Human cytomegalovirus (HCMV) infection is common and affects between 40–100% of the worldwide population. However, the majority of cases are asymptomatic and when severe disease occurs, it is usually restricted to immunocompromised patients. Liver involvement by HCMV differs significantly, accordingly to the immune status of the host. In immunocompromised patients, particularly liver transplant patients, it often causes clinically significant hepatitis. On the other hand, in immunocompetent patients, HCMV hepatitis requiring hospitalization is extremely rare. This review aims to appraise studies regarding the pathophysiology of HCMV hepatitis, including mechanisms of latency and reactivation and its contribution to disease development, clinical presentation, diagnostic modalities and treatment, with a focus on comparing different aspects between immunocompromised and immunocompetent hosts.
Immune checkpoint inhibitors (ICIs) suppress the function of immune checkpoints, which are involved in downregulating immune responses. These lead to an increased activation of the function of T cells, increased release of cytokines, and decreased activity of regulatory T cells. This allows for a more significant and less regulated immune response and subsequent enhanced cytotoxic activity against cancer cells. A number of cancers are now being treated with these agents and this increased use has resulted in more reports of toxicity. While almost every organ can be affected, the skin, gastrointestinal tract, liver, and endocrine glands are most commonly involved. It is necessary that gastroenterologists and hepatologists familiarize themselves with diagnostic steps and management plan in patients with these undesirable outcomes. When assessing for possible ICIs induced hepatotoxicity, it is of utmost importance to use a formal scoring system such as the Roussel Uclaf causality assessment method (RUCAM) to assess for risk factors, alternative causes, and response to cessation and re-exposure of a given drug. While this review is based on studies with and without RUCAM, the conclusions were carefully established mainly from studies that used RUCAM. The aim of this review is to provide information on the epidemiology, risk factors, clinical presentation, diagnostic tools, and management plan based on the most recent studies of immunotherapy-induced hepatotoxicity.
Primary sclerosing cholangitis is a disease affecting around 0.006–0.016% of the population. Of these, around 75% have concomitant inflammatory bowel disease (IBD) according to the most recent epidemiological studies. Several theories have been proposed regarding the pathogenesis of primary sclerosing cholangitis (PSC). These include changes in the function of cholangiocytes, effects of the gut microbiome, association with specific human leukocyte antigen haplotypes and dysregulation of the immune system. However, these do not explain the observed association with IBD. Moreover, there are considerable differences in the frequency and outcomes between patients with PSC and ulcerative colitis compared with PSC and Crohn’s disease. The aim of this review is to appraise the most recent studies that have contributed to the epidemiology, advances in the pathophysiology, and characterization of important clinical aspects of the association of PSC and IBD.
Human infection by Non-Helicobacter pylori-Helicobacter is rare and most commonly transmitted through direct contact with animals. The clinical presentation in most cases is chronic epigastric abdominal pain and it usually leads to chronic gastritis. We present an uncommon case of a patient with acute onset abdominal pain secondary to acute peptic ulcer disease caused by Helicobacter heilmannii who underwent successful treatment. We also conducted a review of the literature to understand the epidemiology, etiology, clinical presentation, and the best diagnostic and treatment modalities for Non-H. pylori-Helicobacter infections.
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