Various Forms Of Liver Disease Research Articles

Every ED Visit is an Opportunity to Talk about Contraception

Every ED Visit is an Opportunity to Talk about Contraception

Phytochemical Characterization, Hepatoprotective Activity on Alcohol-Induced Toxicity of the Aqueous Extract of Curcuma longa (Zingiberaceae) in Wistar Rats

Introduction: Liver or hepatic disease refers to different conditions that affect the liver. Chronic alcohol consumption is one of the most frequent causes of liver disease and accounts for about 55% of liver cirrhosis deaths recorded in Cameroon in 2020. Standard accessible treatments focus on end-stage liver disease with safety and efficacy obstacles. We have a research gap in Cameroon to understand the alternative use of natural products as treatment with a long traditional history of safe use. Curcuma longa has long been a source of traditional and modern medicine. It is commonly used in Cameroon as a spice and herbal product with some level of activity against various forms of liver disease.
 Objective: To phytochemically screen for bioactive metabolites and evaluate the hepatoprotective activity of the aqueous extract of Curcuma longaon alcohol-induced toxicity in Wistar rats.
 Methods: Phytochemical screening was carried out on the aqueous extract obtainedfrom maceration of plant rhizomes. Three doses (125, 250 and 500mg/Kg) of the plant extract and the reference (Silymarin 50mg/Kg) were administered daily (p.o) to rats 30 min before administration of 40% alcohol (2mL/100g p.o) for 21 days. Biochemical parameters such as ALAT, ASAT, GGT, Bilirubin and Lipid profile were quantified and histological studies of the liverwas carried out using standard procedures.
 Results: Phytochemical screening of the aqueous extract of C. longa revealed polyphenols such as flavonoids, tannins, quinones, saponins and phlobatanins. The plant showed hepatoprotective activity by decreasing liver toxicity markers such as ASAT, ALAT, GGT and Bilirubin. Histology revealed dose-dependent protection with 500 mg/Kg showing the most cellular integrity, no central vein occlusion and minimal fibrosis.
 Conclusion: This study indicated the presence of polyphenols like flavonoids and tannins in the aqueous extract of C. longa. The presence of these secondary metabolites in the studied extract justifies its antioxidant and anti-inflammatory properties confirmed by its hepatoprotective effects on alcohol-induced toxicity. This was clearly shown by biochemical and histological parameters. More sensitive and specific methods are required to test for these secondary metabolites in serum.

Endo-hepatology: An emerging field.

Gastroenterologists have long been spearheading the care of patients with various forms of liver disease. The diagnosis and management of liver disease has traditionally been a combination of clinical, laboratory, and imaging findings coupled with percutaneous and intravascular procedures with endoscopy largely limited to screening for and therapy of esophageal and gastric varices. As the applications of diagnostic and therapeutic endoscopic ultrasound (EUS) have evolved, it has found a particular niche within hepatology now coined endo-hepatology. Here we discuss several EUS-guided procedures such as liver biopsy, shear wave elastography, direct portal pressure measurement, paracentesis, as well as EUS-guided therapies for variceal hemorrhage.

Melatonin as a Potential Multitherapeutic Agent.

Melatonin (N-acetyl-5-methoxytryptamine, MEL) is a hormone produced by the pineal gland that was discovered many years ago. The physiological roles of this hormone in the body are varied. The beneficial effects of MEL administration may be related to its influence on mitochondrial physiology. Mitochondrial dysfunction is considered an important factor in various physiological and pathological processes, such as the development of neurodegenerative and cardiovascular diseases, diabetes, various forms of liver disease, skeletal muscle disorders, and aging. Mitochondrial dysfunction induces an increase in the permeability of the inner membrane, which leads to the formation of a permeability transition pore (mPTP) in the mitochondria. The long-term administration of MEL has been shown to improve the functional state of mitochondria and inhibit the opening of the mPTP during aging. It is known that MEL is able to suppress the initiation, progression, angiogenesis, and metastasis of cancer as well as the sensitization of malignant cells to conventional chemotherapy and radiation therapy. This review summarizes the studies carried out by our group on the combined effect of MEL with chemotherapeutic agents (retinoic acid, cytarabine, and navitoclax) on the HL-60 cells used as a model of acute promyelocytic leukemia. Data on the effects of MEL on oxidative stress, aging, and heart failure are also reported.

The role of alcohol use in the aetiology and progression of liver disease: A narrative review and a quantification.

Issues.Alcohol use has been shown to impact on various forms of liver disease, not restricted to alcoholic liver disease.Approach.We developed a conceptual framework based on a narrative review of the literature to identify causal associations between alcohol use and various forms of liver disease including the complex interactions of alcohol with other major risk factors. Based on this framework, we estimate the identified relations for 2017 for the USA.Key Findings.The following pathways were identified and modelled for the USA for the year 2017. Alcohol use caused 35 200 (95% uncertainty interval 32 800–37 800) incident cases of alcoholic liver cirrhosis. There were 1700 (uncertainty interval 1100–2500) acute hepatitis B and C virus (HBV and HCV) infections attributable to heavy-drinking occasions, and 14 000 (uncertainty interval 5900–19 500) chronic HBV and 1700 (uncertainty interval 700–2400) chronic HCV infections due to heavy alcohol use interfering with spontaneous clearance. Alcohol use and its interactions with other risk factors (HBV, HCV, obesity) led to 54 500 (uncertainty interval 50 900–58 400) new cases of liver cirrhosis. In addition, alcohol use caused 6600 (uncertainty interval 4200–9300) liver cancer deaths and 40 700 (uncertainty interval 36 600–44 600) liver cirrhosis deaths.Implications.Alcohol use causes a substantial number of incident cases and deaths from chronic liver disease, often in interaction with other risk factors.Conclusion.This additional disease burden is not reflected in the current alcoholic liver disease categories. Clinical work and prevention policies need to take this into consideration.

Infection with Toxoplasma gondii can promote chronic liver diseases in HIV-infected individuals.

Liver pathologies and infection with Toxoplasma gondii (Nicolle et Manceaux, 1908) are widespread among HIV-infected patients. However, a possible contribution of toxoplasmosis to the development of various forms of liver diseases in HIV-infected individuals has not yet been determined. This research is a retrospective cohort study. Medical cards of 907 HIV-positive patients, including 119 individuals who died, were studied. The patients were divided into two groups: 531 patients were seropositive to T. gondii and 376 seronegative. General liver pathology was more widespread among patients seropositive to T. gondii than in seronegative patients (63.1 ± 2.1% and 51.9 ± 2.6%, respectively, p < 0.001). The association of seropositive to T. gondii with general liver pathology is weak both in the whole cohort (Pearson's contingency coefficient C = 0.112), and among the deceased patients (C = 0.228). Chronic HBV-HCV coinfection was more common in the seropositive than in seronegative individuals as it was found both in entire cohorts (26.0 ± 1.9% and 18.6 ± 2.0%, respectively, p = 0.010) and in died patients (31.0 ± 5.5% and 14.6 ± 5.1%, respectively, p = 0.041). Toxoplasma gondii had a weak role in distributing of HBV-HCV coinfection between cohorts (C = 0.187). In both cohorts in patients with chronic hepatitis, regardless of its etiology, there was no significant difference in alanine transaminase activity (ALT). Cirrhosis of the liver occurred 4.5 times more often in deceased seropositive patients than in the entire seropositive cohort (23.9 ± 5.1 and 5.3 ± 2.0, respectively, p = 0.0006) whereas it no significantly increased in seronegative cohort (10.4 ± 4.4 against 4.8 ± 1.1, p > 0.05). In them T. gondii is weakly involved in cirrhosis formation (C = 0.168). Thus, in HIV-infected patients, T. gondii is a weak nonspecific adjunct that supports chronic liver inflammation and progression of cirrhosis, regardless of etiology, but does not influence the degree of hepatitis activity. The increased prevalence of HBV-HCV coinfection in patients seropositive for T. gondii may be related to their risk factor behaviour associated with uncontrolled blood contacts.

Hepatitis B And Hepatitis C Viral Infections And Associated Factors Among Patients With Diabetes Visiting Gondar Referral Teaching Hospital, Northwest Ethiopia: A Comparative Cross-Sectional Study.

BackgroundThe liver is the major site of Hepatitis B virus and Hepatitis C virus replications. Patients with diabetes tend to be at an increased risk for developing various forms of liver diseases. The infection of the liver can cause or exacerbate diabetes. On the other hand, diabetes can cause or intensify the severity of liver infection. This comparative cross-sectional study was conducted with the aim to determine the prevalence of Hepatitis B and Hepatitis C virus infections and associated factors among patients with diabetes visiting the University of Gondar referral teaching hospital, northwest Ethiopia.ResultsOut of the 610 participants (305 patients with diabetes, 305 people with no diabetes) of the study, 65 (10.7%) were positive for Hepatitis infections, of whom 44 (14.4%) and 21 (6.9%) were positive for at least one of the viruses in patients with diabetes and people with no diabetes, respectively. Out of the diabetic and non-diabetic groups of the study, 26 (8.5%) and 14 (4.6%) (95% CI, 0.96–4.02) were positive for Hepatitis B virus, respectively, while 23 (7.5%) and 7 (2.3%) (95% CI, 1.46–8.68) of the diabetes and non-diabetic groups were positive for Hepatitis C virus, respectively. History of blood transfusion (95% CI, 1.36–12.71) and unprotected sex (95% CI, 1.25–10.15) were significantly associated with Hepatitis B virus infection, while the type of diabetes (95% CI, 1.25–10.89) was associated with anti-Hepatitis C virus positivity.ConclusionPositivity for Hepatitis C virus was significantly associated with Type II diabetes. Blood transfusion and unprotected sex were risk factors for Hepatitis B virus infections. Further studies that elaborate temporal associations and find out explanations for the relationship between diabetes and Hepatitis C viral infections are of paramount importance.

Characterisation of the Serum Metabolic Signature of Cholangiocarcinoma in a United Kingdom Cohort

A distinct serum metabonomic pattern has been previously revealed to be associated with various forms of liver disease. Here, we aimed to apply mass spectrometry to obtain serum metabolomic profiles from individuals with cholangiocarcinoma and benign hepatobiliary diseases to gain an insight into pathogenesis and search for potential early-disease biomarkers. Serum samples were profiled using a hydrophilic interaction liquid chromatography platform, coupled to a mass spectrometer. A total of 47 serum specimens from 8 cholangiocarcinoma cases, 20 healthy controls, 8 benign disease controls (bile duct strictures)and 11 patients with hepatocellular carcinoma (as malignant disease controls) were included. Data analysis was performed using univariate and multivariate statistics. The serum metabolome disparities between the metabolite profiles from healthy controls and patients with hepatobiliary disease were predominantly related to changes in lipid and lipid-derived compounds (phospholipids, bile acids and steroids) and amino acid metabolites (phenylalanine). A metabolic pattern indicative of inflammatory response due to cirrhosis and cholestasis was associated with the disease groups. The abundance of phospholipid metabolites was altered in individuals with liver disease, particularly cholangiocarcinoma, but no significant difference was seen between profiles from patients with benign biliary strictures and cholangiocarcinoma. The serum metabolome in cholangiocarcinoma exhibited changes in metabolites related to inflammation, altered energy production and phospholipid metabolism. This study serves to highlight future avenues for biomarker research in large-scale studies.

Present status of diagnosis and treatment of hepatolenticular degeneration

Hepatolenticular degeneration (HLD) is an autosomal recessive inherited disorder of copper metabolism. The mutations in the ATP7B gene on chromosome 13 leads to the functional defect of ATP7B, which produces pathological deposits of copper in liver, brain, cornea and kidney, with diverse clinical manifestations in various forms of liver disease, nervous system disease and corneal disease (Kayser-Fleischer rings). Early diagnosis and proper treatment can improve the prognosis of hepatolenticular degeneration. Conversely, it may progress to end-stage liver disease or severe motor dysfunction, which seriously affects patient quality of life.

Bile acids regulate cysteine catabolism and glutathione regeneration to modulate hepatic sensitivity to oxidative injury.

Bile acids are signaling molecules that critically control hepatocellular function. Disrupted bile acid homeostasis may be implicated in the pathogenesis of chronic liver diseases. Glutathione is an important antioxidant that protects the liver against oxidative injury. Various forms of liver disease share the common characteristics of reduced cellular glutathione and elevated oxidative stress. This study reports a potentially novel physiological function of bile acids in regulating hepatic sulfur amino acid and glutathione metabolism. We found that bile acids strongly inhibited the cysteine dioxygenase type-1-mediated (CDO1-mediated) cysteine catabolic pathway via a farnesoid X receptor-dependent mechanism. Attenuating this bile acid repressive effect depleted the free cysteine pool and reduced the glutathione concentration in mouse liver. Upon acetaminophen challenge, cholestyramine-fed mice showed impaired hepatic glutathione regeneration capacity and markedly worsened liver injury, which was fully prevented by N-acetylcysteine administration. These effects were recapitulated in CDO1-overexpressing hepatocytes. Findings from this study support the importance of maintaining bile acid homeostasis under physiological and pathophysiological conditions, as altered hepatic bile acid signaling may negatively impact the antioxidant defense mechanism and sensitivity to oxidative injury. Furthermore, this finding provides a possible explanation for the reported mild hepatotoxicity associated with the clinical use of bile acid sequestrants in human patients.

Is the Hepatic Factor a miRNA that Maintains the Integrity of Pulmonary Microvasculature by Inhibiting the Vascular Endothelial Growth Factor?

Background:The “hepatic factor,” a molecule or group of molecules present in the hepatic venous blood, essential for the prevention of the development of pulmonary arteriovenous malfor-mations (PAVMs) and right-to-left shunting has been a conceptual enigma in the understanding of many related conditions.Methods:Patients with various forms of liver diseases including acute hepatic failure, and others with normal hepatic function like hereditary hemorrhagic telangiectasia (HHT), inflammatory and parasitic disorders, cardiogenic hepatopulmonary syndrome (cHPS) and skin disorders like Dyskeratosis con-genita are all known to cause PAVMs. Over a period of the last two decades our understanding of the pathogenesis of PAVMs has changed, but the mechanisms are still not clearly understood. The pres-ence of PAVMs once considered a contraindication for liver transplantation is now a cure for PAVMs in patients with HPS.Results:In this article the molecular mechanisms and the underlying pathogenesis of PAVMs are dis-cussed and the role of microRNA (miRNA) in its pathogenesis is favorably argued. Identifying and preventing or treating the underlying mechanisms will significantly influence the management of a large group of patients who at present cannot be effectively treated with a very poor prognosis. Progressive polycythemia, desaturation, stroke, and infection are serious complications of PAVMs.Conclusion:The clinical data and current understanding leads to the possible role of miRNA, which inhibits Vascular Endothelial Growth Factor (VEGF) synthesis as a pathogenic mechanism for the development of PAVMs.

The hepatic differentiation of adult and fetal liver stromal cells in vitro

The liver has a marked capacity for regeneration. In most cases the liver regeneration is determined by hepatocytes. The regenerative capacity of hepatocytes is significantly reduced in acute or chronic damage. In particular, repair mechanisms are not activated in patients with alcoholic cirrhosis. Organ transplantation or advanced methods of regenerative medicine can help such patients. The promising results were obtained in clinical trials involving patients with various forms of liver disease who received transplantation of autologous bone marrow stem cells. However, to improve the effectiveness of such treatment it is necessary to search for more optimal sources of progenitor cells, as well as to evaluate the possibility of using descendants of these cells differentiated in vitro. In this study we isolated stromal cells from the liver biopsies of three patients with alcoholic cirrhosis, conducted their morphological and phenotypic analysis, and evaluated the hepatic potential of these cells in vitro. The stromal cells isolated from fetal liver were used for comparison. The results of this can serve as a basis for the development of a new method for the treatment of end-stage liver disease. The stromal cells isolated from the liver biopsies for a long time proliferate in a culture and this which makes it possible to expand them to large amounts for subsequent differentiation into hepatocyte-like cells and autologous transplantation.

Emerging Role of High-Mobility Group Box 1 (HMGB1) in Liver Diseases

Damage-associated molecular pattern (DAMP) molecules are essential for the initiation of innate inflammatory responses to infection and injury. The prototypic DAMP molecule, high-mobility group box 1 (HMGB1), is an abundant architectural chromosomal protein that has location-specific biological functions: within the nucleus as a DNA chaperone, within the cytosol to sustain autophagy and outside the cell as a DAMP molecule. Recent research indicates that aberrant activation of HMGB1 signaling can promote the onset of inflammatory and autoimmune diseases, raising interest in the development of therapeutic strategies to control their function. The importance of HMGB1 activation in various forms of liver disease in relation to liver damage, steatosis, inflammation, fibrosis, tumorigenesis and regeneration is discussed in this review.

Mouse Models of Bariatric Surgery.

Morbid obesity is linked to increased incidences of glucose intolerance, Type 2 diabetes mellitus, cardiovascular diseases, various forms of liver disease, and specific forms of cancer. Treatment of obesity by lifestyle modifications (i.e. changes in diet and exercise) and drug therapy is generally ineffective. Bariatric surgery is currently the most effective means of treating obesity and related disorders. We as well as others have developed surgical procedures for application to genetic mouse models that mimic an array of human bariatric surgical procedures used in the treatment of obesity. The application of bariatric surgery to genetic mouse models will broaden our understanding of the role of the gut in metabolic disease. Models that have been developed include gastric banding, sleeve gastrectomy (SG), Roux-en-Y gastric bypass (RYGB) with a complete exclusion of the stomach, duodenal-jejunal bypass (DJB) and biliopancreatic diversion (BPD). The detailed methods of these procedures are provided.

Alcohol consumption and non-communicable diseases: epidemiology and policy implications.

This paper summarizes the relationships between different patterns of alcohol consumption and various on non-communicable disease (NCD) outcomes and estimates the percentage of NCD burden that is attributable to alcohol. A narrative review, based on published meta-analyses of alcohol consumption-disease relations, together with an examination of the Comparative Risk Assessment estimates applied to the latest available revision of Global Burden of Disease study. Alcohol is causally linked (to varying degrees) to eight different cancers, with the risk increasing with the volume consumed. Similarly, alcohol use is related detrimentally to many cardiovascular outcomes, including hypertension, haemorrhagic stroke and atrial fibrillation. For other cardiovascular outcomes the relationship is more complex. Alcohol is furthermore linked to various forms of liver disease (particularly with fatty liver, alcoholic hepatitis and cirrhosis) and pancreatitis. For diabetes the relationship is also complex. Conservatively, of the global NCD-related burden of deaths, net years of life lost (YLL) and net disability adjusted life years (DALYs), 3.4%, 5.0% and 2.4%, respectively, can be attributed to alcohol consumption, with the burden being particularly high for cancer and liver cirrhosis. This burden is especially pronounced in countries of the former Soviet Union. There is a strong link between alcohol and non-communicable diseases, particularly cancer, cardiovascular disease, liver disease, pancreatitis and diabetes, and these findings support calls by the World Health Organization to implement evidence-based strategies to reduce harmful use of alcohol.

The contribution of endoplasmic reticulum stress to liver diseases.

The unfolded protein response (UPR) is an evolutionarily conserved cell signaling pathway that is activated to regulate protein synthesis and restore homeostatic equilibrium when the cell is stressed from increased client protein load or the accumulation of unfolded or malfolded proteins. Once activated, this signaling pathway can either result in the recovery of homeostasis or can activate a cascade of events that ultimately result in cell death. The UPR/endoplasmic reticulum (ER) stress response spectrum and its interplay with other cellular organelles play an important role in the pathogenesis of disease in secretory cells rich in ER, such as hepatocytes. Over the past 2 decades, the contribution of ER stress to various forms of liver diseases has been examined. Robust support for a contributing, as opposed to a secondary role, for ER stress response is seen in the nonalcoholic steatohepatitis, alcoholic liver disease, ischemia/reperfusion injury, and cholestatic models of liver disease. The exact direction of the cause and effect relationship between modes of cell injury and ER stress remains elusive. It is apparent that a complex interplay exists between ER stress response, conditions that promote it, and those that result from it. A vicious cycle in which ER stress promotes inflammation, cell injury, and steatosis and in which steatogenesis, inflammation, and cell injury aggravate ER stress seems to be at play. It is perhaps the nature of such a vicious cycle that is the key pathophysiologic concept. Therapeutic approaches aimed at interrupting the cycle may dampen the stress response and the ensuing injury.

Immunohistochemical Staining of Inflammatory Cells in Liver Biopsy Specimens of Patients With Autoimmune Hepatitis, Primary Biliary Cirrhosis, and Overlap SyndromesThe Authors’ Reply

To the Editor I read with great interest the study by Lee et al1 evaluating IgG and IgM immunohistochemical staining of inflammatory cells in liver biopsy specimens of patients with autoimmune hepatitis (AIH), primary biliary cirrhosis (PBC), and overlap syndromes. The authors report an IgG-predominant infiltrate in all cases of AIH. However, a large proportion (12/26) of PBC cases also showed a predominantly IgG+ infiltrate, which would potentially decrease the usefulness of IgM and IgG immunohistochemical staining in this setting. In contrast with these results, Daniels et al2 reported IgG-predominant infiltrates in all cases of AIH (n = 38) and IgM-predominant infiltrates in the vast majority (16/18 [89%]) of PBC cases. Similarly, our group recently published a study3 evaluating IgM and IgG immunohistochemical staining in various forms of liver disease, including AIH, PBC, primary sclerosing cholangitis …

In Response

In Response We agree with Vos et al.1 that the absence of liver enzyme measurements in some of our patients may be a drawback in our study. However, biochemical hepatic function testing may not offer the key information on hepatocellular dysfunction2 as Vos et al. suggest. Hultcrantz et al.3 described that chronically elevated liver enzymes without symptoms or physical signs of liver disease correspond with various forms of liver disease preferably in the presence of a positive history on alcohol consumption, drug abuse, hepatitis, or obesity. All patients displaying these factors were excluded from our study population, thus removing those patients that may exhibit elevated hepatic enzymes in the absence of physical signs or symptoms of liver disease. Regarding the importance of hemodynamics and indocyanine green plasma disappearance rate (ICG-PDR), we originally intended to use the noninvasive method of ICG measurement, pulse dye densitometry, to measure cardiac output in our study population. To validate the transcutaneous method versus intraarterial measurement of ICG, we performed simultaneous measurements in a subpopulation. In this subpopulation, we had to conclude that, for individual measurement of cardiac output, the transcutaneous measurement of ICG by pulse dye densitometry is not accurate enough.4 For the purpose of this discussion, the measurements of cardiac output versus the ICG-PDR value in the patients in whom we performed arterial blood sampling is shown in Figure 1. The open diamonds represent the patients receiving a propofol induction. Inspection of Figure 1 leads to the conclusion that the absence or presence of propofol did not induce significant hemodynamic changes in this otherwise healthy population nor did it affect ICG-PDR.Figure 1: Representation of cardiac output measurements based on arterial blood indocyanine green (ICG) concentrations versus ICG– plasma disappearance rate (PDR) values determined in patients who underwent simultaneous arterial ICG sampling. The circles represent the measurements in awake subjects; the diamonds represent the measurements during propofol induction.We thus maintain our conclusion4 that ICG-PDR values in a population without clinical signs of liver failure range well below 18% min−1, cited as the cutoff value for hepatic failure and propagated as criterion for clinical intervention. This cutoff value needs to be reconsidered as has been suggested elsewhere.5 We agree with the reviewers that further studies are needed and that the final word on this subject has not yet been written.

The adaptation mechanisms of liver in combined pathologies

The great potential of liver restoration has been described in different liver pathologies. There are various forms of liver diseases. Hence, comparative study of regenerative processes in different pathologies is especially significant for drawing out of modern methods of regenerative therapy.Earlier we have demonstrated that the reparative multiple growth of genome in some population of destructive liver cells occurs after bilateral adrenalectomy. In such conditions the resection of liver initiates a series of quick cell divisions (early mitoses) in the population of hepatocytes and provides partial repairing of liver functional activity. Bile duct ligation within 4 days also initiates the accumulation of polyplody cells in liver for repairing its functional activity. It is significant that at the same time the hepatocyte mitotic activity in cholestatic liver reaches the its maximal value.The aim of the present work was to study the adaptation mechanisms of liver in combined pathologies (bilateral adrenalectomy and cholestasis).The investigations were carried out on 50 adult (150–180 g) rats. Common bile duct ligation was made after 4 days from bilateral adrenalectomy.We have demonstrated that the ploidy of liver parenchymal cells (4c, 4cx2, 8c) significantly increases during 2 days after common bile duct ligation. We have also demonstrated that combined pathologies cause the speeding‐up of mitotic activity, which is explained by stimulating of signal transduction pathways in cholestatic liver in conditions of hormonal disbalance.

Risk Factors For Hepatitis B Virus Transmission In Nigerians: A Case-Control Study

This was a case-control study carried out at gastroenterology unit of the University of Nigeria Teaching Hospital (UNTH) Ituku/Ozalla from January 2008 to April 2010. The cases were consecutive patients with various forms of liver disease who tested positive for Hepatitis B surface (HBsAg). Asymptomatic individuals referred to the unit during the study period after testing positive for HBsAg during screening for blood donation or routine medical examination were also included as cases. The control subjects were age and sex-matched, HBsAgnegative individuals referred for upper gastrointestinal endoscopy.This case-control study of adults with HBV infection revealed that several high risk behaviors and practices for the transmission of this infection are significantly more prevalent among the patients compared to the controls. This means that parenteral transmission of HBV through these high-risk activities may have substantial contribution to disease burden.