Table 1.
Descriptive statistics for the study cohort
| Variables | N=2733 (%) |
|---|---|
| Age in years | |
| < 55 | 644 (23.6) |
| 55–64 | 1148 (42.0) |
| 65+ | 941 (34.4) |
| Sex | |
| Female | 856 (31.3) |
| Male | 1877 (68.7) |
| Race/ethnicity | |
| Non-Hispanic (NH) white | 1373 (50.2) |
| NH-Black | 533 (19.5) |
| Hispanic | 748 (27.4) |
| Other | 79 (2.9) |
| Etiology of liver disease 1 | |
| Active hepatitis C virus (HCV)2 | 521 (19.0) |
| Cured HCV2 | 638 (23.3) |
| Alcoholic liver disease | 439 (16.1) |
| Nonalcoholic fatty liver disease | 822 (30.1) |
| Hepatitis B virus infection3 | 67 (2.4) |
| Autoimmune hepatitis | 117 (4.3) |
| 0Primary biliary cirrhosis | 75 (2.7) |
| Primary sclerosing cholangitis | 22 (0.8) |
| Other etiologies4 | 81 (2.9) |
| Missing | 10 (0.36 |
| Alcohol use | |
| Never | 873 (31.9) |
| Current heavy | 183 (6.7) |
| Current but not heavy | 191 (7.0) |
| Past Heavy | 903 (33.0) |
| Past Not Heavy | 583 (21.4) |
| Smoking | |
| Never | 1087 (39.8) |
| Current | 616 (22.5) |
| Past | 1030 (37.7) |
| Diabetes | |
| No | 1555 (56.9) |
| Yes | 1178 (43.1) |
| Body mass index (kg/m 2 ) | |
| < 25 | 547 (20.0) |
| 25–29 | 864 (31.6) |
| 30–34 | 725 (26.5) |
| 35+ | 597 (21.9) |
| Hypertension | |
| No | 1305 (47.8) |
| Yes | 1428 (52.2) |
| Dyslipidemia | |
| No | 1800 (65.9) |
| Yes | 933 (34.1) |
| Child Pugh Class | |
| A | 1738 (63.6) |
| B | 685 (25.1) |
| C | 119 (4.4) |
| Missing | 191 (6.9) |
Some patients had more than one etiological risk factor. Where possible, we relied on the primary etiology assigned by the treating clinician. Specifically, patients with HCV and excessive alcohol use were classified as patients with HCV. Alcohol related cirrhosis was classified as the underlying risk factor when alcohol was defined as the only risk factors. Nonalcoholic fatty liver disease was defined as the etiology in patients without HCV (active/untreated or resolved HCV), HBV, alcohol, or other etiological risk factors. There could be overlap in etiology in patients with autoimmune hepatitis, primary biliary cholangitis and primary sclerosing cholangitis.
HCV status was defined based on data at the time of cohort enrollment. In total, 908 patients achieved sustained virological response during follow up.
Of the 67 patients with HBV, 24 patients were co-infected with HCV and 11 had co-existing alcohol related liver disease. Only, 32 patients had HBV infection without other risk factors.
Includes patients with hemochromatosis, Wilson’s disease, alpha 1 anti-trypsin deficiency, cryptogenic cirrhosis