SummaryScabies has been diagnosed surprisingly frequently in Germany in recent years, and the use of acaricides has risen markedly. Present figures indicate an increase in the prevalence/incidence of scabies, but do not prove or quantify it for the following reasons: (a) scabies is not a notifiable disease in Germany; (b) the diagnosis is not always confirmed lege artis by means of light microscopy or dermatoscopy (which may lead to a comparatively high proportion of false‐positive diagnoses due to the low overall prevalence of scabies); (c) repeated treatments of the same patient and treatment of contact persons are included in the total number of prescriptions. Therefore, there are no valid data on disease occurrence, either in the current situation or from previous periods.Observations of ineffective treatment with permethrin have led to speculations that Sarcoptes mites are developing resistance to this drug. However, there is little evidence for this assumption.We discuss risk groups (children, elderly people in need of care, migrant health personnel in nursing institutions, refugees, sexually active young adults) and evaluate their possible contribution, albeit in the absence of evidence. None of the groups would be solely responsible for an increased frequency.We have compiled recommendations on how the management of scabies could be improved, and present a way of differentiating permethrin resistance from application errors and/or lack of compliance. The goal is to solve the epidemiological and parasitological questions mentioned above.

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ZusammenfassungDie Diagnose Skabies wird in Deutschland in den letzten Jahren auffallend häufig gestellt, und der Verbrauch an Antiskabiosa ist deutlich gestiegen. Vorliegende Zahlen deuten auf eine Zunahme der Prävalenz/Inzidenz der Skabies hin, beweisen und quantifizieren sie aber nicht, da a) Skabies in Deutschland nicht meldepflichtig ist, b) die Diagnose nicht immer lege artis, also licht‐ oder auflichtmikroskopisch gesichert wird (somit möglicherweise ein relativ hoher Anteil falsch‐positiver Diagnosen in Folge der niedrigen Prävalenz von Skabies), und c) Mehrfachtherapien eines Patienten sowie Behandlung von Kontaktpersonen in die Gesamtzahl der Verordnungen einfließen. Dementsprechend liegen valide Zahlen weder aktuell noch aus früheren Zeiträumen vor. Basierend auf Beobachtungen, dass eine topische Therapie mit Permethrin nicht immer zur Heilung führt, wird zunehmend über eine mögliche Resistenz von Krätzemilben spekuliert. Hierfür gibt es jedoch bislang keinen klaren Beleg.Wir diskutieren die Bedeutung von Risikogruppen (Kinder, ältere pflegebedürftige Menschen, Arbeitnehmerwanderungen im Pflegesektor, Schutzsuchende, sexuell aktive junge Erwachsene) und bewerten deren Bedeutung kritisch angesichts fehlender Evidenzen. Keine kann alleine für eine gestiegene Häufigkeit verantwortlich sein.Wir haben Empfehlungen zusammengestellt, um die Behandlung der Skabies zu optimieren, und stellen Konzepte vor, um Anwendungsfehler und/oder mangelnde Compliance von einer Permethrin‐Resistenz zu unterscheiden. Ziel muss es sein bestehende epidemiologische und parasitologische Wissenslücken zu schließen.

Background: IgA-vasculitis (IgAV) encompasses a systemic form involving kidneys, gut, skin or joints, and a skin-limited form. One characteristic feature of systemic IgAV is deposition of galactosedeficient IgA1 (GD-IgA1) in kidneys (as in IgA-nephropathy). The relevance of GD-IgA1 for cutaneous vasculitis is unknown. Objective: We investigated if GD-IgA1 is deposited perivascularly in systemic and also skin-limited IgAV, and if its serum levels differ between both forms. Methods: In a case control study, deposition of GD-IgA1 was analysed immunohistochemically by KM55-antibody in skin biopsies from 12 patients with skin-limited and 4 with systemic IgAV. GD-IgA1levels were compared by ELISA in sera from 15 patients each with skin-limited and systemic IgAV and from 11 healthy subjects. Results: All biopsies from systemic, but also from skin-limited IgAV revealed perivascular GD-IgA1deposition. The average GD-IgA1-level in serum was significantly higher in systemic than in skinlimited IgAV, despite overlap between both groups. Limitations: Although high GD-IgA1-levels may be predictive of systemic IgAV, patient numbers were too low to determine cutoff values for systemic versus skin-limited IgAV. Conclusion: While perivascular GD-IgA1-deposition is a prerequisite for systemic and skin-limited IgAV, high GD-IgA1-levels in some patients with systemic IgAV suggest a dose-dependent effect of GD-IgA1 in IgAV.

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In IgA vasculitis (IgAV) perivascular deposition of IgA1 immune complexes (IgA-ICs) is traditionally considered the fundamental trigger for polymorphonuclear neutrophil (PMN)–mediated damage. We propose that IgA-IC deposition, although mandatory, is not sufficient alone for IgAV. Serum IgA-IC levels and IgA-IC binding to PMNs were quantified in IgAV patients and controls. Activation of PMNs was evaluated by neutrophil extracellular trap (NET) release, adherence, and cytotoxicity assays and in a flow system to mirror conditions at postcapillary venules. In vitro results were related to findings in biopsies and a mouse vasculitis model. During acute IgAV flares we observed elevated serum levels of IgA-ICs and increased IgA-IC binding to circulating PMNs. This IgA-IC binding primed PMNs with consequent lowering of the threshold for NETosis, demonstrated by significantly higher release of NETs from PMNs activated in vitro and PMNs from IgAV patients with flares compared with surface IgA-negative PMNs after flares. Blocking of FcαRI abolished these effects, and complement was not essential. In the flow system, marked NETosis only occurred after PMNs had adhered to activated endothelial cells. IgA-IC binding enhanced this PMN tethering and consequent NET-mediated endothelial cell injury. Reflecting these in vitro findings, we visualized NETs in close proximity to endothelial cells and IgA-coated PMNs in tissue sections of IgAV patients. Inhibition of NET formation and knockout of myeloperoxidase in a murine model of IC vasculitis significantly reduced vessel damage in vivo. Binding of IgA-ICs during active IgAV primes PMNs and promotes vessel injury through increased adhesion of PMNs to the endothelium and enhanced NETosis.

SummaryVarious studies have already shown that the fatty acid composition of dietary fat has different effects on hemostasis and platelet function. However, knowledge on this topic is incomplete. In the present study, fifty-eight healthy students received either a 4-week rapeseed oil [high content of monounsaturated fatty acids (MUFA) and high n-3/n-6 PUFA ratio], an olive oil (high content of MUFA, low n-3/n-6 PUFA ratio) or a sunflower oil (low content of MUFA, low n-3/n-6 PUFA ratio) diet. In each group, effects on hemostatic parameters were compared with a wash-in diet rich in saturated fatty acids with respect to intermediate-time effects on the hemostatic system and platelet function. With the olive oil diet, a reduction of coagulation factors VIIc, XIIc, XIIa, and Xc was found, whereas sunflower oil led to lower values of coagulation factors XIIc, XIIa, and IXc. In all study groups levels of plasmin-α2-antiplasmin were lower in week 4 than at baseline. Lower fibrinogen binding on platelets was found after the sunflower oil diet, whereas expression of CD62 and spontaneous platelet aggregation were slightly higher after the olive oil diet. However, given the major differences in the fatty acid compositions of the diets, the differences between the groups with respect to hemostasis tended to be small. Therefore, the clinical significance of the present findings remains to be evaluated.

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