Human papillomavirus (HPV) is a DNA tumour virus that is the primary cause of sexually transmitted infections (STIs). The direct connection between HPV and cervical cancer was discovered in 1980, however, many physicians and the general public are still oblivious to the association of HPV and anal cancer; most individuals find out about this relationship after a confirmed diagnosis, and therefore, it is important to raise awareness about HPV as an etiological agent in anal cancer. There is a quadrivalent vaccine available, which prevents an individual from being infected with HPV, thus anal cancer is mainly a preventable cancer when caused by HPV, and ultimately, preventing cancer is better than curing cancer, especially when there is no definite cure.This article aims to review the microbiology, pathophysiology, epidemiology, clinical presentation, diagnostic evaluation, prophylaxis and treatment options for HPV as an etiology agent in anal cancers in light of recent literature.

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Summary Coagulation studies were performed on 104 hospital inpatients with acute infectious hepatitis. Patients with clinical evidence of liver failure were studied separately from those without liver failure. A coagulation defect was found in 57 of the 78 patients without liver failure. This consisted of a prolonged prothrombin time and reduced levels of factors V, VII and X, and plasminogen. The defect was mild in most patients and was not associated with bleeding. A severe coagulation defect was found in all 26 patients with liver failure. Factors II, V, VII and X were markedly reduced. Plasminogen was reduced in all patients, and a low plasma fibrinogen concentration and thrombo‐cytopenia were found in half. One third of the patients studied showed an increase in serum fibrin/ fibrinogen degradation products. It is suggested that in some of these patients disseminated intravascular thrombosis contributed to the coagulation defect. Two patients had evidence of increased fibrinolytic activity. Bleeding occurred in 15 patients with liver failure and required treatment in 10. Fifteen patients with liver failure died. Nine patients with liver failure were treated with exchange transfusions during which a significant improvement of the prothrombin time and a slight reduction in platelet count was observed. Bleeding stopped during exchange transfusions in six of eight patients. It is possible that the improvement of the coagulation defect during exchange transfusions contributed to improved haemostasis.

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in the Western world. Ongoing research has furthered our understanding of NAFLD, the nature of progression of this disease, and its impact on morbidity and mortality. An active form of NAFLD is non-alcoholic steatohepatitis (NASH); it is the most severe subtype, without any current recommended therapies, according to the European Medicines Agency. The development of new therapies presents challenges, notably due to the slow progression of NASH and the clinically relevant endpoints.Correlating new data with effective treatment regimens is an emerging challenge, which will increase our understanding of the factors affecting the NAFLD course. This can enable more appropriate non-invasive prognostic assessments, which can focus on specifically at-risk NAFLD populations for tailored individual treatment. This review article aims to highlight the current developments in the field of NAFLD: pathogenesis, epidemiology, diagnosis, clinical features, and available treatment, including novel targets and therapies.