A patient with a giant aneurysm of the top of the basilar artery presented with severe progressive symptoms of brain-stem compression. There was inadequate collateral circulation to the upper basilar system. She underwent exploration of the aneurysm and, after it was found to be impossible to clip, a tourniquet was placed on the basilar artery for future occlusion with the patient awake. A saphenous vein graft was interposed between the left external carotid and the left posterior cerebral arteries. The previously unruptured aneurysm bled fatally 36 hours after surgery, just before intended occlusion of the basilar artery.
Pseudothrombocytopenia (PTCP) is a laboratory phenomenon that can occur in hospitalized patients, with approximately 0.1 to 0.2% due to ethylenediaminetetraacetic acid (ETDA). The EDTA-dependent mechanism of PTCP occurs due to a conformational change of platelet surface glycoprotein IIb/IIIa (GPIIb/IIIa) caused by EDTA, which allows natural IgM or IgG auto-antibodies to bind to GPIIb/IIIa, leading to platelet agglutination. In most cases, PTCP resolves when a repeat blood sample is drawn in collection tubes containing either citrate or heparin. Here, we report a case of a 23-year-old female presenting with symptoms of gastroenteritis. She exhibited PTCP with blood draws obtained in not only collection tubes containing ETDA, but also with collection tubes containing heparin and citrate, which is highly unusual. The lack of resolution of platelet clumping in collection tubes containing either heparin or citrate suggests that heparin or citrate may also cause conformational changes to platelet surface glycoproteins in a similar mechanism as that of EDTA that allows binding of certain auto-antibodies.
3291 Poster Board III-1 Background: In vitro, dasatinib inhibits proliferation of CD8+ T cells in a dose-dependent manner, associated with decreased secretion of interferon-gamma and granzyme B, as well as arrest of CD8+ T cells in the G0/G1 phase of cell cycle (Blake SJ Blood 2008 Feb.1;111(3):1366-77)). Inhibition of CD8+ T cells has also been shown in blood samples from patients receiving dasatinib compared with their T cell status prior to dasatinib (Cara K.Fraser, Ex.Hema.2009; 37:256-265). These immunosuppressive properties have raised concerns about potential high risk for opportunistic and other infections among patients treated with dasatinib. Aim: Investigate the frequency and characteristics of infectious events in pts with CML in CP treated with dasatinib. Methods: Records from 55 consecutive patients with CML CP treated with dasatinib after imatinib failure were analyzed. Median time from diagnosis to the start of dasatinib therapy was 66 months. The characteristics and management of infectious complications were analyzed for each pt. Results: After a median follow-up of 6 months from the start of therapy, 31 (56%) pts had 53 episodes of infections (Table 1). These included 20 of 34 (58.8%) pts treated with a total daily dose of 140 mg/day, 6 of 8 (75%) treated with 100 mg/day, 2 of 3 (66.7%) treated with 70 mg/day. The one pt treated with 180 mg/day and both patients treated with a dose of 30 mg/day or less (in phase I study) had infections. Most of the infections were localized and not considered related to dasatinib therapy. Blood cultures were done for 5 of the infections (9.4%): 3 were negative and 2 positive (one for coagulase negative staphylococcus and one for streptococcus). Wound cultures were done in 3 pts: one with positive staphylococcus of the foot, one with staphylococcus positive bursitis of the elbow, and one cellulitis with a positive result for MRSA. Other positive cultures included one with a sputum culture positive for MRSA and one with E .coli in a urine culture. 29 (54.7%) of the infectious events required antibiotic therapy; 3 required IV antibiotics, (one with cellulitis, one with an ear infection and one with pneumonia) and one pt needed antiviral treatment for H. zoster. Four patients needed hospital admission; 2 pts had pneumonia, one had cellulitis and positive blood culture, and one had fever and plural effusion. Infections resolved in all 31 pts without complications. ANC at the time of infection was <1 ×109/L in 3 patients (5.5%). Conclusions: This analysis shows that although many patients may develop infections during the course of therapy with dasatinib, these are overwhelmingly common infections, minor, and not related to dasatinib therapy. Opportunistic infections were rare. There is no evidence that dasatinib induces a significant risk of infections in patients with CML in CP. Disclosures: Kantarjian: BMS: Research Funding. Rios:BMS: Honoraria. Cortes:BMS: Research Funding.
Background: Chronic kidney disease is one of the most common diseases. Health care workers in all countries of the world are concerned with the early detection and prevention of kidney diseases. Several novel diagnostic markers are being under investigation nowadays. Tumor necrosis factor-alpha and its receptors are examples. Aim: The present study was conducted to evaluate the role of tumor necrosis factor α receptor 1 (TNFR1) as a biomarker for detection of renal dysfunction. Materials and Methods: The study was carried out for the period from February to June 2019 and included 180 patients (their ages were between 19 and 85 years old) and were divided into 60 patients with renal impairment, 60 hemodialysis patients, and 60 patients with normal renal function (as a control group). Each group included patients with hypertension, patients with diabetes mellitus, and hypertensive- diabetic patients. The patients were attended to Center of Kidney Disease and Transplantation, Dialysis Unit of Baghdad Teaching Hospital – Medical City , Dialysis Unit of Tikrit Teaching Hospital and private laboratory in Samarra City. Urine sample was collected from each patient for bacteriological study and detection the level of TNFR1. Results: The most common pathogen isolated from cultured samples was Escherichia coli. Concentration of urinary TNFR1 in hypertensive and or diabetic with normal kidney function compared with hypertensive or and diabetic renal impairment did not differ statistically significant. Conclusion: Urinary level of tumor necrosis factor receptor 1 (TNFR1) is not important in the diagnosis of renal impairment with the presence of hypertension and or diabetes mellitus. Through statistical comparisons of patients with urinary tract infection (UTI) group and those without UTI group , it seems that UTI does not affect the diagnostic ability of urinary TNFR1. We recommend future studies focusing on serum level of the receptors mentioned above to test their diagnostic potential in renal impairment. In addition, investigating the effect of the immunological causes of renal impairment on the level of TNFR, both in urine and serum.
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