Surgical Treatment of Peripheral Aneurysms in Patients with Behcet’s Disease

AbstractIntroductionOur aim was to report our experience with 23 patients presenting with 32 peripheral aneurysms secondary to Behcet’s disease (BD) and their outcome after vascular surgery.MethodsThe study was retrospective in nature. Except for those presenting with aneurysm rupture, patients underwent surgery after treatment of acute inflammatory lesions. All aneurysms appeared to be pseudo-aneurysms. Graft interposition with polytetrafluoroethylene or saphenous vein was most commonly employed. Postoperatively, all patients were put on immunosuppressive and antiplatelet therapy. Follow-up was done every 6–12 months, complications recorded and managed appropriately.ResultsAll the patients were males. The mean age at diagnosis of a peripheral aneurysm was 41.0 ± 9 years. There were 17 (53%) femoral, 8 (25%) popliteal, two carotid, two external iliac, two brachial and one internal iliac aneurysms. Fourteen (61%) patients had a single peripheral aneurysm while nine had two. Surgery was performed for all initially presenting 23 aneurysms. Six patients with multiple peripheral aneurysms had surgery for their second asymptomatic aneurysm. The mean follow-up period was 84 ± 62 months. Of 29 aneurysms operated on, 7 (24%) anastomotic pseudo-aneurysms and 11 (38%) graft occlusions developed. Five (22%) patients underwent major lower extremity amputations. Six (26%) mortalities were recorded.ConclusionSurgery for peripheral aneurysms in BD is warranted in many instances. Results of operation can be improved by prolonged monitoring. However, despite all efforts, peripheral aneurysm involvement in BD worsens the prognosis

Transmission of Human Immunodeficiency Virus I Drug Resistance - a Case Report. What are the Clinical Implications?

The success of first-line antiretroviral therapy can be challenged by the acquisition of primary drug resistance. Here we report a case where baseline genotypic resistance testing detected resistance conferring nucleoside/nucleotide reverse transcriptase inhibitor (NRTI)-associated mutations, but no primary mutations for protease inhibitor (PI). Subsequent PI-based HAART with boosted saquinavir led to virological treatment success with persistently undetectable viral load. After treatment simplification from saquinavir to an atazanavir based PI-therapy and no change in backbone therapy rapid virological breakthrough occurred. Retrospective analysis displayed preexisting gag cleavage site mutations which may have reduced the genetic barrier in a clinical relevant manner in combination with the already existing NRTI resistance mutations. Alternatively, this effect could be explained with a different antiviral potency for the respective PIs used

Cancer risk in HIV-infected individuals on HAART is largely attributed to oncogenic infections and state of immunocompetence

<p>Abstract</p> <p>Objectives</p> <p>To estimate the cancer risk of HIV-infected patients in the HAART era with respect to a general reference population and to determine risk factors for malignancy.</p> <p>Methods</p> <p>Long term (1996-2009) cancer incidence of the Bonn single centre HIV cohort was compared to the incidence of the reference population of Saarland using standardized incidence ratios (SIR). Poisson regression analysis was used to identify predictors of cancer risk.</p> <p>Results</p> <p>1,476 patients entered the cohort, enabling 8,772 person years of observation. 121 tumours in 114 patients, 7 in-situ and 114 invasive cancers, were identified. Malignancies associated with infectious agents such as Kaposi sarcoma (SIRs: male: 5,683; female: 277), non-Hodgkin lymphoma (SIRs male: 35; female: 18), anal cancer (SIRs male: 88; female: 115) as well a cervical carcinoma (SIR female: 4) and Hodgkin's disease (SIR male: 39) and liver cancer (SIR male: 18) were substantially more frequent in HIV-infected patients than in the general population (p < 0.001, each), whereas all other types of cancer were not increased. Poisson regression identified HAART (incidence rate ratio IRR (95% CI): 0.28 (0.19-0.41), p < 0.001), CD4 count (IRR per 100 cells/μl increase: 0.66 (0.57-0.76), p < 0.001), hepatitis B (IRR: 2.15 (1.10-4.20), p = 0.046) and age (IRR per 10 year increase: 1.23 (1.03 - 1.46), p = 0.023) as independent predictors for the occurrence of any type of cancer.</p> <p>Conclusions</p> <p>HAART and preserved CD4 cells preferentially reduce the risk of malignancies associated with oncogenic infections.</p