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Acute exacerbation of rash is common in patients with atopic dermatitis and has diverse aetiology. We describe a patient with atopic dermatitis who developed a pruritic, burning and weeping rash. The rash quickly worsened and developed into a serious condition for which early diagnosis and treatment are crucial.

Aim. Inflammation is important in heart failure (HF). The role of the immune receptor toll-like receptor 9 (TLR9) in HF is not understood and not investigated in diastolic HF. We investigated the role of TLR9 in a murine diastolic HF model caused by cardiomyocyte SERCA2a excision.Methods and Results. We crossed SERCA2a KO and TLR9 KO mice to generate four mouse lines. Tamoxifen-induced cardiomyocyte SERCA2a gene excision was carried out in mice, causing diastolic HF. After 7.6 weeks, cardiac functions and dimensions were analyzed by echocardiography and heart tissues were processed. HF mice depleted of TLR9 demonstrated reduced survival compared to SERC2a KO mice, with a median life expectancy of 58 days compared to 63 days. Both HF groups displayed increased left atrium size, lung weight, fetal gene expressions, monocyte/macrophage infiltration, and fibrosis. However, there were no significant differences between the groups.Conclusion. In mice with SERCA2a KO-induced diastolic HF, the absence of TLR9 reduced median life expectancy. The cause remains elusive, as all investigated HF parameters were unaltered. Still, these findings support a salutary role of TLR9 in some subsets of HF conditions and underline the importance for future studies on the mechanisms of TLR9 in diastolic HF.

Background Mitochondrial DNA (mtDNA) and possibly nuclear DNA (nDNA) are released as danger-associated molecular patterns during cardiac stress, and may activate several innate immune receptors. The purpose of this study was to investigate the regulation of these danger-associated molecular patterns during human heart failure (HF). Methods and Results Plasma levels of mtDNA and nDNA from HF patients (n = 84) were analyzed by reverse transcriptase-polymerase chain reaction and compared with controls (n = 72). Increased levels of mtDNA were found in New York Heart Association (NYHA) I-II and NYHA III-IV. There was evidence of increased nDNA in NYHA III-IV compared with controls and NYHA I-II. Kaplan-Meier analysis revealed higher mortality in patients with high nDNA levels, whereas high levels of mtDNA were associated with survival. Conclusions Plasma levels of mtDNA and nDNA are elevated in human HF associated with increased and decreased mortality, respectively. This study may suggest a rationale for exploring interventions within inflammatory signaling pathways activated by nucleic acids as novel targets in treatment of HF.

Aim Myocardial infarction (MI) remains a major cause of death and disability worldwide, despite available reperfusion therapies. Inflammatory signaling is considered nodal in defining final infarct size. Activation of the innate immune receptor toll-like receptors (TLR) 9 prior to ischemia and reperfusion (I/R) reduces infarct size, but the consequence of TLR9 activation timed to the onset of ischemia is not known. Methods and results The TLR9-agonist; CpG B was injected i.p. in C57BL/6 mice immediately after induction of ischemia (30 minutes). Final infarct size, as well as area-at-risk, was measured after 24 hours of reperfusion. CpG B injection resulted in a significant increase in circulating granulocytes and monocytes both in sham and I/R mice. Paradoxically, clear evidence of reduced cardiac infiltration of both monocytes and granulocytes could be demonstrated in I/R mice treated with CpG B (immunocytochemistry, myeloperoxidase activity and mRNA expression patterns). In addition, systemic TLR9 activation elicited significant alterations of cardiac inflammatory genes. Despite these biochemical and cellular changes, there was no difference in infarct size between vehicle and CpG B treated I/R mice. Conclusion Systemic TLR9-stimulation upon onset of ischemia and subsequent reperfusion does not alter final infarct size despite causing clear alterations of both systemic and cardiac inflammatory parameters. Our results question the clinical usefulness of TLR9 activation during cardiac I/R.

Bakgrunn Duktalt adenocarcinoma er den vanligste typen kreft i bukspyttkjertelen. I USA og Norge er det den 4. hyppigste kreft-relaterte dødsårsaken. Bukspyttkjertelkreft manifesterer seg med få debuterende symptomer. Kvalme, oppkast, ryggsmerter, gulsott og andre symptomer vises på et sent stadium. Jo lenger tid før diagnose, desto vanskeligere behandling og dårligere prognose. Inoperable pasienter på bakgrunn av lokal avansert kreft som involverer portvenen og v. mesenterica sup., kan tilbys reseksjon, hvis mesenterale kar blir rekonstruert. Denne oppgaven er skrevet for å belyse dette emnet, og oppsummere dagens kunnskap om dødelighet, sykelighet og overlevelse etter denne omfattende kirurgiske prosedyren. Metoder Dette er en litteraturstudie. Søkemotorerene benyttet er PubMed og Google Scholar med ulike søkeord. Jeg har også brukt kreftregisteret.no og kreftforeningen.no. Diskusjon Helt siden Fortner innførte "regional pancreatectomy", har dette temaet vært gjenstand for diskusjon. Spørsmålet er fortsatt om portal-og v. mesenterica sup. reseksjon kan gjøres trygt, og om det kan gjøres med akseptabel sykelighet og dødelighet. Et økende antall sykehus viser en positiv holdning til denne prosedyren, og dagens litteratur tyder også på at dette kan gjøres uten økt dødelighet eller sykelighet. Ved å utføre en slik prosedyre kan vi øke antall pasienter som kan gjennomgå kurativ reseksjon. Derfor bør dette alltid vurderes i tilfeller med mistanke om innvekst i vener. Likevel bør det bare gjøres i nøye utvalgte pasienter på høy-volum sentra, med erfarne kirurger. Videre bør det bare gjøres når negative reseksjon marginer kan forventes. I tillegg til kirurgi bør man også vurdere multimodale behandling. Konklusjon Det er ingen signifikante forskjeller verken i sykelighet, dødelighet eller langsiktig overlevelse etter pancreaticoduodenectomi, med eller uten rekonstruksjon av portvenen og / eller v. mesenterica sup.