Background: Patients with depersonalization disorder (DPD) typically complain about emotional detachment. Previous studies found reduced autonomic responsiveness to emotional stimuli for DPD patients as compared to patients with anxiety disorders. We aimed to investigate autonomic responsiveness to emotional auditory stimuli of DPD patients as compared to patient controls. Furthermore, we examined the modulatory effect of mindful breathing on these responses as well as on depersonalization intensity.
Methods: 22 DPD patients and 15 patient controls balanced for severity of depression and anxiety, age, sex and education, were compared regarding 1) electrodermal and heart rate data during a resting period, and 2) autonomic responses and cognitive appraisal of standardized acoustic affective stimuli in two conditions (normal listening and mindful breathing).
Results: DPD patients rated the emotional sounds as significantly more neutral as compared to patient controls and standardized norm ratings. At the same time, however, they responded more strongly to acoustic emotional stimuli and their electrodermal response pattern was more modulated by valence and arousal as compared to patient controls. Mindful breathing reduced severity of depersonalization in DPD patients and increased the arousal modulation of electrodermal responses in the whole sample. Finally, DPD patients showed an increased electrodermal lability in the rest period as compared to patient controls.
Conclusions: These findings demonstrated that the cognitive evaluation of emotional sounds in DPD patients is disconnected from their autonomic responses to those emotional stimuli. The increased electrodermal lability in DPD may reflect increased introversion and cognitive control of emotional impulses. The findings have important psychotherapeutic implications.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3772934 | PMC |
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0074331 | PLOS |
Cancer Chemother Pharmacol
January 2025
Markey Cancer Center, University of Kentucky, Lexington, KY, USA.
Purpose: Patients with partial or complete DPD deficiency have decreased capacity to degrade fluorouracil and are at risk of developing toxicity, which can be even life-threatening.
Case: A 43-year-old man with moderately differentiated rectal adenocarcinoma on capecitabine presented to the emergency department with complaints of nausea, vomiting, diarrhea, weakness, and lower abdominal pain for several days. Laboratory findings include grade 4 neutropenia (ANC 10) and thrombocytopenia (platelets 36,000).
World J Gastrointest Oncol
January 2025
Department of Clinical Medicine and Surgery, University of Naples Federico II, Naples 80131, Campania, Italy.
Background: Fluoropyrimidines are metabolized in the liver by the enzyme dihydropyrimidine dehydrogenase (DPD), encoded by the gene. About 7% of the European population is a carrier of gene polymorphisms associated with reduced DPD enzyme activity.
Aim: To assess the prevalence of polymorphisms and their impact on fluoropyrimidine tolerability in Italian patients with gastrointestinal malignancies.
Cureus
December 2024
Oncology, Qiannan People's Hospital, Duyun, CHN.
Capecitabine is an oral prodrug metabolized into 5-fluorouracil (5-FU) and serves as a representative anticancer agent. While fluoropyrimidine treatment is usually well-tolerated, a subset of patients unfortunately experiences severe and sometimes life-threatening toxicity related to these compounds. This adverse reaction is frequently attributed to partial or complete deficiencies in the dihydropyrimidine dehydrogenase (DPD) enzyme.
View Article and Find Full Text PDFBiomolecules
December 2024
Department of Medicine and Feinstein Institute for Medical Research, Zucker School of Medicine, Hempstead, NY 11549, USA.
Patients carrying APOL1 risk alleles (G1 and G2) have a higher risk of developing Focal Segmental Glomerulosclerosis (FSGS); we hypothesized that escalated levels of miR193a contribute to kidney injury by activating renin-angiotensin system (RAS) in the APOL1 milieus. Differentiated podocytes (DPDs) stably expressing vector (V/DPD), G0 (G0/DPDs), G1 (G1/DPDs), and G2 (G2/DPDs) were evaluated for renin, Vitamin D receptor (VDR), and podocyte molecular markers (PDMMs, including WT1, Podocalyxin, Nephrin, and Cluster of Differentiation [CD]2 associated protein [AP]). G0/DPDs displayed attenuated renin but an enhanced expression of VDR and Wilms Tumor [WT]1, including other PDMMs; in contrast, G1/DPDs and G2/DPDs exhibited enhanced expression of renin but decreased expression of VDR and WT1, as well as other PDMMs (at both the protein and mRNA levels).
View Article and Find Full Text PDFCancer Chemother Pharmacol
January 2025
Service de Génomique des Tumeurs et Pharmacologie, Hôpital Saint-Louis, Assistance Publique Hôpitaux de Paris, Paris, France.
The enzyme dihydropyrimidine dehydrogenase (DPD) is the primary catabolic pathway of fluoropyrimidines including 5 fluorouracil (5FU) and capecitabine. Cases of lethal toxicity have been reported in cancer patients with complete DPD deficiency receiving standard dose of 5FU or capecitabine. DPD is encoded by the pharmacogene DPYD in which more than 200 variants have been identified.
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