Publications

Background

A common belief is that one quarter to one third of all diabetes cases remain undiagnosed. However, such prevalence estimates may be overstated by epidemiologic studies that do not use confirmatory testing, as recommended by clinical diagnostic criteria.

Objective

To provide national estimates of undiagnosed diabetes by using a confirmatory testing strategy, in line with clinical practice guidelines.

Design

Cross-sectional study.

Setting

National Health and Nutrition Examination Survey results from 1988 to 1994 and 1999 to 2014.

Participants

U.S. adults aged 20 years and older.

Measurements

Confirmed undiagnosed diabetes was defined as elevated levels of fasting glucose (≥7.0 mmol/L [≥126 mg/dL]) and hemoglobin A1c (≥6.5%) in persons without diagnosed diabetes.

Results

The prevalence of total (diagnosed plus confirmed undiagnosed) diabetes increased from 5.5% (9.7 million adults) in 1988 to 1994 to 10.8% (25.5 million adults) in 2011 to 2014. Confirmed undiagnosed diabetes increased during the past 2 decades (from 0.89% in 1988 to 1994 to 1.2% in 2011 to 2014) but has decreased over time as a proportion of total diabetes cases. In 1988 to 1994, the percentage of total diabetes cases that were undiagnosed was 16.3%; by 2011 to 2014, this estimate had decreased to 10.9%. Undiagnosed diabetes was more common in overweight or obese adults, older adults, racial/ethnic minorities (including Asian Americans), and persons lacking health insurance or access to health care.

Limitation

Cross-sectional design.

Conclusion

Establishing the burden of undiagnosed diabetes is critical to monitoring public health efforts related to screening and diagnosis. When a confirmatory definition is used, undiagnosed diabetes is a relatively small fraction of the total diabetes population; most U.S. adults with diabetes (about 90%) have received a diagnosis of the condition.

Primary Funding Source

National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases and National Heart, Lung, and Blood Institute.

More efficacious treatment regimens are needed for tuberculosis, however, drug development is impeded by a lack of reliable biomarkers of disease severity and of treatment effect. We conducted a directed screen of host biomarkers in participants enrolled in a tuberculosis clinical trial to address this need. Serum samples from 319 protocol-correct, culture-confirmed pulmonary tuberculosis patients treated under direct observation as part of an international, phase 2 trial were screened for 70 markers of infection, inflammation, and metabolism. Biomarker assays were specifically developed for this study and quantified using a novel, multiplexed electrochemiluminescence assay. We evaluated the association of biomarkers with baseline characteristics, as well as with detailed microbiologic data, using Bonferroni-adjusted, linear regression models. Across numerous analyses, seven proteins, SAA1, PCT, IL-1β, IL-6, CRP, PTX-3 and MMP-8, showed recurring strong associations with markers of baseline disease severity, smear grade and cavitation; were strongly modulated by tuberculosis treatment; and had responses that were greater for patients who culture-converted at 8weeks. With treatment, all proteins decreased, except for osteocalcin, MCP-1 and MCP-4, which significantly increased. Several previously reported putative tuberculosis-associated biomarkers (HOMX1, neopterin, and cathelicidin) were not significantly associated with treatment response. In conclusion, across a geographically diverse and large population of tuberculosis patients enrolled in a clinical trial, several previously reported putative biomarkers were not significantly associated with treatment response, however, seven proteins had recurring strong associations with baseline radiographic and microbiologic measures of disease severity, as well as with early treatment response, deserving additional study.