FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2964211103> ?p ?o ?g. }

• W2964211103 endingPage "694" @default.
• W2964211103 startingPage "684" @default.
• W2964211103 abstract "Background Cluster analyses have proposed different diabetes phenotypes using age, BMI, glycaemia, homoeostasis model estimates, and islet autoantibodies. We tested whether comprehensive phenotyping validates and further characterises these clusters at diagnosis and whether relevant diabetes-related complications differ among these clusters, during 5-years of follow-up. Methods Patients with newly diagnosed type 1 or type 2 diabetes in the German Diabetes Study underwent comprehensive phenotyping and assessment of laboratory variables. Insulin sensitivity was assessed using hyperinsulinaemic-euglycaemic clamps, hepatocellular lipid content using magnetic resonance spectroscopy, hepatic fibrosis using non-invasive scores, and peripheral and autonomic neuropathy using functional and clinical criteria. Patients were reassessed after 5 years. The German Diabetes Study is registered with ClinicalTrials.gov, number NCT01055093, and is ongoing. Findings 1105 patients were classified at baseline into five clusters, with 386 (35%) assigned to mild age-related diabetes (MARD), 323 (29%) to mild obesity-related diabetes (MOD), 247 (22%) to severe autoimmune diabetes (SAID), 121 (11%) to severe insulin-resistant diabetes (SIRD), and 28 (3%) to severe insulin-deficient diabetes (SIDD). At 5-year follow-up, 367 patients were reassessed, 128 (35%) with MARD, 106 (29%) with MOD, 88 (24%) with SAID, 35 (10%) with SIRD, and ten (3%) with SIDD. Whole-body insulin sensitivity was lowest in patients with SIRD at baseline (mean 4·3 mg/kg per min [SD 2·0]) compared with those with SAID (8·4 mg/kg per min [3·2]; p<0·0001), MARD (7·5 mg/kg per min [2·5]; p<0·0001), MOD (6·6 mg/kg per min [2·6]; p=0·0011), and SIDD (5·5 mg/kg per min [2·4]; p=0·0035). The fasting adipose-tissue insulin resistance index at baseline was highest in patients with SIRD (median 15·6 [IQR 9·3–20·9]) and MOD (11·6 [7·4–17·9]) compared with those with MARD (6·0 [3·9–10·3]; both p<0·0001) and SAID (6·0 [3·0–9·5]; both p<0·0001). In patients with newly diagnosed diabetes, hepatocellular lipid content was highest at baseline in patients assigned to the SIRD cluster (median 19% [IQR 11–22]) compared with all other clusters (7% [2–15] for MOD, p=0·00052; 5% [2–11] for MARD, p<0·0001; 2% [0–13] for SIDD, p=0·0083; and 1% [0–3] for SAID, p<0·0001), even after adjustments for baseline medication. Accordingly, hepatic fibrosis at 5-year follow-up was more prevalent in patients with SIRD (n=7 [26%]) than in patients with SAID (n=5 [7%], p=0·0011), MARD (n=12 [12%], p=0·012), MOD (n=13 [15%], p=0·050), and SIDD (n=0 [0%], p value not available). Confirmed diabetic sensorimotor polyneuropathy was more prevalent at baseline in patients with SIDD (n=9 [36%]) compared with patients with SAID (n=10 [5%], p<0·0001), MARD (n=39 [15%], p=0·00066), MOD (n=26 [11%], p<0·0001), and SIRD (n=10 [17%], p<0·0001). Interpretation Cluster analysis can characterise cohorts with different degrees of whole-body and adipose-tissue insulin resistance. Specific diabetes clusters show different prevalence of diabetes complications at early stages of non-alcoholic fatty liver disease and diabetic neuropathy. These findings could help improve targeted prevention and treatment and enable precision medicine for diabetes and its comorbidities. Funding German Diabetes Center, German Federal Ministry of Health, Ministry of Culture and Science of the state of North Rhine-Westphalia, German Federal Ministry of Education and Research, German Diabetes Association, German Center for Diabetes Research, Research Network SFB 1116 of the German Research Foundation, and Schmutzler Stiftung. Cluster analyses have proposed different diabetes phenotypes using age, BMI, glycaemia, homoeostasis model estimates, and islet autoantibodies. We tested whether comprehensive phenotyping validates and further characterises these clusters at diagnosis and whether relevant diabetes-related complications differ among these clusters, during 5-years of follow-up. Patients with newly diagnosed type 1 or type 2 diabetes in the German Diabetes Study underwent comprehensive phenotyping and assessment of laboratory variables. Insulin sensitivity was assessed using hyperinsulinaemic-euglycaemic clamps, hepatocellular lipid content using magnetic resonance spectroscopy, hepatic fibrosis using non-invasive scores, and peripheral and autonomic neuropathy using functional and clinical criteria. Patients were reassessed after 5 years. The German Diabetes Study is registered with ClinicalTrials.gov, number NCT01055093, and is ongoing. 1105 patients were classified at baseline into five clusters, with 386 (35%) assigned to mild age-related diabetes (MARD), 323 (29%) to mild obesity-related diabetes (MOD), 247 (22%) to severe autoimmune diabetes (SAID), 121 (11%) to severe insulin-resistant diabetes (SIRD), and 28 (3%) to severe insulin-deficient diabetes (SIDD). At 5-year follow-up, 367 patients were reassessed, 128 (35%) with MARD, 106 (29%) with MOD, 88 (24%) with SAID, 35 (10%) with SIRD, and ten (3%) with SIDD. Whole-body insulin sensitivity was lowest in patients with SIRD at baseline (mean 4·3 mg/kg per min [SD 2·0]) compared with those with SAID (8·4 mg/kg per min [3·2]; p<0·0001), MARD (7·5 mg/kg per min [2·5]; p<0·0001), MOD (6·6 mg/kg per min [2·6]; p=0·0011), and SIDD (5·5 mg/kg per min [2·4]; p=0·0035). The fasting adipose-tissue insulin resistance index at baseline was highest in patients with SIRD (median 15·6 [IQR 9·3–20·9]) and MOD (11·6 [7·4–17·9]) compared with those with MARD (6·0 [3·9–10·3]; both p<0·0001) and SAID (6·0 [3·0–9·5]; both p<0·0001). In patients with newly diagnosed diabetes, hepatocellular lipid content was highest at baseline in patients assigned to the SIRD cluster (median 19% [IQR 11–22]) compared with all other clusters (7% [2–15] for MOD, p=0·00052; 5% [2–11] for MARD, p<0·0001; 2% [0–13] for SIDD, p=0·0083; and 1% [0–3] for SAID, p<0·0001), even after adjustments for baseline medication. Accordingly, hepatic fibrosis at 5-year follow-up was more prevalent in patients with SIRD (n=7 [26%]) than in patients with SAID (n=5 [7%], p=0·0011), MARD (n=12 [12%], p=0·012), MOD (n=13 [15%], p=0·050), and SIDD (n=0 [0%], p value not available). Confirmed diabetic sensorimotor polyneuropathy was more prevalent at baseline in patients with SIDD (n=9 [36%]) compared with patients with SAID (n=10 [5%], p<0·0001), MARD (n=39 [15%], p=0·00066), MOD (n=26 [11%], p<0·0001), and SIRD (n=10 [17%], p<0·0001). Cluster analysis can characterise cohorts with different degrees of whole-body and adipose-tissue insulin resistance. Specific diabetes clusters show different prevalence of diabetes complications at early stages of non-alcoholic fatty liver disease and diabetic neuropathy. These findings could help improve targeted prevention and treatment and enable precision medicine for diabetes and its comorbidities." @default.
• W2964211103 created "2019-07-30" @default.
• W2964211103 creator A5001984007 @default.
• W2964211103 creator A5002524981 @default.
• W2964211103 creator A5009401408 @default.
• W2964211103 creator A5016205185 @default.
• W2964211103 creator A5018517341 @default.
• W2964211103 creator A5021542554 @default.
• W2964211103 creator A5031235277 @default.
• W2964211103 creator A5031987417 @default.
• W2964211103 creator A5032951027 @default.
• W2964211103 creator A5034180171 @default.
• W2964211103 creator A5036247938 @default.
• W2964211103 creator A5042433471 @default.
• W2964211103 creator A5044094842 @default.
• W2964211103 creator A5044574961 @default.
• W2964211103 creator A5046010815 @default.
• W2964211103 creator A5047688546 @default.
• W2964211103 creator A5049482906 @default.
• W2964211103 creator A5052469370 @default.
• W2964211103 creator A5053898553 @default.
• W2964211103 creator A5055573058 @default.
• W2964211103 creator A5055720103 @default.
• W2964211103 creator A5057177496 @default.
• W2964211103 creator A5064733533 @default.
• W2964211103 creator A5066435946 @default.
• W2964211103 creator A5066489446 @default.
• W2964211103 creator A5067599146 @default.
• W2964211103 creator A5067604928 @default.
• W2964211103 creator A5067796093 @default.
• W2964211103 creator A5069424368 @default.
• W2964211103 creator A5073351502 @default.
• W2964211103 creator A5074771810 @default.
• W2964211103 creator A5075137497 @default.
• W2964211103 creator A5080149439 @default.
• W2964211103 creator A5082158981 @default.
• W2964211103 creator A5089607608 @default.
• W2964211103 creator A5090648557 @default.
• W2964211103 creator A5091487204 @default.
• W2964211103 date "2019-09-01" @default.
• W2964211103 modified "2023-10-18" @default.
• W2964211103 title "Risk of diabetes-associated diseases in subgroups of patients with recent-onset diabetes: a 5-year follow-up study" @default.
• W2964211103 cites W1521414679 @default.
• W2964211103 cites W1976718118 @default.
• W2964211103 cites W1984637736 @default.
• W2964211103 cites W2018492592 @default.
• W2964211103 cites W2019973807 @default.
• W2964211103 cites W2022313427 @default.
• W2964211103 cites W2086102771 @default.
• W2964211103 cites W2093103330 @default.
• W2964211103 cites W2101099639 @default.
• W2964211103 cites W2118625269 @default.
• W2964211103 cites W2124620553 @default.
• W2964211103 cites W2133275623 @default.
• W2964211103 cites W2162819835 @default.
• W2964211103 cites W2318598002 @default.
• W2964211103 cites W2528138343 @default.
• W2964211103 cites W2531626219 @default.
• W2964211103 cites W2571158149 @default.
• W2964211103 cites W2580009538 @default.
• W2964211103 cites W2590312224 @default.
• W2964211103 cites W2622132351 @default.
• W2964211103 cites W2755781103 @default.
• W2964211103 cites W2766963004 @default.
• W2964211103 cites W2790501791 @default.
• W2964211103 cites W2794371455 @default.
• W2964211103 cites W2800776805 @default.
• W2964211103 cites W2803322171 @default.
• W2964211103 cites W2893710862 @default.
• W2964211103 cites W2899649350 @default.
• W2964211103 cites W2904261387 @default.
• W2964211103 cites W3143409077 @default.
• W2964211103 doi "https://doi.org/10.1016/s2213-8587(19)30187-1" @default.
• W2964211103 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31345776" @default.
• W2964211103 hasPublicationYear "2019" @default.
• W2964211103 type Work @default.
• W2964211103 sameAs 2964211103 @default.
• W2964211103 citedByCount "305" @default.
• W2964211103 countsByYear W29642111032017 @default.
• W2964211103 countsByYear W29642111032018 @default.
• W2964211103 countsByYear W29642111032019 @default.
• W2964211103 countsByYear W29642111032020 @default.
• W2964211103 countsByYear W29642111032021 @default.
• W2964211103 countsByYear W29642111032022 @default.
• W2964211103 countsByYear W29642111032023 @default.
• W2964211103 crossrefType "journal-article" @default.
• W2964211103 hasAuthorship W2964211103A5001984007 @default.
• W2964211103 hasAuthorship W2964211103A5002524981 @default.
• W2964211103 hasAuthorship W2964211103A5009401408 @default.
• W2964211103 hasAuthorship W2964211103A5016205185 @default.
• W2964211103 hasAuthorship W2964211103A5018517341 @default.
• W2964211103 hasAuthorship W2964211103A5021542554 @default.
• W2964211103 hasAuthorship W2964211103A5031235277 @default.
• W2964211103 hasAuthorship W2964211103A5031987417 @default.
• W2964211103 hasAuthorship W2964211103A5032951027 @default.
• W2964211103 hasAuthorship W2964211103A5034180171 @default.
• W2964211103 hasAuthorship W2964211103A5036247938 @default.
• W2964211103 hasAuthorship W2964211103A5042433471 @default.

• next