14 research outputs found

    Inflammatory Bowel Disease Cause-specific Mortality: A Primer for Clinicians

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    Background: Inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC) is perceived to harbor significant morbidity but limited excess mortality, thought to be driven by colon cancer, compared with the general population. Recent studies suggest mortality rates seem higher than previously understood, and there are emerging threats to mortality. Clinicians must be up to date and able to clearly convey the causes of mortality to arm individual patients with information to meaningfully participate in decisions regarding IBD treatment and maintenance of health. Methods: A MEDLINE search was conducted to capture all relevant articles. Keyword search included: “inflammatory bowel disease,” “Crohn's disease,” “ulcerative colitis,” and “mortality.” Results: CD and UC have slightly different causes of mortality; however, malignancy and colorectal cancer–associated mortality remains controversial in IBD. CD mortality seems to be driven by gastrointestinal disease, infection, and respiratory diseases. UC mortality was primarily attributable to gastrointestinal disease and infection. Clostridium difficile infection is an emerging cause of mortality in IBD. UC and CD patients have a marked increase in risk of thromboembolic disease. With advances in medical and surgical interventions, the exploration of treatment-associated mortality must continue to be evaluated. Conclusions: Clinicians should be aware that conventional causes of death such as malignancy do not seem to be as significant a burden as originally perceived. However, emerging threats such as infection including C. difficile are noteworthy. Although CD and UC share similar causes of death, there seems to be some differences in cause-specific mortality

    Hepatitis C in non-hepatic solid organ transplant candidates and recipients: A new horizon

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    Xanthogranulomatous prostatitis presenting as Pseudomonas aeruginosa prostatic abscesses: An uncommon complication after kidney transplantation

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    Xanthogranulomatous (XG) prostatitis is a rare form of granulomatous prostatitis characterized by a benign inflammatory process of non-specific etiology that clinically may mimic carcinoma. Few cases have been reported in the English language medical literature, with only four reported cases presenting as prostatic abscesses. A 70-year-old male with type 2 diabetes mellitus and two previous kidney transplants presented with septic shock secondary to Pseudomonas aeruginosa bacteremia 4 days after undergoing a cystoscopy. Despite appropriate antimicrobial therapy, P. aeruginosa persisted in the blood for a total of 7 days. There were no indwelling prosthetic devices, no complicated pyelonephritis, and no endovascular sources of infection. Upon repeat clinical assessment, the patient reported pelvic pain. A digital rectal examination revealed prostatic tenderness and an endorectal ultrasound confirmed multiple prostatic abscesses. An ultrasound-guided transrectal needle aspirate drained scant purulent fluid and cultures grew the same phenotypic strain of P. aeruginosa. For definitive source control, the patient underwent transurethral resection of the prostate with unroofing of prostatic abscesses. The pathological findings were diagnostic of XG prostatitis. Given the rather acute presentation of this case, our hypothesis is that the prior urological instrumentation likely facilitated bacterial translocation and created the ideal environment for the development of pseudomonal prostatic abscesses resulting in XG inflammation and necrosis. XG prostatitis is a rare entity of uncertain etiology that can result in prostatic abscesses, and surgery is required for definitive diagnosis and management. Keywords: Xanthogranulomatous, Prostatitis, Abscess, Pseudomonas aeruginosa, Transplantatio

    Association between gut colonization of vancomycin-resistant enterococci and liver transplant outcomes

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    Background: Vancomycin-resistant enterococci (VRE) colonization is common in liver transplant recipients and has been associated with worse post-transplant outcomes. Methods: We conducted a retrospective cohort study at the University of Alberta Hospital including patients who underwent a liver transplant between September 2014 and December 2017. Results: Of 343 patients, 68 (19.8%) had pre-transplant VRE colonization and 27 (27/275, 9.8%) acquired VRE post-transplant, 67% were males and the median age was 56.5 years. VRE colonized patients at baseline had higher MELD scores and required longer post-transplant hospitalization. VRE colonization was associated with increased risk of early acute kidney injury (AKI) (64% vs 52%, p = 0. 044), clinically significant bacterial/fungal infection (29% vs 17%, p = 0. 012) and invasive VRE infection (5% vs 1%, p = 0. 017). Mortality at 2-years was 13% in VRE-colonized versus 7% in non-colonized (p = 0.085). On multivariate analysis, VRE colonization increased the risk of post-transplant AKI (HR 1.504, 95% CI: 1.077-2.100, p = 0.017) and clinically significant bacterial or fungal infection at 6 months (HR 2.038, 95%CI: 1.222-3.399, p = 0.006), and was associated with non-significant trend towards increased risk of mortality at 2-years post-transplant (HR 1.974 95% CI 0.890-4.378; p = 0.094). Conclusions: VRE colonization in liver transplant patients is associated with increased risk of early AKI, clinically significant infections, and a trend towards increased mortality at 2-years

    Plasmodium knowlesi Infection in Traveler Returning to Canada from the Philippines, 2023

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    A 55-year-old man sought treatment for an uncomplicated febrile illness after returning to Canada from the Philippines. A suspected diagnosis of Plasmodium knowlesi infection was confirmed by PCR, and treatment with atovaquone/proguanil brought successful recovery. We review the evolving epidemiology of P. knowlesi malaria in the Philippines, specifically within Palawan Island

    European Echinococcus multilocularis Identified in Patients in Canada.

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    Human alveolar echinococcosis is a potentially serious parasitosis caused by the tumorlike larval multiplication of the tapeworm Echinococcus multilocularis. The infection, which usually involves the liver and metastatic spread to distant organs, follows accidental ingestion of parasite eggs released into the environment with the feces of wild and domestic canids. Although this disease has been on the rise in Europe and Asia in recent decades, few cases of locally acquired human alveolar echinococcosis have been confirmed in North America. It has been presumed that the North America strains are less virulent than the Asian and European variants.2 In 2012, the European strain was detected in wildlife in western Canada.3 In 2013, at the Alberta Provincial Laboratory for Public Health, we identified a human case of alveolar echinococcosis.1 Since 2016, six more human cases of alveolar echinococcosis have been identified (see the Supplementary Appendix, available with the full text of this letter at NEJM.org). All the patients presented with hepatic lesions, two with abdominal pain or swelling leading to the imaging that resulted in a diagnosis, one case was diagnosed after surgical excision of a presumptive metastatic lesion, and four cases after incidental findings on imaging performed for unrelated reasons. Three of the patients were receiving immunosuppressive medications, which probably facilitated the development of the parasites.4 The diagnosis of these cases resulted in an estimated annual incidence of 0.059 cases per 100,000 inhabitants, an incidence that is similar to those recorded in endemic areas of Europe.4 Local acquisition of these infections was postulated on the basis of the patients’ travel and exposure histories and on genotyping of the parasite strain. Using sequence analysis of mitochondrial DNA,2 we compared parasitic genotypes responsible for human infections with genotypes of E. multilocularis specimens that had been collected from 77 local animal hosts, including wild canids, domestic dogs, and rodents. (Details are provided in the Supplementary Appendix.) In the animal hosts, three new E. multilocularis strains (ECA, EAB, and ESK) were detected (Fig. 1). These strains resembled the E4 strain found in Austria (AB461395.1) but were distinct because of the presence of three single-nucleotide polymorphisms. The ECA strain, which is unique to Canada and was present in 66 of 77 specimens of wildlife, was detected in five of seven patients with alveolar echinococcosis whose tissues were suitable for sequencing of parasite larvae, a finding that indicates local transmission. Although parasitic genotyping was not possible in samples obtained from one of the patients because of poor DNA quality, the patient’s travel history indicated likely local acquisition. We also found that the patient in whom alveolar echinococcosis had been diagnosed in 2013 had been infected with a European strain of the parasite (see the Supplementary Appendix). However, further characterization of the strain was not possible, and the patient’s travel history, although suggestive of local acquisition, was not conclusive. These data support the hypothesis that the establishment of a European-like strain of E. multilocularis in animal hosts in Canada may result in the emergence of human alveolar echinococcosis in North America
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