Die Leitlinie nimmt Bezug auf die Diagnostik einschließlich begleitender Autoimmunerkrankungen bei Typ-1-Diabetes mellitus, die Insulintherapie und die glykämischen Zielwerte.
Akute Stoffwechselentgleisungen können für Erwachsene in Abhängigkeit von ihrem Ausmaß lebensbedrohlich sein. Dementsprechend sind eine rasche umfassende Diagnostik und Therapie sowie eine enge Überwachung der Vitalparameter und Laborbefunde erforderlich. Bei der Therapie, die sich bei der ketoazidotischen (DKA) und hyperglykämisch-hyperosmolaren (HHS) Form nicht wesentlich unterscheidet, kommt dem Ausgleich des meist beträchtlichen Flüssigkeitsdefizits mit mehreren Litern einer physiologischen kristalloiden Lösung eine vorrangige Rolle zu. Bei den Elektrolyten ist insbesondere auf eine ausgeglichene Serum-Kalium-Konzentration zu achten. Normal-Insulin oder rasch wirksame Analoga können initial als i.v.-Bolus verabreicht werden, in der Folge jedoch kontinuierlich über einen Perfusor. Die Umstellung auf eine subkutane Insulintherapie soll erst bei ausgeglichenem Säure-Basen-Haushalt und zufriedenstellender Glykämie erfolgen.
Die Hyperglykämie ist wesentlich an der Entstehung der Folgeerkrankungen bei Menschen mit Diabetes mellitus Typ 2 beteiligt. Während Lebensstilmaßnahmen die Eckpfeiler jeder Diabetestherapie bleiben, benötigen die meisten Menschen mit Typ-2-Diabetes im Verlauf eine medikamentöse Therapie. Bei der Definition individueller Behandlungsziele stellen die Therapiesicherheit, die Effektivität sowie substanzspezifische, organprotektive Effekte der Therapie die wichtigsten Faktoren dar. Diese nationale Leitlinie fasst die Evidenz aus der aktuellen Datenlage für die klinische Praxis zusammen.
Acute metabolic crises can be potentially life-threatening situations in adults depending on the extent. Therefore, rapid comprehensive diagnostic and therapeutic measures with close monitoring of vital and laboratory parameters are required. The treatment of diabetic ketoacidosis (DKA) and the hyperosmolar hyperglycemic state (HHS) is essentially the same and replacement of the mostly substantial fluid deficit with several liters of a physiological crystalloid solution is the first and most important step. Serum potassium concentrations need to be carefully monitored to guide its substitution. Regular insulin or rapid-acting insulin analogues can be initially administered as an i.v. bolus followed by continuous infusion. Insulin should be switched to subcutaneous injections only after correction of the acidosis and stable glucose concentrations within an acceptable range.
The cardiovascular–renal–liver–metabolic (CKLM) syndrome integrates dysmetabolically driven heart, vascular, kidney, and liver diseases through a shared pathophysiological substrate. In obesity, upregulation of the clearance natriuretic peptide receptor C (NPR-C) in adipose tissue creates a “NP deficiency,” undermining the protective cardiovascular and metabolic actions of endogenous NPs. Recent preclinical data demonstrates that NPR-C functions beyond simple peptide clearance. Through interactions with ligands like CNP, musclin, and osteocrin, NPR-C triggers context-dependent intracellular signaling. In experimental models, independent of systemic NP levels, NPR-C directly modulates cardiac remodeling, podocyte injury, hepatic steatosis, vascular inflammation, and adipocyte function. This review synthesizes NPR-C biology within the CKLM framework. While human validation remains limited, targeting tissue-specific NPR-C pathways represents a promising therapeutic frontier for restoring cardiometabolic homeostasis.
The guidelines summarize the diagnostics of type 1 diabetes mellitus, including accompanying autoimmune diseases, insulin therapy regimens and glycemic target values.
Epidemiological investigations have shown that approximately 2-3% of all Austrians have diabetes mellitus with renal involvement (diabetic kidney disease, DKD). Therefore, this concerns approximately 250,000 people in Austria. The risk of occurrence and progression of DKD can be attenuated by lifestyle interventions as well as optimization of blood pressure, blood glucose control and specific drug classes. These guidelines represent the joint recommendations of the Austrian Diabetes Association and the Austrian Society of Nephrology for the definition, diagnostics and treatment strategies of DKD.
Die in der Diabetes-Klassifikation als Typ-3-Diabetes beschriebenen Krankheitsentitäten umfassen andere spezifische Diabetesformen, welche pathophysiologisch und therapeutisch eine sehr heterogene Krankheitsgruppe darstellen. Diese beinhalten Formen, die aufgrund von genetischen Erkrankungen (monogenetische Formen, neonataler Diabetes, Down-Syndrom, Klinefelter-Syndrom, Turner-Syndrom) oder im Rahmen anderer endokrinologischer Erkrankungen auftreten (z. B. Akromegalie, Cushing-Syndrom, Glukagonom), sowie die an Häufigkeit und Komplexität zunehmenden medikamentös induzierten Diabetesformen (z. B. Therapie mit Glukokortikoiden, Immun-Checkpoint-Inhibitoren, Calcineurininhibitoren, Phosphatidylinositol-3-Kinase-Inhibitoren, hochaktive antiretrovirale Therapie [HAART], Antipsychotika). Ebenfalls in diese Diabeteskategorie fallen pankreoprive Formen (z. B. postoperativ, Zustand nach Pankreatitis, Pankreastumoren, Hämochromatose, zystische Fibrose), seltener infektionsgetriggerte (z. B. kongenitale Rötelninfektion) oder autoimmune Formen (z. B. Stiffman-Syndrom, Anti-Insulin-Rezeptor-Antikörper, Insulin-Autoimmunsyndrom). Die korrekte Zuordnung des Diabetestyps hat unmittelbare therapeutische Auswirkungen für die Betroffenen. Zusätzlich findet sich nicht nur bei pankreopriven Formen, sondern auch bei Diabetes mellitus Typ 1 oder langjährigem Typ-2-Diabetes mellitus häufig eine Assoziation mit einer exokrinen Pankreasinsuffizienz.
Diabetes is associated with a high incidence of diabetic foot and peripheral artery disease and with markedly increased lifetime amputation risk. Here we investigated predictors of reamputation risk and mortality including antidiabetic medication in patients undergoing non-traumatic lower limb amputation (LLA). In an observational longitudinal study, we analyzed 607 patients with diabetes and 500 patients without diabetes who underwent non-traumatic LLA between 2006 and 2022. The primary endpoint was reamputation-free survival. Predictors of subsequent amputations or mortality were analyzed using Cox regression and joint frailty models. Diabetes was independently associated with increased combined reamputation and mortality risk (HR 1.28, 95
Hyperglycemia is substantially involved in the occurrence of complications in people with type 2 diabetes mellitus. While lifestyle interventions remain the cornerstones of diabetes treatment, most people with type 2 diabetes will eventually require pharmacotherapy for improved glycemic management. The definition of individual treatment targets regarding optimal therapeutic efficacy and safety as well as organ-protective effects are the most important factors. These national guidelines summarize the most current evidence-based recommendations for the clinical practice.
Diabetes classified as category 3, usually referred to as type 3 diabetes, encompasses specific types due to other causes. These specific forms of diabetes are clinically and pathophysiologically very heterogeneous. Type 3 diabetes encompasses inherited forms of diabetes (monogenetic diabetes, neonatal diabetes, Down syndrome, Klinefelter syndrome, Turner syndrome), diabetes due to other endocrine disorders (acromegaly, Cushing's disease, glucagonoma) and drug-induced forms, e.g., caused by glucocorticoids, immune checkpoint inhibitors, calcineurin inhibitors, phosphatidylinositol 3 kinase inhibitors, highly active antiretroviral therapy (HAART) and antipsychotics. Additionally, this category includes pancreatogenic forms (after pancreatic surgery, after pancreatitis, pancreatic tumors, hemochromatosis, cystic fibrosis), rare infection-triggered (e.g., congenital rubella syndrome) and autoimmune forms other than type 1 diabetes (e.g., Stiffman syndrome, anti-insulin receptor antibodies, insulin autoimmune syndrome). An exact diagnosis is critical for correct and optimal treatment of affected patients. Exocrine pancreatic insufficiency is not only found in patients with pancreatogenic diabetes but also in patients with type 1 diabetes or long-standing type 2 diabetes.
Introduction:Gestational diabetes (GDM) is not only associated with markedly increased type 2 diabetes risk but is also associated with increased type 1 diabetes risk in later life. The aim of this work was to systematically evaluate the prevalence and clinical relevance of islet autoantibodies in patients with gestational diabetes. Method:A systematic literature search of the predefined keywords "gestational diabetes" or "pregnancy diabetes" and "autoantibodies" in the electronic databases PubMed, ScienceDirect, and ResearchGate from the beginning of the database until November 30, 2025 was performed. The selection of publications was based on the review of studies using predefined inclusion and exclusion criteria. The extracted data obtained were analyzed using meta-analytical techniques. Results:Twenty-one studies including a total of 7760 patients with gestational diabetes were included. Heterogeneity among the analyzed studies was high. The overall prevalence of islet autoantibodies was 10.6% (95% CI 8,2-13,0%) (I2 = 95,9%) in patients with gestational diabetes, which was more than seven-fold higher than in pregnant women without gestational diabetes. Prevalence was highest for ICA and anti-GAD autoantibodies. The prevalence of islet autoantibodies decreased from 10.6% during pregnancy to 3.6% in the postpartum period (95% CI 2.1-5.1%). Conclusion:Our data show a high prevalence of islet autoantibody positivity in patients with gestational diabetes suggesting a relevant pathophysiological role of autoimmunity in a subgroup of affected patients. These data underline the need of postpartum analysis of the autoantibody status and regular follow-up checks in patients with persistent islet autoantibody positivity. Heterogeneity among analyzed studies was high underlining the need of further prospective studies to more clearly define the role of islet autoantibodies in patients with gestational diabetes.
Sodium-glucose cotransporter 2 inhibitors (SGLT2is) have revolutionized the management of type 2 diabetes mellitus, heart failure, and chronic kidney disease (CKD), providing cardiorenal and metabolic benefits that extend beyond glycemic control. While their clinical efficacy is well established, the underlying molecular mechanisms remain only partially understood. This review focuses on current knowledge of SGLT2 expression and regulation in health and metabolic diseases, as well as transcriptional and epigenetic consequences of pharmacological SGLT2 inhibition. Human and experimental studies demonstrate that SGLT2 expression is confined to proximal tubular cells and regulated by insulin, the renin-angiotensin-aldosterone system, the sympathetic nervous system, oxidative stress, and transcriptional and epigenetic pathways. SGLT2 expression follows a biphasic pattern in metabolic disorder-associated CKD: upregulation in early phases and reduction in advanced stages. Evidence from animal models and single-cell transcriptomic studies indicates that SGLT2is normalize metabolic and inflammatory gene networks. To our knowledge, a recent single-cell RNA sequencing study provides the only currently available human dataset linking SGLT2i therapy with tubular metabolic rewiring and suppression of the energy-sensitive mechanistic target of rapamycin complex 1. Collectively, these findings support a model in which SGLT2 inhibition mitigates metabolic stress by restoring energy homeostasis across multiple nephron segments.
Epidemiologische Untersuchungen zeigen, dass etwa 2–3
Emerging evidence supports a bidirectional gut-pancreas axis in which microbial dysbiosis, barrier dysfunction, and altered metabolite fluxes contribute to pancreatogenic diabetes (T3cDM). Whether gut microbial changes reflect systemic metabolic disturbances or primarily arise from exocrine pancreatic insufficiency (EPI) remains unclear. We profiled the gut microbiome of 48 outpatients with T3cDM, type 1 diabetes (T1DM), and healthy controls. Genus-level 16S rRNA data were analyzed using cross-validated LASSO logistic regression and patient-specific community metabolic models. T3cDM showed reduced α-diversity and distinct β-diversity compared with T1DM and controls. Key compositional shifts included enrichment of Enterobacteriaceae (notably Escherichia-Shigella) and Streptococcaceae in T3cDM. LASSO models discriminated T3cDM from T1DM (AUC 0.867; accuracy 0.818), highlighting Blautia, Escherichia-Shigella, Streptococcus, Clostridium, and Faecalibacterium as predictors. Metabolic modelling indicated elevated Escherichia-Shigella growth in T3cDM and disease-specific metabolite fluxes. Gut microbial shifts in T3cDM predominantly reflect EPI rather than systemic metabolic disturbances characteristic of T1DM, underscoring the central role of exocrine pancreatic dysfunction in shaping the gut microbiome and its metabolic activity.
Objectives This study assessed the health-related quality of life (HRQoL) and its relationship with clinical factors and comorbidities in people with type 2 diabetes mellitus (T2DM) treated in primary care settings.Design Cross-sectional study design: This study assessed the HRQoL using a 36-item Short Form Survey (SF-36) tool in eight domains. The HRQoL scores ranged from 0% to 100% for each domain, with higher scores indicating better HRQoL. Linear regression was used to assess the association of HRQoL domain scores with clinical covariates and comorbidities.Setting A countrywide study was conducted on individuals with established T2DM (N=635) attending primary healthcare services for various conditions across nine federal states of Austria from 2021 to 2023.Participants A total of 635 individuals, aged above 50 years and diagnosed with T2DM, were recruited by the attending physician to evaluate their HRQoL in relation to T2DM and its associated comorbidities.Results The mean SF-36 scores for physical functioning (69±28), role-physical (62±42), mental health (72±20), role-emotional (73±41), social functioning (79±25), bodily pain (67±28) and vitality (55±22) were satisfactory, except for general health (41±10). Age and body mass were inversely associated with physical, mental and social HRQoL (p<0.05). Women had lower mental health (β: −5.44 [95% CI −9.43 to −1.44], p<0.05) than men. Smokers and those with cardiovascular and chronic lung diseases reported worse general, mental and physical health and vitality (p<0.05 each). Depression (p<0.001) and multimorbidity (p<0.05) severely deteriorated all HRQoL domains: physical functioning (Depression:−25.34 [95% CI −33.84 to −16.84], p<0.001); (Multimorbidity: −19.37 [95% CI −26.30 to −12.44], p<0.001), physical role limitations (−22.96 [95% CI −36.65 to −9.27], p<0.001); (−18.53 [95% CI −29.59 to −7.48], p<0.001), social functioning (−24.38 [95% CI −32.41 to −16.35], p<0.001); (−8.86 [95% CI −15.66 to −2.07], p<0.05), emotional well-being (−19.80 [95% CI −26.22 to −13.38], p<0.001); (−9.54 [95% CI −14.95 to −4.13], p<0.001), emotional role limitations (−28.26 [95% CI −41.01 to −15.52], p<0.001); (−8.15 [95% CI −18.78 to 2.49], p=0.133), bodily pains (−23.09 [95% CI −32.21 to −13.97], p<0.001); (−14.52 [95% CI −22.08 to −6.95], p<0.001), fatigue (−16.47 [95% CI −23.40 to −9.55], p<0.001); (−13.71 [95% CI −19.39 to −8.03], p<0.001), general health (−7.09 [95% CI −10.40 to −3.78], p<0.001); (−7.14 [95% CI −9.83 to −4.46], p<0.001).Conclusions Our analysis showed that advanced age, obesity, depression, cardiovascular disease, chronic lung diseases and multimorbidity were associated with poor HRQoL of individuals with T2DM at the primary care level. These findings highlight the need for strengthening holistic management in primary care to address the diverse physical, social and emotional needs of individuals with T2DM.
Eine latente Hypothyreose tritt häufig bei älteren Menschen auf, wobei ein moderater Anstieg des TSH im Alter (bis 7ნ mU/L) physiologisch ist. Studien zeigen, dass in diesen Fällen eine Behandlung mit Thyroxin bei Menschen über 65 Jahre meist keine Vorteile bringt, aber potenzielle Risiken hat. Da in der Praxis eine Übertherapie häufig vorkommt, wird eine altersabhängige Interpretation der TSH-Werte und Zurückhaltung bei Erstverordnung empfohlen.
Subclinical hypothyroidism is frequently diagnosed in older patients. However, mild TSH elevations (up to 7 mU/L) with increasing age are physiologic. Studies demonstrate that treatment with levothyroxine in patients older than 65 years is not beneficial but may have potential risks. As overtreatment is often observed, an age-dependent interpretation of TSH levels and a conservative approach to prescription are recommended.
BackgroundDue to the increasing availability and sensitivity of neuroradiological imaging, the number of incidental findings of empty sella (ES) is rising, however, the clinical relevance is not clearly defined.MethodsIn this longitudinal, single-center study patients with first-time diagnosed primary or secondary empty sella were analyzed and followed up for five years. Hormone deficiencies were diagnosed by measuring basal pituitary and target organ hormone levels or dynamic stimulation tests.ResultsOverall, 119 patients, 97 with primary (PES) and 22 with secondary empty sella (SES) were included. At baseline, isolated or total pituitary insufficiency was detected in 34% of patients with PES and 63.6% of patients with SES. While hypogonadism was the most common finding in PES affecting 25.8% of patients, adrenal insufficiency was the most frequent finding in SES affecting 54.5% of patients. Only two patients with intact pituitary function at baseline, one with SES and one with PES, were diagnosed with hormone insufficiency during follow-up.ConclusionsHormone deficiency is common in empty sella, with males and patients with SES being at highest risk. In patients with intact pituitary function at time of diagnosis, the risk of developing hypopituitarism is low thus not justifying regular follow-up assessments.
Introduction: The progression of diabetes status in post-stroke patients remains under-investigated, particularly regarding new treatments for type II diabetes mellitus (DM II), like glucagon-like peptide 1 receptor agonists (GLP-1-RA) and sodium-glucose co-transporter-2 (SGLT-2) inhibitors, which have not been studied in the post-stroke setting. Patients and methods: Eight hundred eighty-four consecutive ischemic stroke patients recruited to our prospective STROKE-CARD Registry were assessed concerning their glycemic status at baseline (normoglycemia, prediabetes, DM II) and change over time within 1 year follow-up. Multivariate logistic regression was performed to identify factors associated with transitioning from normoglycemia to prediabetes or DM II. Additionally, we reviewed ongoing clinical trials for GLP-1-RA and SGLT-2 inhibitors in the context of acute ischemic stroke. Results: At baseline, 44.6% ( n = 394) of individuals had normoglycemia, 33.9% ( n = 300) were prediabetic, and 21.5% had DM II ( n = 190). After 1 year, normoglycemia decreased by 12.1 percentage points ( n = 107), whereas prediabetes and DM II increased by 10.2 percentage ( n = 90) points and 1.9 percentage points ( n = 17), respectively. Statin therapy was the only significant risk factor for progression. 23.4% ( n = 207) of our cohort would have met eligibility criteria for a recent trial on semaglutide in obese non-diabetics with prior cardiovascular disease. However, only one ongoing trial aims at evaluating short-term cardiovascular risk reduction in stroke patients. Discussion: GPrediabetes and DM II are frequent in ischemic stroke patients. Even within an intensified post-stroke disease management setting, a considerable amount of stroke survivors convert to prediabetes or DM II within the first year. Our results demonstrate a notable proportion of patients qualifying inclusion in studies examining the efficacy of GLP-1-RA agonists and SGLT-2 inhibitors in secondary prevention. Conclusion: Given the high prevalence and progression of prediabetes and DM II in stroke survivors, there is a need for clinical trials evaluating the use of GLP-1-RA and SGLT-2 inhibitors in this population.