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.

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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.

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.