The clinical value of glycosylated hemoglobin level in newly diagnosed ketosis-prone type 2 diabetes
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SUBMITTER: Min R
PROVIDER: S-EPMC10667908 | biostudies-literature | 2023 Jan
REPOSITORIES: biostudies-literature
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Project description:Despite advances in diabetes technology and treatment, a majority of children and adolescents with type 1 diabetes (T1D) fail to meet hemoglobin A1c (HbA1c) targets. Among high-income nations, the United States has one of the highest mean HbA1c values. We tracked the HbA1c values of 261 patients diagnosed with T1D in our practice over a 2.5-year period to identify inflection points in the HbA1c trajectory. The HbA1c declined until 5 months postdiagnosis. There was a rise in the HbA1c between the fifth and sixth month postdiagnosis. The HbA1c continued to steadily rise and by 18 months postdiagnosis, the mean HbA1c was 8.2%, which is also our clinic mean. Understanding the HbA1c trajectory early in the course of diabetes has helped to identify opportunities for intensification of diabetes management to flatten the trajectory of HbA1c and improve clinical outcomes.
| S-EPMC7001422 | biostudies-literature
Project description:Ketosis-prone diabetes (KPD) is a widespread, emerging, heterogeneous syndrome characterized by patients who present with diabetic ketoacidosis or unprovoked ketosis but do not necessarily have the typical phenotype of autoimmune type 1 diabetes. Multiple, severe forms of beta-cell dysfunction appear to underlie the pathophysiology of KPD. Until recently, the syndrome has lacked an accurate, clinically relevant and etiologically useful classification scheme. We have utilized a large, longitudinally followed, heterogeneous, multiethnic cohort of KPD patients to identify four clinically and pathophysiologically distinct subgroups that are separable by the presence or absence of beta-cell autoimmunity and the presence or absence of beta-cell functional reserve. The resulting "Abeta" classification system of KPD has proven to be highly accurate and predictive of such clinically important outcomes as glycemic control and insulin dependence, as well as an aid to biochemical and molecular investigations into novel causes of beta-cell dysfunction. In this review, we describe the current state of knowledge in regard to the natural history, pathophysiology, and treatment of the subgroups of KPD, with an emphasis on recent advances in understanding their immunological and genetic bases.
| S-EPMC2528854 | biostudies-literature
Project description:Ketosis-prone type 2 diabetes is recognized as atypical diabetes. These patients are often male, characterized by obesity, sudden onset of ketosis and a transient decrease in insulin secretion capacity that can be recovered with temporal insulin therapy. Here, we report a male patient with ketosis-prone type 2 diabetes who was followed up for 8 years. During the follow-up period, his bodyweight fluctuated and he experienced four episodes of critical ketosis recurrence in association with bodyweight gain. He discontinued insulin therapy after each ketosis episode within the first 4 years, but thereafter, he had to continue insulin therapy because of decreased insulin secretion capacity. Interestingly, his peak bodyweight just before the repeated ketosis episode gradually decreased, and the insulin secretion capacity after the recovery from repeated ketosis decreased in parallel with his peak bodyweight. This long-term clinical course might be a clue to understand the pathophysiology of ketosis-prone type 2 diabetes.
| S-EPMC7078091 | biostudies-literature
Project description: Not available
| S-EPMC162128 | biostudies-literature
Project description:Diabetic ketoacidosis (DKA) has been considered a key clinical feature of Type 1 diabetes mellitus; however, increasing evidence indicates that DKA is also a common feature of Type 2 diabetes (T2DM). Many cases of DKA develop under stressful conditions such as trauma or infection but an increasing number of cases without precipitating cause have been reported in children and adults with T2DM. Such patients present with severe hyperglycemia and ketosis as in Type 1 diabetes mellitus but can discontinue insulin after a few months and maintain acceptable glycemic control on diet or oral agents. This subtype of diabetes has been referred to as ketosis-prone T2DM. In this article, we reviewed the literature on ketosis-prone T2DM and summarized the epidemiology, putative pathophysiology and approaches to management.
| S-EPMC3351851 | biostudies-literature
Project description:BackgroundPrevious studies have reported that abnormal glucose metabolism is associated with poor cancer outcomes. Glycated hemoglobin A1c (HbA1c) is an important indicator of glucose metabolism. This study aimed to investigate the relationship between nondiabetic HbA1c levels and cancer-related mortality.MethodsThis was a retrospective cohort study of Koreans who attended an annual or biennial health checkup program. The study group was categorized based on the quintile of HbA1c level (Q1, 3.0-5.1%; Q2, 5.2-5.3%; Q3, 5.4%; Q4, 5.5-5.6%, Q5, 5.7-6.4%). Cancer-related mortality was determined using the mortality data from the Korea National Statistical Office. Participants with an established diagnosis of diabetes or cancer were excluded. Cancer-related mortality was assessed depending on each HbA1c level with adjustment for factors that could influence mortality.ResultsA total of 589,457 participants were included in this study. During a median follow-up duration of 6.99 years, 1712 cancer-related deaths were reported. The risk of cancer-related mortality was significantly higher in the Q5 group (hazard ratio (HR) 1.23, range 1.02-1.47 in model 1; HR 1.25, range 1.04-1.50 in model 2). HbA1c levels were linearly associated with cancer-related deaths (Ptrend = 0.021 in model 1; 0.013 in model 2). HbA1c level and colorectal, stomach, and lung cancer mortality exhibited a positive relationship, whereas liver cancer-related mortality showed an inverse relationship with HbA1c level (Ptrend = 0.001).ConclusionsOur study showed that abnormal glucose metabolism is significantly associated with cancer-related mortality, and its relationship varies with each type of cancer.
| S-EPMC9570990 | biostudies-literature
Project description:BackgroundKetosis-prone type 2 diabetes (KPD), as a unique emerging clinical entity, often has no clear inducement or obvious clinical symptoms at the onset of the disease. Failure to determine ketosis in time may lead to more serious consequences and even death. Therefore, our study aimed to develop and validate a novel nomogram to predict KPD.MethodsIn this retrospective study, clinical data of a total of 398 newly diagnosed type 2 diabetes in our hospital who met our research standards with an average age of 48.75 ± 13.86 years years old from January 2019 to December 2022 were collected. According to the occurrence of ketosis, there were divided into T2DM groups(228 cases)with an average age of 52.19 ± 12.97 years, of whom 69.74% were male and KPD groups (170cases)with an average age of 44.13 ± 13.72 years, of whom males account for 80.59%. Univariate and multivariate logistic regression analysis was performed to identify the independent influencing factors of KPD and then a novel prediction nomogram model was established based on these independent predictors visually by using R4.3. Verification and evaluation of predictive model performance comprised receiver-operating characteristic (ROC) curve, corrected calibration curve, and clinical decision curve (DCA).Results4 primary independent predict factors of KPD were identified by univariate and multivariate logistic regression analysis and entered into the nomogram including age, family history, HbA1c and FFA. The model incorporating these 4 predict factors displayed good discrimination to predict KPD with the area under the ROC curve (AUC) of 0.945. The corrected calibration curve of the nomogram showed good fitting ability with an average absolute error =0.006 < 0.05, indicating a good accuracy. The decision analysis curve (DCA) demonstrated that when the risk threshold was between 5% and 99%, the nomogram model was more practical and accurate.ConclusionIn our novel prediction nomogram model, we found that age, family history, HbA1c and FFA were the independent predict factors of KPD. The proposed nomogram built by these 4 predictors was well developed and exhibited powerful predictive performance for KPD with high discrimination, good accuracy, and potential clinical applicability, which may be a useful tool for early screening and identification of high-risk population of KPD and therefore help clinicians in making customized treatment strategy.
| S-EPMC10565480 | biostudies-literature
Project description:BackgroundTo evaluate the association of time to reach the target glycosylated hemoglobin (HbA1c) level with long-term durable glycemic control and risk of diabetic complications in patients with newly diagnosed type 2 diabetes mellitus (T2DM).MethodsIn a longitudinal observational cohort, 194 patients with T2DM newly diagnosed between January 2011 and March 2013 were followed up over 6 years. Patients were classified according to the time needed to reach the target HbA1c (<7.0%): <3, 3 to 6 (early achievement group), and ≥6 months (late achievement group). Risks of microvascular complications including diabetic retinopathy, nephropathy, and neuropathy as well as macrovascular events including ischemic heart disease, ischemic stroke, and peripheral arterial disease were assessed by multivariable Cox proportional hazards analysis.ResultsDuring a median follow-up of 6.53 years, 66 microvascular and 14 macrovascular events occurred. Maintenance of durable glycemic control over 6 years was more likely in the early achievement groups than in the late achievement group (34.5%, 30.0%, and 16.1% in <3, 3 to 6, and ≥6 months, respectively, P=0.039). Early target HbA1c achievement was associated with lower risk of composite diabetic complications (adjusted hazard ratio [HR, 0.47; 95% confidence interval [CI], 0.26 to 0.86 in <3 months group) (adjusted HR, 0.50; 95% CI, 0.23 to 1.10 in 3 to 6 months group, in reference to ≥6 months group). Similar trends were maintained for risks of microvascular and macrovascular complications, although statistical significance was not reached for macrovascular complications.ConclusionEarly target HbA1c achievement was associated with long-term durable glycemic control and reduced risk of diabetic complications in newly diagnosed T2DM.
| S-EPMC8164945 | biostudies-literature
Project description:BACKGROUND: Genetic variability of the major subunit (CACNA1E) of the voltage-dependent Ca(2+) channel Ca(V)2.3 is associated to risk of type 2 diabetes, insulin resistance and impaired insulin secretion in nondiabetic subjects. The aim of the study was to test whether CACNA1E common variability affects beta cell function and/or insulin sensitivity in patients with newly diagnosed type 2 diabetes. METHODOLOGY/PRINCIPAL FINDINGS: In 595 GAD-negative, drug naïve patients (mean ± SD; age: 58.5 ± 10.2 yrs; BMI: 29.9 ± 5 kg/m(2), HbA1c: 7.0±1.3) with newly diagnosed type 2 diabetes we: 1. genotyped 10 tag SNPs in CACNA1E region reportedly covering ?93% of CACNA1E common variability: rs558994, rs679931, rs2184945, rs10797728, rs3905011, rs12071300, rs175338, rs3753737, rs2253388 and rs4652679; 2. assessed clinical phenotypes, insulin sensitivity by the euglycemic insulin clamp and beta cell function by state-of-art modelling of glucose/C-peptide curves during OGTT. Five CACNA1E tag SNPs (rs10797728, rs175338, rs2184945, rs3905011 and rs4652679) were associated with specific aspects of beta cell function (p<0.05-0.01). Both major alleles of rs2184945 and rs3905011 were each (p<0.01 and p<0.005, respectively) associated to reduced proportional control with a demonstrable additive effect (p<0.005). In contrast, only the major allele of rs2253388 was related weakly to more severe insulin resistance (p<0.05). CONCLUSIONS/SIGNIFICANCE: In patients with newly diagnosed type 2 diabetes CACNA1E common variability is strongly associated to beta cell function. Genotyping CACNA1E might be of help to infer the beta cell functional phenotype and to select a personalized treatment.
| S-EPMC3302892 | biostudies-literature
Project description:AimsWe investigated quantitative expression, mutual aggregation and relation with hyperglycemia of insulin resistance (IR) and beta-cell dysfunction (BCD) in newly diagnosed type 2 diabetes.MethodsWe assessed IR with euglycemic hyperinsulinemic clamp and BCD with modelled glucose/C-peptide response to oral glucose in 729 mostly drug-naïve patients. We measured glycated hemoglobin, pre-prandial, post-prandial and meal-related excursion of blood glucose.ResultsIR was found in 87.8% [95% confidence intervals 85.4-90.2] and BCD in 90.0% [87.8-92.2] of subjects, ranging from mild to moderate or severe. Approximately 20% of subjects had solely one defect: BCD 10.8% [8.6-13.1] or IR 8.6% [6.6-10.7]. Insulin resistance and BCD aggregated in most subjects (79.1% [76.2-82.1]). We arbitrarily set nine possible combinations of mild, moderate or severe IR and mild, moderate or severe BCD, finding that each had a similar frequency (∼10%). In multiple regression analyses parameters of glucose control were related more strongly with BCD than with IR.ConclusionsIn newly-diagnosed type 2 diabetes, IR and BCD are very common with a wide range of expression but no specific pattern of aggregation. Beta-cell dysfunction is likely to play a greater quantitative role than IR in causing/sustaining hyperglycemia in newly-diagnosed type 2 diabetes.
| S-EPMC9786655 | biostudies-literature