Treatment Options for Chronic Parvovirus Viremia in Pediatric Heart Transplant Patients in a Tertiary Care Center
Poster May 09, 2018
Rachel Cruz, Carla Duff, Diane Krasnopero, Sonya Joychan, David Lindsay, Daime Nieves, Maryssa Ellison, Zsofia Long, Panida Sriaroon, Alfred Asante-Korang, Jolan E. Walter
OBJECTIVE: Parvovirus viremia may occur in pediatric heart transplant patients with secondary T cell lymphopenia and history of thymectomy. While the treatment option for these patients is high dose intravenous immunoglobulin (HDIvIg), it may not be well tolerated in all patients. We present treatment outcomes in three cardiac transplant patients with parvovirus viremia.
RESULTS: Of the three patients, two responded well to treatment; however, one patient’s viral load remained at over one million copies and developed severe side effects of aseptic meningitis with HDIvIg. Compared to the other two cases, this patient had severe reduction of T cell count that likely contributed to the persistence of high viral load. In order to improve this patient’s quality of life as well as reduce the healthcare costs, a new treatment option was explored. Facilitated subcutaneous immunoglobulin treatment was initiated and resulted in a dramatic decrease in parvovirus viral loads with no adverse effects.
CONCLUSION: Pediatric cardiac transplant patients with severely reduced T cell counts may be at risk of developing chronic parvovirus viremia with high viral load. Although most patients respond well to HDIvIg, subcutaneous route may serve as an alternative to treatment refractory cases.
Genome-wide association studies (GWAS) have identified more than 100 genetic loci associated with type 2 diabetes. The majority of these are located in the intergenic or intragenic regions suggesting that the implicated variants may alter chromatin conformation. This, in turn, is likely to influence the expression of nearby or more remotely located genes to alter beta cell function. At present, however, detailed molecular and functional analyses are still lacking for most of these variants. We recently analysed one of these loci and mapped five causal variants in an islet-specific enhancer cluster within the STARD10 gene locus. Here, we aimed to understand how these causal variants influence b-cell function by alteration of the chromatin structure of enhancer clusterREAD MORE