Feasibility of a slower lamotrigine titration schedule for bipolar depression: a naturalistic study

The development of a skin rash is often associated with a rapid escalation of lamotrigine dose. We used lamotrigine to treat 259 patients with Diagnostic and Statistical Manual of Mental Disorders, 4th edition, bipolar depression using either the standard titration schedule (n=132) or a slower titration schedule (n=127) and compared the clinical efficacy and safety of both groups. Clinical efficacy of lamotrigine treatment was assessed using changes in the Clinical Global Impression Scale for Bipolar Disorder-Modified scores during the course of the 12-week treatment A significant reduction of the Clinical Global Impression Scale for Bipolar Disorder-Modified score was observed in both groups and the effect size was large for both groups (standard, 0.75; slower, 0.71). A mixed-effect model of repeated measurement. revealed an increased rate of improvement in the standard titration group that was significant during the first 5 weeks (P<0.001) but became nonsignificant by the final 7 weeks of treatment. The statistically significant reduction in the development of rashes (P=0.005) was a major advantage for patients in the slower titration group. Although the standard titration schedule generally led to faster recovery from depressive symptoms, the slower titration schedule may be an option for patients with a high risk of rash development.Ketter TA, 2008, J PSYCHIATR RES, V43, P13, DOI 10.1016/j.jpsychires.2008.02.007Calabrese JR, 2008, BIPOLAR DISORD, V10, P323Alvestad S, 2007, EPILEPSIA, V48, P1360, DOI 10.1111/j.1528-1167.2007.01109.xKeck PE, 2007, CNS SPECTRUMS, V12, P1Man CBL, 2007, EPILEPSIA, V48, P1015, DOI 10.1111/j.1528-1167.2007.01022.xHirsch LJ, 2006, EPILEPSIA, V47, P318Ostacher MJ, 2006, J CLIN PSYCHIAT, V67, P18*GLAXOSMITHKLINE, 2006, PRESCR INF LAM LAM TKetter TA, 2005, J CLIN PSYCHIAT, V66, P642P-Codrea S, 2005, ACTA NEUROL SCAND, V111, P191, DOI 10.1111/j.1600-0404.2005.00381.xSilverstone PH, 2004, INT CLIN PSYCHOPHARM, V19, P113, DOI 10.1091/01.yic.0000125754.83499.55Chung WH, 2004, NATURE, V428, P486, DOI 10.1038/428486aGueorguieva R, 2004, ARCH GEN PSYCHIAT, V61, P310Katz MM, 2004, NEUROPSYCHOPHARMACOL, V29, P566, DOI 10.1038/sj.npp.1300341Goodwin GM, 2004, J CLIN PSYCHIAT, V65, P432Calabrese JR, 2003, J CLIN PSYCHIAT, V64, P1013Bowden CL, 2003, ARCH GEN PSYCHIAT, V60, P392Choi H, 2003, EXPERT OPIN PHARMACO, V4, P243Calabrese JR, 2002, J CLIN PSYCHIAT, V63, P1012Calabrese JR, 2002, J CLIN PSYCHIAT, V63, P18Frye MA, 2000, J CLIN PSYCHOPHARM, V20, P607Rzany B, 1999, LANCET, V353, P2190Calabrese JR, 1999, J CLIN PSYCHIAT, V60, P79Messenheimer JA, 1998, CAN J NEUROL SCI, V25, pS14Spearing MK, 1997, PSYCHIAT RES, V73, P159COHEN J, 1988, STAT POWER ANAL BEHA

Serum-Derived Neuronal Exosomal microRNAs as Stress-Related Biomarkers in an Atopic Dermatitis Model

Chronic allergic inflammatory skin disease&mdash;atopic dermatitis (AD)&mdash;is characterized by eczema, pruritus, xeroderma, and lichenification. Psychological stress is one cause of this disease; however, psychological stress will also result from the presence of AD symptoms. Previous studies have shown that psychological stress triggers neuroinflammation in the brain, where microRNAs (miRNAs) in the neuronal exosomes (nEVs) were analyzed to identify the composition of the miRNAs in the nEVs and how they were altered by AD. In this study, the AD model was induced by treatment with 2,4-dinitrochlorobenzene (DNCB). The expression patterns of neuroinflammation markers, such as brain-derived neurotrophic factor, cyclooxygenase-2, and glial fibrillary acidic protein, were subsequently evaluated over time. Among these groups, there was a significant difference in DNCB 14 days expression compared with the control; therefore, nEVs were isolated from serum and next-generation sequencing was performed. The results demonstrate that 9 miRNAs were upregulated and 16 were downregulated in the DNCB 14 days compared with the control. Previous studies have shown that some of these miRNAs are associated with stress and stress-induced depression, which suggests that the miRNAs in nEVs may also be stress-related biomarkers