Rare occurrence of fatal Candida haemulonii peritonitis in a diabetic CAPD patient

A 68-year-old diabetic chronic kidney disease patient on continuous ambulatory peritoneal dialysis for two years developed Candida haemulonii peritonitis without any predisposing factors. There is no effective treatment for this fungus. A peritoneal biopsy showed morphological changes of acute inflammation and chronicity.     

Use of Laboratory Tests to Guide Initiation of Autologous Hematopoietic Progenitor Cell Collection by Apheresis: Results From the Multicenter Hematopoietic Progenitor Cell Collection by Apheresis Laboratory Trigger Survey

Limited literature describes the value of laboratory “triggers” to guide collection of peripheral blood (PB) hematopoietic progenitor cells (HPCs) by apheresis [HPC(A)]. We used a web-based survey to determine which parameters are used to initiate autologous HPC(A) collection in adult and pediatric patients and to identify common practice patterns. Members of the AABB Cellular Therapy Product Collection and Clinical Practices Subsection and the American Society for Apheresis HPC Donor Subcommittee drafted and developed relevant survey questions. A web link to the survey was distributed by electronic newsletter or email. Responses from 67 programs that perform autologous HPC(A) collections, including academic medical centers (n = 46), blood centers (n = 10), community hospitals (n = 5), and a variety of other medical institutions (n = 6), were analyzed. Ninety-three percent (62/67) of programs used a laboratory parameter to initiate HPC(A) collection. In both adult (40/54, 74%) and pediatric (29/38, 76%) patients, the PB CD34 + cell count was the most common parameter used to initiate HPC(A) collection. The median PB CD34 + trigger value was 10/μL for both patient populations. Among centers routinely using the PB CD34 + cell count to initiate apheresis, 51% (22/43) first sent the test before the patient presented for collection. Although more than 90% of centers used a laboratory test to trigger apheresis in cytokine-mobilized (44/48) or chemomobilized patients (50/53), only 57% (30/53) used a laboratory trigger if the patient was mobilized with granulocyte colony-stimulating factor plus plerixafor. Forty-two percent (21/50) of programs that routinely measured the PB CD34 + count before collection and discontinued further HPC(A) collection based on product CD34 + cell yield also stopped if the PB CD34 + value before apheresis was considered too low to proceed. Most programs use the PB CD34 + cell count to trigger autologous HPC(A) collection. Some centers also use this parameter to stop further collections. Laboratory tests are used less frequently to initiate apheresis when patients are mobilized with plerixafor. These data reveal ongoing diversity in clinical practices and suggest that consensus guidelines on use of laboratory parameters may further optimize HPC(A) collection.     

Aortic Remodelling in Chronic Nicotine-Administered Rat

Vascular remodelling is an adaptive mechanism, which counteracts pressure changes in blood circulation. Nicotine content in cigarette increases the risk of hypertension. The exact relationship between nicotine and vascular remodelling still remain unknown. Current study was aimed to determine the effect of clinically relevant dosage of nicotine (equivalent to light smoker) on aortic reactivity, oxidative stress markers and histomorphological changes. Twelve age-matched male Sprague-Dawley rats were randomly divided into two groups, i.e.: normal saline as control or 0.6 mg/kg nicotine for 28 days (i.p., n=6 per group). On day-29, the rats were sacrificed and the thoracic aorta was dissected immediately for further studies. Mean arterial pressure (MAP) and pulse pressure (PP) of nicotine-treated vs. control were significantly increased (p<0.05). Nicotine-treated group showed significant (p<0.05) increase tunica media thickness, and decrease in lumen diameter, suggesting vascular remodelling which lead to prior hypertension state. The phenylephrine (PE)-induced contractile response in nicotine group was significantly higher than control group (ED₅₀=1.44×10⁵ M vs. 4.9×10⁶ M) (p<0.05~0.001). However, nicotine-treated rat showed significantly lower endothelium-dependent relaxation response to acetylcholine (ACh) than in control group (ED₅₀=6.17×10⁷ M vs. 2.82×10⁷ M) (p<0.05), indicating loss of primary vascular function. Malondialdehyde (MDA), a lipid peroxidation marker was significantly higher in nicotine group. Superoxide dismutase (SOD) enzymatic activity and glutathione (GSH) were all reduced in nicotine group (p<0.05) vs. control, suggesting nicotine induces oxidative imbalance. In short, chronic nicotine administration impaired aortic reactivity, probably via redox imbalance and vascular remodelling mechanism.