ABSTRACT
Background: The main aim of this study is to find out the effect of valproic acid on platelet count and to know the possible risk factors for thrombocytopenia in patients taking valproate (VPA). Methods: On 72 patients having psychiatric indication, a longitudinal observational study was designed and conducted from February 2012 to July 2013 at Department of Psychiatry (out-patient department) of Pt. Jawahar Lal Nehru Memorial Medical College and Dr. Bhim Rao Ambedkar Memorial Hospital, Jail Road, Raipur, Chhattisgarh. Platelet count was monitored and determined using an automatic coulter analyzer. The patients were followed up to 6 months. Statistical tool standard deviation ± was used for statistical analysis. p<0.05 is considered as statistically significant. Results: Total percentage of thrombocytopenia was found to be 12.5%; among that males constitute 9.8% and females 19.04%. The maximum number of cases falls in the age group between 51 and 60 years (55.5%). The major diagnostic group was reported to be consisted of mania (40.4%), followed by resistant cases of schizophrenia (25%) and then bipolar affective disorder (23.6%). The study indicated that maximum patients suffered from mild thrombocytopenia (11.1%) and (1.4%) patients have moderate thrombocytopenia. The mean time from exposure to VPA therapy to the first episode of thrombocytopenia was reported 92 days. Conclusions: Our findings underlined the importance of monitoring platelet counts in patients treated with VPA. This monitoring should be continued indefinitely on monthly basis. The studies indicate that the demands of more vigilant monitoring of patients should occur in age of 50-60 years, and result of entire studies indicates that females were found to be subjected to incidences of thrombocytopenia especially.
ABSTRACT
ABSTRACT: Cholesterol is an essential structural component of mammalian cell membranes and plays crucial roles in intracellular transport, cell signalling and regulation etc. Proper regulation of cholesterol homeostasis in the body is important for human health. Recently, plenty of new findings reveal the molecular mechanism of cholesterol uptake, which may provide new insights on our understanding of cholesterol homeostasis. In this review, we summarized recent progress in cholesterol biology and hoping to provide new perspectives on the regulation of cholesterol transport and metabolism. ABBREVIATIONS: ER, endoplasmic reticulum; SCAP, sterol regulatory element binding protein cleavage activating protein; (HMG-CoAR), hydroxyl methyl glutaryl CoA (HMG-CoA) reductase; NPC1, Niemann–Pick C1 protein; SSD, sterol-sensing domain; SRE, sterol regulatory element; LDLR, low density lipoprotein receptor; APOE, Apoproteins E; VLDL, very low density lipoprotein; LDL, low density lipoprotein; HDL, high density lipoprotein; LXRs, liver X receptors; SR, scavenger receptors; SR-A, scavenger receptor-A; NADPH oxidase, nicotinamide adenine dinucleotide phosphate-oxidase; ACAT, acyl CoA: cholesterol acyltransferase; ACAT-1, Acyl coenzyme-A: cholesterol acyltransferase-1; FC, free cholesterol; M1, classical activation macrophage;M2, alternative activation macrophage; CEs, Cholesterol ester; (IFN)-γ, interferon; TLR, Toll-like receptor; Th2,Thelper, IL, interleukin; GM-CSF, granulocyte macrophage colony-stimulating factor (GM-CSF), LPS, lipopolysaccharide; TNF, tumor necrosis factor; (TGF)-β, transforming growth factor; HB-EGF, heparin binding epidermal growth factor; IGF, insulin-like growth factor; CC, chemokines; IDO, indole amine 2,3-dioxygenase.