Association between response to lithium augmentation and the combined DEX/CRH test in major depressive disorder

Bschor, Tom; Baethge, Christopher; Adli, Mazda; Eichmann, Uta; Ising, Marcus; Uhr, Manfred; Modell, S.; Künzel, Heike; Müller‐Oerlinghausen, B.; Bauer, Michael

doi:10.1016/s0022-3956(02)00088-2

Cited by 22 publications

(17 citation statements)

References 28 publications

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“…The underlying mechanisms of action involved in the potentiatory effect of lithium is still unclear and several hypotheses have been suggested such as activity and modulation on serotonin (5-HT) neurotransmission and endocrine systems [36][37][38] . Initially, de Montigny and colleagues [17,39] postulated that a pharmacodynamic action mediated via the serotonergic systems may ac-count for the synergistic effect of lithium when added to a tricyclic antidepressant.…”

Section: Mechanisms Of Lithium Augmentationmentioning

confidence: 99%

“…Further evidence for a 'true' augmentation effect derived from animal studies showed that, in contrast to lithium alone, the addition of lithium to antidepressant treatment with the SSRI, citalopram potentiated presynaptic serotonergic function in rats [41] . Specifically, some authors suggested that the effect of lithium on 5-HT neurotransmission could be linked to a partial agonist activity on 5-HT1B autoreceptors or to a modulatory activity on these receptors [38] . In a recent series of experiments, the effects of lithium were investigated in a battery of standard behavioral tests (e.g.…”

Section: Mechanisms Of Lithium Augmentationmentioning

confidence: 99%

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Lithium’s Emerging Role in the Treatment of Refractory Major Depressive Episodes: Augmentation of Antidepressants

Adli²,

et al. 2010

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Background: The late onset of therapeutic response and a relatively large proportion of nonresponders to antidepressants remain major concerns in clinical practice. Therefore, there is a critical need for effective medication strategies that augment treatment with antidepressants. Methods: To review the available evidence on the use of lithium as an augmentation strategy to treat depressive episodes. Results: More than 30 open-label studies and 10 placebo-controlled double-blind trials have demonstrated substantial efficacy of lithium augmentation in the acute treatment of depressive episodes. Most of these studies were performed in unipolar depression and included all major classes of antidepressants, however mostly tricyclics. A meta-analysis including 10 randomized placebo-controlled trials has provided evidence that lithium augmentation has a statistically significant effect on the response rate compared to placebo with an odds ratio of 3.11, which corresponds to a number-needed-to-treat of 5. The meta-analysis revealed a mean response rate of 41.2% in the lithium group and 14.4% in the placebo group. One placebo-controlled trial in the continuation treatment phase showed that responders to acute-phase lithium augmentation should be maintained on the lithium-antidepressant combination for at least 12 months to prevent early relapses. Preliminary studies to assess genetic influences on response probability to lithium augmentation have suggested a predictive role of the –50T/C single nucleotide polymorphism of the GSK3β gene. Conclusion: Augmentation of antidepressants with lithium is currently the best-evidenced augmentation therapy in the treatment of depressed patients who do not respond to antidepressants.

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Section: Mechanisms Of Lithium Augmentationmentioning

confidence: 99%

Section: Mechanisms Of Lithium Augmentationmentioning

confidence: 99%

Lithium’s Emerging Role in the Treatment of Refractory Major Depressive Episodes: Augmentation of Antidepressants

Adli²,

et al. 2010

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“…Six of these depressed subjects did not receive 1-year post-treatment ratings; five were lost to follow-up and one missed the 1-year follow-up. Remission was defined as at least a 50% decrease from HAM-D 24 baseline score and a score of p10 at the 1-year assessment (Bschor et al, 2002;Bschor et al, 2003;Keller, 2004;Lin et al, 1998;Paykel et al, 1995;Roose and Suthers, 1998;Smith et al, 2002). All subjects were treated with antidepressant medications during the year.…”

Section: Subjectsmentioning

confidence: 99%

Higher 5-HT1A Receptor Binding Potential During a Major Depressive Episode Predicts Poor Treatment Response: Preliminary Data from a Naturalistic Study

Parsey

Olvet

Oquendo

et al. 2006

Neuropsychopharmacol

206

122

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Serotonin 1A (5-HT 1A ) binding potential (BP) as assessed by positron emission tomography (PET) is higher in major depressive disorder (MDD) in association with the higher expressing GG genotype of the 5-HT 1A C-1019G polymorphism. We hypothesize that higher 5-HT 1A BP and the GG genotype predict remission failure on antidepressant treatment. We determined 5-HT 1A BP by PET and 5-HT 1A C-1019G genotype in 43 controls and 22 medication-free MDD subjects. MDD was treated naturalistically and remission was defined as 450% reduction and a score of p10 on the 24 item Hamilton Scale 1 year after initiation of treatment after scanning. Despite equivalent treatment, nonremitters have higher pretreatment cortical BP and the GG genotype is over-represented compared with remitters. Higher 5-HT 1A BP, perhaps due to greater gene expression, may predict antidepressant medication nonremission. The findings should be tested in a controlled prospective treatment study.

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“…Although the research still remains to be performed aimed at understanding and determining the cortisol net-effects of both hypo- and hypercortisolism in bipolar disorder, there are studies indicating that both treatment regimens that lower as well as elevate the cortisol levels can have positive effects on depressive symptomatology. Lithium augmentation has in depressive disorder been shown to increase HPA-axis activity and further, this increase has been associated with short-term treatment efficiency [63], [64]. There is a pilot study showing promising results with low-dose prednisolone treatment of treatment-resistant depressive disorder patients exhibiting hypocortisolism [65].…”

Section: Discussionmentioning

confidence: 99%

Relative Hypo- and Hypercortisolism Are Both Associated with Depression and Lower Quality of Life in Bipolar Disorder: A Cross-Sectional Study

et al. 2014

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BackgroundDepression in unipolar and bipolar disorders is associated with hypothalamic-pituitary-adrenal-axis (HPA-axis) hyperactivity. Also, unipolar disorder has recently been shown to exhibit HPA-axis hypoactivity. We studied for the first time how HPA-axis hypo- and hyperactivity relate to depression and disease burden in bipolar disorder. We were interested in studying hypocortisolism; characterized by increased HPA-axis negative feedback sensitivity and lower basal cortisol levels together with the opposite HPA-axis regulatory pattern of hypercortisolism.MethodsThis cross-sectional study includes 145 type 1 and 2 bipolar outpatients and 145 matched controls. A dexamethasone-suppression-test (DST) measures the negative feedback sensitivity and a weight-adjusted very-low-dose DST was employed, which is sensitive in identifying hypocortisolism and hypercortisolism. The 25th and 75th percentiles of control post-DST values were used as cut-offs identifying patients exhibiting relative hypo-, and hypercortisolism. Self-report questionnaires were employed: Beck-Depression-Inventory (BDI), Montgomery-Åsberg-Depression-Rating-Scale (MADRS-S), World-Health-Organization-Quality-of-Life-Assessment–100 and Global-Assessment-of-Functioning.ResultsPatients exhibiting relative hypocortisolism expectedly exhibited lowered basal cortisol levels (p = 0.046). Patients exhibiting relative hypercortisolism expectedly exhibited elevated basal levels (p<0.001). Patients exhibiting relative hypocortisolism showed 1.9–2.0 (BDI, p = 0.017, MADRS-S, p = 0.37) and 6.0 (p<0.001) times increased frequencies of depression and low overall life quality compared with patients exhibiting mid post-DST values (eucortisolism). Adjusted Odds Ratios (OR:s) for depression ranged from 3.8–4.1 (BDI, p = 0.006, MADRS-S, p = 0.011) and was 23.4 (p<0.001) for life quality. Patients exhibiting relative hypercortisolism showed 1.9–2.4 (BDI, p = 0.017, MADRS-S, p = 0.003) and 4.7 (p<0.001) times higher frequencies of depression and low overall life quality compared with patients exhibiting eucortisolism. Adjusted OR:s for depression ranged from 2.2–2.7 (BDI, p = 0.068, MADRS-S, p = 0.045) and was 6.3 (p = 0.008) for life quality.LimitationsThe cross-sectional design and lack of pre-established reference values of the DST employed.ConclusionsRelative hypocortisolism and relative hypercortisolism were associated with depression and lower life quality, providing novel insights into the detrimental role of stress in bipolar disorder.

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Association between response to lithium augmentation and the combined DEX/CRH test in major depressive disorder

Cited by 22 publications

References 28 publications

Lithium’s Emerging Role in the Treatment of Refractory Major Depressive Episodes: Augmentation of Antidepressants

Lithium’s Emerging Role in the Treatment of Refractory Major Depressive Episodes: Augmentation of Antidepressants

Higher 5-HT1A Receptor Binding Potential During a Major Depressive Episode Predicts Poor Treatment Response: Preliminary Data from a Naturalistic Study

Relative Hypo- and Hypercortisolism Are Both Associated with Depression and Lower Quality of Life in Bipolar Disorder: A Cross-Sectional Study

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