Incidence, course, and outcome of Clostridium difficile infection in children with hematological malignancies or undergoing hematopoietic stem cell transplantation.

Clostridium difficile infection (CDI) is one of the most common causes of nosocomial infectious diarrhea in children during anticancer therapy or undergoing hematopoietic stem cell transplantation (HSCT) in Europe. Immunosuppression in these patients is a risk factor for CDI. Malignant diseases, age, acute graft-versus-host disease (aGVHD), HLA mismatch, or use of total body irradiation may play an important role in CDI course. The aim of this study was to evaluate the incidence, course, and outcome of CDI in children treated for malignancy or undergoing HSCT. Between 2012 and 2015, a total number of 1846 patients were treated for malignancy in Polish pediatric oncological centers (PHO group) and 342 underwent transplantation (HSCT group). In PHO group, episodes of CDI occurred in 210 patients (14%). The incidence of CDI was higher in patients with hematological malignancies in comparison to that with solid tumors. Patients with acute myeloblastic leukemia had shorter time to episode of CDI than those with acute lymphoblastic leukemia. Patients over 5 years and treated for acute leukemia had more severe clinical course of disease in PHO group. In HSCT group, CDI occurred in 29 (8%) patients. The incidence of CDI was higher in patients transplanted for acute leukemia. The recurrence rate was 14.7% in PHO and 20.7% in HSCT patients. CDI incidence was highest in patients with hematological malignancies. Most of patients experienced mild CDI. Age < 5 years and diagnosis other than acute leukemia were the positive prognostic factors influencing clinical CDI course.

Lack of local anesthetic properties of lidocaine gel in an experimental model.

INTRODUCTION: Many reports negate the anesthetic properties of lidocaine gel placed in the urethra during catheterization. The anesthetic action of lidocaine is inseparably associated with the toxic action of this compound on cells. MATERIALS AND METHODS: A primary rabbit urothelial cell culture (PRUCC) was previously established as a monolayer. The effect of 2% lidocaine gel on the viability of the PRUCC was assessed and compared with the cytotoxic effect of decreasing concentrations of lidocaine solution. Cell viability was evaluated after 1-hour exposure using the trypan blue exclusion test. RESULTS: The 2% lidocaine gel did not show cytotoxic properties after 1 h of incubation on a PRUCC. The 2 and 1% lidocaine solutions induced statistically significant decreases in the viability of the PRUCC after 1 h of incubation. CONCLUSIONS: Experimental tests evaluating the cytotoxicity of local anesthetics may prove to be an objective measure of the accessibility of these substances to cells and their anesthetic action.

Kidney preserving solutions containing lidocaine may increase urological complication rate after renal transplantation: an in vitro study.

OBJECTIVE: The frequency of urological complications after renal transplantation is up to 12%. Some authors consider that lidocaine addition to preservation solutions produces a favorable influence on allograft function. However, lidocaine may influence urinary tract epithelial cells. The aim of this work was to establish the influence of lidocaine on cultured primary rabbit urothelial cells (PRUC) as a tool to understand mechanisms of urological complications after kidney transplantation. DESIGN AND METHODS: A PRUC culture was established from an 8-month-old male rabbit bladder. The cells were cultured alone and then with in various concentrations of lidocaine for 24 hours or 1 hour. After an additional 24 hours, cell viability was assessed by the trypan blue exclusion test. Student's t test was used for statistical analysis, with significance set at P < .05. RESULTS: The cytotoxic effects of lidocaine on PRUC were concentration dependent. One-hour exposure of PRUC culture to 0.5 or 1.0% lidocaine decreased cell viability. Both lidocaine concentrations decreased cell viability in PRUC culture after a 24-hour incubation; even 0.25% lidocaine caused changes in the PRUC culture morphology after a 1-hour incubation. Cells became rounded and detached from the growth surface. No cells were observed in the monolayer after 1-hour incubation with 1% of lidocaine. CONCLUSIONS: The toxic effects of lidocaine on PRUC may forecast problems with supplementation of kidney preservation solutions, leading to impaired epithelial layer healing with an increased risk of urological complications.

High extracellular GABA levels in hippocampus--as a mechanism of neuronal protection in cerebral ischemia in adrenalectomized gerbils.

Adrenalectomy protects the brain from delayed neuronal damage that occurs following transient forebrain ischemia in gerbils. Gamma-amino butyric acid (GABA) and GABA-mimetic drugs also have a neuro-protective effect. In this study we estimated the extracellular glutamate and GABA levels in the hippocampus during transient forebrain ischemia in adrenelectomized gerbils (n = 8) compared to controls (n = 6). Duration of ischemia was 10 min, and glutamate and GABA levels were measured with in vivo microdialysis. Microdialysis was started 2 h after the placement of a probe (to stabilise baseline) and samples were collected at 10-min intervals. The pattern of glutamate release did not show any difference between adrenelectomized animals and controls. Adrenelectomized animals showed marked increase in GABA levels during ischemia and upto 30 min after ischemia (P = 0.0287, 2-way ANOVA for repeated measurements). The enhanced GABA release may be one of the possible mechanisms of neuronal protection against ischemia in adrenelectomized gerbils.

Decreased glutamate release during hypothyroidism may contribute to protection in cerebral ischemia.

Hypothyroidism protects the brain from the effects of transient forebrain ischemia in gerbils. The mechanism for this protection is not fully understood. In this study we looked at the release of glutamate during ischemia in gerbils exposed to surgical hypothyroidism (n = 7), chemical hypothyroidism (n = 8), and surgical hypothyroidism thyroxine-treated (n = 3) and compared them to control euthyroid animals (n = 8). The duration of ischemia was 10 min. Glutamate release was measured with in vivo microdialysis. Microdialysis analysis began 2 h after the placement of the probes (to stabilize the baseline) and collections were obtained in 10-min samples. During ischemia, there was an increase in the release of glutamate that returned to the baseline within 20 min following the insult. In animals made hypothyroid surgically and chemically, the extent of glutamate release was significantly lower than that in the controls. The release of glutamate in the surgically hypothyroid thyroxine-treated animals was similar to that in controls. The attenuated glutamate release could be a mechanism of protection during ischemia in hypothyroid gerbils.