Journal of diabetes and its complications最新文献

Background

A quarter of people with diabetes develop foot ulcer in their lifetime and are six times more likely to require a major lower limb amputation compared to the general population. Risk stratification tools can reliably identify those at the highest risk of ulceration, but it remains unclear if screening for foot complications can prevent limb loss in people with diabetes.

Aims

The aim of this systematic review was to determine whether population-based foot screening in people with diabetes reduces lower limb complications as assessed by development of foot ulceration, minor and major lower limb amputations, hospitalisation, or death.

Methods

MEDLINE, Embase, Emcare and CINAHL databases were searched to identify randomised and non-randomised controlled trials and observational studies (cohort, case-control and cross-sectional surveys). The screening process, study quality assessment and data extraction were performed by two independent reviewers.

Results

Following abstract screening and assessment for eligibility, five out of 10,771 identified studies were included in the analysis. Of these studies, one demonstrated 24 % reduction in development of new ulceration following introduction of screening. Major amputations decreased by between 17 and 96 % in three studies. Hospitalisation rates were contradictory, with one study showing doubling in hospital admissions and another one reduction by 33 %. One study demonstrated no impact of screening on minor or major amputation rates. None of the studies addressed the effect of foot screening on all-cause mortality.

Conclusions

The number and quality of studies to support population-based foot screening to prevent lower limb complications in people with diabetes is low. Current evidence suggests variable impact of screening on important clinical outcomes.

Aims

To investigate circulating angiogenic cells in adults with prediabetes and the effect of a structured exercise program.

Methods

A cohort of adults with overweight/obesity and either normal glucose (NG) or prediabetes were randomised to receive exercise (Exercise) (as twice weekly supervised combined high intensity aerobic exercise and progressive resistance training, and once weekly home-based aerobic exercise) or an unsupervised stretching intervention (Control) for 12 weeks. Circulating angiogenic T cells, muscle strength, and cardiovascular disease risk factors, including blood lipids, arterial stiffness, central haemodynamic responses, and cardiorespiratory fitness (VO₂peak) in those with prediabetes (n = 35, 16 Control, 19 Exercise) and NG (n = 37, 17 Control, 20 Exercise) were analysed at baseline and after the 12-week intervention.

Results

At baseline, compared with NG those with prediabetes demonstrated reduced VO₂peak, angiogenic CD31⁺CD8⁺ T cells and VEGFR2⁺CD4⁺ T cells, and increased systolic blood pressure. CD31⁺ T cells were negatively correlated with cardiovascular disease (CVD) risk. Compared with Control, exercise training increased muscle strength, VO₂peak, and CD31⁺CD4⁺ and CD31⁺CD8⁺ T cells in NG and prediabetes.

Conclusions

Circulating angiogenic CD31⁺ T cells are decreased in people with prediabetes and are enhanced with exercise training. Exercise increases CD31⁺ T cells, and through this mechanism it is proposed that it may reduce CVD risk.

Trial registration

Australian New Zealand Clinical Trials Registry number: ACTRN12617000552381.

Aims

Glycogenic hepatopathy is associated with significant psychosocial consequences and health costs. Metabolic Dysfunction-Associated Steatotic Liver Disease and glycogenic hepatopathy are frequently confused as “fatty liver” when seen on ultrasonography. We wished to examine liver fat and glycogen content in groups defined based on metabolic and liver disease phenotypes.

Methods

This case-control study undertaken in a tertiary hospital used nuclear proton magnetic resonance spectroscopy (¹H-MRS) to examine liver fat and glycogen content in five clinical groups, each containing five participants: 1. type 1 diabetes with glycogenic hepatopathy, 2. satisfactorily controlled type 1 diabetes with no liver disease, 3. poorly controlled type 1 diabetes without liver disease, 4. a control group of body mass index- and age-matched individuals without diabetes or liver disease, and 5. hepatic steatosis.

Results

Fat content was highest in the hepatic steatosis (median 15.4 %, IQR 10.0–19.3) and glycogenic hepatopathy (median 6.5 %, IQR 4.5–9.1) groups and compared to both of these groups was lower in the control group (median 1.0 %, IQR 0.7–1.1, p 0.002 and 0.022), the T1DM group with satisfactory control (median 0.3 %, IQR 0.2–0.6, p < 0.001 and <0.001), and the T1DM group with poor control without liver disease (median 1.1 %, IQR 0.9–1.1, p 0.001 and 0.012).

No participants from the type 1 diabetes poor control, type 1 diabetes satisfactory control or the no diabetes groups had ¹H-MRS-diagnosed hepatic steatosis.

¹H-MRS glycogen content could not be interpreted in the majority of those with glycogenic hepatopathy because of interference from the fat signal.

Conclusions

In cases diagnosed with glycogenic hepatopathy there may be significant concomitant fat accumulation, compounding the already elevated cardiovascular risk in this cohort.

The technique of ¹H-MRS has not been demonstrated to be useful for diagnosing glycogenic hepatopathy.

Aims

To investigate the prevalence of diabetic polyneuropathy (DPN), cardiac autonomic neuropathy (CAN) and sudomotor dysfunction in children and adolescents with type 1 diabetes using bedside modalities. Secondly, to evaluate the co-existence of these types of diabetes neuropathies.

Methods

Cross-sectional study including 221 children and adolescents with type 1 diabetes. DPN was assessed by vibration sensation threshold and sural nerve conductance, CAN by cardiac reflex tests and sudomotor function by electrochemical skin conductance.

Results

Median (interquartile range) age was 14.2 (11.9, 16.5) years, diabetes duration 4.8 (2.7, 7.7) years and Hba1c 7.1 (6.6, 7.9) %, (54: 49, 63 mmol/mol). Three had retinopathy; all had normal albuminuria. DPN was present in 40 %, early CAN in 17 %, established CAN in 3 % and sudomotor dysfunction in the feet in 5 %. Of these, 60 % had one type of neuropathy, while 35 % had two types. Only 1 participant manifested all three types of neuropathies.

Conclusions

Bedside modalities demonstrated a high prevalence of neuropathy in children and adolescents with type 1 diabetes, despite good glycemic outcome, short diabetes duration and absence of complications. A lack of co-existing neuropathies was shown, underscoring the need for multiple screening modalities.

Introduction

Methods

Results

Conclusion

Objective

Methods

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Conclusion

Aims

Methods

Results

Conclusion

Background

Given sparse relevant data, the aim of this study was to determine whether Helicobacter pylori infection, including cytotoxin-associated gene-A (CagA) producing strains, is associated with dementia in type 2 diabetes (T2DM).

Methods

Longitudinal data from 1115 participants in the community-based Fremantle Diabetes Study Phase I (mean age 64.0 years, 48.0 % males; 38.0 % H. pylori seronegative, 24.3 % H. pylori seropositive/CagA seronegative, and 37.7 % H. pylori/CagA seropositive at baseline) were analyzed.

Results

During up to 19 years of follow-up, 50.3 % and 83.5 % of participants without and with incident dementia, respectively, died. In Cox proportional hazards models, H. pylori/CagA seropositivity (hazard ratio (95 % CI) 1.68 (1.15, 2.46), P = 0.008), but not H. pylori seropositivity/CagA seronegativity (P = 0.541) was an independent predictor of incident dementia, but neither H. pylori seropositivity/CagA seronegativity nor H. pylori/CagA seropositivity were significant predictors in competing risks models (P ≥ 0.280).

Conclusions

Although CagA seropositivity in T2DM may have a contributory etiologic role in the risk of dementia, this may be through its association with reduced cardiovascular/all-cause mortality.