METHODS: We estimated mortality using natural history models for acute hepatitis infections and GBD's cause-of-death ensemble model for cirrhosis and liver cancer. We used meta-regression to estimate total cirrhosis and total liver cancer prevalence, as well as the proportion of cirrhosis and liver cancer attributable to each cause. We then estimated cause-specific prevalence as the product of the total prevalence and the proportion attributable to a specific cause. Disability-adjusted life-years (DALYs) were calculated as the sum of years of life lost (YLLs) and years lived with disability (YLDs).
FINDINGS: Between 1990 and 2013, global viral hepatitis deaths increased from 0·89 million (95% uncertainty interval [UI] 0·86-0·94) to 1·45 million (1·38-1·54); YLLs from 31·0 million (29·6-32·6) to 41·6 million (39·1-44·7); YLDs from 0·65 million (0·45-0·89) to 0·87 million (0·61-1·18); and DALYs from 31·7 million (30·2-33·3) to 42·5 million (39·9-45·6). In 2013, viral hepatitis was the seventh (95% UI seventh to eighth) leading cause of death worldwide, compared with tenth (tenth to 12th) in 1990.
INTERPRETATION: Viral hepatitis is a leading cause of death and disability worldwide. Unlike most communicable diseases, the absolute burden and relative rank of viral hepatitis increased between 1990 and 2013. The enormous health loss attributable to viral hepatitis, and the availability of effective vaccines and treatments, suggests an important opportunity to improve public health.
FUNDING: Bill & Melinda Gates Foundation.
METHODS: A cross-sectional investigation was conducted at General Penang Hospital, Malaysia. Demographic criteria and laboratory tests of patients were investigated. Controlled glycemia (CG) was recognized as glycated hemoglobin (HbA1c) ≤7% depending on American Diabetes Association guidelines 2018. Charlson Comorbidity Index (CCI) was used to estimate the confounding influence of co-morbidities and predict ES-10Y. Data was managed by IBM-SPSS 23.0.
RESULTS: A total of 400 cases categorized to (44.25%) patients with CG, and (55.75%) cases had uncontrolled glycemia (UCG). HbA1c mean in CG and UCG group was (6.8 ± 0.9 vs 9.5 ± 1.6, P-value: 0.001). Fasting blood glucose was (7 ± 2.3 vs. 9.9 ± 4.3, P-value: 0.001) in CG and UCG group. CCI was (3.38 ± 2.38 vs. 4.42 ± 2.70, P-value: 0.001) and, ES-10Y was (62% vs 46.2%, p-value: 0.001) in CG vs. UCG respectively. Spearman test indicates a negative correlation between CG and CCI (r: 0.19, p-value: 0.001). Logistic regression confirmed HbA1c as a significant predictor of CCI (r2: 0.036, P-value: 0.001). CG has a positive correlation with survival (r: 0.16, P-value: 0.001) and logistic regression of survival (r2: 0.26, P-value: 0.001).
CONCLUSIONS: More than one-half of the investigated persons had UCG. Controlled HbA1c was associated with lower co-morbidities and higher ES-10Y.