BACKGROUND
Depression, anxiety and somatization are the most common mental disorders in primary care as well as medical specialty populations; each is present in at least 5-10% of patients and frequently comorbid with one another. An efficient means for measuring and monitoring all three conditions would be desirable.


METHODS
Evidence regarding the psychometric and pragmatic characteristics of the Patient Health Questionnaire (PHQ)-9 depression, generalized anxiety disorder (GAD)-7 anxiety and PHQ-15 somatic symptom scales are synthesized from two sources: (1) four multisite cross-sectional studies (three conducted in primary care and one in obstetric-gynecology practices) comprising 9740 patients, and (2) key studies from the literature that have studied these scales.


RESULTS
The PHQ-9 and its abbreviated eight-item (PHQ-8) and two-item (PHQ-2) versions have good sensitivity and specificity for detecting depressive disorders. Likewise, the GAD-7 and its abbreviated two-item (GAD-2) version have good operating characteristics for detecting generalized anxiety, panic, social anxiety and post-traumatic stress disorder. The optimal cutpoint is > or = 10 on the parent scales (PHQ-9 and GAD-7) and > or = 3 on the ultra-brief versions (PHQ-2 and GAD-2). The PHQ-15 is equal or superior to other brief measures for assessing somatic symptoms and screening for somatoform disorders. Cutpoints of 5, 10 and 15 represent mild, moderate and severe symptom levels on all three scales. Sensitivity to change is well-established for the PHQ-9 and emerging albeit not yet definitive for the GAD-7 and PHQ-15.


CONCLUSIONS
The PHQ-9, GAD-7 and PHQ-15 are brief well-validated measures for detecting and monitoring depression, anxiety and somatization.

Iconography : The Patient Health Questionnaire Somatic, Anxiety, and Depressive Symptom Scales: a systematic review

This revision of the 2005 British Association for Psychopharmacology guidelines for the evidence-based pharmacological treatment of anxiety disorders provides an update on key steps in diagnosis and clinical management, including recognition, acute treatment, longer-term treatment, combination treatment, and further approaches for patients who have not responded to first-line interventions. A consensus meeting involving international experts in anxiety disorders reviewed the main subject areas and considered the strength of supporting evidence and its clinical implications. The guidelines are based on available evidence, were constructed after extensive feedback from participants, and are presented as recommendations to aid clinical decision-making in primary, secondary and tertiary medical care. They may also serve as a source of information for patients, their carers, and medicines management and formulary committees.

/pdf/evidence-based-pharmacological-treatment-of-anxiety-3shxwfbh66.pdf

Evidence-based pharmacological treatment of anxiety disorders, post-traumatic stress disorder and obsessive-compulsive disorder: A revision of the 2005 guidelines from the British Association for Psychopharmacology

2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has raised many questions about the management of patients with chronic obstructive pulmonary disease (COPD) and whether modifications of their therapy are required. It has raised questions about recognizing and differentiating coronavirus disease (COVID-19) from COPD given the similarity of the symptoms. The Global Initiative for Chronic Obstructive Lung Disease (GOLD) Science Committee used established methods for literature review to present an overview of the management of patients with COPD during the COVID-19 pandemic. It is unclear whether patients with COPD are at increased risk of becoming infected with SARS-CoV-2. During periods of high community prevalence of COVID-19, spirometry should only be used when it is essential for COPD diagnosis and/or to assess lung function status for interventional procedures or surgery. Patients with COPD should follow basic infection control measures, including social distancing, hand washing, and wearing a mask or face covering. Patients should remain up to date with appropriate vaccinations, particularly annual influenza vaccination. Although data are limited, inhaled corticosteroids, long-acting bronchodilators, roflumilast, or chronic macrolides should continue to be used as indicated for stable COPD management. Systemic steroids and antibiotics should be used in COPD exacerbations according to the usual indications. Differentiating symptoms of COVID-19 infection from chronic underlying symptoms or those of an acute COPD exacerbation may be challenging. If there is suspicion for COVID-19, testing for SARS-CoV-2 should be considered. Patients who developed moderate-to-severe COVID-19, including hospitalization and pneumonia, should be treated with evolving pharmacotherapeutic approaches as appropriate, including remdesivir, dexamethasone, and anticoagulation. Managing acute respiratory failure should include appropriate oxygen supplementation, prone positioning, noninvasive ventilation, and protective lung strategy in patients with COPD and severe acute respiratory distress syndrome. Patients who developed asymptomatic or mild COVID-19 should be followed with the usual COPD protocols. Patients who developed moderate or worse COVID-19 should be monitored more frequently and accurately than the usual patients with COPD, with particular attention to the need for oxygen therapy.

Global Initiative for the Diagnosis, Management, and Prevention of Chronic Obstructive Lung Disease. The 2020 GOLD Science Committee Report on COVID-19 and Chronic Obstructive Pulmonary Disease

Handbook of Psychiatric Measures

The early stages of the COVID-19 pandemic have focused on containing SARS-CoV-2 infection and identifying treatment strategies. While controlling this communicable disease is of utmost importance, the long-term effect on individuals with non-communicable diseases (NCD) is significant. Although certain NCDs appear to increase the severity of COVID-19 and mortality risk, SARS-CoV-2 infection in survivors with NCDs may also affect the progression of their pre-existing clinical conditions. Infection containment measures will have substantial short- and long-term consequences; social distancing and quarantine restrictions will reduce physical activity and increase other unhealthy lifestyles, thus increasing NCD risk factors and worsening clinical symptoms. Vitamin D levels might decrease and there might be a rise in mental health disorders. Many countries have made changes to routine management of NCD patients, e.g., cancelling non-urgent outpatient visits, which will have important implications for NCD management, diagnosis of new-onset NCDs, medication adherence, and NCD progression. We may have opportunities to learn from this unprecedented crisis on how to leverage healthcare technologies and improve procedures to optimize healthcare service provision. This article discusses how the COVID-19 outbreak and related infection control measures could hit the most frail individuals, worsening the condition of NCD patients, while further jeopardizing the sustainability of the healthcare systems. We suggest ways to define an integrated strategy that could involve both public institutional entities and the private sector to safeguard frail individuals and mitigate the impact of the outbreak.

/pdf/the-potential-long-term-impact-of-the-covid-19-outbreak-on-35jgzuvyyo.pdf

The potential long-term impact of the COVID-19 outbreak on patients with non-communicable diseases in Europe: consequences for healthy ageing.

This review provides a brief summary of what is known about the anxiolytic mechanism of action of pregabalin, a highly selective, high-affinity ligand of the P/Q type of voltage-gated calcium channel (CaV). Evidence from in vivo models of neuronal hyperexcitability suggests that pregabalin reduces synaptic release of neurotransmitters in selected CNS regions including the cortex, olfactory bulb, hypothalamus, amygdala, hippocampus, cerebellum and dorsal horn of the spinal cord. Release of neurotransmitters from the synaptic vesicle, and propagation of neurotransmission, requires the vesicle to fuse with the presynaptic membrane. Pregabalin binding to the α2δ type 1 protein of the P/Q type CaV reduces the availability of Ca2+ required for membrane fusion and exocytosis of neurotransmitters. Evidence that the anxiolytic mechanism of action of pregabalin is mediated by binding to the α2δ type 1 protein comes from animal models, which have demonstrated a structure-activity relationship between the affinity of ligands for the α2δ type 1 protein and their potency in models of anxiety such as the Vogel conflict test. Furthermore, the anxiolytic activity of pregabalin is lost in transgenic mice with specific point mutations in the CaV α2δ type 1 protein. Pregabalin-mediated reduction in calcium currents has also been shown to result in a significant inhibition of the release of neurotransmitters implicated in pa-thological anxiety such as glutamate and monoamine neurotransmitters. However, further research is needed to confirm that these effects contribute to the anxiolytic mechanism of action of pregabalin. Finally, pregabalin may also act by inhibiting synaptogenesis of excitatory neurons formed in response to chronic stress or anxiety, or more acutely inhibit the trafficking of CaV to the plasma membrane.

Elucidating the mechanism of action of pregabalin: α(2)δ as a therapeutic target in anxiety.

Sleep disturbance is a cardinal symptom in both DSM-IV and ICD-10 criteria for generalized anxiety disorder (GAD). This review summarizes the results of clinical trials and pooled analyses that provide data on pregabalin's effect on sleep disturbance in patients diagnosed with GAD. The hypothesized mechanism of action of pregabalin is distinctly different from other anxiolytics. Pregabalin binds to a membrane α2δ subunit protein to inhibit release in excited central nervous system neurons of neurotransmitters implicated in pathological anxiety. Treatment with pregabalin has been found to be associated with significant improvement in GAD-related sleep disturbance across seven placebo-controlled clinical trials. Treatment with pregabalin is associated with improvement in all forms of insomnia and improvement in sleep has been found to be correlated with reduction in functional impairment and improvement in quality of life on subjective global measures. Results of a mediational analysis suggest that 53% of the effect of pregabalin on sleep disturbance was due to a direct effect and 47% was due to an indirect effect, mediated through prior reduction in anxiety symptom severity. In patients with GAD, improvement in sleep has been found to be associated with a reduction in daytime sleepiness. However, dose-related sedation is reported, typically in the first 2 wk of treatment, in approximately 10-30% of patients, depending on the dose used and the speed of titration. Insomnia is a common component of the clinical presentation of GAD and pregabalin appears to be an efficacious treatment for this often chronic and disabling symptom.

Effects of pregabalin on sleep in generalized anxiety disorder

Discontinuation effects following cessation of 12 and 24 wk of pregabalin treatment for generalized anxiety disorder (GAD) were evaluated in a placebo- and lorazepam-controlled, randomized, double-blind, multicentre trial conducted in 16 countries. The study design consisted of two 12-wk treatment periods (periods 1 and 2), each followed by a 1-wk taper and two post-discontinuation assessments, one immediately following the taper and one 1-wk post-taper. Patients were assigned to receive an initially flexible dose of pregabalin 450–600 mg/d, pregabalin 150–300 mg/d, or lorazepam 3–4 mg/d for 6 wk; responders continued fixed-dose therapy for 6 additional weeks. Patients entering period 2 continued on the same fixed dose or switched to placebo. Discontinuation effects were evaluated with the Physician Withdrawal Checklist (PWC) and reported discontinuation-emergent signs and symptoms. Rebound anxiety was measured with the Hamilton Anxiety Rating Scale. GAD symptoms improved with all treatments and improvements were maintained over 12 and 24 wk. Low levels of discontinuation symptoms were evident in all treatment groups. For patients who received active treatment during both periods, mean (95% confidence interval) increases on the PWC from last visit on active treatment to the second post-discontinuation assessment were: pregabalin 450–600 mg/d: 2.8 (1.6–3.9), pregabalin 150–300 mg/d: 1.7 (0.7–2.8), lorazepam 3–4 mg/d: 2.2 (1.0–3.5). Rates of rebound anxiety were also low at both 12 and 24 wk (0–6%). This suggests that risk of discontinuation symptoms and rebound anxiety are low for pregabalin after 12 and 24 wk of treatment.

Pregabalin long-term treatment and assessment of discontinuation in patients with generalized anxiety disorder.

Objective:This review aims to summarize meta-analyses and other relevant data relating to the efficacy and safety of the various treatment options for generalized anxiety disorder (GAD) in Europe. In addition, it will provide an overview of the prevalence, burden, and recognition of the disorder, with a view to raise awareness of GAD and inform primary care practitioners.Research design and methods:Relevant research or review articles on psychological or pharmacological treatments for GAD published in the English language between March 2006 and March 2012 were identified via a literature search in PubMed and ISI Web of Knowledge and from the Cochrane Library. Other relevant references/clinical guidelines were individually selected by the authors.Results:Prevalence rates of GAD vary across Europe but its economic and social burden is increasing. A large proportion of patients with GAD present with symptoms in primary care. However, due to the disorder’s complexity and the incidence of comorbid dise...

Rita Prieto

Papers

The potential long-term impact of the COVID-19 outbreak on patients with non-communicable diseases in Europe: consequences for healthy ageing.

Elucidating the mechanism of action of pregabalin: α(2)δ as a therapeutic target in anxiety.

Effects of pregabalin on sleep in generalized anxiety disorder

Pregabalin long-term treatment and assessment of discontinuation in patients with generalized anxiety disorder.

Comprehensive review of generalized anxiety disorder in primary care in Europe.