thomas Merlin C MC Forsblom Carol C Groop Per-Henrik PH

Scientific reports 20210115 1

We investigated the association between diet and risk of hospitalisation for diabetic ketoacidosis (DKA) or hypoglycaemia in type 1 diabetes. Food records were used to assess dietary intake. Data on DKA and hypoglycaemia hospitalisations, within two years of dietary assessments, were obtained from registries. Analyses were conducted with and without macronutrient substitution. Data were available from 1391 participants, 28 (2.0%) and 55 (4.0%) of whom were hospitalised due to DKA or hypoglycaemi ...[more]

PMID: 33452386

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Project description:Diabetic ketoacidosis (DKA) is a serious complication of complete insulin deficiency and insulin resistance in Type 1 diabetes (T1D). This results in the body producing high levels of serum ketones in an attempt to compensate for the insulin deficiency and decreased glucose utilization. DKA's metabolic and immunologic dysregulation results in gradual increase of systemic and cerebral oxidative stress, along with low grade systemic and cerebral inflammation and the development of pretreatment subclinical BE. During treatment the early progression of oxidative stress and inflammation is hypothesized to advance the possibility of occurrence of crisis of clinical brain edema (BE), which is the most important cause of morbidity and mortality in pediatric DKA. Longitudinal neurocognitive studies after DKA treatment show progressive and latent deficits of cognition and emphasize the need for more effective DKA treatment of this long-standing conundrum of clinical BE, in the presence of systemic osmotic dehydration, metabolic acidosis and immune dysregulation. Candidate biomarkers of several systemic and neuroinflammatory pathways prior to treatment also progress during treatment, such as the neurotoxic and neuroprotective molecules in the well-recognized tryptophan (TRP)/kynurenine pathway (KP) that have not been investigated in DKA. We used LC-MS/MS targeted mass spectrometry analysis to determine the presence and initiation of the TRP/KP at three time points: A) 6-12 hours after initiation of treatment; B) 2 weeks; and C) 3 months following DKA treatment to determine if they might be involved in the pathogenesis of the acute vasogenic complication of DKA/BE. The Trp/KP metabolites TRP, KYN, quinolinic acid (QA), xanthurnenic acid (XA), and picolinic acid (PA) followed a similar pattern of lower levels in early treatment, with subsequent increases. Time point A compared to Time points B and C were similar to the pattern of sRAGE, lactate and pyruvic acid. The serotonin/melatonin metabolites also followed a similar pattern of lower quantities at the early stages of treatment compared to 3 months after treatment. In addition, glutamate, n-acetylglutamate, glutamine, and taurine were all lower at early treatment compared to 3 months, while the ketones 3-hydroxybutaric acid and acetoacetate were significantly higher in the early treatment compared to 3 months. The two major fat metabolites, L-carnitine and acetyl-L-carnitine (ALC) changed inversely, with ALC significantly decreasing at 2 weeks and 3 months compared to the early stages of treatment. Both anthranilic acid (AA) and 3-OH-anthranilic acid (3OH-AA) had overall higher levels in the early stages of treatment (A) compared to Time points (B and C). Interestingly, the levels of AA and 3OH-AA early in treatment were higher in Caucasian females compared to African American females. There were also differences in the metabolite levels of QA and kynurenic acid (KA) between genders and between races that may be important for further development of custom targeted treatments. We hypothesize that the TRP/KP, along with the other inflammatory pathways, is an active participant in the metabolic and immunologic pathogenesis of DKA's acute and chronic insults.

Project description:Objective:This study aims to estimate the length of stay and hospitalisation cost of hypoglycaemia, and to identify determinants of variation in the length of stay and hospitalisation cost among individual patients with type 1 or 2 diabetes mellitus. Methods:A cross-sectional study was conducted using inpatients records for patients with diabetes mellitus who had been hospitalised due to hypoglycaemic events in two private hospitals in Amman, Jordan between January 2009 and May 2017. All hospitalisation costs were inflated to the equivalent costs in 2017. Hospitalisation cost was estimated from the patient's perspective in Jordanian dinars (JOD). Descriptive analyses and correlation between sociodemographic or clinical characteristics with the cost and length of stay were explored. Predictors of hypoglycaemic hospitalisation cost and length of stay were determined using logistic regression. Results:During the study period a total of 126 patients with diabetes mellitus were hospitalised due to an incident of hypoglycaemia. The mean patient age was 64.2 (SD=19.6) years; half were male. Patients admitted for hypoglycaemia stayed in hospital for a median duration of two days (IQR=2 days). The median cost of hospitalisation for hypoglycaemia was 163.2 JOD (USD 230.1) (IQR=216.3 JOD). We found that the Glasgow coma score was positively associated with length of stay (0.345, p=0.008), and older age was correlated with higher hospitalisation cost (0.207, p=0.02). Patients with a family history of diabetes had higher hospitalisation costs and longer duration of stay (0.306 and 0.275, p<0.05). In addition, being a male patient (0.394, p<0.05) and with an absence of smoking history was associated with longer duration of stay (0.456, p<0.01), but not with higher hospitalisation cost. Conclusions:Costs associated with the incidence of hypoglycaemic events are not low and constitute a large cost component of managing and treating diabetes mellitus. Male patients and patients having a family history of diabetes should receive extra care and education on the prevention of hypoglycaemic events, and a treatment de-intensification approach should be considered if necessary, so we can prevent its associated hospitalisation costs and length of stay.

Project description:BackgroundLactulose is approved for the symptomatic treatment of constipation, a gastrointestinal (GI) complication common in individuals with diabetes. Lactulose products contain carbohydrate impurities (e.g., lactose, fructose, galactose), which occur during the lactulose manufacturing process. These impurities may affect the blood glucose levels of individuals with type 2 diabetes mellitus (T2DM) using lactulose for the treatment of mild constipation. A previous study in healthy subjects revealed no increase in blood glucose levels after oral lactulose intake. However, it is still unclear whether the intake of lactulose increases blood glucose levels in individuals with diabetes.AimTo evaluate the blood glucose profile after oral lactulose intake in mildly constipated, non-insulin-dependent subjects with T2DM in an outpatient setting.MethodsThis prospective, double-blind, randomized, controlled, single-center trial was conducted at the Clinical Research Center at the Medical University of Graz, Austria, in 24 adult Caucasian mildly constipated, non-insulin-dependent subjects with T2DM. Eligible subjects were randomized and assigned to one of six treatment sequences, each consisting of four treatments stratified by sex using an incomplete block design. Subjects received a single dose of 20 g or 30 g lactulose (crystal and liquid formulation), water as negative control or 30 g glucose as positive control. Capillary blood glucose concentrations were measured over a period of 180 min post dose. The primary endpoint was the baseline-corrected area under the curve of blood glucose concentrations over the complete assessment period [AUCbaseline_c (0-180 min)]. Quantitative comparisons were performed for both lactulose doses and formulations vs water for the equal lactulose dose vs glucose, as well as for liquid lactulose vs crystal lactulose. Safety parameters included GI tolerability, which was assessed at 180 min and 24 h post dose, and adverse events occurring up to 24 h post dose.ResultsIn 24 randomized and analyzed subjects blood glucose concentration-time curves after intake of 20 g and 30 g lactulose were almost identical to those after water intake for both lactulose formulations despite the different amounts of carbohydrate impurities (≤ 3.0% for crystals and approx. 30% for liquid). The primary endpoint [AUCbaseline_c (0-180 min)] was not significantly different between lactulose and water regardless of lactulose dose and formulation. Also with regard to all secondary endpoints lactulose formulations showed comparable results to water with one exception concerning maximum glucose level. A minor increase in maximum blood glucose was observed after the 30 g dose, liquid lactulose, in comparison to water with a mean treatment difference of 0.63 mmol/L (95% confidence intervals: 0.19, 1.07). Intake of 30 g glucose significantly increased all blood glucose endpoints vs 30 g liquid and crystal lactulose, respectively (all P < 0.0001). No differences in blood glucose response were observed between the different lactulose formulations. As expected, lactulose increased the number of bowel movements and was generally well tolerated. Subjects experienced only mild to moderate GI symptoms due to the laxative action of lactulose.ConclusionBlood glucose AUCbaseline_c (0-180 min) levels in mildly constipated, non-insulin dependent subjects with T2DM are not affected by the carbohydrate impurities contained in 20 g and 30 g crystal or liquid lactulose formulations.

Dataset Information

Dietary intake and hospitalisation due to diabetic ketoacidosis and hypoglycaemia in individuals with type 1 diabetes.

Publications

Dietary intake and hospitalisation due to diabetic ketoacidosis and hypoglycaemia in individuals with type 1 diabetes.

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