Gastroentrology & Hepatology

Author, shares series of cases to illustrate homoeopathic therapeutic strategies in acute viral hepatitis. The stage of disease, dominant miasm and assessment of susceptibility are some of the considerations in prescribing.

https://hpathy.com/homeopathy-papers/understanding-homoeopathic-therapeutic-strategyin-acute-viral-hepatitis/

Cholelithiasis of the main bile duct in children Résumé Introduction: La présence d'un calcul dans la voie biliaire principale peut être primitive ou provenir de la vésicule biliaire. L'objectif de cette étude est à travers une description clinique, de discuter les approches thérapeutiques de la lithiase de la voie biliaire principale du nourrisson. Cas clinique : Nourrisson de 50 jours présente à J+45 de vie une chlolestase clinique et biologique. A

Jasminum multiflorum Burm. f. (J. multiflorum) is an ornamental plant with traditional medicinal importance. This study aims to evaluate the activity of J. multiflorum isolated compounds against hepatocellular carcinoma cells infected with hepatitis C virus (HCV) in vitro. The in vitro anti-viral and anti-oncogenic-related activity were validated by anchorage-independent assay plus transwell migration/invasion and spreading assay. In addition to chromatographic isolation of the active metabolites. The flower extract demonstrated a significant antiviral potential through reducing active viral replication by more than 90%. Study results credit this to specific reduction of viral NS5A and cellular EphA2 protein levels. Molecular docking analysis proved the role of the isolated compounds especially multifloroside, jasfloroside A and jasfloroside B as possible anti HCV molecules.

Depression is a public disorder worldwide. Despite the widespread use of venlafaxine in the treatment of depression, it has been associated with the incidence of toxicities. Hence, the goal of the current investigation was to evaluate the mechanisms of venlafaxine–induced cell death in the model of the freshly isolated rat hepatocytes. Methods: Collagenase-perfused rat hepatocytes were treated with venlafaxine and other agents. Cell damage, reactive oxygen species (ROS) formation, lipid peroxidation, mitochondrial membrane potential decline, lysosomal damage, glutathione (GSH) level were analyzed. Moreover, rat liver mitochondria were isolated through differential centrifugation to assess respiratory chain functionality. Results: Our results demonstrated that venlafaxine could induce ROS formation followed by lipid peroxidation, cellular GSH content depletion, elevated GSSG level, loss of lysosmal membrane integrity, MMP collapse and finally cell death in a concentration-dependent manner. N-acetyl cysteine, taurine and quercetine significantly decreased the aforementioned venlafaxine-induced cellular events. Also, radical scavenger (butylatedhydroxytoluene and α-tocopherol), CYP2E1 inhibitor (4-methylpyrazole), lysosomotropic agents (methylamine and chloroquine), ATP generators (L-gluthamine and fructose) and mitochondrial pore sealing agents (trifluoperazine and L-carnitine) considerably reduced cytotoxicity, ROS generation and lysosomal leakage following venlafaxine treatment. Mitochondrion dysfunction was concomitant with the blockade of the electron transfer complexes II and IV of the mitochondrial respiratory system. Conclusion: Therefore, our data indicate that venlafaxine induces oxidative stress towards hepatocytes and our findings provide evidence to propose that mitochondria and lysosomes are of the primary targets in venlafaxine-mediated cell damage

In Iranian traditional medicine, it is believed that constipation treatment and using of laxative if needed during pregnancy can reduce many of the pregnancy complications. Recommendations related to pregnancy constipation in Iranian traditional medicine textbooks included: nutritional recommendations such as eating fatty soups, medicinal recommendations such as Cassia fistula and Rosa damascene, non-nutritional recommendations such as mild walking and enema, and contraindications and cautions such as avoidance of spicy, bitter and astringent foods. In conventional medicine similar to traditional medicine, first-line treatment for pregnancy constipation is diet and lifestyle modification.

Planning for a Baby:  https://youtu.be/2iwLh6XCnq8

Pregnancy with IBD: https://youtu.be/br0kciD8xJk

Motherhood with IBD: https://youtu.be/TQjt8pnMv4I


Our aim is to provide an understanding of the experience of women with inflammatory bowel disease (IBD) who have made the transition to motherhood. A total of 22 mothers with IBD were recruited from around the United Kingdom. Semi-structured interviews were conducted and analyzed using thematic analysis. The central concept—Blurred Lines—offers a novel frame for understanding the transition to motherhood with IBD through identifying parallels between having IBD and becoming, and being, a mother. Parallels clustered into three main themes: Need for Readiness, Lifestyle Changes, and Monitoring Personal and Physical Development. Hence, women with IBD are in some ways well prepared for the challenges of motherhood even though, as a group, they tend to restrict their reproductive choices. We recommend health professionals initiate conversations about reproduction early and provide a multidisciplinary approach to pregnancy and IBD in which women have confidence that their ongoing treatment will be integrated successfully with their maternity care.

In writing this book, I have tried to focus on the most important updates in medicine that have been emerging during the past decade; novel diseases, novel investigations, and newly approved medications. Needless to say, COVID-19 and its SARS-CoV-2 will be encountered in each chapter, in addition to occupying a unique position in the chapter on infectious diseases.

The other aspect that I think is very crucial to tackle is women’s health and pregnancy. Once again, such a topic has been addressed in each and every chapter. There are no separate chapters for geriatrics, clinical sciences, and pharmacology (including therapeutics and toxicology); their questions have been distributed throughout the book’s chapters. Each answer is followed by an explanation and a reference (source) and/or additional (further) reading. In this way, you can go there; skim the whole subject if you are interested to get more information.

I did my best to avoid regurgitated subjects and themes (which have been encompassed by many books, including me, during the past 20 years). Although many questions appear to be difficult and may fit part II examinations, I believe these questions (and their explanation) will strengthen your background and help you prepare well for part II. Remember, the goal is to find and fill in the gaps in your knowledge.

The methods of postgraduate teaching, training, and accreditation have evolved considerably during the past decade. The strike of the COVID-19 crisis was a huge blow to this remarkable progression yet has taught us many endless lessons. I always say, “Even the best-informed trainee cannot answer all the questions.” The purpose of this book is to self-assess. 100, 1000, or 10000 questions will never cover the entire curriculum/syllabus. Medicine is a huge ocean, and once you dive in, you have to swim to stay alive. 

In writing this book, I tried my best to guide you on how you approach part II written examinations, how to skim the data, and how to conclude your answer. The subjects I have chosen apply the rule of “the common is common”. I formulated the scenarios and their explanation in a way that, I hope, will inform you of the core feature of decision-making. It’s an art. I have tried to focus on some important updates in medicine that have been emerging during the past decade; novel diseases, novel investigations, and newly approved medications. COVID-19 (and its SARS-CoV-2) and women’s health will be encountered many times. Remember, the goal is to find and fill in the gaps in your knowledge. 

Undoubtedly, if you are well-prepared, you will pass the examination very easily. No need to panic when you hear your colleagues’ past [bad] experiences. Lack of preparation is the single most common reason for failure. Remember, practice makes perfect. Read, practice, and self-assess; that’s it!

Good luck with your career and exams!

Hepatocellular carcinoma (HCC) is a significant global health problem with high morbidity and mortality. Its incidence is increasing exponentially worldwide with a close overlap between annual incidence and death rates. Even though significant advances have been made in HCC treatment, fewer than 20% of patients with HCC are suitable for potentially curative treatment. Hereditary hemochromatosis (HH) is an important genetic risk factor for HCC. HH is an autosomal recessive disorder of iron metabolism, characterised by elevated iron deposition in most organs including the liver, leading to progressive organ dysfunction. HCC is a complication of HH, nearly always occurring in patients with cirrhosis and contributes to increased mortality rates. Identifying the susceptibility of development of HCC in HH patients has gained much traction. This review summarises the current knowledge with regard to the association of HH and HCC in order to encourage further research. In this review, we focus particularly on HFE gene-related HH. Herein, we highlight and discuss emerging clinical research which addresses the prevalence of HCC in HH patients and the coincidence of HH with other risk factors for HCC development. We also focus on the therapeutic tools in the management of HCC associated with HH.

Liver cancer stem cells (LCSCs), a small subpopulation that constitutes liver cancer heterogeneity, play a vital role in cancer initiation, invasion, recurrence, metastasis, and resistance to chemo-radiotherapy. It is believed that therapies targeting LCSCs can improve the efficacy of conventional chemotherapy and radiotherapy by completely eliminating tumors while preventing recurrence. Therefore, during last decades, numerous surface markers for LCSCs have been identified and characterized in many subtypes of liver cancer, especially in hepatocellular carcinoma (HCC). These well-recognized surface markers significantly promote the therapeutic efficacy that identifies, targets and destroys LCSCs. Meanwhile, there have been intensive studies that aim to investigate the molecular mechanism of how stemness contributes to liver cancer relapse, recurrence and resistance. However, liver cancer stemness seems to be regulated by a hierarchical organization and crosstalk of a wide variety of signaling pathways. Using individual or few LCSC surface markers may not be able to completely reveal the intrinsic stemness hierarchy. From an integrated perspective, understanding of recent advances in LCSC surface markers remains important and urgent. In this review, we concentrate on demonstrating the indispensable roles of LCSC surface markers in identification and characterization of multiple cancer stages including initiation, invasion, metastasis, resistance and highlighting the cutting-edge therapeutic strategies against cancer stem cells in HCC.

The multiplicity and phenotype of intratumoral immune infiltrate have been shown to influence the clinical outcome of hepatocellular carcinoma (HCC), thus providing a strong rationale to therapeutic interventions aimed at restoring the dysfunctional immune response against the tumor. Improving the knowledge of the complex interactions between transformed hepatocytes, nonparenchymal resident cells, and infiltrating immune cells (characterizing the HCC microenvironment) will be instrumental to increase the success rate of existing immunotherapeutic strategies and to identify new potential targets for intervention or biomarkers to optimize the selection of candidate patients.

Patients with hepatocellular carcinoma (HCC) often present with underlying liver disease and significant comorbidities, limiting treatment tolerance. With the development of improved toxicity models and highly conformal radiation delivery systems, external beam radiotherapy has become a valuable treatment option for liver cancer. Using cutting edge technology, stereotactic ablative radiotherapy (SABR) allows for the delivery of ablative doses in few fractions while sparing uninvolved liver tissue. This approach permits dose escalation and precise tumor targeting with minimal risk of radiation induced liver disease. This review clarifies SABR's role alongside liver-directed treatments such as radiofrequency ablation, transarterial radioembolization, and transarterial chemoembolization in the management of HCC. It also examines the promising potential of SABR combined with immunotherapy to treat advanced HCC.

Hepatocellular carcinoma (HCC) is the most lethal and common type of liver cancer with limited treatment options at the advanced stage. The use of immune checkpoint inhibitor (ICI) based immunotherapy is exponentially increasing in the treatment of patients with advanced solid tumors. The expression of immune checkpoints on tumor cells leading to lower activity of T-cells is one of the major mechanisms of immune escape. Checkpoint blockade immunotherapies with antibodies against PD-1, PD-L1 or CTLA-4 are being investigated in clinical trials in HCC patients. ICIs have improved survival in patients with inoperable advanced stage HCC where other curative treatments are not applicable. However, the response rates remain low with only a small subset of patients responding to this therapy. There is an unmet need to identify predictive markers to select those HCC patients who would benefit from ICI therapies. Importantly, epithelial-to-mesenchymal transition (EMT), a major process driving HCC invasion and metastasis by regulating the phenotypic cellular switching from epithelial to mesenchymal state, has been implicated as a resistance mechanism associated with ICI therapies. The role of EMT as a regulator of immune checkpoint molecule in HCC is just emerging. However, the consequence of EMT as a resistance mechanism in HCC patients undergoing ICI treatments remains unexplored. In this review, we summarize the recent clinical studies with ICIs in HCC and highlight the trials underway featuring novel monotherapies and combinatorial approaches based on immune and non-immune therapies. We will discuss the ongoing efforts to discover new immune checkpoint molecules in HCC as potential drug targets. We also highlight the role of EMT in facilitating therapy resistance in HCC treated with ICIs and discuss potential strategies to circumvent resistance in ICI treated HCC patients.

Most patients diagnosed with hepatocellular carcinoma (HCC) present with advanced or metastatic disease. The lack of therapeutic options in the treatment of advanced HCC accounts for its high mortality and recurrence rate. HCC is known as an immunogenic tumor, which develops in chronically inflamed livers. Anti-PD-1/PD-L1 antibodies (immune checkpoint inhibitors, ICB) were approved by the FDA to treat advanced HCC in patients previously treated with sorafenib as a second line. This has opened up a new era of anticancer treatment, although the response rate of HCC to anti-PD-1/PD-L1 antibodies is only around 20%. Other than ICB treatment, adoptive cell transfer, dendritic cell-based vaccines and oncolytic therapy are currently under clinical trials. In this review, different immunotherapy approaches for HCC is presented. Current knowledge on the mechanisms of action for each approach is discussed and relevant, ongoing clinical trials are presented. We also discuss the future of immunotherapy and combination treatment for HCC patients.

Primary liver cancer is one of the leading causes of cancer-related deaths worldwide. China has more than 55% liver cancer cases globally. The development of hepatocellular carcinoma (HCC) was caused by a variety of risks factors, including chronic inflammation by virus, alcohol consumption and non-alcoholic steatohepatitis. Emerging evidence has notarized inflammation as a critical component of HCC progression. The development of HCC is a multistep process which may originate from liver chronic injury and inflammation to subsequent fibrosis and/or cirrhosis and finally HCC. A large number of studies indicate that chemokines and cytokines are candidates linking molecules between inflammation and liver cancer. Here, we will describe a few of the key cytokines and chemokines and signal pathways which are involved in the inflammation of HCC. Inhibitors of inflammation for the prevention and overcoming antitumor immunity for treatment of liver cancer are promising candidates for the future management of patients with HCC.

Non-alcoholic fatty liver disease (NAFLD) is now the most common cause of liver disease worldwide, and represents an increasingly important cause of hepatocellular carcinoma (HCC). As the prevalence of NAFLD has increased, the burden of NAFLD-related HCC has been rising in parallel. This is particularly evident in Western countries, where NAFLD is estimated to account for 10%-59% of all HCC. NAFLD-related HCC can occur in the presence or absence of cirrhosis, and, while those with cirrhosis remain at the greatest risk, factors such as steatohepatitis, age, genetic polymorphisms, type 2 diabetes mellitus and obesity also appear have an impact on the risk of developing HCC in NAFLD. In this review, we present the epidemiology of NAFLD-related HCC from a Western perspective, highlighting gaps in current knowledge and future directions for research in this field.

Hepatocellular carcinoma (HCC) is often associated with pre-existing chronic liver pathologies of different origin infections of hepatitis B virus (HBV) and hepatitis C virus. Clinically, the diagnosis and therapy for HCC are very important for the prognosis of patients. However, current methods for HCC diagnosis and therapy have no an optimal accuracy due to the tumor heterogeneity and the frequent late diagnosis. This review summarizes the new advances in molecular diagnosis and therapy of HCC, based on the recent novel biomarkers and new therapeutic strategies for HCC, including alpha-fetoprotein-L3, glypican-3, heat shock protein 90, dickkopf WNT signaling pathway inhibitor 1, paraoxonase 1, highly up-regulated in liver cancer. Moreover, epigenetic regulation, signal pathway, cellular and molecular targets for the immunotherapy, tumor microenviroment and genome sequencing analysis may serve as the molecular expression signatures in clinical practice. For promising new treatment strategy of HCC, targeting molecular therapy based on the restoration of tumor suppressor genes lost and inhibition of oncogenic genes is attractive. The new clinical trials for other molecular-targeted agents, including pembrolizumab, nivolumab, tivantinib, lenvatinib, cabozantinib, and ramucirumab, are ongoing in clinic. Interestingly, anti-HBV drugs display an amazing therapy for HBV-related HCC. In future, the global determination of more biomarkers may provide new insights into the diagnosis of HCC. More importantly, the diagnostic markers should be used to trace patient's follow-up disease progression, guiding doctors to judge and prescribe drugs for status of an illness, prognosis and other processes.

Hepatocellular carcinoma (HCC) is the most recurrent hepatic malignancy and the third in the cancer-related casualties in the west. The frequently-documented causes of HCC are chronic liver infections by hepatitis B virus or hepatitis C virus, nonalcoholic fatty liver disease, cirrhosis, exposure to aflatoxins and tobacco smocking, etc. Clinical presentation of this fatal disease ranges from asymptomatic to upper abdominal pain or common health conditions like weight loss or lethargy. Among current surveillance strategy for suspected patients, liver imaging and serum alpha fetoprotein estimation has been regularly recommended. However, sensitivity of this diagnostic methodology especially in early detections, often suffers from compromised sensitivity and selectivity. Various image based and serological biomarkers for HCC has been introduced in recent decades with varied sensitivity as stand-alone or combined diagnostic protocol. The current article will review the status of HCC diagnosis with respect to common diagnostic protocol, and upcoming novel biomarkers.

With the highest annual fatality ratio (mortality-to-incidence ratio), reported for a human cancer, hepatocellular carcinoma (HCC) ranks as the third leading cause of cancer-related deaths worldwide and its distribution is not uniform. In Sub-Saharan Africa (SSA), HCC is the second leading cause of cancer-related deaths for men and the fourth for women in 2020, with average age-standardised mortality rates of 8.2 and 4.2 per 100,000 persons/year, respectively. In this region, HCC presents in younger age groups and has a median survival rate of ~3-4 months. The major risk factors for HCC include viral [hepatitis B virus (HBV), hepatitis C virus (HCV) and hepatitis D virus (HDV)] and environmental [dietary aflatoxin and iron overload] factors, with more than 50% being attributable to HBV, which is endemic in SSA. HCC control efforts in SSA are faced with a number of unique challenges, including resource restrictions, a paucity of good data, few cancer registries, inaccessibility of treatment for HBV and HCV, co-infection with human immunodeficiency virus (HIV), exposure to co-carcinogen aflatoxin B1, unique (sub)genotypes of HBV and changing natural history and aetiology of HCC as a result of antiretroviral therapy rollout for HIV and changing lifestyles. The unique features of HCC in SSA, together with the challenges faced in its prevention and appropriate public health intervention, diagnosis and treatment, all suggest that HCC in SSA is deserving of an in depth understanding by further focused research. Considerable motivation of policymakers, work and resources are required to reduce the burden of this cancer on the subcontinent.

Hepatocellular carcinoma (HCC) is a major and increasing cause of clinical and economic burden worldwide. Now that there are effective therapies to control or eradicate viral aetiologies, the landscape of HCC is changing with alcoholic and metabolic liver diseases becoming major catalysts. The pathogenesis of HCC is complex and incompletely understood, hampering improvements in therapy. Animal models are essential tools for advancing study on the cellular and molecular processes in HCC and for screening potential novel therapies. Many models of hepatocarcinogenesis have been established using various methods including genetic engineering, chemotoxic agents and dietary manipulation to direct implantation of tumour cells. However, none of these can accurately replicate all features found in human diseases. In this review, we provide an overview of different mouse models of HCC with a particular focus on cancer arising from alcoholic liver disease, non-alcoholic fatty liver disease and hereditary haemochromatosis. We also highlight their strengths and limitations and provide perspectives for future study.

Hepatocellular carcinoma (HCC) is the main tumor of the liver and is the sixth most frequently diagnosed tumor in the world. It is the evolution of chronic hepatic injury secondary to different etiologies. Chronic hepatitis B virus and hepatitis C virus infection, chronic alcoholic hepatitis, as well as non-alcoholic fatty liver disease are the most common causes behind the development of HCC. The introduction of effective prophylaxis and treatment against hepatitis B, the recent use of highly effective hepatitis C treatments, as well as lifestyle changes observed in recent decades in the general population causing an increase in obesity and metabolic syndrome have led to significant epidemiological change in HCC in relation to the changed etiologic prevalence of liver injury. Increasing evidence was emerging, emphasizing how the development of HCC is a complex and multifactorial process. The knowledge of the molecular mechanisms involved is important for the understanding of the basic factors of the development of hepatocarcinogenesis and of possible therapeutic approaches. Several pathogenic mechanisms and clinical expression of HCC occur in relation to the different etiologies of the underlying liver disease. The different clinical behavior of HCC often makes diagnosis difficult at an early stage, that is necessary for an effective therapeutic approach. This review analyzes the possible different pathogenic mechanisms involved in the development of HCC and emphasizes the different epidemiological and clinical aspects of HCC observed in the most common forms of liver diseases of viral and non-viral origin.

In multistep hepatocarcinogenesis, sizable lesions can precede the development of hepatocellular carcinoma (HCC). These lesions are currently classified as low grade (LG)-and high grade (HG)-dysplastic nodules. Following international guidelines recommending the surveillance of cirrhotic patients, a growing number of 1-2 cm hepatocellular nodules are recognized including early hepatocellular carcinoma (eHCC) and DN the latter accounting for as many as 70% of nodules < 1 cm. HG-DN are currently considered the most advanced HCC precursors. The histological diagnosis of low-grade dysplastic nodule (LG-DN), high-grade dysplastic nodule (HG-DN) and eHCC in small liver biopsies requires a comprehensive stepwise morphological and immunocytochemical approach. By imaging the differential diagnosis among these lesions is a challenge. According to vascular enhancement at dynamic computed tomography (CT) or magnetic resonance imaging (MRI) these precursors are classified as hypo-vascular/ indeterminate nodules even though distinction between LG-DN and HG-DN is almost impossible. The introduction of gadoexetic acid-enhanced MRI has represented an extremely important advance in this field allowing a better differentiation of dysplastic lesions from eHCC and progressed HCC. Additional MRI features as diffusion-weighted imaging further improved diagnostic accuracy of imaging. According to Liver Imaging Reporting and Data System (LI-RADS), either CT/MRI or Contrast-Enhanced Ultrasound LI-RADS, the dysplastic lesions should be categorized as LR-3 or LR-4. Natural history of these lesions confirmed that HCC can develop from HG-DN but which nodule and when it will undergo malignant transformation is not predictable. The search and validation of radiological and tissue markers able to select lesions more prone to HCC development, is currently underway. Whether and how HG-DN should be ablated or closely followed up is currently debated.

Present study reports an update on the molecular interaction of antiviral drugs with viral and host cell components during hepatitis C virus (HCV) infection. In addition to the traditional therapeutic drug regimen, termed as standard of care, some recent drugs have been added in the existing regimen used for HCV infection. These drugs were categorized as direct-acting antivirals (DAAs) agents and "other agents", with their efficacious impact in the control of HCV infection. They target both viral proteases and host cell receptor proteins/enzymes involved in HCV entry into the cell, replication, and assembly to check their propagation both in situ as well as in cell to cell transmission. Recent studies have reported a significant rise in sustained virological response after the use of these drugs both alone and in combination with pegylated interferon-α (PegIFN-α) plus ribavirin. Recently, DAAs have been reported to be highly effective in eradication of HCV infection, especially liver cirrhosis, reducing but not avoiding the occurrence of liver cancer. Some studies have demonstrated that the presence of resistant HCV variants, arising during viral replication, may be controlled by the new drug regimen. It is important to note here that all these drugs are influenced by viral as well as host factors including basic viral load, HCV genotypes, IFN action, interleukin 28B polymorphism and some liver and metabolic diseases, etc. This is an area with ongoing investigations to explore more antiviral agents that may address new challenges in HCV therapy.

Aims: A cross-sectional research study on the seroprevalence of hepatitis B and listeriosis co-infection among patients attending Sickbay Hospital, Ahmadu Bello University, Zaria was carried out, with view to characterize, identify and to determine the antimicrobial sensitivity profile of Methodology: A total of 100 venous blood samples were collected from consenting patients presented to the study area suspected with hepatic disorders. The samples were centrifuged and the blood sera were obtained. The sera were qualitatively screened for HBsAg by immunochromatographic technique using rapid diagnostic device kit. Reactive sera for HBsAg were further confirmed by ELISA kits. Listeria monocytogenes was isolated from the HBV seropositive samples by standard methods and identified using biochemical characterizations. Results: The results showed that the overall seroprevalence of hepatitis B was found to be 11 (11%) in the study area, with females and males accounting for 3 (8.6%) and 8 (12.3%) seroprevalences respectively. The prevalence of hepatitis B — listeriosis co-infection was found to be 4 (36.4%). A statistical relationship (p= .56) was found between hepatitis B— listeriosis co-infection and the age of the patients. There is no significant difference between the prevalence of Hepatitis B — Listeriosis co-infection and the gender. All sex has equal chance of contacting the disease. Conclusion: The seroprevalence of 11% HBsAg obtained in this study signifies high endemicity of HBV infection in the study area. There is presence of mixed infections of hepatitis B and listeriosis in the study area. The Listeria monocytogenes isolated from HBV seropositive patients was found to be highly sensitive to Penicillin (100%) and Ampicillin (100%) but resistant to Chloramphenicol (0%), Ofloxacin (0%) and Gentamicin (0%).

Hepatocellular carcinoma (HCC) carries an unfavorable prognosis and novel therapeutic strategies are needed. Until now, only few systemic agents have improved survival in patients with advanced stage disease. Immunotherapy changed the landscape in several tumor types by producing unprecedented clinical outcomes with a favorable safety profile. Liver presents a particular immune-suppressive microenvironment and HCC develops in a background of chronic inflammation in the vast majority of cases. In this regard, immunotherapy may be a suitable strategy. Preliminary research focused on therapies involving immune cells and anti-tumor immune response for HCC has shown encouraging preliminary results. Immune checkpoint inhibitors, such the anti-PD-1/PD-L1 monoclonal antibodies, have provided durable responses in patients with advanced stage disease, although the pioneers phase III trials did not confirm survival superiority over the available agents. Cancer vaccines, adoptive cellular therapies and combinations of local modalities with immunotherapy are promising approaches under active research.