Prolonged impact of the COVID-19 pandemic on self-harm hospitalizations in France: A nationwide retrospective observational study.

BACKGROUND: The first wave of the COVID-19 pandemic in France was associated with a reduced number of hospitalizations for self-harm, with the exception of older people. The on-going pandemic may have both sustained and delayed effects. METHODS: Data were extracted from the French national hospital database (PMSI), a nationwide exhaustive database. The number of self-harm hospitalizations (ICD-10 codes X60-84) between September 1, 2020 and August 31, 2021 (N = 85,679) was compared to 2019 (N = 88,782) using Poisson regression models. RESULTS: There was a decrease in the total number of self-harm hospitalizations during the studied period versus 2019 (-3.5%; Relative Risk [RR] [95% Confidence Intervals] = 0.97 [0.96-0.97]; p < 0.0001). However, sex and age effects were identified. While adults aged 30-59-years-old showed a decrease (monthly decreases: -12.6 to -15.0%), we found an increase in adolescent girls (+27.7%, RR = 1.28 [1.25-1.31]; p < 0.0001), notably since January 2021. Moreover, the numbers were similar to 2019 in adolescent boys, in youths aged 20-29 years, and in people aged 70 and more. Hospitalizations in intensive care units decreased (-6.7%, RR = 0.93 [0.91-0.96]; p < 0.0001) and deaths at hospital following self-harm remained stable (+0.6%, Hazard Ratio = 0.99 [0.91-1.08], p = 0.79). CONCLUSIONS: During this second stage, the number of self-harm hospitalizations remained at a lower level than in the prepandemic period. However, significant variations over time, age, and sex were observed. Young people (notably adolescent girls) appear to have particularly suffered from the persistence of the pandemic, while older people did not show any decrease since the beginning. Vigilance and continuing prevention are warranted.

Type A competitiveness traits correlate with downregulation of c-Fos expression in patients with type 1 diabetes.

AIM: Type A personality has been associated with increased survival in people with type 1 diabetes (T1D). Systemic low-grade inflammation may play a critical role, as suggested in recent reports, although the links between the inflammatory circulating transcriptome and Type A remain unknown. This prompted our exploration of the potential associations between Type A personality and c-Fos gene expression, a candidate gene closely linked to inflammatory processes, in T1D. METHODS: Type A personality was assessed by Bortner questionnaire in patients with T1D, and two subscales - 'speed' and 'competitiveness' - were used to measure these specific dimensions of Type A. Expression of the c-Fos gene was assessed by a quantitative real-time polymerase chain reaction technique. RESULTS: This pilot study included 20 men with T1D. Multivariable analyses showed an independent inverse association between Type A competitiveness score and c-Fos expression, while a regression model adjusted for age, body mass index and HbA1c levels revealed a significant inverse relationship between c-Fos transcripts and Type A competitiveness (P = 0.003). CONCLUSION: This strong association between Type A competitiveness and reduced c-Fos expression is in line with recent data suggesting a psychobiological influence of the Type A profile in T1D via inflammatory pathways.

Mast cells' involvement in inflammation pathways linked to depression: evidence in mastocytosis.

Converging sources of evidence point to a role for inflammation in the development of depression, fatigue and cognitive dysfunction. More precisely, the tryptophan (TRP) catabolism is thought to play a major role in inflammation-induced depression. Mastocytosis is a rare disease in which chronic symptoms, including depression, are related to mast cell accumulation and activation. Our objectives were to study the correlations between neuropsychiatric features and the TRP catabolism pathway in mastocytosis in order to demonstrate mast cells' potential involvement in inflammation-induced depression. Fifty-four patients with mastocytosis and a mean age of 50.1 years were enrolled in the study and compared healthy age-matched controls. Depression and stress were evaluated with the Beck Depression Inventory revised and the Perceived Stress Scale. All patients had measurements of TRP, serotonin (5-HT), kynurenine (KYN), indoleamine 2,3-dioxygenase 1 (IDO1) activity (ratio KYN/TRP), kynurenic acid (KA) and quinolinic acid (QA). Patients displayed significantly lower levels of TRP and 5-HT without hypoalbuminemia or malabsorption, higher IDO1 activity, and higher levels of KA and QA, with an imbalance towards the latter. High perceived stress and high depression scores were associated with low TRP and high IDO1 activity. In conclusion, TRP metabolism is altered in mastocytosis and correlates with perceived stress and depression, demonstrating mast cells' involvement in inflammation pathways linked to depression.

Potential influence of Type A personality on plasma C-reactive protein levels in people with diabetes.

AIM: Type A personality, although classically known as a factor linked to increased vascular risk, has recently been associated with increased survival in patients with diabetes. As low-grade inflammation predicts a poor outcome, the present study explored the potential associations between Type A and plasma levels of C-reactive protein (CRP) in diabetes. METHODS: Type A personality was assessed by the Bortner questionnaire in people with diabetes. The association between Type A and plasma CRP levels was examined by multivariable linear regression, and structural equation modelling (SEM) was performed to determine the impact of the major clinical, biological and psychological confounders. RESULTS: The study included 626 participants with type 1 and type 2 diabetes from the Diabetes and Psychological Profile study. Multivariable analyses showed an independent inverse association between Type A score and CRP levels. The structural model adjusted for age, gender, diabetes type and duration, body mass index (BMI), smoking status, alcohol abuse, oral antidiabetic and statin treatments, HbA1c levels, lipids, perceived stress, anxiety and depression revealed significant associations between CRP and Type A (ß=-0.135, 95% CI: -0.242, -0.028; P=0.014), BMI (ß=0.194, 95% CI: 0.038, 0.350; P=0.015) and HDL cholesterol (ß=-0.132, 95% CI: -0.245, -0.020; P=0.014). CONCLUSION: Our present study data indicate that Type A personality is independently associated with lower CRP levels. This lower level of inflammation might explain the better clinical outcomes associated with Type A personality in patients with diabetes.

[Telomeres in the brain cortex of depressive patients]. / Longueur des télomères dans le cortex des patients atteints de troubles dépressifs.

BACKGROUND: Telomeres are complex structures formed by the end of the DNA molecule at the tip of chromosomal arms. The telomeric sequence, which results from the repetition of the hexanucleotide TTAGGG, is partly single strand and is associated with more than ten proteins, including the enzyme telomerase. Because of the characteristics of the DNA replication process, only telomerase is able to elongate the telomeric sequence. Since the telomerase gene is repressed in virtually all the somatic cells, telomeres progressively shorten at each S phase of the cell cycle, and this shortening is accelerated by oxidative stress. A critically shortened telomere activates the genetic program of cell senescence and/or apoptosis. The telomere length measured in peripheral blood leucocytes is considered a reliable marker of biological age, mortality risk and exposure to various pathological conditions, including cardiovascular disease, dementia and metabolic syndrome. Telomere erosion has been observed in psychiatric disorders including schizophrenia and mood disorders, suggesting an accelerated aging of 10 to 20 years. Whether this peripheral dynamic is reflected by a similar pattern in the brain remains unknown. To address this issue, we have measured the telomere length in the occipital DNA cortex of 24 patients with major depressive disorder and 12 controls (donated by the Stanley Research Institute). METHODOLOGY: The mean telomere length has been evaluated by a real time quantitative PCR technique, which amplified the telomere sequence and a reference single copy sequence. Results have been expressed by the ratios of Ct obtained for the two amplification curves. RESULTS: The mean Ct values were strictly identical (0.79 ± 0.001) and the 36 PCR curves were coincident. DISCUSSION: This study demonstrates for the first time that there is no shortening of telomeres in the cortex of patients with depressive disorder. Previous results have shown that in normal tissues telomeres length is inversely correlated to age, even in non proliferating tissues, but that the change is minimal in the brain. Thus, although consistent evidence for the role of a systemic and brain inflammation associated oxidative stress in depression has been provided, it must be concluded that the cerebral state of telomeres is not affected by the mechanism operating in the leucocytes. This observation raises the issue of the relation between the psychiatric pathological process and the peripheral telomere marker. It suggests the existence of specific telomere stabilizing factors in the cortex cells.

[Efficacy of escitalopram vs paroxetine on severe depression with associated anxiety: data from the "Boulenger" study]. / Efficacité de l'escitalopram vs paroxétine sur les formes de dépressions sévères avec symptômes anxieux associés. Données issues de l'étude "Boulenger": escitalopram versus paroxétine.

Several recent studies have underlined the importance of anxiety in major depressive disorders. It has been shown that anxiety was responsible for worsening of depression and reduction of the efficacy of the antidepressant treatment. While it is well known that SSRI are efficient in treating depression or anxiety disorders, the authors tried to determine the influence of baseline anxiety on the response to SSRI treatment in patients with severe depression receiving either escitalopram or paroxetine. In a 24-week double-blind clinical trial, 459 patients with a primary diagnosis of severe major depressive disorder were randomised to receive escitalopram (20mg) or paroxetine (40mg). Post hoc analyses of efficacy in patients with a baseline HAM-A total score less or equal to 20 (n=171) or greater than 20 (n=280) were based on analysis of covariance. (ANCOVA) (ITT, LOCF). At week 24, the mean change from baseline in MADRS total score was -24.2 for escitalopram-treated patients (n=141) and -21.5 for paroxetine treated patients (n=139) (p<0.05, between both groups) in high baseline anxiety patients (HAM-A>20) and the mean change from baseline in HAM-A total score was -17.4 (escitalopram) and -15.1 (paroxetine) (p<0.05, between both groups). As far as complete remitters (CGI-S=1) after 24-week treatment were concerned, their number was significantly higher with escitalopram in the case of marked baseline anxiety. No difference was shown in the low baseline anxiety group. Looking for the influence of baseline anxiety on SSRI treatment effects, the authors showed that antidepressant efficacy of 20mg escitalopram was better than 40mg paroxetine for patients highly depressed with comorbid anxiety symptoms and that, contrary to paroxetine, escitalopram maintained sustained antidepressant activity in patients featuring increased baseline anxiety levels.

Fatigue in patients with cardiovascular disease.

Fatigue is a frequent complaint during cardiovascular disease and can sometimes constitute the first clinical manifestation of this disease. It is responsible for deterioration of the quality of life and prognosis. Although physical and mental fatigue are often intimately interrelated, these two aspects of fatigue correspond to different pathophysiological mechanisms and different clinical features and the neurobiological links between the two are only just beginning to be studied. Physical fatigue is related to loss of efficacy of the effector muscle, due to multiple causes: mismatch of cardiac output during exercise, muscle and microcirculatory deconditioning, neuroendocrine dysfunction, associated metabolic disorders. Mental fatigue corresponds to predominantly depressive mood disorders with a particular entity, vital exhaustion. The diagnostic approach is designed to eliminate other organic causes of fatigue. Functional tests investigating physical (exercise capacity) and mental dimensions (mood disorders) can be used to analyse their respective roles and to propose personalized management, in which rehabilitation has an essential place due to its global approach. The objective of this reduction of fatigue is threefold: to improve independence, to improve quality of life and to limit morbidity and mortality.