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Published on: April 28, 2020
Association Between Khat (Catha edulis) Consumption and Hepatocellular Enzyme Elevation: A Hospital-Based
Ahmed Ibrahim Farah1,2,3, Jama Mohamed4, Nega Berhe5
1College of Medicine and Health Sciences, University of Hargeisa, Hargeisa, Somaliland.
Background:
Khat (Catha edulis) is a widely consumed stimulant in East Africa, but its role in hepatocellular alterations remains debated.
Objectives:
This study evaluated the association between khat consumption patterns and subclinical liver injury in Somaliland.
Design:
A hospital-based case-control study.
Methods:
The study was conducted at Hargeisa Group Hospital (N = 260). Biochemical markers were compared among current, past, and non-chewing controls. Because khat use was absent among females, multivariable logistic regression was restricted to males (n = 188). Serum AST, ALT, and bilirubin were analyzed using the Kruskal-Wallis H test and bootstrap BCa 95% confidence intervals.
Results:
Current khat chewers exhibited significantly higher median AST (76.50 vs. 39.50 U/L), ALT (75.00 vs. 42.50 U/L), and total bilirubin (1.45 vs. 0.30 mg/dL) levels than non-chewers (all p < 0.001). Biochemical markers in past chewers did not differ significantly from controls (p > 0.05). Total bilirubin >3 mg/dL was observed across all groups but was more prevalent among current chewers (37.3%) than non-chewers (30.9%) and past chewers (6.3%) (p = 0.003). ALT >3× ULN was more frequent among current chewers (p = 0.020), whereas AST >3× ULN did not differ significantly (p = 0.256). Current khat chewing independently predicted hepatocellular injury (AOR = 3.73; 95% CI: 1.40-9.95; p = 0.009). A dose-response pattern was observed, with consumption ≥250 g/session (AOR = 2.45; p = 0.038) and duration >10 years (AOR = 5.08; p = 0.001) associated with increased odds of injury.
Conclusion:
Active khat consumption among males was associated with dose-dependent subclinical hepatocellular injury. The absence of abnormalities in past chewers may suggest stabilization after cessation. Given the observational design, these findings should be interpreted as associations rather than evidence of causality and warrant prospective studies with comprehensive hepatobiliary assessment.
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