TAG: "Liver disease"

Six months of fish oil reverses liver disease in kids with intestinal failure


UCLA study finds promising results with fish oil.

Isabella Piscione following her fish oil treatment

Isabella Piscione following her fish oil treatment

Children who suffer from intestinal failure, most often caused by a shortened or dysfunctional bowel, are unable to consume food orally. Instead, a nutritional cocktail of sugar, protein and fat made from soybean oil is injected through a small tube in their vein.

For these children, the intravenous nutrition serves as a bridge to bowel adaptation, a process by which the intestine recovers and improves its capacity to absorb nutrition. But the soybean oil, which provides essential fatty acids and calories, has been associated with a potentially lethal complication known as intestinal failure–associated liver disease, which may require a liver and/or intestinal transplant. Such a transplant can prevent death, but the five-year post-transplant survival rate is only 50–70 percent.

Previous studies have shown that replacing soybean oil with fish oil in intravenous nutrition can reverse intestinal failure–associated liver disease. However, the necessary duration of fish oil treatment had not been established in medical studies.

Now, a clinical trial conducted at the Children’s Discovery and Innovation Institute at Mattel Children’s Hospital UCLA has found that, compared with soybean oil, a limited duration (24 weeks) of fish oil is safe and effective in reversing liver disease in children with intestinal failure who require intravenous nutrition. The researchers believe that fish oil may also decrease the need for liver and/or intestinal transplants — and mortality — associated with this disease.

The researchers’ study, “Six Months of Intravenous Fish Oil Reverses Pediatric Intestinal Failure Associated Liver Disease,” is published online in the Journal of Parenteral and Enteral Nutrition.

“With this particular study, we set out to determine if a finite period of six months of intravenous fish oil could safely reverse liver damage in these children, and we have had some promising results,” said lead author Dr. Kara Calkins, an assistant professor in the department of pediatrics in the division of neonatology and developmental biology at UCLA. “But because intravenous fish oil is not yet approved by the Food and Drug Administration and is much more costly than soybean oil, it is typically not covered by insurance. As a result, this oil is considered experimental and is currently available only under special protocols. If it proves safe and effective for patients, we hope it would eventually be available for wider use.”

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Discovery could improve liver transplant success


Natural substance found in blood vessels stimulates organ and tissue regeneration.

Bruce Hammock, UC Davis

Bruce Hammock, UC Davis

Researchers from multiple institutions, including UC Davis and Harvard Medical School, have discovered a novel and natural means that could increase the success of human liver transplants and speed the recovery of both the patient and the donor.

The study is especially significant because of the desperate shortage of livers among thousands of very ill patients, said lead researcher Dipak Panigrahy of Harvard Medical School, in work published online in the July 29 edition of Proceedings of the National Academy of Sciences (PNAS).

According to the American Liver Foundation website, 1,848 patients died in 2005 while waiting for a donated liver to become available. “Currently, about 17,000 adults and children have been medically approved for liver transplants and are waiting for donated livers to become available. The waiting list grows every year.”

The researchers found that a natural substance in blood vessels stimulates organ and tissue regeneration.

“The endothelium of blood vessels generate the lipid mediators called epoxyeicosatrienoic acids or EETs,” explained Panigrahy, assistant professor of pathology at Harvard Medical School and the Center of Vascular Biology Research at the Beth Israel Deaconess Medical Center, Boston. “EETs stimulate blood vessel formation, and organ regeneration is dependent on blood vessel formation. However, the role of EETs in organ regeneration is unknown. Our research shows that EETs stimulate organ and tissue regeneration.”

The 28-member discovered that “systemic administration of EETs significantly increased liver and lung regeneration by 23 percent to 46 percent when compared to control mice post partial liver resection,” Panigrahy said.

“This can be very useful in transplant both for the donor and the recipient in getting full function back with liver transplant,” said researcher and co-author Bruce Hammock, a distinguished professor of entomology with a joint appointment at the UC Davis Comprehensive Cancer Center.

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Free hepatitis B screenings offered on May 19


UC Davis event targets Asian-American adults.

A UC Davis medical student prepares to draw blood for hepatitis screening test.

Asian Americans and adult children of foreign-born Asian Americans are invited to a free hepatitis B screening event Sunday (May 19) at the UC Davis Comprehensive Cancer Center.

The event, from 10 a.m. to 2 p.m., is being held in recognition of Asian Pacific Islander Heritage Month and National Hepatitis Testing Day. It is funded with a federal grant aimed at boosting hepatitis B screening and preventing liver cancer in the Asian-American community.

“Our goal is to screen 1,000 foreign-born or children of foreign-born Asian Americans who are 18 years of age or older, and who are from areas where hepatitis B is endemic,” said Julie Dang, a community health program supervisor at the UC Davis Comprehensive Cancer Center and study program manager.

One of every 10 Asian Pacific Islanders has hepatitis, and most do not know they have been infected because often there are no symptoms. Untreated, hepatitis B virus can lead to liver cancer. Nearly 80 percent of liver cancer cases in Asian Americans can be directly traced to the Hepatitis B virus infection.

Screening participants who test negative and need vaccination will be put on a waiting list and contacted when vaccines become available.  All participants will receive a phone call and a result letter regarding their status.

“Individuals who test positive will receive individual counseling sessions to help them understand their status and get referrals for  care,” said Dang.

Additional event offerings will include risk-factor screenings (hepatitis C, diabetes and blood pressure), health education and light refreshments. All participants will receive a $10 Walmart gift card for their contribution to the study.

The event is co-sponsored by the Asian American Network for Cancer Awareness, Research and Training (AANCART), a national organization that is headquartered at the cancer center

The UC Davis Comprehensive Cancer Center is at 4501 X St. in Sacramento. To RSVP for the event, please contact Tina Fung at (916) 734-5371, or email her at tina.fung@ucdmc.ucdavis.edu.

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Home-based health visits increase hepatitis screening rates for Hmong Americans


First-of-kind study finds effectiveness of health care worker visits.

Twenty-four percent of Hmong study subjects who learned about hepatitis B and liver cancer were later screened.

In the first study of its kind, lay health workers increased screening rates for hepatitis B virus (HBV) and knowledge about the disease among a group of Asian Americans, known as the Hmong, UC Davis researchers have found. The study appears online today (April 23) in Cancer Epidemiology, Biomarkers & Prevention.

Hmong Americans, who originate from the mountainous areas of Laos, are at elevated risk for chronic hepatitis B — the major risk factor for liver cancer. They’re also at greater risk than either white or other Asian Americans for poor outcomes from liver cancer.

Although Hmong Americans often have health insurance, cultural and language barriers can prevent access to adequate screening for hepatitis B and liver cancer,  according to study author Moon Chen Jr., professor and associate director for cancer control at UC Davis, who led the research effort.

“Compared to other Asian Americans, liver cancer tends to be found at a later stage among the Hmong, and the survival rate is very low. While the overall survival rate for liver cancer is 10 percent, Hmong people who are diagnosed with the disease usually live for less than a year, and often for as little as a month or two,” said Chen.

“We wanted to decrease the probability of earlier death from liver cancer among the Hmong and increase the probability of earlier detection,” said Chen, who is also principal investigator for the Asian American Network for Cancer Awareness Research and Training (AANCART), the National Cancer Institute’s National Center for Reducing Asian American Cancer Health Disparities.

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Teen liver transplant recipient to honor donor at 2013 Rose Parade


Alfonso Garcia is spreading the word about the value of organ donation.

Alfonso Garcia and his parents pose with the UCSF medical team that cared for him during his 2010 life-saving liver transplant.

Alfonso Garcia still carries around a baseball cap that belonged to a 22-year-old man who passed away in 2010 having never met him. But the cap is just a small token of an even bigger reminder that the 18-year-old college freshman carries with him every day: the man’s liver, which saved Garcia’s life.

Since receiving the liver transplant at UC San Francisco, Garcia has made it a mission to spread the word about the value of organ donation by sharing the memory of his hero, George Becker, who died after a bad sinus infection spread to his brain.

Years later, Garcia still “thinks about George every day,” he said. “I don’t take anything for granted.”

As part of that mission, Garcia was selected by UCSF and the California Transplant Donor Network to ride on the Donate Life “Journeys of the Heart” float at the 2013 Tournament of Roses Parade in Pasadena on Tuesday, Jan. 1., in honor of Becker. The float will bear a florograph of Becker – a portrait made of flowers.

Garcia – whose father, Oscar Garcia, is a respiratory therapist at UCSF – was 15 years old when he was diagnosed with Wilson’s disease, a genetic disorder in which too much copper accumulates in the body’s tissues, causing damage to the liver and nervous system. His health was deteriorating quickly and he needed a liver transplant immediately.

Becker, who signed up to be an organ donor on his driver’s license when he was 16, ended up being the right match. And Garcia’s UCSF medical team – which included transplant surgeon Ryutaro Hirose, M.D.; Philip Rosenthal, M.D., medical director of the Pediatric Liver Transplant Program; Emily Perito, M.D., a clinical fellow in pediatrics and gastroenterology; and nurse practitioner Susan Diaz, M.S.N. – performed a successful transplant.

“It’s something that I appreciate and hold very close to my heart, the people at UCSF,” said Garcia, now a healthy, strong young man who just started attending the University of San Francisco. “Growing up, seeing my dad go to work every day, I didn’t know the significance of that until the day I was under the care of UCSF. I was like, ‘Wow, these people do an incredible job day in and day out to care for people and save people’s lives.’”

Recognized as a world leader in organ transplantation since 1964, the UCSF Organ Transplant Service has performed transplants for more than 10,000 patients and has played a key role in defining the field. The UCSF Liver Transplant Program, designated as a “Center of Excellence” by the U.S. Department of Health and Human Services, performs more liver transplants than any other hospital in Northern California – more than 2,300 liver transplants for adults and children since it began in 1988.

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Rose Parade tribute to a Bruin who saved lives

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Gene found that turns carbs into fat


UC Berkeley discovery could provide new target for treatments.

Fatty liver tissue

Image courtesy of The Sul Lab

A gene that helps the body convert that big plate of holiday cookies you just polished off into fat could provide a new target for potential treatments for fatty liver disease, diabetes and obesity.

Researchers at the University of California, Berkeley, are unlocking the molecular mechanisms of how our body converts dietary carbohydrates into fat, and as part of that research, they found that a gene with the catchy name BAF60c contributes to fatty liver, or steatosis.

In the study, to be published online Dec. 6 in the journal Molecular Cell, the researchers found that mice that have had the BAF60c gene disabled did not convert carbohydrates to fat, despite eating a high-carb diet.

“This work brings us one step forward in understanding fatty liver disease resulting from an excessive consumption of carbohydrates,” said the study’s senior author, Hei Sook Sul, professor at UC Berkeley’s Department of Nutritional Science and Toxicology. “The discovery of this role of BAF60c may eventually lead to the development of treatment for millions of Americans with fatty liver and other related diseases.”

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Most liver transplant candidates receive donation offers


UCSF study finds transplant wait-list deaths are not just due to organ availability.

Jennifer Lai, UC San Francisco

Most liver transplant candidates who died or were removed from the transplant list actually received one or more liver donation offers, according to a recent UC San Francisco study.

“What we found challenges the simplistic view that transplant dynamics are driven simply by organ availability,” said lead author, Jennifer Lai, M.D., assistant clinical professor in the UCSF Division of Gastroenterology and Hepatology. “Efforts to reduce wait-list mortality must target all aspects of mismatch between supply and demand.” 

Recognized as a world leader in organ transplantation since 1964, the UCSF Organ Transplant Service has performed transplants for more than 10,000 patients and has played a key role in defining the field. The UCSF Liver Transplant Program, designated as a “Center of Excellence” by the U.S. Department of Health and Human Services, performs more liver transplants than any other hospital in Northern California – over 2,300 liver transplants for adults and children since it began in 1988.

For this study, the research team analyzed data from 33,389 candidates listed in the United Network for Organ Sharing (UNOS)/Organ Procurement and Transplantation Network (OPTN) registry during the time frame of Feb. 1, 2005, to Jan. 31, 2010. Out of the candidates who had died or been delisted, 84 percent received one or more liver offers prior to death/delisting, indicating that they had an opportunity to undergo transplantation. Reasons for liver offer refusals were reported as donor quality/age or other donor-related factors, size compatibility or recipient readiness.

“Understanding the real-time factors involved in the decisions regarding liver transplant offers is vital to improving the wait-list process,” said senior author, John Roberts, M.D., professor of surgery and chief of the UCSF Division of Transplantation. “While some of the factors are beyond control, others can be managed.”

Simply increasing the availability of deceased donor livers or the number of offers may not necessarily reduce wait-list mortality, according to the study, published in the leading journal in its field, Gastroenterology. Instead, the study suggests that efforts must be made to understand multiple factors involving candidates, donors and transplant centers to help influence what is often a complex and dynamic decision to accept or decline a liver offer.

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New drug successfully halts fibrosis in animal model of liver disease


Study suggests a NOX inhibitor could provide effective treatment for the disease.

David Brenner, UC San Diego

A study published in the online journal Hepatology reports a potential new NADPH oxidase (NOX) inhibitor therapy for liver fibrosis, a scarring process associated with chronic liver disease that can lead to loss of liver function.

“While numerous studies have now demonstrated that advanced liver fibrosis in patients and in experimental rodent models is reversible, there is currently no effective therapy for patients,” said principal investigator David A. Brenner, M.D.,  vice chancellor for Health Sciences and dean of the School of Medicine at the University of California, San Diego. “This new study provides important validation of the role of NOX in liver fibrosis, and suggests that a NOX inhibitor could provide an effective treatment for this devastating disease.”

Most chronic liver diseases are associated with progressive fibrosis, which is triggered by the loss of liver cells and the activation of inadequate wound healing pathways. In addition, oxidative stress — which results from an inappropriate balance between the production and clearance of highly reactive molecules involved in cell signaling called reactive oxidative species (ROS) — leads to aberrant tissue repair in the liver.

When the liver is injured — for example, through hepatitis or alcohol abuse — HSCs are activated to become myofibroblasts, cells which play a crucial role in wound healing and the body’s response to inflammation by recruiting immune cells called macrophages to the injury site. This process, triggered by intracellular signalling pathways involving NOX, can result in an abundance of scarring and eventually result in the loss of organ function.

By inhibiting NOX, the researchers theorized that myofibroblast activation and macrophage recruitment could be interrupted, preventing further fibrosis and potentially allowing regression of established fibrosis.

They assessed the effectiveness of treatment with GKT137831 — a NOX1/4 inhibitor developed by Genkyotex SA of Geneva, Switzerland — in mouse models, and found that treatment with this NOX inhibitor suppressed ROS production, as well as NOX and fibrotic gene expression.

“These data highlight the excellent pharmacological properties of GKT137831 and the broad potential for its use in fibrotic diseases,” said Patrick Page, chief development officer at Genkyotex and contributor to the study.

According to Brenner, the next steps include a clinical trial with this drug in patients with liver fibrosis.

Additional contributors include Tomonori Aoyama, UC San Diego and Juntendo University School of Medicine, Tokyo; Yong-Han Paik, Yonsei University College of Medicine, Seoul, Korea; Sumio Watanabe, Juntendo University; Benoît Laleu, Francesca Gaggini, Laetitia Fioraso-Cartier, Sophie Molangpo, Freddy Heitz, Cédric Merlot and Cédric Szyndralewiez, GenKyoTex SA, Geneva.

The study was funded in part by grants 1 R24 DK090962, 5 P50 AA011999 and 5 R01 GM041804 from the National Institutes of Health and by the American Liver Foundation.

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Deadly liver cancer may be triggered by cells changing identity


UCSF researchers triggered cellular transformation — and caused tumors to form in mice — by activating just two genes.

Holger Willenbring, UC San Francisco

A rare type of cancer thought to derive from cells in the bile ducts of the liver may actually develop when one type of liver cell morphs into a totally different type, a process scientists used to consider all but impossible. UC San Francisco researchers triggered this kind of cellular transformation — and caused tumors to form in mice — by activating just two genes. Their discovery suggests that drugs that are able to target those genes may provide a way to treat the deadly cancer, known as cholangiocarcinoma. It also shows, yet again, how the process of scientific discovery involves serendipity as well as skill.

The study appears as an advanced online publication today (July 16) in the Journal of Clinical Investigation and will appear later in the August print edition.

The two cell types, hepatocytes and biliary cells, exist side by side in the liver, but don’t normally change their “stripes” — their cellular function — let alone turn into each other. Scientists have therefore assumed that hepatocellular carcinomas, the most common kind of liver cancer, start in the hepatocytes and that cholangiocarcinomas, the bile duct cancers, start in the biliary cells.

Hepatocytes, which form the bulk of the liver, “are very good at making other hepatocytes,” said Holger Willenbring, Ph.D., an associate professor of surgery, a member of the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research at UCSF, and a senior author of the study. “They can divide many times but are restricted in the progeny they produce. They either produce more hepatocytes or, if something goes wrong, can cause hepatocellular carcinomas.”

The study started when Xin Chen, Ph.D., an assistant professor of bioengineering and therapeutic sciences and a senior author of the manuscript, tried to make something go wrong in the hepatocytes as a way to explore the origins of hepatocellular carcinoma. Chen and her group hoped to induce the cancer in mice by activating oncogenes, genes that trigger cancer.

Things did go awry in the hepatocytes — but not in the way the researchers expected. In specific conditions, mice developed cholangiocarcinoma instead of hepatocellular carcinoma. “We were very surprised,” Chen recalls. “How did that happen?”

The two scientists figured some of the genes they had activated might have reprogrammed the hepatocytes in a way that turned them into aberrant biliary cells, capable of forming tumors. Their chief suspects were two genes, NOTCH, which is known to be involved in the embryonic development of bile ducts, and AKT, which has been shown to play a role in many tumors.

The scientists used bits of bacterial DNA called plasmids as delivery vehicles to boost levels of NOTCH and AKT in the liver. Three-and-a-half weeks after injecting these plasmids into mice, small white growths appeared on the surface of their livers and, by five weeks, the tumors had spread through the liver. Now the scientists needed to trace the origins of these cancer cells.

Willenbring’s lab had previously developed a method for labeling mouse hepatocytes so that they, and any cell they turned into, would glow. They put this “hepatocyte fate-tracing” system to work and were able to show that the cancerous cells that formed bile duct tumors had in fact started out as hepatocytes.

For many years, scientists had believed that development of cells proceeded in one direction, moving step-by-step from primordial stem cells to fully differentiated adult cells. In recent years, researchers have shown that, by turning on certain genes, mature cells can go back in time to become stem cells or even move sideways to become other kinds of adult cell.

“This highlights how readily one cell can be converted into another and how cancer can do it for you very efficiently,” Willenbring said. “For us, it’s fairly shocking. It only took two oncogenes and it all happened in a few weeks.”

The findings also help explain another puzzle: why the incidence of bile duct cancer is higher in people with hepatitis. “Since hepatitis doesn’t do anything to biliary cells that didn’t quite make sense,” Willenbring said

Now there’s a new way to look at it, he suggests. As hepatocytes and their genomes become disarrayed by disease, Willenbring says, they may activate oncogenes in much the same way their experiment did, causing the cells to change identity and become cancerous.

Having shown that NOTCH and AKT are the triggers in this tumor-inducing process, Chen and her team are now hunting for therapies. Working with colleagues from Genentech Inc., they are testing antibodies that may blunt the activity of the genes and halt or reverse the growth of bile duct cancers in mice. “The preliminary results with the therapeutic antibodies are very encouraging,” Chen says. If they find the right formula, they may have an answer for a currently untreatable cancer.

Biao Fan, Yann Malato, Diego F. Calvisi, Syed Naqvi, Nataliya Razumilava, Silvia Ribback, Gregory J. Gores, Frank Dombrowski and Matthias Evert contributed to the research.

Funding support came from the California Institute of Regenerative Medicine, National Institutes of Health, Deutsche Forschungsgemeinschaft and the China Scholarship Council.

UCSF is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care. For further information, please visit www.ucsf.edu.

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Liver disease expert joins UC Davis faculty


Yu-Jui Yvonne Wan will serve as professor and vice chair of research.

Yu-Jui Yvonne Wan

Yu-Jui Yvonne Wan, a national leader in the study of liver diseases whose work focuses on the role of retinoids and their receptors in control of liver function, joined the Department of Pathology and Laboratory Medicine at UC Davis as professor and vice chair of research on July 1.

Wan also will serve as scientific director of a new biorepository program, working with Senior Associate Dean for Research Lars Berglund to develop a master plan to expand and unite current biorepositories into a comprehensive tissue-banking service spanning the health system. She also will participate in the Human Anatomical Specimen and Tissue Oversight Committee chaired by Executive Associate Dean Fred Meyers and will report to Department of Pathology and Laboratory Medicine Chair Lydia Pleotis Howell.

“Dr. Wan is an award-winning researcher and mentor with more than 30 years’ experience in academic medicine,” Howell said. “Her work on retinoic acid, vitamin A and related nuclear receptors is advancing knowledge of liver cell differentiation, proliferation, metabolism and disease processes, including cancer, metabolic syndrome, obesity, alcoholic liver disease and cardiovascular disease. In addition, her emphasis on translational research and education complements existing efforts under way in our stem cell biology, cancer and pharmacogenomics programs. The department and I are excited to have Dr. Wan lead integration of our clinical and research faculty into multidisciplinary collaborations that will create innovative solutions to scientific and health care problems.”

Wan came from the University of Kansas Medical Center, where she was a professor of pharmacology, toxicology and therapeutics, program leader of the Cancer Biology Program and director of the Liver Center. Before that, she was a professor of pathology at UCLA. She is recognized for establishing the Human Liver Depository, which has become an indispensible resource for scientists worldwide seeking liver tissue, serum and blood for studies. The repository contains more than 1,500 liver specimens with extensive corresponding patient data.

Wan has received many honors and awards, including the 2010 Chancellor’s Club Research Award from the University of Kansas, SIG Elsevier Mentoring Award from the Society of Toxicology, California’s Distinguished Women in Research Award and Richard Weitzman Award. She received her doctorate in pathology from Hahnemann University (now Drexel University College of Medicine) and began her career in the pathology department at UCLA.

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Hepatitis: UCSF & San Francisco at ground zero


UCSF with several initiatives to address potentially life-threatening condition.

Viral hepatitis chronically infects between 3.5 and 5.2 million people in the U.S. and more than 30,000 in San Francisco, alone — but only about 1 in 3 people who are infected know it, according to a report by the U.S. Department of Health and Human Services.

San Francisco is a clinical hot spot for viral hepatitis infection, and UCSF is at the forefront in research, public health programs, and clinical trials to prevent and fight the potentially life-threatening condition.

UCSF faculty and staff in the schools of dentistry, medicine, nursing and pharmacy and UCSF Medical Center are engaged in a range of efforts, sometimes joined by students, often with partners in San Francisco city and county government and in affected populations. They aim to educate individuals at risk for the disease about prevention and vaccination, to identify people who are infected and to ensure that those who need treatment receive it.

Among the UCSF initiatives are:

  • a free screening clinic in Chinatown
  • the use of a new computerized check-in system in UCSF Medical Center’s acute care clinic that screens for individuals at risk for hepatitis B and expedites follow-up care
  • public health awareness programs aimed at highly affected populations, including Vietnamese Americans, who have a 1-in-7 incidence of hepatitis B
  • screening and prevention outreach for injection drug users at high risk for hepatitis C infection
  • participation in the coordination and improvement of citywide activities, such as the San Francisco Hep B Free program
  • testing new treatments
  • investigating the causes of chronic infection and why vulnerability to chronic infection and treatment responses vary among individuals.

Viral hepatitis primarily is caused by three unrelated viruses — hepatitis A, B and C viruses. All attack the liver, but hepatitis B and hepatitis C are largely responsible for an increasing number of liver cancer deaths. There are effective vaccines for hepatitis A and hepatitis B, but not for hepatitis C.

Potential exposures to hepatitis B are often due to infected blood, unprotected sex or mother-to-child transmission during birth. Unlike newborns, most untreated, newly infected adults clear the infection.

In San Francisco, hepatitis B is common because of the large Asian-American population in which the disease has been passed down from mother to newborn over many generations. A goal of the Health and Human Services action plan is to eliminate mother-to-child transmission.

Hepatitis C is transmitted most easily through exposure to infected blood, and compared to hepatitis B is more apt to become a chronic infection in newly infected adults.

Nationwide, hepatitis C virus has surpassed HIV as a cause of death, according to a U.S. Centers for Disease Control and Prevention (CDC) report published earlier this year. Injection drug users may be at greater risk of being infected with hepatitis C than with human immunodeficiency virus (HIV). Millions of baby boomers were infected before testing became available to screen blood products.

In May, the CDC proposed draft recommendations calling for people in the U.S. born between 1945 and 1965 to be screened for hepatitis C. In the U.S., more than 1 million in this age group are believed to be unknowingly, chronically infected.

Although hepatitis C infection rates have dropped considerably, infection is still epidemic among injection drug users. HIV prevention has led to lower rates of infection, but still more than half of injection drug users are infected with hepatitis C. Locally, prevention, testing and counseling for hepatitis C have become public health priorities.

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More than 1/4 L.A. homeless adults have hepatitis C


Nearly 1/2 don’t know it.

Lillian Gelberg, UCLA

Recent government studies show that hepatitis C, which can destroy the liver and necessitate a liver transplant, now kills more American adults than AIDS, and new UCLA research shows just how prevalent the disease is among homeless adults in downtown Los Angeles.

In a study published in the July–August issue of Public Health Reports, researchers found that 26.7 percent of homeless adults tested and surveyed in downtown Los Angeles’ skid row were infected with the hepatitis C virus (HCV) — more than 10 times the 2 percent rate among the general U.S. population. Of those surveyed, 46.1 percent were unaware that they were infected. Four percent of the sample were HIV-positive.

Few of the infected homeless adults surveyed had ever received any treatment for their HCV, said Dr. Lillian Gelberg, professor of family medicine at the David Geffen School of Medicine at UCLA, who led the study with Dr. Marjorie Robertson of the Public Health Institute’s Alcohol Research Group. Less than 3 percent of those who knew they were infected had ever been treated.

“Their hepatitis C can result in high costs to the public and the health care system if progression of their disease is not halted through treatment,” said Gelberg, who is also a professor of public health at the UCLA Fielding School of Public Health. “The costs of their untreated hepatitis C may start escalating soon, as many are approaching 20 years of infection, which is the point at which we see escalating risk for liver cirrhosis and end-stage liver disease, requiring expensive health services utilization and liver transplantation.”

The study surveyed 534 homeless adults from 41 shelters and meal programs in the skid row area between June 2003 and February 2004. Most were males and the majority were African Americans. Each was tested for hepatitis B and C and for HIV. Overall, the researchers found that HCV prevalence was significantly higher among those homeless individuals who had injected drugs or been in prison; who were 40 years of age and older; who had less education; or who were U.S.-born.

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