Background: Hepatitis C virus (HCV) infection is the global epidemic of this century, affecting almost 100 million people, and it is now the leading cause of liver-related mortality and liver transplantation. Interferon (IFN)-α was introduced as the first treatment for chronic hepatitis C but had several limitations, including factors that cause unresponsiveness to therapy, such as viral and host factors. The availability of non-interferon antiviral agents, direct-acting antivirals (DAAs), has led to a major paradigm shift in the treatment of HCV infection. This therapy has been shown to achieve higher cure rates and minimal side effect profiles in clinical trials. This study is aimed to determine the correlation between host factors, such as age, gender, and body mass index (BMI) with virological response to DAA treatment in hepatitis C patients. Result: Observational research with a retrospective cohort approach was conducted at Wahidin Sudirohusodo Hospital, Makassar, Indonesia, from April 2021 to October 2021. The virological response was assessed using HCV-RNA quantitative and sustained virological response (SVR) 12 weeks after therapy. The research was conducted on 86 subjects consisting of 57 men and 29 women with a mean age of 48.69±13.94 years and mean BMI of 23.17±3.71 kg/m², with SVR12 up to 90.7%. Study analysis did not find a significant correlation between age, gender, and BMI, with virological response SVR12 of chronic hepatitis C patients with direct-acting antiviral (p>0.05). Conclusion: Age, gender, and body mass index do not influence the success of DAA therapy.

Peutz-Jeghers syndrome (PJS) is a rare autosomal dominant disorder characterised by mucocutaneous pigmentation, gastrointestinal polyps and an increased risk of gastrointestinal and other cancers. We report an Indonesian woman, aged 28, with black spots on her lips who had multiple polyps extending from the stomach to the rectum. Her father and a son also had mucocutaneous lesions but they did not undergo gastrointestinal investigations. All three had mutations in the serine/threonine kinase 11 gene (STK11).