Abstract Objective: To investigate the optimal timing of initial intravenous immunoglobulin (IVIG) treatment in Kawasaki disease (KD) patients. Methods: KD patients were classified as the early group (day 1-4), conventional group (day 5-7), conventional group (day 8-10), and late group (after day 10). Differences among the groups were analyzed by ANOVA and Chi-square analysis. Predictors of IVIG resistance and the optimal cut-off value were determined by multiple logistic regression analyses and receiver operating characteristic (ROC) curve analysis. Results: There were no significant differences in IVIG resistance among the 4 groups (p = 0.335). The sensitivity analysis also confirmed no difference in the IVIG resistance between those who started the initial IVIG ≤ day 7 of illness and those who received IVIG >day 7 of illness (p = 0.761). In addition, patients who received IVIG administration more than 7 days from the onset had a higher proportion of coronary artery abnormalities (p = 0.034) and longer length of hospitalization (p = 0.033) than those who started IVIG administration less than 7 days. The optimal cut-off value of initial IVIG administration time for predicting IVIG resistance was >7 days, with a sensitivity of 75.25% and specificity of 82.41%. Conclusions: IVIG therapy within 7 days of illness is found to be more effective for reducing the risk of coronary artery abnormalities than those who received IVIG >day 7 of illness. IVIG treatment within the 7 days of illness seems to be the optimal therapeutic window of IVIG. However, further prospective studies with long-term follow-up are required.

Resumo: Introdução: A doença diverticular do apêndice vermiforme (DDA) tem uma incidência de 0,004 a 2,1% em peças de apendicectomia. DDA está de forma variável associada a perfuração e malignidade. Reportamos uma experiência unicêntrica de DDA. O objectivo primário é validar a associação de DDA com apendicite complicada ou malignidade, e o objectivo secundário é validar os critérios de Systemic Inflammatory Response Syndrome (SIRS) e o score de quick Sepsis-related Organ Failure Assessment (qSOFA). Métodos: Os relatórios histopatológicos de 2,305 peças de apendicectomia de Janeiro 2011 a Dezembro de 2015 foram revistos. Apendicite aguda foi verificada em 2,164 (93,9%) peças. A histologia das restantes 141 (6,1%) revelou: apêndice normal (n = 110), DDA (n = 22), endometriose do apêndice (n = 6) e apêndice ausente (n = 3). As características demográficas dos doentes, perfil clínico, dados cirúrgicos e perioperatórios dos doentes com DDA foram avaliados. Modified Alvarado score, Andersson score, SIRS criteria, e o qSOFA scores foram calculados retrospectivamente. Resultados: A incidência de DDA foi de 0,95%. Dez doentes (45,5%) tinham diverticulite. A idade média dos doentes com DDA foi de 39,5 anos (âmbito 23-87) com predominância masculina (n = 12, 54,5%). A mediana do Modified Alvarado score foi de 8 (âmbito 4-9), e a mediana do Andersson score foi de 5 (âmbito 2-8). Quatorze doentes (63,6%) tinham SIRS e nenhum tinha um qSOFA score alto. Oito doentes (36,4%) tinham apendicite complicada (perfuração n = 2; abcesso n = 6). Onze (50%) doentes foram submetidos a apendicectomia laparoscópica. Verificaram-se 3 readmissões aos 30 dias e nenhuma morte. Conclusão: DDA é uma entidade clínica e patológica distinta e está associada a apendicite complicada.

Abstract: Introduction : Diverticular disease of the vermiform appendix (DDA) has an incidence of 0.004 to 2.1% in appendicectomy specimens. DDA is variably associated with perforation and malignancy. We report a single-center experience of DDA. The primary aim is to validate the association of DDA with complicated appendicitis or malignancy, and the secondary aim is to validate systemic inflammatory response syndrome (SIRS) criteria and quick Sepsis-related Organ Failure Assessment (qSOFA) scores. Methods: The histopathology reports of 2,305 appendicectomy specimens from January 2011 to December 2015 were reviewed. Acute appendicitis was found in 2,164 (93.9%) specimens. Histology of the remaining 141 (6.1%) patients revealed: normal appendix (n = 110), DDA (n = 22), endometriosis of appendix (n = 6), and an absent appendix (n = 3). Patient demographics, clinical profile, operative data, and perioperative outcomes of DDA patients are studied. Modified Alvarado score, Andersson score, SIRS criteria, and qSOFA scores were retrospectively calculated. Results: The incidence of DDA was 0.95%. Ten patients (45.5%) had diverticulitis. The mean age of DDA patients was 39.5 years (range 23-87), with male preponderance (n = 12, 54.5%). The median Modified Alvarado score was 8 (range 4-9), and the median Andersson score was 5 (range 2-8). Fourteen patients (63.6%) had SIRS, and none had a high qSOFA score. Eight patients (36.4%) had complicated appendicitis (perforation [n = 2] or abscess [n = 6]). Eleven (50%) patients underwent laparoscopic appendicectomy. There were three 30-day readmissions and no mortality. Conclusion: DDA is a distinct clinical pathology associated with complicated appendicitis.

Caspase recruitment domain-containing protein 9 (Card9) is located upstream of the nuclear factor kappa B (NF-κB) and p38 mitogen-activated protein kinase (MAPK) inflammatory pathways. This study investigated the therapeutic effect and potential mechanism of pioglitazone in rats with severe acute pancreatitis (SAP). SAP was induced by a retrograde infusion of 5.0% sodium taurocholate into the biliopancreatic duct of Sprague Dawley rats (n=54), which were then treated with pioglitazone. Blood and pancreatic tissues were harvested at 3, 6, and 12 h after SAP induction. Pancreatic pathological damage was evaluated by hematoxylin and eosin staining. Serum amylase, serum pro-inflammatory cytokines, and pancreatic myeloperoxidase (MPO) activities were determined by enzyme-linked immunosorbent assay. The expression of Card9 mRNA and protein in pancreatic tissues was detected by real-time polymerase chain reaction and western blotting. Pioglitazone had a therapeutic effect in treating rats with SAP by decreasing the level of amylase activity, ameliorating pancreatic histological damage, decreasing serum pro-inflammatory cytokine levels and tissue MPO activity, and downregulating the expression of NF-κB, p38MAPK, and Card9 mRNAs and proteins (P<0.05). The present study demonstrated that the inhibition of Card9 expression could reduce the severity of SAP. Card9 has a role in the pathogenic mechanism of SAP.