Depression Treatment: The Temporal Relationship Between Depression and Rheumatoid Arthritis Disease Activity, Treatment Persistence and Response: A Systematic Review.
The temporal relationship between depression and rheumatoid arthritis disease activity, treatment persistence and response: a systematic review.
Filed under: Depression Treatment
Rheumatology (Oxford). 2012 Dec 11;
Rathbun AM, Reed GW, Harrold LR
Objective. To determine whether depression has a temporal association with RA disease activity, treatment persistence and response to therapy.Methods. We performed a systematic review encompassing an electronic database search of all published literature since the availability of biologic response modifiers (beginning in 1998) investigating the impact of depression on downstream RA disease progression and treatment.Results. Only seven articles that evaluated temporal relationships between depression and RA outcomes comprising disease activity, treatment persistence and response to therapy, were included in the review. Results from these studies suggest that depression may exacerbate pain and disease activity and decrease the efficacy of pharmacological (i.e. biologic and non-biologic DMARDs) and some non-pharmacological (e.g. cognitive behavioural therapy) RA treatments.Conclusion. Given the available evidence, depression probably has a temporal influence on RA disease progression and treatment. However, it is unclear whether these observed effects are due to a response tendency on patient-reported outcomes created from negative cognitive perceptions, immunologically mediated processes that increase inflammation or behavioural changes that lead to decreased physical activity and a greater sensitivity to pain.
HubMed – depression
A nosological review of depressive disorders based on observations in clinical practice, Part 2: a working typology for clinicians.
Filed under: Depression Treatment
Australas Psychiatry. 2012 Dec 12;
Restifo S
OBJECTIVE: The purpose of this paper is to examine the essential nosological differentiation between melancholic and non-melancholic forms of depression with a view to promoting a meaningful, working typology for clinicians. The paper primarily comprises observations and reflections drawn from clinical practice. CONCLUSIONS: The most specific symptoms of melancholic depression are described, as are the main varieties of non-melancholic ‘depression’, including demoralisation, grief, loneliness, existential depression and depressive personality.
HubMed – depression
Polymorphisms of the serotonin transporter gene and post-stroke depression: a meta-analysis.
Filed under: Depression Treatment
J Neurol Neurosurg Psychiatry. 2012 Dec 12;
Mak KK, Kong WY, Mak A, Sharma VK, Ho RC
BACKGROUND: Polymorphisms of the gene encoding the serotonin transporter-specifically, length variation in the serotonin-transporter-linked polymorphic region (5-HTTLPR), a single-nucleotide polymorphism in the 5-HTTLPR (rs25531), and variable number of tandem repeats (VNTR) in the second intron 2 (STin2)-have been implicated in the development of post-stroke depression (PSD). OBJECTIVE: To evaluate the association between polymorphisms of the serotonin transporter gene and PSD in the medical literature. METHODS: Random-effects meta-analyses were conducted on cross-sectional, case-control and cohort studies examining relations between polymorphisms of the gene encoding the serotonin transporter and the risk of developing PSD. RESULTS: Four studies comprising 260 stroke patients with PSD and 381 without were included. Our analyses showed a significant and positive association between the homozygous short variation (S) allele genotype of the 5-HTTLPR (SS) and PSD (random-effects pooled OR 2.05, 95% CI 1.41 to 2.98, z=3.79, p<0.001). Our analyses also showed a significant and negative association between the homozygous long variation (L) allele genotype of the 5-HTTLPR (LL) and PSD (random-effects OR 0.52, 95% CI 0.27 to 0.97, z=-2.07, p=0.039). No statistically significant association of PSD with heterozygous S and L allele genotype for 5-HTTLPR or other polymorphisms with rs25531 and STin2 VNTR was found. Heterogeneity and publication bias were not statistically significant. The major limitation of this meta-analysis is that we could not assess the interaction between stroke, environmental stress and PSD. CONCLUSIONS: The 5-HTTLPR SS genotype may be a risk factor for PSD. The 5-HTTLPR LL genotype showed a significant negative association with PSD. Further research to assess the sensitivity and specificity of predicting the risk of developing PSD by screening for the 5-HTTLPR genotype in stroke patients is required. HubMed – depression
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