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We describe the implementation of a novel electronic platform for specialty referral and consultation, eConsult Mental Health. This innovation aims to address mental health care access and coordination challenges in the nation's second largest public health system in Los Angeles. eConsult Mental Health is one of the largest documented electronic platforms to facilitate the integration of behavioral health services in primary care. Although implementation has been met with barriers unique to mental health care, eConsult Mental Health appears to be a promising tool to expand the spectrum of care for Los Angeles County safety net primary care providers in patient-centered medical homes. [ABSTRACT FROM AUTHOR]

Lack of timely access to specialty care is a significant problem among disadvantaged populations, such as those served by the Los Angeles County Department of Health Services. In 2012 the department implemented an electronic system for the provision of specialty care called the eConsult system, in which all requests from primary care providers for specialty assistance were reviewed by specialists. In many cases, the specialist can address the primary care provider's question via an electronic dialogue, thereby eliminating the need for the patient to see a specialist in person. We observed rapid growth in the use of eConsult: By 2015 the system was in use by over 3,000 primary care providers, and 12,082 consultations were taking place per month, compared to 86 in the third quarter of 2012. The median time to an electronic response from a specialist was one day, and 25 percent of eConsults were resolved without a specialist visit. Three to four years after implementation, the median time to a specialist appointment decreased significantly, while the volume of visits remained stable. eConsult systems are a promising and sustainable intervention that could improve access to specialist care for underserved patients. [ABSTRACT FROM AUTHOR]

Background: Studies document increasing rates of hospitalization among patients with inflammatory bowel disease, but temporal trends for in-hospital mortality among patients with inflammatory bowel disease are not characterized. We sought to determine whether in-hospital mortality changed over a 13-year period among nationwide hospitalizations associated with inflammatory bowel disease. We additionally sought to identify factors correlated with mortality. Methods: We used the National Hospital Discharge Survey, a large nationally representative database, for the years 1994 through 2006. Age- and mortality-adjusted rates of in-hospital mortality and standardized mortality ratios were calculated for four time periods. Logistic regression analysis was used to assess associations between advancing time and mortality in adjusted analyses. Results: 150 (0.9%) of 17,393 hospitalizations for patients with inflammatory bowel disease ended in death. Age-adjusted in-hospital mortality decreased from 3.6 deaths per 1,000 hospital days in 1994-96 to 2.4 per 1,000 in 2003-06; standardized mortality ratio decreased from 0.33 to 0.27. Similar trends were seen for patients with ulcerative colitis, but mortality did not change over time among patients with Crohn's disease. Multivariable logistic regression analysis confirmed the significance of these changes in mortality, with 17% decreased odds of in-hospital death per three-year period (P= 0.012). Subject age (OR 1.06 per year, P<0.001), Charlson comorbidity index (OR 1.29 per 1-point increase, P<0.001), and diagnosis of ulcerative colitis (versus Crohn's disease, OR 1.41, P =.042) were also associated with in-hospital mortality. Conclusions: The odds of in-hospital mortality among hospitalized patients with inflammatory bowel disease decreased by 17% per 3-year period from 1994 to 2006 in analysis adjusted for age and comorbidity status, in this large, nationally representative database. Multiple factors likely contribute to these trends. [ABSTRACT FROM AUTHOR]

OBJECTIVES: Morbidity and mortality due to liver disease and cirrhosis vary significantly by race/ethnicity in the United States. We examined the prevalence of liver disease risk factors among blacks, Mexican Americans, and whites, including elevated aspartate aminotransferase and alanine aminotransferase activity, infection with viral hepatitis B or hepatitis C, alcohol intake, obesity, diabetes, and metabolic syndrome. METHODS: Data were obtained from the Fourth National Health and Nutrition Examination Survey (NHANES IV). A logistic regression was used to examine the association of race/ethnicity to liver disease risk factors, controlling for the demographic and socioeconomic variables. RESULTS: Mexican-American men and women are the most likely to have elevated aminotransferase activity. Among men, Mexican Americans are more likely than whites to be heavy/binge drinkers, and blacks are more likely to have hepatitis B or hepatitis C. Among women, Mexican Americans are more likely than whites to be obese and diabetic, and less likely to be heavy/binge drinkers; blacks are more likely than whites to have hepatitis B or hepatitis C, be obese or diabetic, and less likely to be heavy/binge drinkers. CONCLUSIONS: In this national sample, the prevalence of risk factors for liver disease varies by race/ethnicity. Mexican Americans and blacks have a greater risk of developing liver disease than their white counterparts. These findings are consistent with the observed racial/ethnic disparities in morbidity and mortality due to chronic liver disease and contribute to the efforts to identify the causes of these disparities. This information can be used by health professionals to tailor screening and intervention programs. [ABSTRACT FROM AUTHOR]

Chemotaxis (i.e., directed migration) of hepatic stellate cells to areas of inflammation is a requisite event in the liver's response to injury. Previous studies of signaling pathways that regulate stellate cell migration suggest a key role for focal adhesions, but the exact function of these protein complexes in motility remains unclear. Focal adhesions attach a cell to its substrate and therefore must be regulated in a highly coordinated manner during migration. To test the hypothesis that focal adhesion turnover is an essential early event for chemotaxis in stellate cells, we employed a live-cell imaging technique in which chemotaxis was induced by locally stimulating the tips of rat stellate cell protrusions with platelet-derived growth factor-BB (PDGF). Focal adhesions were visualized with an antibody directed against vinculin, a structural component of the focal adhesion complex. PDGF triggered rapid disassembly of adhesions within 6.25 mm, subsequent reassembly by 12.5 mm, and continued adhesion assembly in concert with the spreading protrusion until the completion of chemotaxis. Blockade of adhesion disassembly by growing cells on fibronectin or treatment with nocodazole prevented a chemotactic response to PDGF. Augmentation of adhesion disassembly with ML-7 enhanced the chemotactic response to PDGF. These data suggest that focal adhesion disassembly is an essential early event in stellate cell chemotaxis in response to PDGF. [ABSTRACT FROM AUTHOR]

The contractile force generated by hepatic stellate cells in response to endothelin-1 contributes to sinusoidal blood flow regulation and hepatic fibrosis. This study's aim was to directly test the widely held view that changes in cytosolic Ca2+ concentration ([Ca2+]i) mediate stellate cell force generation. Contractile force generation by primary cultures of rat hepatic stellate cells grown in three-dimensional collagen gels was directly and quantitatively measured using a force transducer. Stellate cell [Ca2+]i, myosin activation, and migration were quantified using standard techniques. [Ca2+]i was modulated using ionomycin, BAPTA, KCl, and removal of extracellular Ca2+ Removal of extracellular Ca2+ did not alter endothelin-1-stimulated force development or [Ca2+]i. lonomycin, a Ca2+ ionophore, triggered an increase in [Ca2+]i that was three times greater than that stimulated by endothelin-1, but only induced 16% of the force and 38% of the myosin regulatory light chain (MLC) phosphorylation induced by endothelin-1. Physiological increases in [Ca2+]i induced by hyperkalemia had no effect on contractile force. Loading BAPTA, a Ca2+ chelator, in stellate cells completely blocked endothelin-1-induced increases in [Ca2+]i but had no effect on endothelin-1-stimulated force generation or MLC phosphorylation. In contrast, Y-27632, a selective rho-associated kinase inhibitor, inhibited endothelin-1-stimulated force generation by at least 70% and MLC phosphorylation by at least 80%. Taken together, these observations indicate that changes in [Ca2+]i are neither necessary nor sufficient for contractile force generation by rat stellate cells. Our results challenge the current model of contractile regulation in hepatic stellate cells and have important implications for our understanding of hepatic pathophysiology. [ABSTRACT FROM AUTHOR]

Intestinal response to injury requires coordinated regulation of the tension exerted by subepithelial myofibroblasts (SEM). However, the signals governing relaxation of intestinal SEM have not been investigated. Our aim was to test the hypothesis that signal transduction pathways initiated by C-type natriuretic peptide (CNP) induce intestinal SEM relaxation. We directly quantified the effects of CNP on isometric tension exerted by cultured human colonic SEM. We also measured the effects of CNP on cGMP content, myosin regulatory light chain (MLC) phosphorylation, and cytosolic Ca[sup 2+] concentration. CNP induced relaxation of SEM within 10 s. By 10 min, relaxation reached a plateau that was sustained for 2 h. CNP-induced relaxation was saturable, with a maximal decrease in tension (51.7 ± 3.8 dyn) observed at 250 nM. SEM relaxation in response to CNP constituted ∼23% of total basal tension. CNP increased intracellular cGMP content and reduced MLC phosphorylation. Effects of CNP on cGMP and MLC exhibited the same dose dependence as CNP-induced relaxation. MLC phosphorylation decreased within 2 min of CNP exposure and was sustained for at least 45 min. CNP also stimulated a large transient increase in cytosolic Ca[sup 2+] concentration that occurred within 30 s and was nearly complete by 1 min. We also observed that calyculin-A, a potent inhibitor of MLC phosphatase, completely abolished the reduction in MLC phosphorylation induced by CNP. These results suggest that CNP induces intestinal SEM relaxation through cGMP-associated reductions in MLC phosphorylation. Moreover, these findings raise the possibility that CNP plays a role in intestinal wound healing. guanosine 3',5'-cyclic monophosphate; contraction; myosin; subepithelial myofibroblast; intestine [ABSTRACT FROM AUTHOR]

Cirrhosis, a pathological condition defined by deranged hepatic architecture resulting from progressive fibrosis, is the final common pathway through which nearly all chronic diseases of the liver produce morbidity and mortality. Historically, treatments for hepatic fibrosis have been directed against specific causes of chronic liver injury, and include corticosteroids for autoimmune hepatitis, interferon for hepatitis B and C, and iron depletion for haemochromatosis. However, there is no effective treatment for most causes of chronic liver disease. Fortunately, the past decade has witnessed great advances in our understanding of the fundamental pathophysiological mechanisms underlying fibrosis of the liver. It is now recognised that hepatic stellate cells (myofibroblast-like cells that encircle the sinusoids) are primarily responsible for hepatic fibrosis and subsequent progression to cirrhosis. In response to liver injury stellate cells undergo a phenotypic transformation that is termed activation, and characterised by chemotaxis, proliferation, contraction, fibrogenesis, and extracellular matrix degradation. Under conditions of persistent injury the behavioural responses of these stellate cells act in concert to bring about fibrosis of the liver. Recent investigations elucidating the signal transduction pathways that link hepatic injury to stellate cell function suggest novel targets at which treatment for fibrosis may be directed. For example, antagonism of TGF-β receptor signaling has been shown to modulate fibrosis in animal models. This work, as well as other studies in both humans and animals, indicates that hepatic fibrosis may be slowed or reversed. These results suggest that a rational approach to treatment can be developed based on our detailed understanding of the molecular and cellular mechanisms underlying cirrhosis, which will have a major impact on the clinical management of patients with chronic liver disease. [ABSTRACT FROM AUTHOR]

The role of G protein-coupled receptors and their ligands in intestinal epithelial cell signaling and proliferation is poorly understood. Here, we demonstrate that arginine vasopressin (AVP) induces multiple intracellular signal transduction pathways in rat intestinal epithelial IEC-18 cells via a V1A receptor. Addition of AVP to these cells induces a rapid and transient increase in cytosolic Ca2+ concentration and promotes protein kinase D (PKD) activation through a protein kinase C (PKC)-dependent pathway, as revealed by in vitro kinase assays and immunoblotting with an antibody that recognizes autophosphorylated PKD at Ser916. AVP also stimulates the tyrosine phosphorylation of the nonreceptor tyrosine kinase proline-rich tyrosine kinase 2 (Pyk2) and promotes Src family kinase phosphorylation at Tyr418, indicative of Src activation. AVP induces extracellular signal-related kinase (ERK)-1 (p44mapk) and ERK-2 (p42mapk) activation, a response prevented by treatment with mitogen-activated protein kinase kinase (MEK) inhibitors (PD-98059 and U-0126), specific PKC inhibitors (GF-I and Ro-31-8220), depletion of Ca2+ (EGTA and thapsigargin), selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (tyrphostin AG-1478, compound 56), or the selective Src family kinase inhibitor PP-2. Furthermore, AVP acts as a potent growth factor for IEC-18 cells, inducing DNA synthesis and cell proliferation through ERK-, Ca2+-, PKC-, EGFR tyrosine kinase-, and Src-dependent pathways. [ABSTRACT FROM AUTHOR]

OBJECTIVE:Hemodialysis patients with hepatitis B surface antigen (HBsAg) are considered to have the hepatitis B virus (HBV) and are segregated to limit transmission. However, transient de novo HBsAg has been identified in hemodialysis patients shortly after vaccination. Our hypothesis is that immunization rather than actual HBV infection is the most common cause of de novo HBsAg among hemodialysis patients.METHODS:We performed a prospective study between January, 1998 and June, 2000 of de novo HBV infection in over 2400 hemodialysis patients who were screened monthly for HBsAg using a standard enzyme immunoassay. Positive results were confirmed with a neutralization assay. If the confirmatory test was positive, anti-hepatitis B core antibody IgM testing was performed.RESULTS:We identified nine patients with de novo HBsAg confirmed with the neutralization assay. In eight of the nine patients with de novo HBsAg (89%), HBsAg was temporally related to HBV immunization. In none of these eight patients was there a detectable anti-hepatitis B core antibody IgM, an elevated ALT level, or clinical history suggestive of recent hepatitis. The mean age (± SD) of the four men and four women was 56.4 ± 18.8 yr. HBsAg was detectable within 3 days of immunization in most patients.CONCLUSION:Our results suggest that HBV immunization is the most common cause of detectable HBsAg in hemodialysis patients. Hemodialysis patients should not be screened for HBV within a week of immunization, and caution should be exercised when interpreting HBsAg seropositivity within 4 wk of HBV immunization. [Copyright &y& Elsevier]

Tests the hypothesis that hepatic stellate cells (HSC) contraction and relaxation around the sinusoid control hepatic blood flow in rats by modulating sinusoidal resistance. Comparison of force generation by non-muscle cell types; Quantitative measurements of HSC contraction and relaxation; HSC response to agonists and antagonists.

The objective of this study was to analyze a series of patients with Enterococcus faecium infection following transjugular intrahepatic portosystemic shunts (TIPS) in order to define the risk factors, outcome, and role of treatment including hepatic transplantation. This study is a case series from a tertiary referral center for liver transplantation. The medical records of four patients referred to one teaching hospital in San Francisco between 1990 and 1995 for evaluation or management of Enterococcal infection following TIPS were reviewed. A review of the microbiology records of all 314 patients who underwent TIPS at that institution and a MEDLINE search were performed to assess whether any other cases existed. The effect of therapy on survival was assessed, in particular, the repeated use of TIPS and prolonged courses of antibiotics. All four patients had thrombosis of their TIPS at the time of diagnosis of enterococcal bacteremia. All were treated with prolonged courses of intravenous antibiotics. One patient had echocardiographic evidence of subacute bacterial endocarditis with chronic aortic insufficiency. In all cases, liver transplantation was contraindicated in the acute setting because of uncontrolled endovascular infection. Two of four patients survived; these were the only two patients who had had a successful repeat TIPS. Enterococcal bacteremia is a rare complication following TIPS but carries a high mortality. It usually occurs in the setting of technically difficult TIPS with shunt thrombosis. Management should be focused on long term antibiotics and attempts at reestablishment of portal decompression with another TIPS. Liver transplantation should not be considered until the infection is cleared. Prophylaxis for Enterococcus species should be considered in technically difficult or unsuccessful TIPS. [ABSTRACT FROM AUTHOR]

The author discusses the importance of communication between primary care specialists (PCPs) and specialists. The author says that the interaction of the health care providers is the key to provide quality health care to the patient. He cites three practice traits that are related to the communication of both physicians such as adequate time during patient visit or consultation, the receipt of efficient reports particularly in patients with chronic conditions and nurses' monitoring of chronic patients.

To achieve the benefits of the patient-centered medical home (PCMH) model, the American College of Physicians has issued a policy paper addressing the relationship between specialist and subspecialist physicians and PCMH practices. This paper represents a significant step toward improving care coordination and quality by demonstrating that this model is supported by numerous specialties and subspecialties, recognizing the importance of building a strong medical neighborhood, and providing a framework that will foster improvements in care at the interface of PCMHs and PCMH neighbors (PCMH-Ns). Construction of a well-functioning medical neighborhood will, however, require some refinements. First, the proposed interaction typology between PCMHs and PCMH-Ns must be expanded to include innovative forms of interaction that do not depend on traditional office visits, but for which there are clear incentives. Second, the recommended care coordination agreements must be better standardized for the sake of practicality. Finally, genuine dialogue between PCMH and PCMH-N practices needs to be realized. [ABSTRACT FROM AUTHOR]

The authors reflect on the improvement of primary and specialty care. They argue that indications for referral and integrated decision support are exceptions to the health care system rules. A study on referral process was conducted at a university medical center and has resulted to communication inefficiency. They note that C. B. Forrest's proposal on typology can establish mutual duties for medical practitioners and will improve the quality of communication between physicians.

The article presents the authors' comments on whether an ideal biomarker exists for the progression of nonalcoholic fatty liver disease (NAFLD) in humans. They state that an ideal biomarker should have the characteristics including, it should be minimally invasive, it should allow repetitive measurements and should be able to identify early stages of the disease. They suggest that biomarkers for NAFLD require a combination of advanced techniques like genomics with polymorphism.

The authors discuss a clinician- and health care organization-informed approach to reduce clinical practice variation across the Los Angeles Department of Health Services (LADHS) by developing and implementing expected practices (EPs). They enumerate several steps involved in the approach to reducing variation in clinical practice, such as the establishment of Specialty-Primary Care work groups. They also elaborate on the use of EPs.

Comments on a study conducted by Ron Roizen et al, and published in the August 1999 issue of `Western Journal of Medicine,' which examined the relation between ethanol use and death from cirrhosis in the United States. Significance and drawbacks of the study; Results of the study; Pathogenesis of liver disease; Influence of societal changes on ethanol consumption.

The authors focus on the consideration of the electronic (e)Referral as a new model for the integration of primary and specialty care. The authors mention that health information technology is being utilized by eReferral for the association of primary care providers (PCPs) and specialists. They add that eReferral can help in the achievement of better care for individuals, populations, and lower costs if it will be widely adopted.

: PurposeTo assess the evidence supporting the efficacy of weight reduction for patients with nonalcoholic fatty liver.: MethodsPotentially relevant studies were identified by a computerized search of databases and a manual search of abstracts from scientific meetings. Studies were included if they reported histology, serum aminotransferase levels, or radiological imaging of the liver in obese adult patients who had undergone weight reduction. Weight reduction regimens included diet, exercise, antiobesity medications, gastric bypass, gastroplasty, or any combination of these interventions. Studies involving jejunoileal or small bowel bypass surgery were excluded.: ResultsWe identified 517 potentially relevant studies, of which 15 met the inclusion criteria: one randomized controlled trial (in abstract form), two nonrandomized controlled trials, nine case series, one retrospective review, and two case reports. Three studies included more than 50 patients, whereas nine studies had 25 or fewer patients. Twelve studies used behavioral, dietary, or pharmacologic therapy for weight reduction, and three studies used surgical interventions. Although all 15 studies demonstrated overall improvement in the measurements of liver outcome after weight reduction, more than half did not report histologic results.: ConclusionDespite general acceptance that weight reduction is an effective therapy for nonalcoholic fatty liver, this systematic review found little data to support or refute this recommendation. [Copyright &y& Elsevier]

A small percentage of human immunodeficiency virus (HIV)-infected individuals, termed elite controllers, are able to spontaneously control HIV replication in blood. As the gastrointestinal mucosa is an important site of HIV transmission and replication as well as CD4+ T-cell depletion, it is important to understand the nature of the immune responses occurring in this compartment. Although the role of the HIV-specific CD8+ T-cell responses in mucosal tissues has been described, few studies have investigated the role of mucosal HIV-specific CD4+ T cells. In this study, we assessed HIV-specific CD4+ T-cell responses in the rectal mucosa of 28 "controllers" (viral load [VL] of <2,000 copies/ml), 14 "noncontrollers" (VL of >10,000 copies/ml), and 10 individuals on highly active antiretroviral therapy (HAART) (VL of <75 copies/ml). Controllers had higher-magnitude Gag-specific mucosal CD4+ T-cell responses than individuals on HAART (P < 0.05), as measured by their ability to produce gamma interferon (IFN-γ), interleukin-2 (IL-2), tumor necrosis factor alpha (TNF-α), and macrophage inflammatory protein 1β (MIP-1β). The frequency of polyfunctional mucosal CD4+ T cells was also higher in controllers than in noncontrollers or individuals on HAART (P < 0.05). Controllers with the strongest HIV-specific CD4+ T-cell responses possessed class II HLA alleles, HLA-DRB1*13 and/or HLA-DQB1*06, previously associated with a nonprogression phenotype. Strikingly, individuals with both HLA-DRB1*13 and HLA-DQB1*06 had highly polyfunctional mucosal CD4+ T cells compared to individuals with HLA-DQB1*06 alone or other class II alleles. The frequency of polyfunctional CD4+ T cells in rectal mucosa positively correlated with the magnitude of the mucosal CD8+ T-cell response (Spearman's r = 0.43, P = 0.005), suggesting that increased CD4+ T-cell "help" may be important in maintaining strong CD8+ T-cell responses in the gut of HIV controllers. [ABSTRACT FROM AUTHOR]

Previous studies have suggested that polyfunctional mucosal CD8= T-cell responses may be a correlate of protection in HIV controllers. Mucosal T-cell breadth and/or specificity may also contribute to defining protective responses. In this study, rectal CD8= T-cell responses to HIV Gag, Env, and Nef were mapped at the peptide level in four subject groups: elite controllers (n = 16; viral load [VL], <75 copies/ml), viremic controllers (n = 14; VL, 75 to 2,000 copies/ml), noncontrollers (n = 14; VL, >10,000 copies/ml), and antiretroviral- drug-treated subjects (n = 8; VL, <75 copies/ml). In all subject groups, immunodominant CD8= T-cell responses were generally shared by blood and mucosa, although there were exceptions. In HIV controllers, responses to HLA-B27- and HLA-B57-restricted epitopes were common to both tissues, and their magnitude (in spot-forming cells [SFC] per million) was significantly greater than those of responses restricted by other alleles. Furthermore, peptides recognized by T cells in both blood and rectal mucosa, termed "concordant," elicited higher median numbers of SFC than discordant responses. In magnitude as well as breadth, HIV Gag-specific responses, particularly those targeting p24 and p7, dominated in controllers. Responses in noncontrollers were more evenly distributed among epitopes in Gag, Env, and Nef. Viremic controllers showed significantly broader mucosal Gag-specific responses than other groups. Taken together, these findings demonstrate that (i) Gag-specific responses dominate in mucosal tissues of HIV controllers; (ii) there is extensive overlap between CD8= T cells in blood and mucosal tissues, with responses to immunodominant epitopes generally shared by both sites; and (iii) mucosal T-cell response breadth alone cannot account for immune control. [ABSTRACT FROM AUTHOR]

Although hepatic myofibroblast (HMF) migration contributes to the development of fibrosis, the mechanisms coordinating this movement are uncertain. We determined the effects of lysophosphatidic acid (LPA) and platelet-derived growth factor-BB (PDGF) on actin polymerization, FAK tyrosine phosphorylation, and migration of cultured human HMFs. LPA (0.4–100 μM) stimulated migration, FAK tyrosine phosphorylation, and stress fiber assembly with a sigmoidal dose response. PDGF (1–250 ng/ml) stimulated migration, FAK tyrosine phosphorylation, and actin polymerization with a bell-shape dose–response characterized by a maximum at 10–25 ng/ml. Concentrations of cytochalasin D, which abolished FAK tyrosine phosphorylation, also blocked LPA- and PDGF-induced migration. A dose of 1–10 ng/ml PDGF acted synergistically with LPA (10 μM) to stimulate FAK tyrosine phosphorylation and migration, whereas higher concentrations of PDGF (100–250 ng/ml) inhibited FAK tyrosine phosphorylation and migration in response to LPA (10 μM). These data indicate that PDGF and LPA coordinately govern the migration of HMFs by differentially regulating FAK and suggest a novel model in which PDGF, acting as an amplifier/attenuator of LPA-induced signaling, facilitates HMF accumulation within injured areas of the liver. [Copyright &y& Elsevier]

A decision-analysis model was developed to compare the strategies to maintain hepatitis B virus (HBV) immunity in hemodialysis patients who responded to the primary HBV vaccine. Our hypothesis is that the routine, annual administration of the vaccine booster to all hemodialysis patients (non-screening strategy) is more cost-effective than the current strategy of vaccination based on anti-HBs titers (screening strategy). Under baseline assumptions, the screening strategy was less costly and was associated with fewer HBV infections than the non-screening strategy. The results of our model did not support our hypothesis, and indicate that regularly screening patients for HBV immunity before revaccination is less costly and more effective than the empiric vaccination of hemodialysis patients. [Copyright &y& Elsevier]