Exploring Liver Damage in Hepatitis C Patients: A Case Study on Medication-Induced Injury

I appreciate the information you provided in your initial discussion regarding the pathophysiology of hepatitis C, and the effects of medications on the liver. I feel that exports tend to pay less attention to the side effects of medications on the liver among patients with hepatitis C. This issue may lead to negative patient outcomes, further health complications, and even death sometimes.

According to Andrade et al. (2019), Liver induced injury is a concern in most healthcare settings but is normally overlooked even though it might progress to a chronic illness that may eventually lead to hepatic failure. Once the situation progresses to hepatic failure, it will need a liver transplant to resolve, and the chances of death are also high.

Andrade et al. (2019) state that the medications may lead to either intrinsic or idiosyncratic reactions that lead to liver damage. These reactions can occur together in some cases. Liver injury due to intrinsic reactions is dose-dependent and predictable. Liver damage due to idiosyncratic reactions, on the other hand, is not dose-dependent and unpredictable.

They are divided into subtypes such as immuno-allergic and metabolic idiosyncratic reactions. Overall, Higher daily doses that go above 50mg/day are highly correlated with detrimental hepatic events such as liver transplant, liver failure, and death (Andrade et al., 2019). However, there is no correlation with lower does.

Experts believe that drug doses also play some role in idiosyncratic liver damage. Liver damage may escalate further by transmitting inflammatory signals and hepatic injury to neighboring cells via other gap junctions (Andrade et al., 2019).  The incidences of drug-related liver damage are quite high. Andrade et al. (2019 state that the estimated annual incidence is between 10 and 15 per 10,000 to 100,000 persons. However, the actual numbers might be higher since diagnosis is normally not easy.

I also feel that you did well explaining the pathophysiology aspect of hepatitis C. To add, the hepatitis C virus is a spherical, enveloped, positive strand of RNA virus. This pathogen encodes a polyprotein, which in turn, can be processed into at least 10 types of proteins (the nucleocapsid protein, the structural protein, the core, and others) (Basit et al., 2022).

It also encodes for two proteins (NS2 and p7) which are responsible for the production of vision. The viral RNA enters the hepatocyte through endocytosis. Its positive-stranded RNA is then translated into ten mature peptides. Both viral and host proteases cleave the peptides, which then form a replication complex in the endoplasmic reticulum (Basit et al., 2022).

The hepatitis C virus (HCV) can be detected in the plasma between 1 and 4 weeks of exposure. Viremia reaches its peak between 8 and 12 weeks of infection. The pathophysiology of the hepatitis C virus is a bit complex. The initial symptoms of the disease tend to be non-specific including malaise, fatigue, joint pain, and others (Basit et al., 2022). Later the disease may present symptoms of end liver disease such as cyanosis, palmar erythema, gynecomastia, and others.

Reference

Andrade, R. J., Chalasani, N., Björnsson, E. S., Suzuki, A., Kullak-Ublick, G. A., Watkins, P. B., & Aithal, G. P. (2019). Drug-induced liver injury. Nature Reviews Disease Primers5(1), 1-22. https://doi.org/10.12701/yujm.2019.00297

Basit, H., Tyagi, I., & Koirala, J. (2022). Hepatitis C. StatPearls [Internet]. https://www.ncbi.nlm.nih.gov/books/NBK430897/

NEXT

 

Order this paper