Cargando…

Abstract 71: Preserved beta cell function in long standing type 1 diabetes mellitus

Background: Maturity onset diabetes of young (MODY) may be misdiagnosed as type 1 or type 2 diabetes mellitus and there may be an overlap between MODY and type 1 diabetes. The presence of persistent endogenous insulin, after the “honey-moon period” has ended, should lead to evaluation of secondary c...

Descripción completa

Detalles Bibliográficos
Autores principales: Vivek, K, Reddy, D Sandeep, Sharmila, P, Rao, P Srinivas, Danda, Vijay Sheker Reddy
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer - Medknow 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9067813/
http://dx.doi.org/10.4103/2230-8210.342188
_version_ 1784700090598817792
author Vivek, K
Reddy, D Sandeep
Sharmila, P
Rao, P Srinivas
Danda, Vijay Sheker Reddy
author_facet Vivek, K
Reddy, D Sandeep
Sharmila, P
Rao, P Srinivas
Danda, Vijay Sheker Reddy
author_sort Vivek, K
collection PubMed
description Background: Maturity onset diabetes of young (MODY) may be misdiagnosed as type 1 or type 2 diabetes mellitus and there may be an overlap between MODY and type 1 diabetes. The presence of persistent endogenous insulin, after the “honey-moon period” has ended, should lead to evaluation of secondary causes of diabetes including MODY. Aim: To identify subjects with preserved beta cell function; utilizing urinary C-peptide/creatinine ratio (UCPCR) in those, who have been diagnosed and treated as Type 1 diabetes mellitus. Methodology: Hospital based cross sectional study, between February 2019 and February 2021 in 100 Subjects diagnosed as Type 1 DM for more than 3 years. Results: Mean age and duration of DM 14.17 years and 5.3years respectively. Among 18 who had family history of D.M, 7 subjects had 3 generation involvement. GAD antibodies (68%) were more prevalent compared to IA 2 antibodies (56%). 49% had presence of both Anti GAD and IA2 auto antibodies. Mean UCPCR was 0.17. UCPCR >0.2 (suggestive of preserved endogenous insulin secretion) was present in 8 subjects among study population. Among these 8 subjects, 4 subjects had history of DKA episodes, 3 subjects had family history of D.M. 3 subjects did not have either of the auto antibodies. Compared to UCPCR <0.2, subjects with UCPCR >0.2 had statistically significant lower Hba1c (p=0.005), high UCPCR values (p=0.001), high MODY probability scores (p=0.004). Conclusions: UCPCR can be used as a screening tool to identify cases who need further evaluation for secondary causes, including genetic testing for MODY.
format Online
Article
Text
id pubmed-9067813
institution National Center for Biotechnology Information
language English
publishDate 2022
publisher Wolters Kluwer - Medknow
record_format MEDLINE/PubMed
spelling pubmed-90678132022-05-05 Abstract 71: Preserved beta cell function in long standing type 1 diabetes mellitus Vivek, K Reddy, D Sandeep Sharmila, P Rao, P Srinivas Danda, Vijay Sheker Reddy Indian J Endocrinol Metab Abstracts … Esicon 2021 Background: Maturity onset diabetes of young (MODY) may be misdiagnosed as type 1 or type 2 diabetes mellitus and there may be an overlap between MODY and type 1 diabetes. The presence of persistent endogenous insulin, after the “honey-moon period” has ended, should lead to evaluation of secondary causes of diabetes including MODY. Aim: To identify subjects with preserved beta cell function; utilizing urinary C-peptide/creatinine ratio (UCPCR) in those, who have been diagnosed and treated as Type 1 diabetes mellitus. Methodology: Hospital based cross sectional study, between February 2019 and February 2021 in 100 Subjects diagnosed as Type 1 DM for more than 3 years. Results: Mean age and duration of DM 14.17 years and 5.3years respectively. Among 18 who had family history of D.M, 7 subjects had 3 generation involvement. GAD antibodies (68%) were more prevalent compared to IA 2 antibodies (56%). 49% had presence of both Anti GAD and IA2 auto antibodies. Mean UCPCR was 0.17. UCPCR >0.2 (suggestive of preserved endogenous insulin secretion) was present in 8 subjects among study population. Among these 8 subjects, 4 subjects had history of DKA episodes, 3 subjects had family history of D.M. 3 subjects did not have either of the auto antibodies. Compared to UCPCR <0.2, subjects with UCPCR >0.2 had statistically significant lower Hba1c (p=0.005), high UCPCR values (p=0.001), high MODY probability scores (p=0.004). Conclusions: UCPCR can be used as a screening tool to identify cases who need further evaluation for secondary causes, including genetic testing for MODY. Wolters Kluwer - Medknow 2022-03 /pmc/articles/PMC9067813/ http://dx.doi.org/10.4103/2230-8210.342188 Text en Copyright: © 2022 Indian Journal of Endocrinology and Metabolism https://creativecommons.org/licenses/by-nc-sa/4.0/This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.
spellingShingle Abstracts … Esicon 2021
Vivek, K
Reddy, D Sandeep
Sharmila, P
Rao, P Srinivas
Danda, Vijay Sheker Reddy
Abstract 71: Preserved beta cell function in long standing type 1 diabetes mellitus
title Abstract 71: Preserved beta cell function in long standing type 1 diabetes mellitus
title_full Abstract 71: Preserved beta cell function in long standing type 1 diabetes mellitus
title_fullStr Abstract 71: Preserved beta cell function in long standing type 1 diabetes mellitus
title_full_unstemmed Abstract 71: Preserved beta cell function in long standing type 1 diabetes mellitus
title_short Abstract 71: Preserved beta cell function in long standing type 1 diabetes mellitus
title_sort abstract 71: preserved beta cell function in long standing type 1 diabetes mellitus
topic Abstracts … Esicon 2021
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9067813/
http://dx.doi.org/10.4103/2230-8210.342188
work_keys_str_mv AT vivekk abstract71preservedbetacellfunctioninlongstandingtype1diabetesmellitus
AT reddydsandeep abstract71preservedbetacellfunctioninlongstandingtype1diabetesmellitus
AT sharmilap abstract71preservedbetacellfunctioninlongstandingtype1diabetesmellitus
AT raopsrinivas abstract71preservedbetacellfunctioninlongstandingtype1diabetesmellitus
AT dandavijayshekerreddy abstract71preservedbetacellfunctioninlongstandingtype1diabetesmellitus