Showing papers by "William J. Tremaine published in 2017"
TL;DR: Estimated incidence rates for UC and CD in Olmsted County are among the highest in the United States, and male sex and younger age were significantly associated with a higher incidence rate of CD.
307 citations
TL;DR: The cumulative probability of perianal or rectovaginal fistulizing disease has decreased over time and the associated proctectomy rate in the prebiologic era vs the biologic era using a population-based cohort of Crohn's disease patients is re-estimated.
Abstract: Background This study sought to re-estimate the cumulative incidence of perianal or rectovaginal fistulas and the associated proctectomy rate in the prebiologic era vs the biologic era using a population-based cohort of Crohn's disease (CD) patients. Methods The medical records of 414 residents of Olmsted County, Minnesota, who were diagnosed with CD between 1970 and 2010 were reviewed. The cumulative incidence of perianal or rectovaginal fistulas from time of CD diagnosis and the cumulative rate of proctectomy from date of first perianal or rectovaginal fistula diagnosis were estimated using the Kaplan-Meier method. Results Eighty-five patients (20.5%) diagnosed with CD between 1970 and 2010 had at least 1 perianal or rectovaginal fistula episode between January 1, 1970, and June 30, 2016. The cumulative incidence of perianal or rectovaginal fistulas was 18% after 10 years, 23% after 20 years, and 24% after 30-40 years from CD diagnosis. The cumulative incidence of perianal or rectovaginal fistulas was significantly lower in patients diagnosed in 1998 or after than in patients diagnosed before 1998 (P = 0.03, log-rank). Among 85 patients developing perianal or rectovaginal fistulas, 16 patients (18.8%) underwent proctectomy for the treatment of perianal or rectovaginal fistulas during follow-up. Conclusions In a population-based inception cohort of CD, one-fifth of patients were diagnosed with at least 1 perianal or rectovaginal fistula. The cumulative probability of perianal or rectovaginal fistulizing disease has decreased over time.
70 citations
TL;DR: Microscopic colitis is a common cause of chronic diarrhoea and various treatment options have been described, but there are limited data describing outcomes of corticosteroid‐sparing treatments.
Abstract: SummaryBackground
Microscopic colitis (MC) is a common cause of chronic diarrhoea. Various treatment options have been described, but there are limited data describing outcomes of corticosteroid-sparing treatments.
Aim
To evaluate the outcomes of patients with active MC treated with immune modulators.
Methods
All patients seen at Mayo Clinic, Rochester between January 1, 1997 and November 30, 2016 with a histological diagnosis of MC were identified. Patients treated with an immune modulator of interest were selected and clinical outcomes recorded.
Results
Seventy-three MC patients (50 collagenous colitis and 23 lymphocytic colitis) with a median disease duration of 24 months (range, 7-60) were included. The indications for treatment were budesonide-refractoriness in 66%, budesonide dependence in 29%, and budesonide intolerance in 5%. Median age was 51.8 years (range, 43.4-63.1) and 61 (84%) were female. Thiopurines were used in 49 patients (67%) for a median of 4 months (range, 1.5-15). Complete and partial response occurred in 43% and 22% respectively. Adverse effects resulting in therapy cessation occurred in 17 patients (35%). Twelve patients (16%) were treated with methotrexate for a median of 14 months (3-18.8). Complete and partial response occurred in 58% and 17%, respectively. Anti-TNF therapy was used in 10 patients (14%) for a median of 4 months (range, 2.3-5.5). Complete response occurred in four patients and partial response in four patients.
Conclusions
The majority of patients with active MC responded to thiopurines, methotrexate, or anti-TNF therapy. Larger controlled studies are required to confirm the efficacy and safety of these medications in MC.
30 citations
TL;DR: Routine administration of PJP prophylaxis in patients with IBD treated with corticosteroids, immunosuppressants, and biologics may not be warranted, although it should be considered for high‐risk groups, such as patients receiving triple therapy.
23 citations
TL;DR: The majority of budesonide-experienced patients with active microscopic colitis did not respond to pentoxifylline, however, it was well-tolerated, with 1 patient achieving long-term remission and one-third of the cohort having a partial response.
5 citations
TL;DR: The patient was diagnosed with UC after consultations, through the acute and short course, enlarged spleen and enlarged cervical lymph nodes during the relapse could not match UC well, and the pathologists found cryptitis and crypt abscess with a complete mucosal structure in the slides.
Abstract: ogists found a small lymphoproliferative lesion (Fig. 2B) in the rectum biopsy with an immunohistochemistry result of CD7++, CD202, and EBV-encoded small RNA+. To exclude the diagnosis of lymphoma, we reexamined the colonoscopy and took 32 pieces of biopsies. None of the biopsies showed even a LPD change. He was diagnosed with EBV-associated enteritis accompanied with EBV-associated LPD. We speculate that CAEAE can turn into LPD, which is a precancerous condition to lymphoma4,5 (Fig. 2). Chronic active EBV infection is a rare disorder, especially in gastrointestinal tract, which usually takes the form of LPD rather than a simple inflammation. There are only 3 cases of EBV-infected enteritis with no involvement of an underlying LPD in immunocompetent adult reported in the English literature worldwide till now.6–8 The patients all recovered from supportive treatment and the long-term follow-ups are unknown. We believe this to be the first reported case of CAEAE in an immunocompetent adult. The prognosis of CAEAE is unknown. We know that LPD is a precancerous condition5 and we have reported a case with LPD developed into lymphoma.4 From this case, we know that CAEAE would turn into LPD one day and should be monitored closely. EBV-associated colitis is hard but important to distinguish from IBD. IBD is associated with a higher prevalence of opportunistic infections, including EBV infections, for the damaged intestinal immune barrier or on immunosuppressive medications.3 The thiopurine therapy would impair the T cell activity, and thus decreased immunosurveillance of latent EBV infection and facilitate the reactivation EBV. EBV infection will cause relapses or deteriorations in patients with IBD. Before making a diagnosis of IBD, we should rule out all the infected diseases including EBV infection. In this case, the patient was diagnosed with UC after consultations, through the acute and short course, enlarged spleen and enlarged cervical lymph nodes during the relapse could not match UC well. The pathologists found cryptitis and crypt abscess with a complete mucosal structure in the slides. But cryptitis and crypt abscess not only exist in UC but also in some virusinfected enteritis. The diagnosis of CAEAC should be supported by medical history and pathological findings. In conclusion, the diagnosis of CAEAE should be supported by medical history and pathological findings. EBV infection in intestinal can also cause a recurrent infection in an immunocompetent individual and develop into LPD someday. So CAEAE should be monitored closely for it is a precancerous disease. Our patient has been free of symptoms since the last discharge and he is very closely followed.
3 citations
TL;DR: It is shared by the concerns of Fernandez-Banares and Gisbert that higher doses of budesonide over the long term may be associated with higher risk of steroid-related side effects, but there is not aware of robust evidence thatHigher doses (ie 6 mg/d) are riskier than lowdose budesonid (ie 3mg/d), and in the absence of such data, it is not clear that maintenance treatment with immunomodulators is safer than budeson
Abstract: SIRS, We appreciate the comments of Drs. Fernandez-Banares and Gisbert on our article. We agree that our definition of budesonide dependence was broad, namely recurrence of diarrhoea after budesonide discontinuation. We also agree with their clinically important recommendation that maintenance budesonide should be used at the lowest effective dose, to minimise the risk of steroid-related side effects and cost, as noted in reviews from the USA and Europe. An average dose of 4.5 mg/d was more effective than placebo in a randomised trial, and in clinical practice, doses as low as 3 mg/d or even 3 mg every other day may be effective for maintenance. The Spanish Microscopic Colitis Group demonstrated the effectiveness of this strategy in a group of patients with collagenous colitis, and also reported that a subset of patients requires higher doses. In this study, only NSAID use at diagnosis was predictive of the need for higher maintenance doses of budesonide. We aimed to study doseresponse in our cohort treated with maintenance budesonide, but in a substantial proportion of patients in this retrospective study, we only knew the starting dose of budesonide but not the lowest dose used to maintain remission. We share the concerns of Fernandez-Banares and Gisbert that higher doses of budesonide over the long term may be associated with higher risk of steroid-related side effects, but we are not aware of robust evidence that higher doses (ie 6 mg/d) are riskier than lowdose budesonide (ie 3 mg/d). In the absence of such data, we prefer a broader definition of budesonide dependence to include any patient requiring long-term treatment for symptom control. As recommended previously, patients on maintenance budesonide should be monitored for the adverse events, particularly those on higher doses. Furthermore, it is not clear that maintenance treatment with immunomodulators is safer than budesonide, even at a dose of 69 mg/d, and therefore we tend to restrict use of immunomodulators to patients who are actually experiencing a side effect on budesonide.
1 citations