Abstract Background Elevated serum levels of parathyroid hormone (PTH), one of the main regulators of calcium homeostasis and vitamin D metabolism, have been proposed as predictors of mortality. The impact of type 2 diabetes mellitus (T2DM) on the putative association between PTH and mortality has not been investigated thus far. Aim The aim of our study was to investigate the impact of T2DM on the power of PTH to predict mortality risk. Methods Serum PTH levels were determined in 904 consecutive Caucasian patients referred to coronary angiography for the evaluation of established or suspected stable coronary artery disease (CAD), including 235 patients with T2DM. Prospectively, deaths were recorded over a mean follow-up period of 6.3 years. Results PTH at baseline did not differ significantly between patients with and without T2DM (P = .307). Cox regression analysis revealed that the serum PTH level strongly predicted all-cause mortality in patients with T2DM (hazard ratio [HR] = 2.35 [1.37-4.03]; P = .002), whereas PTH did not predict all-cause mortality in patients without T2DM (HR = 1.04 [0.81-1.32]; P = .766). The interaction term PTH × T2DM was significant (P = .006), indicating a significantly stronger impact of PTH on mortality risk in patients with T2DM than in individuals without diabetes. The impact of PTH on mortality risk in patients with T2DM remained significant after adjustment for glycated hemoglobin A1c, diabetes duration, classical cardiovascular risk factors, serum levels of vitamin D, and kidney function (HR = 2.10 [1.10-4.10]; P = .030). Conclusion We conclude that PTH is a significantly stronger predictor of all-cause mortality in patients with T2DM than in those without T2DM.

Glycated hemoglobin

10.1210/clinem/dgaa512

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P4772Elevated parathyroid hormone is associated with an increased mortality risk in type 2 diabetes

European Heart Journal (2018)

Axel Muendlein Andreas Leiherer Christoph H. Saely Kathrin Geiger Eva Maria Brandtner

On behalf of the

10.1093/eurheartj/ehy563.p4772

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Non-Suitability of Levator Ani Method as an Index of Anabolic Effect of Steroids

Experimental Biology and Medicine (1957)

M. E. Nimni Kathrin Geiger

Injection of androgens such as testosterone propionate or Norethandrolone in normal and castrated male rats promotes growth of the m. levator ani even on protein-free diets. Based on these and other experiments, it is assumed that the growth of this muscle is a sex-linked function. It is. therefore, concluded that the hormone-induced growth of this muscle is not an appropriate index for the general “myotropic.” i.e. anabolic effects of steroid compounds.

Testosterone propionate

Anabolic steroid

Levator ani

Anabolic Agents

10.3181/00379727-94-23025

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Citations (22)

Title Page / Table of Contents

Neurodegenerative Diseases (2007)

Barbara Bettegazzi Marija Mihailovich Vitor Sousa Daniele Zacchetti Evelina Chieregatti

Table of contents

Table (database)

10.1159/000104849

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Plasma omentin significantly predicts cardiovascular events independently from the presence and extent of angiographically determined baseline coronary artery disease

Atherosclerosis (2015)

Christoph H. Saely Andreas Leiherer A Muendlein Alexander Vonbank Philipp Rein

Coronary atherosclerosis

10.1016/j.atherosclerosis.2015.04.510

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Permanent Middle Cerebral Artery Occlusion in Sheep: A Novel Large Animal Model of Focal Cerebral Ischemia

Journal of Cerebral Blood Flow & Metabolism (2008)

Johannes Boltze Annette Förschler Björn Nitzsche Daniela Waldmin Anke Hoffmann

As effective stroke treatment by thrombolysis is bound to a narrow time window excluding most patients, numerous experimental treatment strategies have been developed to gain new options for stroke treatment. However, all approaches using neuroprotective agents that have been successfully evaluated in rodents have subsequently failed in clinical trials. Existing large animal models are of significant scientific value, but sometimes limited by ethical drawbacks and mostly do not allow for long-term observation. In this study, we are introducing a simple, but reliable stroke model using permanent middle cerebral artery occlusion in sheep. This model allows for control of ischemic lesion size and subsequent neurofunctional impact, and it is monitored by behavioral phenotyping, magnetic resonance imaging, and positron emission tomography. Neuropathologic and (immuno)-histologic investigations showed typical ischemic lesion patterns whereas commercially available antibodies against vascular, neuronal, astroglial, and microglial antigens were feasible for ovine brain specimens. Based on absent mortality in this study and uncomplicated species-appropriate housing, long-term studies can be realized with comparatively low expenditures. This model could be used as an alternative to existing large animal models, especially for longitudinal analyses of the safety and therapeutic impact of novel therapies in the field of translational stroke research.

Stroke

Animal model

Brain ischemia

10.1038/jcbfm.2008.89

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Betatrophin Predicts Cardiovascular Events Independently from the Presence of Type 2 Diabetes and Coronary Artery Disease

Diabetes (2018)

Andreas Leiherer Axel Muendlein Kathrin Geiger Christoph H. Saely Eva‐Maria Brandtner

Betatrophin, also known as ANGPTL8 or lipasin is a nutritionally-regulated protein secreted by the liver and adipose tissue. It is associated with type 2 diabetes mellitus (T2DM) and lipid metabolism. Whether betatrophin is associated with the risk for cardiovascular events is unknown and is addressed in the present study. We measured betatrophin in 553 patients undergoing coronary angiography for the evaluation of established or suspected stable coronary artery disease (CAD) and prospectively recorded cardiovascular events in these patients during a follow-up period of up to 8 years. During follow-up, 301 cardiovascular events occurred. The incidence of cardiovascular events was significantly higher in patients with T2DM (n=161) than in those who did not have diabetes (47.2% vs. 34.4%; p=0.005). Betatrophin was significantly and inversely associated with cardiovascular events both univariately (HR 0.64 [95% CI 0.47-0.87], p=0.004) and after full adjustment including T2DM and baseline CAD (HR 0.55 [95% CI 0.40-0.76], p<0.001). The inclusion of betatrophin to a basic prediction model for the cardiovascular event risk significantly increased model performance (NRI=0.188, p<0.01). In conclusion, this study for the first time shows that betatrophin predicts cardiovascular events independently from conventional risk factors including the presence of T2DM. Disclosure A. Leiherer: None. A. Muendlein: None. K. Geiger: None. C.H. Saely: None. E. Brandtner: None. J. Ebner: None. B. Larcher: None. A. Mader: None. P. Fraunberger: None. H. Drexel: None.

10.2337/db18-160-or

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Citations (1)