Search

Aims/Introduction Diabetic polyneuropathy (DPN) develops in the early stage of diabetes. However, no common diagnostic protocol has yet been established. Here, to verify that the flicker electroretinogram using a hand‐held device can detect the early dysfunction of the peripheral nervous system in patients with diabetes, we investigated the correlation between the progression of DPN and neuroretinal dysfunction. Materials and Methods In total, 184 participants with type 1 or 2 diabetes underwent a flicker electroretinogram (ERG) using a hand‐held device RETeval™ and nerve conduction study. Participants were also evaluated for intima‐media thickness, ankle‐brachial index, toe brachial index and brachial‐ankle pulse wave velocity. Parameters of the nerve conduction study were used to diagnose the severity according to Baba’s classification. A multiple regression analysis was used to examine the associations of ERG parameters with the severity of DPN categorized by Baba’s classification. Diagnostic properties of the device in DPN were evaluated using a receiver operating characteristic curve. Results A multiple regression model to predict the severity of DPN was generated using ERG. In the model, moderate‐to‐severe DPN was effectively diagnosed (area under the receiver operating characteristic curve 0.692, sensitivity 56.5%, specificity 78.3%, positive predictive value 70.6%, negative predictive value 66.1%, positive likelihood ratio 2.60, negative likelihood ratio 0.56). In the patients without diabetic retinopathy, the implicit time and amplitude in ERG significantly correlated with the parameters of the nerve conduction study, brachial‐ankle pulse wave velocity and intima‐media thickness. Conclusions Electroretinogram parameters obtained by the hand‐held device successfully predict the severity of DPN. The device might be useful to evaluate DPN., The progression of diabetic retinopathy and the dysfunction of neuroretina evaluated using the mydriasis‐free flicker electroretinogram showed a significant correlation. In patients without apparent diabetic retinopathy, the electroretinogram data correlated with parameters indicating vascular dysfunction, and with parameters indicating diabetic polyneuropathy, such as data of a nerve conduction study. Therefore, the electroretinogram data might reflect the neural and vascular impairments of the retina in patients with diabetes. The electroretinogram data were able to be used to predict the severity of diabetic polyneuropathy.

Aims/Introduction Although nerve conduction study (NCS) using a standard electromyography system (EMGS) is considered to be the gold standard in evaluating diabetic polyneuropathy, this examination requires expensive equipment and well‐trained technicians. We aimed to validate a point‐of‐care device, NC‐stat/DPNCheck™, that has been developed for widespread use of NCS in diabetic polyneuropathy. Materials and Methods Diabetes patients underwent two kinds of NCS: DPNCheck™ and electromyography system. Inter‐/intrarater reliability of DPNCheck™ were also determined by the intraclass correlation coefficient. Results A total of 57 patients were evaluated. The parameters of NCS between the two methods correlated well (r = 0.7734 for the sural nerve conduction velocity, r = 0.6155 for the amplitude of sural nerve action potential). The intraclass correlation coefficients were excellent (intrarater: the velocity 0.767, the amplitude 0.811; interrater: the velocity 0.974, the amplitude 0.834). Conclusions The point‐of‐care device has excellent reproducibility and good agreement with standard electromyography system. The device might be useful to evaluate diabetic polyneuropathy.

Background: Diabetic complications (DCs) are conventionally classified as micro- or macro-angiopathies. However, in the case of diabetic neuropathy (DPN), it is thought that impairments of neurons and glial cells of the peripheral nervous system, which do not consist of the vascular system, occupy a pivotal role in the pathology. Furthermore, recent accumulated evidences indicate that diabetic retinopathy (DR) which has been mentioned as a microangiopathy, should be also considered as adisease with complex pathogenesis consist of neurodegeneration and angiopathy. Based on this fact, we hypothesized that retinal function can predict the presence or absence of early stage DCs. The current study aimed to elucidate the relationship between DCs and retinal function in diabetic patients (DM) using a handheld device of electroretinogram (ERG) RETevalTM. Methods: Subjects: 175 hospitalized DM. Microvascular complications were assessed using urine albumin creatinine ratio (ACR) measurements, digital retinal images, and nerve conduction studies. Atherosclerosis was assessed utilizing baPWV, ABI, TBI, and carotid IMT. The Pearson’s or Spearman’s coefficient was used for data analysis. Results: Patient background: 112 males, average 60.4±14.0 years old, mean duration of disease 10.7±11.3 years, and mean HbA1c 10.1±2.3%. Prevalence of DCs were 29.4% of DR, 32.9% of nephropathy (DN), and 43.8% of DPN. Relationships with significant correlation between indices of ERG and DCs: ERG latency (LAT) and DR (p = 0.003); ERG amplitude (AMP) and DR (p < 0.001), DN (p = 0.024), or DPN (p = 0.019). Relationships with significant correlation between indices of ERG and indices of DCs: LAT and minimal F-wave latency of the tibial nerves or sural nerve NCVs; AMP and T-Chol, LDL-C, eGFR, urinary C-peptide, ACR, IMT, baPWV, TBI, or SNAP of the sural nerves. Conclusion: AMP and LAT were correlated with prevalence of DCs and their indices. The handheld ERG might predict DCs. Disclosure M. Kawai: None. T. Himeno: None. Y. Yamada: None. E. Asano: None. Y. Sugiura: None. H. Shimoda: None. Y. Shibata: None. M. Kondo: None. S. Tsunekawa: None. H. Kamiya: Speaker's Bureau; Self; Astellas Pharma Inc., Eli Lilly Japan K.K., MSD K.K., Novartis Pharma K.K., Novo Nordisk Oharma Ltd., Ono Pharmaceutical Co., Ltd., Sanofi K.K. J. Nakamura: Research Support; Self; Astellas Pharma Inc., Boehringer Ingelheim Pharmaceuticals, Inc., Daiichi Sankyo Company, Limited, Eli Lilly and Company, Japan Tobacco Inc., Kissei Pharmaceutical Co., Ltd., Merck Sharp & Dohme Corp., Novartis Pharmaceuticals Corporation, Novo Nordisk Inc., Ono Pharmaceutical Co., Ltd., Sanofi K.K., Sumitomo Dainippon Pharma Co., Ltd., Taisho Pharmaceutical Co., Ltd., Takeda Pharmaceutical Company Limited. Speaker's Bureau; Self; Astellas Pharma Inc., AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Daiichi Sankyo Company, Limited, Eli Lilly and Company, Kowa Pharmaceu. Co. Ltd., Merck Sharp & Dohme Corp., Mitsubishi Tanabe Pharma Corporation, Novartis Pharmaceuticals Corporation, Novo Nordisk Inc., Ono Pharmaceutical Co., Ltd., Sanofi K.K., Takeda Pharmaceutical Company Limited, Terumo Medical Corporation.

We present a case of a 32-year-old diabetic woman with Prader-Willi syndrome who developed severe ketoacidosis caused by a sodium-glucose cotransporter 2 (SGLT2) inhibitor, a novel class of antihyperglycemic agents, during a strict low-carbohydrate diet. At admission, a serum glucose level of 191 mg/dL was relatively low, though laboratory evaluations showed severe ketoacidosis. This is the first report of ketoacidosis caused by a SGLT2 inhibitor. It is necessary to not only pay attention when using a SGLT2 inhibitor in patients following a low-carbohydrate diet, but also to start a low-carbohydrate diet in patients treated with a SGLT2 inhibitor because of a high risk for developing ketoacidosis.