Evaluating the effectiveness of using negative pressure wound therapy in the preservation of the infected prosthetic aortic graft.

BACKGROUND: Infected deep sternal infection due to an associated infection of the prosthetic aortic graft is a devastating condition. Standard management requires the removal of the graft and substituting it with a new one. Often, removal of the prosthetic graft is close to impossible. Negative pressure wound therapy is currently the treatment of choice for patients with deep sternal infection. However, its use in deep sternal infection with exposed infected prosthetic aortic graft has not been well described. METHODS: Eight patients were included in this study. All had type A aortic dissection of the ascending aorta and/or aortic arch. RESULTS: There were 7 men and 1 woman. The median age was 53 years old (range 33-81 years old). The median number of days from the initial aortic operation to the diagnosis of infection was 20 days (range 14-52). The median length of stay in the intensive care unit was 17 days (range 6-338 days). The median time interval from the initial debridement to reconstruction was 20 days (range 6-43 days). The median number of times negative pressure wound therapy was changed was 4 (range 2-9). The most common flap used for reconstruction was the pectoralis major musculocutaneous flap in 7 patients, a free antero-lateral thigh flap in 1 patient, and pedicled omental flap in combination with pectoralis major musculocutaneous flap in 1 patient. One patient had persistent recurrent infection of the graft despite negative pressure wound therapy and flap reconstruction. The median length of follow-up was 38.5 months (range 4-120 months). CONCLUSION: This small study suggests that negative pressure wound therapy could be used successfully for the management of deep sternal infection due to infected prosthetic aortic grafts. In most cases, it eliminated the need to replace the infected prosthetic aortic graft in high-risk patients.

Chronic Pancreatitis Correlates With Increased Risk of Cerebrovascular Disease: A Retrospective Population-Based Cohort Study in Taiwan.

The aim of this study is to explore whether there is a relationship between chronic pancreatitis and cerebrovascular disease in Taiwan. Using the claims data of the Taiwan National Health Insurance Program, we identified 16,672 subjects aged 20 to 84 years with a new diagnosis of chronic pancreatitis from 2000 to 2010 as the chronic pancreatitis group. We randomly selected 65,877 subjects aged 20 to 84 years without chronic pancreatitis as the nonchronic pancreatitis group. Both groups were matched by sex, age, comorbidities, and the index year of diagnosing chronic pancreatitis. The incidence of cerebrovascular disease at the end of 2011 was measured. The multivariable Cox proportional hazards regression model was used to measure the hazard ratio (HR) and 95% confidence interval (CI) for cerebrovascular disease risk associated with chronic pancreatitis and other comorbidities. The overall incidence of cerebrovascular disease was 1.24-fold greater in the chronic pancreatitis group than that in the nonchronic pancreatitis group (14.2 vs. 11.5 per 1000 person-years, 95% CI = 1.19-1.30). After controlling for confounding factors, the adjusted HR of cerebrovascular disease was 1.27 (95% CI = 1.19-1.36) for the chronic pancreatitis group as compared with the nonchronic pancreatitis group. Woman (adjusted HR = 1.41, 95% CI = 1.31-1.51), age (every 1 year, HR = 1.04, 95% CI = 1.04-1.05), atrial fibrillation (adjusted HR = 1.23, 95% CI = 1.02-1.48), chronic kidney disease (adjusted HR = 1.48, 95% CI = 1.31-1.67), chronic obstructive pulmonary disease (adjusted HR = 1.27, 95% CI = 1.16-1.40), diabetes mellitus (adjusted HR = 1.82, 95% CI = 1.72-1.92), hypertension (adjusted HR = 1.66, 95% CI = 1.56-1.76), and peripheral atherosclerosis (adjusted HR = 1.26, 95% CI = 1.06-1.51) were other factors significantly associated with cerebrovascular disease. Chronic pancreatitis is associated with increased hazard of subsequent cerebrovascular disease.

Serum vascular adhesion protein-1 level predicts risk of incident cancers in subjects with type II diabetes.

BACKGROUND: Serum vascular adhesion protein-1 (VAP-1) predicts cancer-related mortality in diabetic subjects. However, whether serum VAP-1 predicts cancer incidence or cancer progression remains unclear. We conducted a cohort study to investigate whether serum VAP-1 and related clinical variables predict incident cancers in type II diabetic subjects. METHODS: From 1996 to 2003, we enrolled 568 type II diabetic subjects who were free of cancer at baseline. Serum VAP-1 at enrollment was measured by time-resolved immunofluorometric assay. Chronic kidney disease (CKD) was defined as estimated glomerular filtration rate <60 mL/min per 1.73 m(2). The subjects were followed until first occurrence of cancer or until December 31, 2011. RESULTS: During a mean follow-up of 11.3 years, 71 subjects developed incident cancers. The HRs for incident cancers in subjects with highest tertile of serum VAP-1 and in subjects with CKD were 2.95 [95% confidence interval (CI), 1.31-6.63; P = 0.009] and 2.29 (95% CI, 1.18-4.44; P = 0.015), respectively, after multivariate adjustment. There was an interaction between serum VAP-1 and CKD on the risk of incident cancers (P = 0.01 for log-transformed VAP-1 × CKD). The relationship among serum VAP-1, CKD, and incident cancers was similar if death was considered in the competing risk models or if subjects with shorter follow-up period were excluded. CONCLUSIONS: Higher serum VAP-1 and CKD can independently predict future development of cancers in type II diabetic subjects. IMPACT: Physicians should be aware of the early signs of cancer in diabetic individuals with elevated VAP-1 or renal dysfunction. More aggressive treatment strategies might be considered.

Role of uric acid in the link between arterial stiffness and cardiac hypertrophy: a cross-sectional study.

OBJECTIVES: Hyperuricaemia has been linked to atherosclerosis; however, there is limited evidence about its association with arterial stiffness and cardiac hypertrophy, which are associated with adverse cardiovascular outcomes. We studied the association of hyperuricaemia with an increased risk of arterial stiffness and cardiac hypertrophy in a population participating in a health-screening programme. METHODS: In subjects who underwent health screening from 2005 to 2007, arterial stiffness was measured by brachial-ankle pulse wave velocity (baPWV), whereas cardiac hypertrophy was determined by plain chest radiography and electrocardiography. Polychotomous logistic regression was used to identify associations of hyperuricaemia with arterial stiffness and cardiac hypertrophy, after adjusting for the presence of metabolic syndrome. RESULTS: Of the total 9375 subjects enrolled, 1324 (14.5%) had hyperuricaemia. Subjects with hyperuricaemia had a significantly higher baPWV [1618.8 (379.3) cm/s] than those without it [1501.8 (334.9) cm/s]. Cardiac hypertropy was observed in 1047 (11.2%) subjects. Hyperuricaemia was associated with cardiac hypertrophy with an odds ratio (OR) of 1.53 (95% CI 1.32, 1.77). Polychotomous logistic regression showed that hyperuricaemia was associated with ORs (95% CI) for coexisting abnormal baPWV and cardiac hypertrophy of 1.75 (95% CI 1.24, 2.47) and 1.41 (95% CI 1.04, 1.91) in men and women, respectively, after adjusting for age, proteinuria, high high-sensitive CRP, abnormal ankle-brachial index or a number of metabolic syndrome components present. CONCLUSION: Hyperuricaemia was associated with arterial stiffness and cardiac hypertrophy. Hyperuricaemia, along with other risk factors related to atherosclerosis, could play a role in the development of cardiac hypertrophy by increasing arterial stiffness.

Gout: an independent risk factor for all-cause and cardiovascular mortality.

OBJECTIVE: The relation of gout and hyperuricaemia to cardiovascular diseases has been well documented. This study investigates the survival impact of both gout and hyperuricaemia. METHODS: The subjects of this study comprised participants of a health screening programme conducted by the Chang Gung Memorial Hospital in Taiwan from 2000 to 2006. The status and causes of death were ascertained by the Taiwan National Death Registry 2000-07. Cox proportional hazard model was performed to examine the association. RESULTS: Among 61 527 subjects, 1383 deaths (198 cardiovascular deaths) were identified, corresponding to a crude mortality rate of 4.86 deaths per 1000 person-years. Crude mortality rates were 4.50, 5.61 and 10.46 deaths per 1000 person-years for subjects with normouricaemia, hyperuricaemia and gout, respectively. Compared with subjects with normouricaemia, the hazard ratios (HRs) of all-cause mortality were 1.46 (95% CI 1.12, 1.91) for individuals with gout and 1.07 (95% CI 0.94, 1.22) for those with hyperuricaemia, respectively, after adjustments were made for age, sex, component number of metabolic syndrome and proteinuria. The adjusted HRs of cardiovascular mortality were 1.97 (95% CI 1.08, 3.59) for individuals with gout and 1.08 (95% CI 0.78, 1.51) for those with hyperuricaemia. Moreover, the risk of all-cause or cardiovascular mortality for gout remained unchanged when limiting the data to those with an estimated glomerular filtration of >60 ml/min/1.73 m(2). CONCLUSION: This study demonstrates a link of gout, not hyperuricaemia, with a higher risk of death from all causes and cardiovascular diseases.

The sequence heterogenicities among 16S rRNA genes of Salmonella serovars and the effects on the specificity of the primers designed.

Previously, we have reported a 16S rDNA targeted polymerase chain reaction (PCR) method for the specific detection of Salmonella serovars [J. Appl. Bacteriol. 80 (1996) 659]. The target sites of its primers, i.e. 16SFI and 16SIII, according to the data in GenBank, were found mismatched to the corresponding sequences of some Salmonella serovars, such as those of S. Houten, S. Chingola, S. Bareilly, and S. Weltevreden. Accordingly, a PCR method using a nonspecific primer MINf combined with a primer modified from our 16SFI primer, i.e. the primer MINr, was developed and displayed better detection specificity [Int. J. Food Microbiol. 80 (2003) 67]. In this study, we show the sequence heterogenicity at the primer 16SFI targeting sites for some Salmonella serovars. Thus, the sequence used for designing of PCR primers might be just one of the several possible sequences. Such a situation may lead to the misjudgment on evaluation of the specificity of the primers if this was only based on the data in GenBank. Strains of the above described Salmonella serovars with target sequences from GenBank mismatched to the primer 16SF1 were reidentified and their PCR results were confirmed. Meanwhile, their 16SFI/16SIII primer annealing sites were sequenced and the sequences obtained were found completely and highly homologous to those of 16SFI and complementary to those of 16SIII primer, respectively.