Published online Dec 28, 2016. doi: 10.4254/wjh.v8.i36.1623
Peer-review started: July 3, 2016
First decision: August 5, 2016
Revised: September 16, 2016
Accepted: November 1, 2016
Article in press: November 2, 2016
Published online: December 28, 2016
To identify significant liver disease [including nodular regenerative hyperplasia (NRH)] in asymptomatic Didanosine (DDI) exposed human immunodeficiency virus (HIV) positive patients.
Patients without known liver disease and with > 6 mo previous DDI use had liver stiffness assessed by transient elastography (TE). Those with alanine transaminase (ALT) above upper limit normal and/or TE > 7.65 kPa underwent ultrasound scan (U/S). Patients with: (1) abnormal U/S; or (2) elevated ALT plus TE > 7.65 kPa; or (3) TE > 9.4 kPa were offered trans-jugular liver biopsy (TJLB) with hepatic venous pressure gradient (HVPG) assessment.
Ninety-nine patients were recruited, median age 50 years (range 31-70), 81% male and 70% men who have sex with men. Ninety-five percent with VL < 50 copies on antiretroviral therapy with median CD4 count 639 IU/L. Median DDI exposure was 3.4 years (range 0.5-14.6). Eighty-one had a valid TE readings (interquartile range/score ratio < 0.3): 71 (88%) < 7.65 kPa, 6 (7%) 7.65-9.4 kPa and 4 (6%) > 9.4 kPa. Seventeen (17%) met criteria for TJLB, of whom 12 accepted. All had HVPG < 6 mmHg. Commonest histological findings were steatosis (n = 6), normal architecture (n = 4) and NRH (n = 2), giving a prevalence of previously undiagnosed NRH of 2% (95%CI: 0.55%, 7.0%).
A screening strategy based on TE, liver enzymes and U/S scan found a low prevalence of previously undiagnosed NRH in DDI exposed, asymptomatic HIV positive patients. Patients were more likely to have steatosis highlighting the increased risk of multifactorial liver disease in this population.
Core tip: Human immunodeficiency virus positive patients are at increased risk of liver disease. The aetiology is often multifactorial and includes exposure to antiretroviral therapy. We used a simple screening strategy based on transient elastography, liver enzymes and ultrasound scan to identify that 2% of asymptomatic patients exposed to Didanosine in a clinical cohort had undiagnosed nodular regenerative hyperplasia. A further 6% had undiagnosed steatosis. Implementation of a screening strategy enables identification of liver disease and initiation of earlier targeted interventions in this high-risk group.