Improving Depression Screening in Underserved Populations in a Large Urban Academic Primary Care Center: A Provider-Centered Analysis and Approach.

Screening for depression is paramount to identify patients with depression and link them to care, yet only 29% of patients in the primary care center (PCC) were screened for depression in 2016. A baseline survey identified provider barriers to depression screening, including lack of time, support staff, and referral resources. The purpose of this project was to increase depression screening in the PCC using the Patient Health Questionnaire (PHQ-2/9). The authors created an educational program for staff and providers that included referral resources, treatment guidelines, and a decision-support tool in the electronic medical record. A retrospective chart review was performed, from January 2016 to June 2017, to determine the percentage of patients who received annual depression screening. During the program, the PCC saw an increase in depression screening rates. Thus, it is possible to overcome barriers to depression screening in a primary care setting by providing resources and education to clinicians.

Chronic medical conditions based obesity phenotypes: A two-step cluster analysis of a representative sample of obese American adults.

BACKGROUND AND OBJECTIVE: Although obesity is a heterogeneous disease, little is known regarding chronic medical conditions (CMCs) that defines variability in obese populations. The characterization of obese populations using CMCs rather than categorization using BMI alone can advance understanding of obesity. The aims of this study are to phenotype obesity in a large representative sample of non-Hispanic White (NHW), non-Hispanic Black (NHB) and Mexican American (MA) obese adults using CMCs, and assess relationship between resulting phenotypes and self-rated health (SRH). METHODS: Sex-specific two-step cluster analysis was used to phenotype obese participants (n = 12,547) to CMC-based clusters. The prevalence of CMCs and lifestyle risk factors in each cluster was assessed. Sex and race/ethnic specific association between cluster membership and SRH was determined using odds ratio (OR) from logistic regression analysis. RESULTS: Distinct subgroups of obese men and women were observed: moderate dyslipidemic healthy young obese men, hypertensive-dyslipidemic middle-age obese men, hypertensive young obese men, hypertensive-dyslipidemic-asthmatic middle-age obese men, and syndemic elderly obese men, healthy young obese women, hypertensive-dyslipidemic middle-age obese women, dyslipidemic young adult obese women, syndemic middle-age obese women, and syndemic elderly obese women. Participants in the more CMCs symptomatic clusters reported high rates of behavioral risk factors and showed significantly greater odds of poor SRH than participants in the less symptomatic clusters. Compared to obese persons who are asymptomatic for CMCs, syndemic elderly obese and women men had much higher increased ORs for poor SRH with values of 3.88 [95% CI = 2.41-6.26], 3.96 [95% CI = 1.86-8.30] and 7.25 [95% CI = 2.41-9.6] for NHW, NHB and MA men, respectively. The corresponding ORs for women are 4.08 [95% CI = 2.71-6.14], 4.01 [95% CI = 2.40-6.69], and 2.62 [95% CI = 1.32-5.19], respectively. CONCLUSION: Obesity treatment and intervention should consider heterogeneity within obese persons and pay greater attention to obesity related co-morbidities and metabolic manifestations.

Diffuse Idiopathic Pulmonary Neuroendocrine Cell Hyperplasia (DIPNECH) with liver metastases.

Diffuse Idiopathic Pulmonary Neuroendocrine Cell Hyperplasia (DIPNECH) is a rare pulmonary disorder characterised by classic radiological findings and symptoms of obstructive lung disease. DIPNECH is considered a precursor to carcinoid tumours in the lungs. In this case, we describe a patient with years of unexplained dry cough presenting with 2 weeks of progressive nausea and vomiting, and found to have massive hepatomegaly on examination. By CT-PE, she was diagnosed with DIPNECH, and abdominal MRI revealed metastatic carcinoid tumours. Despite its non-specific presentation, DIPNECH has characteristic radiological findings of mosaic attenuation with numerous pulmonary nodules. DIPNECH requires early identification and close surveillance to prevent progression to carcinoid tumours. Thus, it is critical for frontline providers to consider this diagnosis as part of their differential when other common causes of obstructive lung disease have been ruled out.

Nocardia-induced granulocyte macrophage colony-stimulating factor is neutralized by autoantibodies in disseminated/extrapulmonary nocardiosis.

BACKGROUND: Nocardia species cause infections in both immunocompromised and otherwise immunocompetent patients, although the mechanisms defining susceptibility in the latter group are elusive. Anticytokine autoantibodies are an emerging cause of pathogen-specific susceptibility in previously healthy human immunodeficiency virus-uninfected adults, including anti-granulocyte macrophage colony-stimulating factor (GM-CSF) autoantibodies with cryptococcal meningitis. METHODS: Plasma from patients with disseminated/extrapulmonary nocardiosis and healthy controls was screened for anticytokine autoantibodies using a particle-based approach. Autoantibody function was assessed by intranuclear staining for GM-CSF-induced STAT5 phosphorylation in normal cells incubated with either patient or normal plasma. GM-CSF-mediated cellular activation by Nocardia was assessed by staining for intracellular cytokine production and intranuclear STAT5 phosphorylation. RESULTS: We identified neutralizing anti-GM-CSF autoantibodies in 5 of 7 patients studied with central nervous system nocardiosis and in no healthy controls (n = 14). GM-CSF production was induced by Nocardia in vitro, suggesting a causative role for anti-GM-CSF autoantibodies in Nocardia susceptibility and dissemination. CONCLUSIONS: In previously healthy adults with otherwise unexplained disseminated/extrapulmonary Nocardia infections, anti-GM-CSF autoantibodies should be considered. Their presence may suggest that these patients may be at risk for later development of pulmonary alveolar proteinosis or other opportunistic infections, and that patients may benefit from therapeutic GM-CSF administration.

Melatonin increases survival and inhibits oxidative and amyloid pathology in a transgenic model of Alzheimer's disease.

Increased levels of a 40-42 amino-acid peptide called the amyloid beta protein (A beta) and evidence of oxidative damage are early neuropathological markers of Alzheimer's disease (AD). Previous investigations have demonstrated that melatonin is decreased during the aging process and that patients with AD have more profound reductions of this hormone. It has also been recently shown that melatonin protects neuronal cells from A beta-mediated oxidative damage and inhibits the formation of amyloid fibrils in vitro. However, a direct relationship between melatonin and the biochemical pathology of AD had not been demonstrated. We used a transgenic mouse model of Alzheimer's amyloidosis and monitored over time the effects of administering melatonin on brain levels of A beta, abnormal protein nitration, and survival of the mice. We report here that administration of melatonin partially inhibited the expected time-dependent elevation of beta-amyloid, reduced abnormal nitration of proteins, and increased survival in the treated transgenic mice. These findings may bear relevance to the pathogenesis and therapy of AD.