Effekt von Basalinsulin-Inkretinmimetischer Therapie bei Typ-2-Diabetikern nach Myokardrevaskularisation auf die Hypoglykämierate

Der Einsatz inkretinmimetischer Therapie bei Typ 2 Diabetes mellitus kann zu einem reduzierten Insulinbedarf mit weniger Hypoglykämien und Reduktion der kardialen Mortailtät führen. Ziel des Studienvorhabens ist es, die Auswirkung Basalinsulin-Inkretinmimetischer Therapie im Vergleich zu insulingeführter bzw. im Vergleich zu oral antidiabetischer Therapie auf das Auftreten von Hypoglykämien, das Überleben, Rehospitalisierungsraten, den HbA1c sowie den Body Mass Index bei operativ oder interventionell myokardrevaskularisierten Patienten mit kardiovaskulärem Höchstrisiko, retro- und prospektiv in einem „real-world“ Patientenkollektiv zu untersuchen. Die Daten der vorliegenden Studie weisen auf einen überraschend niedrigen Gebrauch von inkretinmimetischer Therapie hin, welcher durch die Studienlage nicht erklärbar ist. Ferner bestätigte sich im Nachbeobachtungszeitraum eine erhöhte Inzidenz von symptomatischen Hypoglykämien bei insulingeführten versus OAD-geführten Typ-2-Diabetikern.The use of incretin mimetic therapy in type 2 diabetes mellitus can lead to reduced insulin requirement with less hypoglycaemia and a reduction in cardiac mortality. The aim of the study project is to determine the effect of basal insulin-incretin mimetic therapy compared to insulin-controlled or compared to oral antidiabetic therapy on the occurrence of hypoglycaemia, survival, rehospitalization rates, HbA1c and body mass index in surgically or interventionally myocardial revascularized patients with highest cardiovascular risk to examine retrospectively and prospectively in a "real-world" patient group. The data of the present study indicate a surprisingly low use of incretin mimetic therapy, which cannot be explained by the study situation. Furthermore, an increased incidence of symptomatic hypoglycaemia in insulin-controlled versus OAD-controlled type 2 diabetics was confirmed in the follow-up period

Varicella zoster virus-specific hyperimmunoglobulin in the adjuvant treatment of immunocompromised herpes zoster patients : a case series

Introduction: Immunocompromised patients are at increased risk for herpes zoster (HZ)-associated complications. Despite standard therapy with systemic antiviral drugs and analgesics, complications are frequently encountered, including generalization of lesions or persistent neuropathic pain, so-called post-herpetic neuralgia (PHN). Given the scarcity of literature and awareness of therapeutic options to improve patient outcomes, especially for vulnerable patient groups, here we describe a strategy based on early intensification of treatment with a varicella zoster virus-specific hyperimmunoglobulin (VZV-IgG), which is approved in the adjuvant treatment of HZ. Methods: For this case series, we selected four cases of HZ in patients with impaired immunity due to hemato-oncologic disease or immunosuppressive treatment who presented with either existing generalized lesions and/or severe pain or with other risk factors for a complicated HZ course such as PHN. They were considered to be representative examples of different patient profiles eligible for intensification of treatment by the addition of VZV-IgG to virostatic therapy. Case Report: All patients showed a rapid response to combined treatment with VZV-IgG and a virostatic agent. In two patients who had generalized lesions, the formation of new lesions ceased 1 day after VZV-IgG infusion. One patient, with mantle cell lymphoma, achieved complete healing of the lesions 9 days after diagnosis of HZ, a rare occurrence compared to similar cases or cohorts. A patient with HZ in the cervical region showed a good response after a single dose of VZV-IgG. None of the patients developed post-zoster-related complications. Combination therapy of a virostatic agent and VZV-IgG was well tolerated in these four cases. Conclusion: This case series demonstrates highly satisfactory treatment effectiveness and tolerability for VZV-IgG in the adjuvant treatment of immunocompromised HZ patients and supports early intensification of HZ therapy in patients at high risk of severe disease progression

Talent Development in Achievement Domains: A Psychological Framework for Within- and Cross-Domain Research

Achievement in different domains, such as academics, music, or visual arts, plays a central role in all modern societies. Different psychological models aim to describe and explain achievement and its development in different domains. However, there remains a need for a framework that guides empirical research within and across different domains. With the talent-development-in-achievement-domains (TAD) framework, we provide a general talent-development framework applicable to a wide range of achievement domains. The overarching aim of this framework is to support empirical research by focusing on measurable psychological constructs and their meaning at different levels of talent development. Furthermore, the TAD framework can be used for constructing domain-specific talent-development models. With examples for the application of the TAD framework to the domains of mathematics, music, and visual arts, the review provided supports the suitability of the TAD framework for domain-specific model construction and indicates numerous research gaps and open questions that should be addressed in future research

Dermatologische Differentialdiagnosen von idiopathischen entzündlichen Muskelerkrankungen

ZusammenfassungDie Hautsymptome sind für die Differenzialdiagnose der Myositiden wichtig, da sie einmal entscheidend für die Unterscheidung der Dermatomyositis und des Anti-Synthetase-Syndroms von den anderen Autoimmun-Myositiden sind, und da sie bei Myositiden im Rahmen von Overlap Syndromen Hinweise auf die zugrunde liegenden Autoimmunerkrankungen (Lupus erythematodes, systemische Sklerose u. a.) geben können. Daher sollte bei Patienten mit einer Myositis eine genaue Inspektion der Haut erfolgen. Fast pathognomonisch für die Dermatomyositis ist die Trias aus symmetrischem, fliederfarbenem Erythem auf den Oberlidern (heliotropes Erythem), Erytheme oder flache Papeln oder Plaques über den proximalen interphalangealen und metacarpophalangealen Fingergelenken (so genannte Gottron Papeln) und Erytheme über Knien, Ellenbogen oder Knöcheln (so genanntes Gottron Zeichen). Daneben gibt es eine Reihe weiterer, typischer Hautsymptome (peitschenabdruckartige Erytheme, Poikilodermie, dystrophe Nagelhäutchen, Vaskulitiden, Juckreiz). Beim Anti-Synthetase-Syndrom treten neben einem Raynaud Phänomen als charakteristisches Symptom die sog. Mechanikerhände („mechanic‘s hands“) auf, d. h. Hyperkeratosen und Fissuren lateral an den Fingern. Klinisch und histologisch sind die Hautsymptome beim LE nicht eindeutig von denen der Dermatomyositis zu trennen, auch wenn es einige Unterschiede gibt. Die Hauteffloreszenzen sprechen nicht immer gut auf die Therapien der Myositis an. Ein Rückgang wurde unter Glukokortikoiden, Methotrexat, IVIG, Mycophenolatmofetil und Rituximab beobachtet. Als systemische Therapie gegen die Hautbeteiligung hat Hydroxychloroquin Wirksamkeit gezeigt, manchmal nur in Kombination mit Mepacrin. Zur zusätzlichen topischen Behandlung eignen sich Glukokortikoide und Calcineurin-Inhibitoren. Eine generelle Maßnahme ist der konsequente Sonnenschutz.</jats:p

Bullous drug reaction after pembrolizumab administration : two case reports

Zu den schweren, blasenbildenden Arzneimittelreaktionen an der Haut gehören das Stevens-Johnson-Syndrom (SJS) und die toxisch epidermale Nekrolyse (TEN). Allopurinol, Antikonvulsiva, Sulfonamidantibiotika und nichtsteroidale Antirheumatika vom Oxicam-Typ sind wiederholt als Auslöser beschrieben. Zunehmend rücken auch Immuntherapien als Auslöser schwerer Hautreaktionen in den Fokus. Vorgestellt werden 2 Patienten mit bullösen Hauterscheinungen nach Gabe des Checkpointinhibitors Pembrolizumab. Da das klinische Bild nicht immer eine zweifelsfreie Einordnung zulässt, ist eine histologische Mitbeurteilung vielfach unverzichtbar

Pathophysiology and clinical manifestations of immune complex vasculitides

Immune complex (IC) vasculitides present inflammations of vessel walls associated with perivascular deposition of immunoglobulins (Igs), mostly ICs. They encompass systemic and skin-limited variants of IgA vasculitis (IgAV), cryoglobulinemic vasculitis (CV), rheumatoid, lupus, and hypocomplementemic vasculitides, serum sickness cutaneous IgM/IgG (non-IgA) vasculitis, and recurrent macular (hypergammaglobulinemic or exertion-induced) vasculitis. Serum sickness and CV fulfill the criteria of a type III hypersensitivity immune reaction as large lattices of the IC precipitate at vessel walls and activate polymorphonuclear neutrophils (PMNs). Immunoglobulin-A vasculitis differs with regard to the causes of perivascular deposition of ICs since here many IgA1 molecules are hypoglycosylated (Gd-IgA1), which appears to facilitate their perivascular deposition in skin and mesangium (via e.g. CD71). The reasons for increased generation of immunoglobulins or formation of IC and their perivascular deposition in either skin or systemic organs are different and not fully explored. A common denominator of OC vasculitides is the activation of PMNs near the vessel wall via Fcy or Fcα receptors. Acute episodes of IgAV additionally require PMNs to become preactivated by IgA1 or by IC already in circulation. This intravascular priming results in increased adherence and subsequently vessel-destructive NETosis when they encounter IgA deposited at the vessel walls. Binding of IgA1 to PMNs in blood stream is associated with increased serum levels of hypogalactosidated IgA1. The characteristic clinical picture of IgAV (and also of so-called IgG/IgM vasculitis) comprises palpable or retiform purpura with a clear predilection for lower legs, probably due to stasis-related reduction in blood velocity, while in other IC vasculitides, additional factors influence the sites of vasculitides. Our knowledge of distinct forms and different pathophysiological pathways of IC vasculitides may lead to in efficacious or targeted therapies. Antibodies to complement components or intestinal budesonide for IgAV are promising agents (the latter suppresses the pathophysiologically related IgA nephropathy by reducing the generation of mucosal IgA

Pathophysiology and clinical manifestations of immune complex vasculitides

Immune complex (IC) vasculitides present inflammations of vessel walls associated with perivascular deposition of immunoglobulins (Igs), mostly ICs. They encompass systemic and skin-limited variants of IgA vasculitis (IgAV), cryoglobulinemic vasculitis (CV), rheumatoid, lupus, and hypocomplementemic vasculitides, serum sickness cutaneous IgM/IgG (non-IgA) vasculitis, and recurrent macular (hypergammaglobulinemic or exertion-induced) vasculitis. Serum sickness and CV fulfill the criteria of a type III hypersensitivity immune reaction as large lattices of the IC precipitate at vessel walls and activate polymorphonuclear neutrophils (PMNs). Immunoglobulin-A vasculitis differs with regard to the causes of perivascular deposition of ICs since here many IgA1 molecules are hypoglycosylated (Gd-IgA1), which appears to facilitate their perivascular deposition in skin and mesangium (via e.g. CD71). The reasons for increased generation of immunoglobulins or formation of IC and their perivascular deposition in either skin or systemic organs are different and not fully explored. A common denominator of OC vasculitides is the activation of PMNs near the vessel wall via Fcy or Fcα receptors. Acute episodes of IgAV additionally require PMNs to become preactivated by IgA1 or by IC already in circulation. This intravascular priming results in increased adherence and subsequently vessel-destructive NETosis when they encounter IgA deposited at the vessel walls. Binding of IgA1 to PMNs in blood stream is associated with increased serum levels of hypogalactosidated IgA1. The characteristic clinical picture of IgAV (and also of so-called IgG/IgM vasculitis) comprises palpable or retiform purpura with a clear predilection for lower legs, probably due to stasis-related reduction in blood velocity, while in other IC vasculitides, additional factors influence the sites of vasculitides. Our knowledge of distinct forms and different pathophysiological pathways of IC vasculitides may lead to in efficacious or targeted therapies. Antibodies to complement components or intestinal budesonide for IgAV are promising agents (the latter suppresses the pathophysiologically related IgA nephropathy by reducing the generation of mucosal IgA.</jats:p