Serotonin gene polymorphisms and lifetime mood disorders in predicting interferon-induced depression in chronic hepatitis C

Cozzolongo, Raffaele; Porcelli, Piero; Cariola, Filomena; Giannuzzi, Vito; Lanzilotta, Elsa; Gentile, Mattia; Sonnante, Gabriella; Leandro, Gioacchino

doi:10.1016/j.jad.2015.04.056

Cited by 15 publications

(11 citation statements)

References 76 publications

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“…Kraus et al (2007) found that homozygosity for the G allele of the 5-HTR1A (C1019G) polymorphism in the promoter region of the 5-HT1A receptor gene conferred a higher risk for the development of IFN-induced depression compared to carriers with at least one C allele. In accordance with previous study, Cozzolongo et al (2015) demonstrated that this C-1019G polymorphism within the transcriptional control region of the 5-HTR1A gene independently predicted the incidence of IFN-induced depression in patients with CH-C. Thirdly, relevant to the metabolism of serotonin, much more attention has been paid on IDO, which breaks down TRP, the primary amino acid precursor for serotonin. Although the IDO enzyme seems to be involved in the pathophysiology of IFN-induced depression, Galvao-de Almeida et al (2011) suggested that there was no influence of the variants in the IDO gene and the diagnosis of IFN-related depression in the Brazilian population.…”

Section: Evidence For Genomic Influence In Modulating Depressionsupporting

confidence: 86%

Depression and Chronic Liver Diseases: Are There Shared Underlying Mechanisms?

Huang

Liu

2017

Front. Mol. Neurosci.

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The occurrence of depression is higher in patients with chronic liver disease (CLD) than that in the general population. The mechanism described in previous studies mainly focused on inflammation and stress, which not only exists in CLD, but also emerges in common chronic diseases, leaving the specific mechanism unknown. This review was to summarize the prevalence and risk factors of depression in CLD including chronic hepatitis B, chronic hepatitis, alcoholic liver disease, and non-alcoholic fatty liver disease, and to point out the possible underlying mechanism of this potential link. Clarifying the origins of this common comorbidity (depression and CLD) may provide more information to understand both diseases.

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Section: Evidence For Genomic Influence In Modulating Depressionsupporting

confidence: 86%

Depression and Chronic Liver Diseases: Are There Shared Underlying Mechanisms?

Huang

Liu

2017

Front. Mol. Neurosci.

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“…148 In agreement, several studies have shown that life stressors, including chronic pain or infection, interact with the rs6295 genotype for anxiety, depression and susceptibility to hospitalization for depression. 51,81,146,[149][150][151] However, in 1 study, although the G allele, childhood or later life stress were each associated with substance abuse, psychiatric hospitalization and suicide, there was no interaction between genotype and trauma in a highly stressed cohort. 61 Similarly, other studies did not find an association between rs6295/ stress and depression.…”

Section: Environmental Risk: Stress × Genotype Interactionmentioning

confidence: 65%

“…48 Furthermore, several other 5-HT-, monoamine-, or stress-related genes have also been associated with major depression. 49,50 The HTR1A G carrier or GG genotype has also been associated with increased 5-HT 1A autoreceptors, 23,41 major depression, 51 amygdala reactivity to fearful stimuli [52][53][54][55][56] and increased hippocampal volume. 57 In addition, associations have been reported between the G carrier or the GG genotype and disordered eating in female adolescents, 58 panic disorder 59 or panic disorder without agoraphobia, 60 substance abuse and psychiatric hospitalization.…”

Section: Functional 5-ht Polymorphisms and Major Depressionmentioning

confidence: 99%

Genetic, epigenetic and posttranscriptional mechanisms for treatment of major depression: the 5-HT1A receptor gene as a paradigm

Albert

François

Vahid-Ansari

2019

jpn

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Major depression and anxiety are highly prevalent and involve chronic dysregulation of serotonin, but they remain poorly understood. Here, we review novel transcriptional (genetic, epigenetic) and posttranscriptional (microRNA, alternative splicing) mechanisms implicated in mental illness, focusing on a key serotonin-related regulator, the serotonin 1A (5-HT 1A) receptor. Functional single-nucleotide polymorphisms and stress-induced DNA methylation of the 5-HT 1A promoter converge to differentially alter pre-and postsynaptic 5-HT 1A receptor expression associated with major depression and reduced therapeutic response to serotonergic antidepressants. Major depression is also associated with altered levels of splice factors and microRNA, posttranscriptional mechanisms that regulate RNA stability. The human 5-HT 1A 3′-untranslated region is alternatively spliced, removing microRNA sites and increasing 5-HT 1A expression, which is reduced in major depression and may be genotype-dependent. Thus, the 5-HT 1A receptor gene illustrates the convergence of genetic, epigenetic and posttranscriptional mechanisms in gene expression, neurodevelopment and neuroplasticity, and major depression. Understanding gene regulatory mechanisms could enhance the detection, categorization and personalized treatment of major depression.

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“…There are many opinions about the mechanism of IFN-induced depression. It was found that having been exposed to mood disorders in the past and carrying G allele variation of 5-hydroxytryptamine receptor 1-A (HTR1-A) significantly influenced the increase in IFN-induced depression [27]. Besides, reduced glucocorticoid negative feedback sensitivity leading to flattening of the diurnal cortisol slope [28], direct effect on central serotonin neurotransmission [29][30][31][32], activation of indoleamine 2,3-dioxygenase which indirectly converts tryptophan to kynurenine [33], and a decrease in the levels of brain-derived neurotrophic factor after IFN treatment might have played a role in the etiology of IFN-induced depression [34].…”

Section: Discussionmentioning

confidence: 99%

Depression and anxiety disorders during pegylated interferon treatment in patients with chronic hepatitis B

Sertöz

Tunçel

Taşbakan

et al. 2017

Psychiatry and Clinical Psychopharmacology

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Objectives: Interferon (IFN) treatment has many neuropsychiatric side effects such as depression and anxiety disorder. Although untreated depression is a major contributor to dosage reduction or premature discontinuation of the IFN treatment, it is found that depressive symptoms among patients undergoing hepatitis C virus (HCV) treatment are commonly overlooked during routine clinical interviews. Besides depression, anxiety disorders are shown to affect adherence to pegylated IFN (Peg-IFN) treatment in patients with hepatitis C. Despite the occurrence of neuropsychiatric side effects of IFN treatment being widely reported in patients with hepatitis C, there are few studies studying patients infected with hepatitis B virus (HBV). The aim of this prospective study was to evaluate the incidence and risk factors of depressive and anxiety disorders that occur during Peg-IFN treatment of patients with HBV. Methods: The sample consisted of volunteer patients who were diagnosed with HBV infection and who were decided to receive IFN treatment. During the study period, all consecutive patients with HBV infection and who would have IFN treatment were informed about the study and invited to participate. Thirty-seven chronic hepatitis B (CHB) patients were recruited for the study, but four of them were excluded due to psychiatric diagnosis at the initiation of the treatment. Therefore, the sample consisted of 33 patients with CHB, meeting the inclusion criteria. The participants had psychiatric assessment before the treatment and at 1st, 3rd, 6th, and 12th months. At each visit, the subjects were assessed with Clinical Global Impressions Scale, Hamilton Rating Scale for Depression (HRSD), and Hamilton Anxiety Rating Scale (HAM-A). Results: Among the 33 patients with HBV, 22 (66.7%) were men. Mean age was 35.97 ± 10.73 years. While follow-up, 6 patients dropped out from the study. Also, 13 patients were excluded from the study as they developed depression and/or anxiety disorder. Mean baseline HRSD and HAM-A scores were smaller than the following visits' scores. The difference was not statistically significant only for the 12th month assessments. Totally 14 (42.4%) patients developed depression/anxiety disorder during 1 year follow-up. Six (42.86%) of them received the diagnosis at the 1st month, 3 (21.43%) at the 3rd, 4 (28.57%), at 6th months, and 1 (7.14%) at the 12th month. When we compared the patients who developed depression/anxiety disorder with the patients who did not develop any psychiatric disorder, we found that the mean baseline HRSD score (t = 2.303, p = .028) and female percentage (p = .017) were statistically significantly higher in the depression/anxiety disorder group. Conclusions: There is an incidence of 42.4% for depression and/or anxiety disorders during Peg-IFN treatment. Females and patients with subsyndromal depressive symptoms should be referred to a psychiatrist and closely monitored especially for the first three months of the IFN treatment. ARTICLE HISTORY

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Serotonin gene polymorphisms and lifetime mood disorders in predicting interferon-induced depression in chronic hepatitis C

Cited by 15 publications

References 76 publications

Depression and Chronic Liver Diseases: Are There Shared Underlying Mechanisms?

Depression and Chronic Liver Diseases: Are There Shared Underlying Mechanisms?

Genetic, epigenetic and posttranscriptional mechanisms for treatment of major depression: the 5-HT1A receptor gene as a paradigm

Depression and anxiety disorders during pegylated interferon treatment in patients with chronic hepatitis B

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