IMPORTANCE Medical students are at high risk for depression and suicidal ideation. However, the prevalence estimates of these disorders vary between studies.OBJECTIVE To estimate the prevalence of depression, depressive symptoms, and suicidal ideation in medical students.DATA SOURCES AND STUDY SELECTION Systematic search of EMBASE, ERIC, MEDLINE, psycARTICLES, and psycINFO without language restriction for studies on the prevalence of depression, depressive symptoms, or suicidal ideation in medical students published before September 17, 2016. Studies that were published in the peer-reviewed literature and used validated assessment methods were included.DATA EXTRACTION AND SYNTHESIS Information on study characteristics; prevalence of depression or depressive symptoms and suicidal ideation; and whether students who screened positive for depression sought treatment was extracted independently by 3 investigators. Estimates were pooled using random-effects meta-analysis. Differences by study-level characteristics were estimated using stratified meta-analysis and meta-regression. MAIN OUTCOMES AND MEASURESPoint or period prevalence of depression, depressive symptoms, or suicidal ideation as assessed by validated questionnaire or structured interview.RESULTS Depression or depressive symptom prevalence data were extracted from 167 cross-sectional studies (n = 116 628) and 16 longitudinal studies (n = 5728) from 43 countries. All but 1 study used self-report instruments. The overall pooled crude prevalence of depression or depressive symptoms was 27.2% (37 933/122 356 individuals; 95% CI, 24.7% to 29.9%, I 2 = 98.9%). Summary prevalence estimates ranged across assessment modalities from 9.3% to 55.9%. Depressive symptom prevalence remained relatively constant over the period studied (baseline survey year range of 1982-2015; slope, 0.2% increase per year [95% CI, −0.2% to 0.7%]). In the 9 longitudinal studies that assessed depressive symptoms before and during medical school (n = 2432), the median absolute increase in symptoms was 13.5% (range, 0.6% to 35.3%). Prevalence estimates did not significantly differ between studies of only preclinical students and studies of only clinical students (23.7% [95% CI, 19.5% to 28.5%] vs 22.4% [95% CI, 17.6% to 28.2%]; P = .72). The percentage of medical students screening positive for depression who sought psychiatric treatment was 15.7% (110/954 individuals; 95% CI, 10.2% to 23.4%, I 2 = 70.1%). Suicidal ideation prevalence data were extracted from 24 cross-sectional studies (n = 21 002) from 15 countries. All but 1 study used self-report instruments. The overall pooled crude prevalence of suicidal ideation was 11.1% (2043/21 002 individuals; 95% CI, 9.0% to 13.7%, I 2 = 95.8%). Summary prevalence estimates ranged across assessment modalities from 7.4% to 24.2%. CONCLUSIONS AND RELEVANCEIn this systematic review, the summary estimate of the prevalence of depression or depressive symptoms among medical students was 27.2% and that of suicidal ideation was 11.1%. Further research is nee...

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Objective To characterize HIV-infected patients with neuro-symptomatic CSF ‘escape,’ defined as detectable CSF HIV RNA in the setting of treatment-suppressed plasma levels or CSF RNA >1 log higher than plasma RNA. Design Retrospective case series. Setting 4 urban medical centers in the United States and Europe. Subjects Virologically controlled HIV-infected patients on antiretroviral therapy (ART) with progressive neurologic abnormalities who were determined to have CSF ‘escape.’ Intervention Optimization of ART based upon drug susceptibility and presumed CNS exposure. Main outcome measures Levels of CSF HIV RNA and inflammatory markers, clinical signs and symptoms, magnetic resonance imaging findings. Results 10 patients presented with new neurological abnormalities, which included sensory, motor, and cognitive manifestations. Median CSF HIV RNA was 3900 copies/mL (range 134-9056), while median plasma HIV RNA was 62 copies/mL (range <50-380). Median CD4+ T cell count was 482 cells/mm3 (range, 290-660). All patients had been controlled <500 copies/mL for median 27.5 months (range, 2-96) and 5/10 had been suppressed <50 copies/mL for median 19.5 months (range, 2-96). Patients had documentation of a stable ART regimen for median 21 months (range 9-60). All had CSF pleocytosis or elevated CSF protein; 7/8 had abnormalities on MRI; and 6/7 harbored CSF resistance mutations. Following optimization of ART, 8/9 patients improved clinically. Conclusions The development of neurologic symptoms in patients on ART with low or undetectable plasma HIV levels may be an indication of CSF ‘escape.’ This study adds to a growing body of literature regarding this rare condition in well-controlled HIV infection.

Background The biological processes associated with postacute sequelae of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (PASC) are unknown. Methods We measured soluble markers of inflammation in a SARS-CoV-2 recovery cohort at early (&lt;90 days) and late (&gt;90 days) timepoints. We defined PASC as the presence of 1 or more coronavirus disease 2019 (COVID-19)–attributed symptoms beyond 90 days. We compared fold-changes in marker values between those with and without PASC using mixed-effects models with terms for PASC and early and late recovery time periods. Results During early recovery, those who went on to develop PASC generally had higher levels of cytokine biomarkers including tumor necrosis factor–α (1.14-fold higher mean ratio [95% confidence interval {CI}, 1.01–1.28]; P = .028) and interferon-γ–induced protein 10 (1.28-fold higher mean ratio [95% CI, 1.01–1.62]; P = .038). Among those with PASC, there was a trend toward higher interleukin 6 levels during early recovery (1.29-fold higher mean ratio [95% CI, .98–1.70]; P = .07), which became more pronounced in late recovery (1.44-fold higher mean ratio [95% CI, 1.11–1.86]; P &lt; .001). These differences were more pronounced among those with a greater number of PASC symptoms. Conclusions Persistent immune activation may be associated with ongoing symptoms following COVID-19. Further characterization of these processes might identify therapeutic targets for those experiencing PASC.