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Different role of zinc transporter 8 between type 1 diabetes mellitus and type 2 diabetes mellitus
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Diabetes can be simply classified into type 1 diabetes mellitus and type 2 diabetes mellitus. Zinc transporter 8 (ZnT8), a novel islet autoantigen, is specifically expressed in insulin‐containing secretory granules of β‐cells. Genetic studies show that the genotypes of SLC30A8 can determine either protective or diabetogenic response depending on environmental and lifestyle factors. The ZnT8 protein expression, as well as zinc content in β‐cells, was decreased in diabetic mice. Thus, ZnT8 might participate in insulin biosynthesis and release, and subsequently involved deteriorated β‐cell function through direct or indirect mechanisms in type 1 diabetes mellitus and type 2 diabetes mellitus. From a clinical feature standpoint, the prevalence of ZnT8A is gradiently increased in type 2 diabetes mellitus, latent autoimmune diabetes in adults and type 1 diabetes mellitus. The frequency and epitopes of ZnT8‐specific T cells and cytokine release by ZnT8‐specific T cells are also different in diabetic patients and healthy controls. Additionally, the response to ZnT8 administration is also different in type 1 diabetes mellitus and type 2 diabetes mellitus. In the present review, we summarize the literature about clinical aspects of ZnT8 in the pathogenesis of diabetes, and suggest that ZnT8 might play a different role between type 1 diabetes mellitus and type 2 diabetes mellitus. 相似文献
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Kota Tsuruya Kazuya Anzai Shunsuke Shioyama Ayano Ito Yoshitaka Arase Shunji Hirose Yasuhito Tanaka Hidekazu Suzuki Tatehiro Kagawa 《Hepatology research》2021,51(2):239-244
A 71-year-old man was diagnosed with B-cell chronic lymphocytic leukemia. He was negative for hepatitis B surface antigen (HBsAg), positive for antibodies against the hepatitis B surface and core, and negative for hepatitis B virus (HBV)-DNA before starting chemotherapy. A total of 13 months after the initiation of ibrutinib (a Bruton's tyrosine kinase inhibitor), the patient's alanine aminotransferase levels suddenly increased to 427 U/L. As the level of serum HBV-DNA increased to 5.2 logIU/mL, a diagnosis of HBV reactivation was made, whereas the patient remained negative for HBsAg. The patient's serum alanine aminotransferase levels normalized after the initiation of entecavir at a dose of 1 mg/day. However, it took >1 year to achieve an undetectable level of HBV-DNA, even with an add-on therapy of tenofovir disoproxil fumarate. Interestingly, the patient remained negative for HBsAg throughout the clinical course owing to triple HBsAg escape mutations: Q101K, M133L, and G145A. 相似文献
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Martial Hamon MD Gilles Lemesle Olivier Tricot Thibaud Meurice Michel DeneveXavier Dujardin MD Jean Michel Brufau Jerome Bera Nicolas Lamblin Christophe Bauters 《Journal of the American College of Cardiology》2014
Background
Although there is evidence that patients who experience major bleeding after an acute coronary event are at higher risk of death in the months after the event, the incidence and impact on outcome of bleeding beyond 1 year of follow-up in patients with stable coronary artery disease (CAD) are largely unknown.Objectives
The goal of this study was to assess the incidence, source, determinants, and prognostic impact of major bleeding in stable CAD.Methods
We prospectively included 4,184 consecutive CAD outpatients who were free from any myocardial infarction (MI) or coronary revascularization for >1 year at inclusion. Follow-up was performed at 2 years, with major bleeding defined as a type ≥3 bleed using the Bleeding Academic Research Consortium (BARC) definition.Results
There were 51 major bleeding events during follow-up (0.6%/year). Most events were BARC type 3a bleeds with 12 fatal bleeds (type 5). In most cases (54.9%), the site of bleeding was gastrointestinal. Major bleeding was significantly associated with mortality (adjusted hazard ratio: 2.89; 95% confidence intervals: 1.73 to 4.83; p < 0.0001). The increased risk of bleeding associated with vitamin K antagonist (VKA) treatment was particularly evident when VKA was combined with an antiplatelet therapy (APT). In contrast, the risk of cardiovascular death, MI, or nonhemorrhagic stroke did not differ in patients who received VKA + APT versus patients on VKA alone.Conclusions
In patients with stable CAD (i.e., >1 year, with no acute events), major bleeding events are rare, but such events are an independent predictor of death. When oral anticoagulation is required, concomitant APT should not be prescribed in the absence of a recent cardiovascular event. 相似文献6.
Hepatitis B virus (HBV) reactivation under systemic chemotherapy or immunosuppressive therapy is a serious complication among HBV-resolved patients. Some medications, such as more than 2 weeks of corticosteroid therapy, can influence HBV reactivation; therefore, screening tests that measure hepatitis B surface antigen (HBsAg), hepatitis B core antibody, and hepatitis B surface antibody before therapy are required. Additionally, because HBV reactivation has been reported in patients positive for HBsAg treated with immune checkpoint inhibitors (ICIs), the prophylactic administration of nucleos(t)ide analogues prior to administering ICIs is recommended for HBsAg-positive patients. Under these circumstances, highly sensitive novel biomarkers are expected to be used for the early diagnosis of HBV reactivation. A fully automated high-sensitivity HBsAg assay (detection limit: 5 mIU/ml) by Lumipulse HBsAg-HQ, with 10-fold higher sensitivity than that of conventional assays, is currently used. Furthermore, ultra-sensitive HBsAg assays using a semi-automated immune complex transfer chemiluminescence enzyme immunoassay (ICT-CLEIA; detection limit: 0.5 mIU/ml) have been developed. Recently, a fully automated, novel high-sensitivity hepatitis B core-related antigen assay (iTACT-HBcrAg; cut-off value: 2.1 Log U/mL) has been developed and reported. The utility of ICT-CLEIA and iTACT-HBcrAg for the diagnosis of HBV reactivation appears comparable to the use of HBV DNA. In this review, we provide the latest information related to medications that influence HBV reactivation and recently developed novel biomarkers that predict and monitor HBV reactivation. 相似文献
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Aims To determine the occurrence of diabetic ketoacidosis (DKA) in adult Type 2 and Type 1 diabetic patients in Northern Sweden and to determine whether DKA presents with a different clinical picture in Type 2 compared with Type 1 diabetic subjects. Methods All adult patients from a hospital catchment area in Northern Sweden with diagnosed DKA episodes during 1997–2000 were included in a retrospective study. Medical records and laboratory reports were analysed. Results During the years 1997 to 2000, the average annual incidence rate for DKA was 5.9 per 100 000 adult inhabitants. Twenty‐five patients developed DKA, eight (32%) had Type 2 diabetes, while 17 (68%) had Type 1 diabetes. Type 2 diabetic patients with DKA were older and had higher levels of C‐peptide than Type 1 diabetic patients. On admission because of DKA, a similar degree of hyperglycaemia was present in Type 1 and Type 2 patients. Metabolic acidosis was more severe in Type 1 compared with Type 2 diabetic patients. In 50% of the Type 2 diabetic patients, diabetes was diagnosed at the episode of DKA. Conclusions DKA occurs in Caucasian Type 2 diabetic patients within a Swedish population. Although the frequency of DKA is much higher in Type 1 diabetic patients, Type 2 diabetes may account for as much as one‐third of the overall DKA cases. 相似文献
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Dysmorphic erythrocytes are superior to hematuria for indicating non‐diabetic renal disease in type 2 diabetics
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Zhe‐yi Dong Yuan‐da Wang Qiang Qiu Kai Hou Li Zhang Jie Wu Han‐yu Zhu Guang‐yan Cai Xue‐feng Sun Xue‐guang Zhang Mo‐yan Liu Jia Kou Xiang‐mei Chen 《Journal of diabetes investigation.》2016,7(1):115-120
Aims/Introduction
There are sparse and limited studies on erythrocyte morphology in renal biopsy identifying nephropathic patients among type 2 diabetics. The present study sought to clarify the predictive value of dysmorphic erythrocytes in type 2 diabetics with non‐diabetic renal disease and influences on hematuria.Materials and Methods
We examined 198 patients with type 2 diabetes who underwent kidney biopsies between 2012 and 2013. Hematuria was defined as >3 or >10 red blood cells per high‐power field (RBCs/hpf) in urine sediment. If >80% of the erythrocytes were dysmorphic, glomerular hematuria was diagnosed. Clinical findings and predictive value of dysmorphic erythrocytes were compared between patients with hematuria (n = 19) and those without (n = 61). The potential risk factors for hematuria among diabetic nephropathy patients were also screened.Results
There was a statistically significant difference between the diabetic nephropathy group and the non‐diabetic renal disease group (6.6 vs 16.8%; P = 0.04) when the demarcation point of hematuria was 10 RBCs/hpf. When the definition of hematuria was based on an examination of urinary erythrocyte morphology, a marked difference was seen (3.3 vs 24.8%; P < 0.001). Glomerular hematuria showed high specificity and a positive predictive value (0.97 and 0.94, respectively) in non‐diabetic renal disease. A multivariate analysis showed that nephrotic syndrome was significantly associated with hematuria (odds ratio 3.636; P = 0.034).Conclusions
Dysmorphic erythrocytes were superior to hematuria for indicating non‐diabetic renal disease in type 2 diabetics. Nephrotic syndrome was an independent risk factor for hematuria. 相似文献10.
Norie Yamada Asako Murayama Masaaki Shiina Hussein Hassan Aly Masashi Iwamoto Senko Tsukuda Koichi Watashi Tomohisa Tanaka Kohji Moriishi Hironori Nishitsuji Masaya Sugiyama Masashi Mizokami Kunitada Shimotohno Masamichi Muramatsu Kazumoto Murata Takanobu Kato 《Hepatology research》2020,50(3):283-291
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Analysis of pancreatic volume in acute‐onset,slowly‐progressive and fulminant type 1 diabetes in a Japanese population
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Tomoyasu Fukui Toshiyuki Hayashi Takeshi Yamamoto Makoto Ohara Saki Yamamoto Tetsuro Kobayashi Tsutomu Hirano 《Journal of diabetes investigation.》2018,9(5):1091-1099
Aims/Introduction
A decrease in the size of the pancreas is observed in islet autoantibody‐positive non‐diabetic donors and acute‐onset type 1 diabetes irrespective of the diabetes duration. Little is known, however, about the relationship between the size of the pancreas and type 1 diabetes subtypes, including fulminant type 1 diabetes.Materials and Methods
We examined the pancreatic volume (PV) in 44 adult patients with type 1 diabetes (16 acute‐onset type 1 diabetes, 18 slowly progressive type 1 diabetes and 10 fulminant type 1 diabetes) and 39 age‐ and body mass index‐matched non‐diabetic controls. PV was measured by computed tomography. The ability to secrete insulin was assessed by stimulated C‐peptide after intravenous glucagon administration.Results
PV was significantly correlated with bodyweight in both control participants and type 1 diabetes patients. The PV index (PVI; PV/bodyweight) was decreased by 39% in type 1 diabetes compared with that in controls. PVI was significantly decreased in acute‐onset type 1 diabetes patients and slowly progressive type 1 diabetes patients (both P < 0.0001), but not in fulminant type 1 diabetes patients (P = 0.10), compared with control participants. In cases patients with recent‐onset type 1 diabetes (0–7 days post‐diagnosis), PVI was significantly decreased in acute‐onset type 1 diabetes patients (n = 8, P = 0.0005), but not in fulminant type 1 diabetes patients (n = 7, P = 0.44), compared with controls. PVI showed no correlations with the diabetes duration, C‐peptide levels, glycated hemoglobin, glutamic acid decarboxylase autoantibody levels, serum amylase or daily total insulin dose in type 1 diabetes subtypes.Conclusions
The present results show that patients with acute‐onset type 1 diabetes and slowly progressive type 1 diabetes have small pancreases irrespective of the diabetes duration or C‐peptide levels. In contrast to earlier findings on acute‐onset type 1 diabetes, we found no reduction of PVI at the onset of fulminant type 1 diabetes. 相似文献12.
Effect of serum 25‐hydroxyvitamin D3 on insulin resistance and β‐cell function in newly diagnosed type 2 diabetes patients
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Mingjing Bao Limei Liu Yang Xian Jichuan Wu Pengqiu Li 《Journal of diabetes investigation.》2016,7(2):226-232
Aims/Introduction
To evaluate serum 25‐hydroxyvitamin D3 (25(OH)D3) in newly diagnosed type 2 diabetes patients and to explore the associations of 25(OH)D3 with insulin resistance and β‐cell function.Materials and Methods
A total of 97 newly diagnosed type 2 diabetes patients and 69 healthy controls were recruited. Serum 25(OH)D3 was determined using high‐pressure liquid chromatography. Insulin resistance was measured using a homeostasis model assessment of insulin resistance (HOMA‐IR). β‐Cell function was determined using the HOMA β‐cell function index (HOMA‐β), early‐phase insulin secretion index (ΔI30/ΔG30) and area under the insulin curve (AUCins). Correlation analysis was carried out using Pearson''s correlation and multiple stepwise regression analysis.Results
Serum 25(OH)D3 was much lower in patients with newly diagnosed type 2 diabetes (t = −13.00, P < 0.01), and the prevalence of hypovitaminosis 25(OH)D3 was 62.9% (61/97) in diabetic patients. Among the diabetic patients, patients with hypovitaminosis 25(OH)D3 showed higher glycosylated hemoglobin and AUCglu (P < 0.01) as well as lower HOMA‐β, ΔI30/ΔG30 and AUCins. Serum 25(OH)D3 was independently positively correlated with ΔI30/ΔG30 and AUCins (P < 0.05), but was not significantly correlated with either HOMA‐IR or HOMA‐β. Only triglycerides, glycosylated hemoglobin and ΔI30/ΔG30 emerged as independent factors associated with serum 25(OH)D3 in both diabetes patients and the health control group.Conclusions
The present results further showed a low serum 25(OH)D3 concentration in patients with newly diagnosed type 2 diabetes. 25(OH)D3 deficiency is associated with disturbances in glucose metabolism and lipid metabolism. Serum 25(OH)D3 is not correlated with basal insulin resistance or β‐cell function, but is significantly positively correlated with glucose‐stimulated insulin secretion and β‐cell function. 相似文献13.
Y. Derraz H. Benamer T. Lefèvre B. Chevalier T. Hovasse R. Chaito P. Garot M.-C. Morice Y. Louvard 《Annales de cardiologie et d'angeiologie》2013
Background
The mother and child “5-in-6” technique using the Heartrail II catheter is a novel tool allowing stent delivery in challenging lesions, when conventional techniques have failed.Methods
A total of 147 consecutive patients underwent percutaneous coronary intervention (PCI) using the “5-in-6” Heartrail II catheter was restrospectively identified in the Institut Cardiovasculaire Paris Sud, (Jacques-cartier hospital), Institut hospitalier Claude-Galien (Claude-Galien hospital) and European hospital of Paris between July 2009 and September 2012.Results
Ten interventional cardiologists treated 147 patients with the new device. The patients mean age was 68.5 ± 21.5 years, 78% were men. Radial access was used in 128 cases (87.9%). The treated vessels were the right coronary artery in 82%, left anterior descending in 22%, left circumflex in 18%, marginal branch in 9%, the posterior descending artery in three patients, retroventricular artery in one patient and a saphenous graft in two patients. Most lesions (70%) had American Heart Association/American College of Cardiology (AHA/ACC) type B2 or C, and greater than 50% were located in distal vessel segments. Mean lesion length was 16 ± 4 mm, which is indicative of long lesion. Most (62%) lesions were moderately to heavily calcified and 22 (14%) were chronic total occlusions. Problems with stent delivery were due to poor guide catheter support or excessive calcification. Introduction of the “Heartrail II” catheter allowed successful stent delivery in 139 cases (94%).Conclusion
The “5 in 6” Heartrail II catheter is a simple and easy-to-use device that can improve the success of stent delivery in challenging coronary interventions. 相似文献14.
Type 1 diabetes mellitus results from the progressive and specific autoimmune destruction of insulin‐secreting pancreatic B‐cells, which develops over a period of years and continues after the initial clinical presentation. The ultimate goal of therapeutic intervention is prevention or reversal of the disease by the arrest of autoimmunity and by preservation/restoration of B‐cell mass and function. Recent clinical trials of antigen‐specific or non‐specific immune therapies have proved that modulation of islet specific autoimmunity in humans and prevention of insulin secretion loss in the short term after the onset of disease is achievable. The identification of suitable candidates for therapy, appropriate dosage and timing, specificity of intervention and the side‐effect profile are crucial for the success of any approach. Considering the complexity of the disease, it is likely that a rationally designed approach of combined immune‐based therapies that target suppression of B‐cell specific autoreactivity and maintenance of immune tolerance, coupled with islet regeneration or replacement of the destroyed B‐cell mass, will prove to be most effective in causing remission/reversal of disease in a durable fashion. 相似文献
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Kunal N. Karmali David C. Goff Jr. Hongyan Ning Donald M. Lloyd-Jones 《Journal of the American College of Cardiology》2014
Background
The 2013 American College of Cardiology/American Heart Association updated cholesterol guidelines recommend the use of Pooled Cohort Equations to estimate 10-year absolute risk for atherosclerotic cardiovascular disease (ASCVD) in primary prevention.Objectives
This study sought to systematically examine the Pooled Cohort Equations to determine risk factor levels required to exceed risk thresholds outlined in new cholesterol guidelines.Methods
We entered continuous risk factor levels in isolation and in specified combinations with the risk tool, and we observed predicted risk output patterns. We used the 10-year ASCVD risk threshold of ≥7.5% as a clinically relevant risk threshold.Results
We demonstrated that a hypothetical man or woman can reach clinically relevant risk thresholds throughout the eligible age spectrum of 40 to 79 years of age, depending on the associated risk factor burden in all race-sex groups. Age continues to be a major determinant of 10-year ASCVD risk for both men and women. Compared with the previous risk assessment tool used in cholesterol guidelines, the inclusion of a stroke endpoint and use of race-specific coefficients permit identification of at-risk African Americans and non-Hispanic white women at much younger ages and lower risk factor levels.Conclusions
These data provide context of specific risk factor levels and groups of individuals who are likely to have 10-year ASCVD risk estimates ≥7.5%. Age continues to be a major driver of risk, which highlights the importance of the clinician-patient discussion before statin therapy is initiated. 相似文献20.
Wei Tang Huiying Liang Ying Cheng Jiao Yuan Gan Huang Zhiguang Zhou Lin Yang 《Journal of diabetes investigation.》2021,12(6):963-969
Aims/IntroductionType 1 diabetes mellitus is a T cell‐mediated autoimmune disease. However, the determination of the autoimmune status of type 1 diabetes mellitus relies on islet autoantibodies (Abs), as T‐cell assay is not routinely carried out. This study aimed to investigate the diagnostic value of combined assay of islet antigen‐specific T cells and Abs in type 1 diabetes mellitus patients.Materials and MethodsA total of 54 patients with type 1 diabetes mellitus and 56 healthy controls were enrolled. Abs against glutamic acid decarboxylase (GAD), islet antigen‐2 and zinc transporter 8 were detected by radioligand assay. Interferon‐γ‐secreting T cells responding to glutamic acid decarboxylase 65 and C‐peptide (CP) were measured by enzyme‐linked immunospot.ResultsThe positive rate for T‐cell responses was significantly higher in patients with type 1 diabetes mellitus than that in controls (P < 0.001). The combined positive rate of Abs and T‐cell assay was significantly higher than that of Abs assay alone (85.2% vs 64.8%, P = 0.015). A significant difference in fasting CP level was found between the T+ and T– groups (0.07 ± 0.05 vs 0.11 ± 0.09 nmol/L, P = 0.033). Furthermore, levels of fasting CP and postprandial CP were both lower in the Ab−T+ group than the Ab−T− group (fasting CP 0.06 ± 0.05 vs 0.16 ± 0.12 nmol/L, P = 0.041; postprandial CP 0.12 ± 0.13 vs 0.27 ± 0.12 nmol/L, P = 0.024).ConclusionsEnzyme‐linked immunospot assays in combination with Abs detection could improve the diagnostic sensitivity of autoimmune diabetes. 相似文献