April 14, 2012

Inked or infected: Tattooing comes with risks

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By Jeffrey Kreisberg

04.14.12 | 03:30 pm

There was a time not long ago when those sporting multiple tattoos were thought to be sociopaths. I’m talking about bikers, gang bangers, and prisoners — you know the type — freaks, like Lisbeth, in “The Girl with the Dragoon Tattoo”.

Let’s fast forward to today. Body piercing and tattooing has become more and more popular among teens and young adults; they’re easy to get and quick and some are quite beautiful. Even minors can even get them with parental consent. It is estimated that 36% of Americans under 30 have skin designs.

But don’t let peer pressure and the ease of getting one stop you (and your parents) from carefully considering the risks, like infection.

Tatoo seekers should realize that we’re dealing with needles and blood here! Never mind injecting dangerous unregulated dyes, which may cause cancer, under your skin.

We’re also talking about viral infections spread by contaminated blood; viruses like hepatitis C and HPV. Point of fact, hepatitis C causes more American deaths than HPV.

The problem with being infected with hepatitis C is that most people don’t have early (acute) symptoms of disease and don’t even know they have the virus until it destroys their liver (chronic disease). If you have acute symptoms, they might include fatigue, loss of appetite, nausea, vomiting, dark urine, jaundice, joint pain, and fever.

Approximately 3.2 million Americans are infected with hepatitis C of whom 75 to 85 percent will have chronic infections. Infection with hepatitis C is the leading cause of liver transplants in America and contrary to hepatitis A and B, there is no vaccine for hepatitis C.

While sharing needles during illegal drug use is the biggest risk factor for contracting hepatitis C, there are increasing numbers of cases caused by some very common activities including tattooing, piercings, manicures and pedicures. In fact, it is estimated that tattooing may increase your risk of hepatitis C infection 2-to-3-fold.

However, there’s no need to panic. With proper precautions, these risks can be avoided. And, if you think you may have been infected you can be tested and treated.

To mitigate the risk of infection, be sure you go to a licensed tattoo parlor (a license should be prominently displayed). Do not let your friends tattoo you!

Since tattoo and body piercing instruments come in contact with blood and bodily fluids, infection is possible if instruments are used on more than one person without being sterilized or without proper hygiene. Professionals are required by law to have sterile instruments. I doubt your friends have an autoclave to sterilize instruments. Also, ask if the tattoo dyes have been kept in sterile containers — it is not required and could also be a source of infections.

Even if your tattoo parlor is licensed it's better to be safe than sorry. Here are some things you can check for yourself to be certain your tattoo parlor is safe.

  • Treat a tattoo as you would any other medical procedure. You want a tattoo parlor to be at least as clean as your doctor’s office.
  • Ask to see the tools the artist will use. The needles should be new, sterilized, and wrapped — no exceptions. The ink should be in small pots meant for single-use and anything that touches your skin should not be reused. And the artist should wear gloves.
  • Make sure the work area is free of any possible contamination from items like purses and cell phones.

Tattoos can be beautiful, artistic expressions of our inner selves. Just be sure you know the risks and go to a professional tattoo artist.

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Silent epidemic calls out for cure

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Kerri-Ann Smith ... "People think hepatitis C equals drug use." Photo: Simon Alekna

April 15, 2012

WHEN healthcare worker Kerri-Anne Smith started feeling constantly exhausted, she put it down to being a single mother raising four children while working and studying.

It was only during a course on blood-borne viruses that Ms Smith, from Toongabbie, west of Sydney, suspected she might have contracted an infection from a blood transfusion many years earlier.

She saw her doctor and her suspicions were proved correct: she had contracted hepatitis C, a slow-acting virus that can cause severe liver damage.

Two new treatments, approved by the Therapeutic Goods Administration this year and described as a medical breakthrough will give hope to patients such as Ms Smith, who was devastated by her diagnosis in 1994, 10 years after her blood transfusion.

''I was really shocked. I went to pieces, actually, and I felt I couldn't tell anyone,'' she said.

The stigma of having a condition closely associated with intravenous drug use was almost as bad as the symptoms, Ms Smith said, which included extreme fatigue and aches and pains.

''I had four small children and lived in a small community,'' she said. ''I didn't want anyone to know. I didn't want the kids being told that they couldn't have friends over to play. I hid it for the first eight years. There is a lot of ignorance about how it is transmitted.

''People think hep C equals drug use. I call it discrimination by assumption.''

Hepatitis C is often called the silent epidemic. It can take up to 15 years after infection for its sufferers to show any symptoms.

Ms Smith feared liver disease might also be her fate. She suffered from the hepatitis C strain genotype-1, the most common form of the disease in Australia and the hardest to treat.

It accounts for about half of hepatitis C cases but does not respond well to standard therapy.

The TGA has approved two new drugs, boceprevir and telaprevir, for people suffering genotype-1. They belong to a new class of medicine known as direct-acting antivirals, which work by preventing the hepatitis C virus from replicating in people with genotype-1.

Treatment takes about half the time of standard therapy and has a cure rate of up to 80 per cent.

Ms Smith was one of the first people in Australia to undergo treatment as part of a trial at Westmead Hospital with telaprevir and says that while the side effects, which included depression and skin rashes, were unpleasant, it was worth it.

''The side effects were a small price to pay if it meant not dying from end-stage liver disease.''

A price has not been set for the two treatments in Australia and both drugs are awaiting listing on the Pharmaceutical Benefits Scheme.

In the US, a course of treatment costs between $US48,000 and $US85,000 ($46,000 to $82,000), according to the medical news service MedPage Today. But the chief executive of Hepatitis NSW, Stuart Loveday, believes the treatments are cost effective.

''It's far more economical to fund treatment for those people who need it and will benefit from it rather than allow them to progress to severe liver disease,'' Mr Loveday said.

''That will be an even greater burden down the track on Australia's healthcare system. The cost of a liver transplant is about $130,000. That's just for the operation. Then there is an annual maintenance cost of about $15,000 per year.''

Professor Geoff McCaughan, the head of the liver immunobiology program at the Centenary Institute and director of the AW Morrow Gastroenterology and Liver Centre in Sydney, said the two new treatments were the first in a whole series of direct-acting antiviral medication.

''It is a major breakthrough,'' he said.

''They are the first stepping stone in a whole swag of new drugs which are in the pipeline. They will focus on shorter duration of therapy which can help people with all genotypes of hepatitis C.''

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Published on: 2012-04-12

Spirulina platensis, a cynobacterium used frequently as a dietary supplement had been found to exhibit many immune-stimulating and antiviral activities. It had been found to activate macrophages, NK cells, T cells, B cells, and to stimulate the production of Interferon gamma (IFN-gamma) and other cytokines.

Natural substances isolated from Spirulina platensis had been found to be potent inhibitors against several enveloped viruses by blocking viral absorption/penetration and some replication stages of progeny viruses after penetration into cells. We aimed to study whether this dietary supplement possesses any therapeutically feasible activity worthy of further larger controlled clinical evaluation.

Methods: Sixty six patients with chronic hepatitis C virus infection and eligible for inclusion had been randomized to either Spirulina or Silymarin treated groups for a period of six months treatment.The two groups were followed up and blindly compared for early (after 3 months) and end of 6 months treatment virological response.

The effects of both treatments on each of alanine aminotransferase (ALT), Chronic Liver Disease Questionnaire scores (CLDQ), Arizona Sexual Experience Scale scores (ASEX) and the occurrence of any attributable adverse events were also compared.

Results: Among the 30 patients who had been treated with Spirulina and completed the 6 months protocol, 4 patients (13.3%) had a complete end of treatment virological response and 2 patients (6.7%) had a partial end of treatment response defined as significant decrease of virus load of at least 2-logs10. Though the proportion of responders in Spirulina group was greater than in the Silymarin group, the difference was not statistically significant at the end of both 6 months (p = 0.12) and 3 months treatment (p = 0.22) by Exact test.

Alanine aminotransferase as well as CLDQ and ASEX scores were found to be more significantly improved in Spirulina than in Silymarin treated group.

Conclusions: Our results could suggest a therapeutically feasible potential for Spirulina platensis in chronic HCV patients, worthy to conduct a larger sized and longer study to confirm these safety and efficacy encouraging results.WHO Clinical Trial Registration ID:ACTRN12610000958088 http://apps.who.int/trialsearch/trial.aspx?trialid=ACTRN12610000958088

Author: Mostafa YakootAmel Salem
Credits/Source: BMC Gastroenterology 2012, 12:32

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Liver Cancer Predictors in Chronic Hepatitis B Identified

By: MARY ANN MOON, Oncology Report Digital Network

04/12/12

In patients with chronic hepatitis B who are negative for hepatitis B e antigen and have low viral loads, serum levels of hepatitis B surface antigen can be used to predict risk for hepatocellular carcinoma (HCC), Dr. Tai-Chung Tseng and colleagues reported in the May issue of Gastroenterology.

In such patients, high levels of hepatitis B surface antigen (HBsAg) indicate higher risk for liver cancer, regardless of low hepatitis B DNA levels, said Dr. Tseng of the Buddhist Tzu Chi General Hospital Taipei, and associates.

HBV DNA levels are considered the major driver of disease progression in patients with chronic hepatitis B, and those with low viral loads are usually considered to be at low risk for developing HCC. However, even these patients still carry some risk for the malignancy, with an estimated annual incidence of 0.06%.

"Therefore, identification of factors predictive of HCC other than viral load in these ‘low-risk’ patients remains [imperative]," the investigators wrote (Gastroenterology 2012 Feb. 13 [doi:10.1053/j.gastro.2012.02.007]).

"Recently, HBsAg quantification has become increasingly recognized as a marker for evaluating viral replication and possible host immune control over HBV infection. A lower HBsAg level is associated with ... a lower risk of hepatitis activity," they noted.

So Dr. Tseng and colleagues assessed a large cohort of treatment-naive patients who had chronic HBV infection with genotypes B or C, but no cirrhosis. The study subjects and had been enrolled in a study of HBsAg loss in 1985-1995, and study enrollment later was extended until 2000.

The study population comprised 2,688 HBV carriers aged 28 and older at baseline who underwent frequent liver function tests, serum sampling, and abdominal ultrasonography for HCC surveillance. Approximately 61% of them were men.

The average duration of follow-up was 14.7 years (range, 2.5 to 25.8 years). A total of 191 patients developed HCC during that time, with an overall incidence of 4.8 cases per 1,000 person-years.

The average interval between baseline and development of HCC was 11 years (range, 2.5 to 24.5 years).

As expected, HBeAg positivity, higher levels of HBV DNA, and higher levels of alanine aminotransferase all were associated with a higher rate of HCC. Other factors known to raise the risk of HCC did so in this study, including older age, male gender, and infection with genotype C.

HBsAg level also was found to correlate with HCC risk, in a dose-response manner. However, it was not as strong as the other predictors in the study population as a whole or in the subgroup of patients who were HBeAg positive.

But the researchers were particularly interested in patients who were HBeAg-negative and had low viral loads, and thus were lacking the two risk factors that best predicted HCC risk.

In a univariate analysis, the hazard ratio (HR) for developing HCC was 5.4 in such patients who had a high (1,000 IU/mL or greater) HBsAg level, compared with those who had an HBsAg level lower than 1,000 IU/mL.

Further multivariate analysis showed that a high HBsAg level remained an independent risk factor for HCC, with an HR of 13.7.

"These data suggest that HBsAg level may complement HBV DNA level in predicting HCC development," especially in patients with low viral loads, Dr. Tseng and colleagues said.

They proposed that patients with low viral loads but high HBsAg levels "may harbor more hepatocytes with HBV integration than those who have a low HbsAg level. Therefore, the higher risk of HCC ... may be attributed to the increased genomic instability as a result of integrated viral sequences, which play an important role in hepatocarcinogenesis."

In this study population, the subgroup of patients who had both a low HBV DNA level and a low HBsAg level showed a cumulative incidence of HCC of only 0.2%, which is similar to the level reported in control subjects in previous studies. Thus, a low HbsAg level accompanied by a low HBV DNA level appears to reflect adequate host immune control against HBV infection and can be used to identify patients at low risk for developing HCC.

Clinicians "urgently require a good indictor to stop nucleotide analogue therapy in HBeAg-negative patients. If an HbsAg level of less than 1000 IU/mL could be reliably used to define low-risk or inactive HBV carriers, we may adopt this cutoff level as the intermediate treatment goal," assuming that the results of this study are confirmed in future research, the authors wrote.

This study was supported by the Buddhist Tzu-Chi General Hospital Taipei Branch, the National Taiwan University Hospital, the Department of Health, and the National Science Council. Dr. Tseng’s associates reported ties to Abbott, Bayer, Bristol-Myers Squibb, Gilead Sciences, GlaxoSmithKline, Merck Sharp & Dohme, Novartis, and Roche.

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Timing Key in Rewriting Addict's Memory

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By Kristina Fiore, Staff Writer, MedPage Today

Published: April 13, 2012

Reviewed by Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston and Dorothy Caputo, MA, BSN, RN, Nurse Planner

Using a type of exposure therapy to wipe out the emotional triggers that drive drug addiction may be most effective when the brain is in the process of recalling and re-storing memories, Chinese researchers found.

Calling up a drug-related memory just before having "extinction" therapy -- seeing drug-related cues without being able to use -- was associated with diminished cravings in rat and human models, Lin Lu, PhD, of Peking University in Beijing, and colleagues reported in Science.

Performing this type of emotional-memory-scrambling as a memory is "reconsolidating" may eventually provide a means of treating addiction, according to David Epstein, PhD, of the National Institute on Drug Abuse (NIDA), a co-author on the paper.

The idea behind memory reconsolidation is that once a patient consciously recalls a memory, it has to be stored in the brain as a new memory all over again. It can be altered, however, during that process.

Epstein explained that by itself, extinction therapy -- similar to exposure therapy, which tempers PTSD symptoms in veterans by having them relive the traumatic moment -- doesn't work all that well in drug addiction because it doesn't weaken the initial memory that drives the user to seek out more drugs.

"It's only new learning that's superimposed on top of an old memory that stubbornly sticks around," he said.

But if you perform extinction during memory reconsolidation and that memory is vulnerable to interference, Epstein said, it can be weakened.

"So when you do the extinction [during reconsolidation], you're doing more than just creating the usual new learning," he said. "You're overwriting the old memory."

Researchers have already tinkered with emotional-memory reconsolidation in addicts by using pharmacologics, mainly propranolol (Inderal), but also in animal models with other agents not approved for use in humans. So Lu and colleagues' aim was to be able to interfere with the process without using any drugs.

In a series of experiments in rats, they found that those addicted to cocaine or heroin had no interest in the drugs after having reconsolidation and extinction -- but only if the reminder occurred 10 minutes or an hour before extinction therapy.

Drug-seeking behaviors returned if 6 hours had elapsed between the memory trigger and the exposure therapy, the researchers reported.

"The timing is really crucial," Epstein said. "It reflects the limited time window during which memories are vulnerable to disruption."

In another model in which the rats were able to self-administer drugs, only those that had reconsolidation and extinction -- not extinction alone -- were less likely to resume drug-seeking behaviors a month later, they found.

Lu and colleagues then tested the treatment in Chinese heroin addicts who'd had medically supervised detoxification and were inpatients at a treatment facility.

Patients had either extinction therapy alone, or memory retrieval -- a 5-minute video of heroin use -- either 10 minutes or 6 hours before extinction therapy in which they were exposed to drug images and paraphernalia but not given any drugs.

Only those who had the 10-minute interval between the memory trigger and extinction therapy had significantly reduced cravings (P<0.01) and a trend toward decreases in blood pressure (P=0.09) that were sustained for about 6 months, the researchers reported, noting, however, that there were no changes in heart rate.

"That's kind of astonishing considering how nonintrusive and how seemingly inconsequential this procedure is," Epstein said.

But he noted that the trial reveals nothing about what would happen to the heroin addicts if they were exposed to the real-world environmental cues that got them hooked in the first place.

One of the next steps, he said, would be to conduct similar trials in an outpatient setting. No such U.S.-based trial is planned, but Epstein said NIDA is currently conducting an outpatient trial that uses propranolol to interfere with memory reconsolidation in addicts -- although it "would be nice to be able to do it completely behaviorally," he said.

In terms of potential neural mechanisms, reconsolidation and extinction have been shown to depend on activation of N-methyl-D-aspartate (NMDA) receptors, the researchers said. In their study, they also saw increased expression of protein kinase C in the infralimbic cortex and diminished expression in the basolateral amygdala.

This may lead to structural changes in neurons that stabilize memory, they wrote.

In an accompanying editorial, Amy Milton, PhD, and Barry Everitt, PhD, of the University of Cambridge in England, agreed that "targeting maladaptive memories that play an important role in the persistence of addictive behavior may provide a new avenue for treatment interventions."

The study was supported by the National Basic Research Program of China, the Natural Science Foundation of China, and the National Institute on Drug Abuse.

Neither the researchers nor the editorialists reported any conflicts of interest.

Primary source: Science
Source reference:
Xue YX, et al "A memory retrieval-extinction procedure to prevent drug craving and relapse" Science 2012; 366: 241-245.

Additional source: Science
Source reference:
Milton AL, Everitt BJ "Wiping drug memories" Science 2012; 336: 167-168.

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Liver cancer can be caused by excess growth hormone

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Saturday, April 14th 2012, 12:14 PM

Vienna, April 14 — In a major discovery, Austrian scientists have found that the overproduction of a growth hormone can cause liver cancer.

The scientists at the Ludwig Boltzmann Institute for Cancer Research have shown that overproduction of growth hormone, led by hormonal or metabolic disorders, greatly accelerated the development of tumour diseases and caused liver cancer, Xinhua reported.

The growth hormone, however, is very difficult to detect, they added.

Liver cancer is the fifth most common cancer in the world and the third most common cause of tumour-associated deaths. So far, viral infections such as hepatitis B, hepatitis C and excessive alcohol consumption are considered the main culprits for causing liver cancer.

The scientists' studies aimed to understand the mechanism of a signalling molecule, known as STAT 5, in the development of liver cancer due to the overproduction of growth hormone.

Through experiments on mice, the scientists were able to show that this signalling pathway protects the liver in a healthy condition and can regulate metabolic processes essentially.

The overproduction of the growth hormone can also lead to kidney diseases and organ failure, said the report.

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By Brett Chase Apr 13, 2012 9:15 am

Both medical and investor communities will scrutinize results from an experimental, next-generation treatment for the liver-destroying virus hepatitis C.

It’s just about showtime for Gilead Sciences (GILD) and its experimental hepatitis C drug.

When specialist doctors from around the world gather in Spain next week to learn about new drugs in development for liver diseases, data for Gilead’s GS-7977 will be closely scrutinized and among the most anticipated research presented. The company hopes to show it has a real potential winner of a drug to treat the liver-wasting virus hepatitis C.

The big medical meeting, the International Liver Conference, begins Wednesday, and some scientific abstracts have been released in advance of the five-day gathering. However, a pair of key studies for Gilead’s drug are still embargoed until presentations starting Thursday. Gilead and a host of rivals are trying to develop an all-oral and better treatment regimen for hepatitis C. There has been a lot of excitement in the medical community and the investment world over Gilead’s drug.

“We have very high expectations for GS-7977,” Stifel Nicolaus analyst Joel Sendek says in a recent note recommending Gilead’s stock.

He is counting on the drug to spur future growth. Gilead is so dominant among HIV drug makers (with about 70% of the treatment market) that it’s unlikely to expand as rapidly in the future, he says.

Gilead also begins losing patent protection on HIV drugs later this decade, which is a key reason the company is expanding into hepatitis. A better hepatitis treatment potentially would bring in billions of dollars in new annual revenue. Gilead clearly has high hopes for 7977 as it was the strategic drug acquired with the recent $11 billion takeover of Pharmasset. (See Gilead Plans $11 Billion Takeover of Pharmasset to Gain Hepatitis Drugs.)

Shares of Gilead are up 12% this year but fell earlier this week. The stock closed at $45.72 Thursday.

While there are a number of other companies vying for the next generation of hepatitis C treatments, none of them made such a big wager on an acquisition. Among the other companies racing to bring a new hepatitis drug to market: Abbott Laboratories (ABT), Bristol-Myers Squibb (BMY), Merck (MRK), Vertex Pharmaceuticals (VRTX), Idenix Pharmaceuticals (IDIX) and Roche (RHHBY.PK). Abbott was among the companies whose hepatitis research was released earlier in advance of the Spain conference and turned some heads with impressive study data. (See Abbott Laboratories Rises to Record High on Hepatitis Drug Study.) A Bristol-Myers drug is being tested with Gilead’s 7977 in research to be presented at the medical meeting.

Hepatitis C is being carried by millions of people and many of them don’t even know they have the virus. As many as 170 million people worldwide have a chronic infection, according to one estimate. More than 3 million Americans are estimated to be chronically infected, according to government figures.

Vertex and Merck launched two much improved treatments for the virus last year.

The research focus now is to create a new class of drugs.

Twitter: @brettchase

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Health topics: What Is Hepatitis C? – Symptoms

Stethascope

Saturday, April 14, 2012

The hepatitis C virus, or HCV, is one of the most common causes of chronic liver disease. In some cases it leads to chronic hepatitis, cirrhosis and certain types of liver cancer. Hepatitis means “inflammation of the liver” and the hepatitis A, B and C forms are the most common in Western countries. All three types are associated with acute hepatitis. But only hepatitis B and C are associated with chronic liver disease. Vaccines are currently available to prevent hepatitis A and B, but there is no vaccine for hepatitis C.

HCV is primarily transmitted through contact with infected blood and has already affected an estimated 4 million Americans. Millions more are infected worldwide. Because symptoms often take years, if not decades, to appear, the U.S. Centers for Disease Control and Prevention estimates that 65 percent to 70 percent of those infected are unaware they have the disease.

What Is Hepatitis C?

Individuals react to the hepatitis C virus very differently. Approximately 15 percent of infected individuals will experience a full recovery within six months and will clear the virus from their systems. Most of these people will not even be aware they were ill, though virtually all will have some sort of liver cell injury. Some 85 percent develop chronic hepatitis. That means the virus may progressively damage their livers over time. Of those, most will develop chronic liver disease. The liver disease’s severity is highly variable. At one end of the spectrum are those with mild, stable hepatitis who never develop significant liver disease. At the other end are those with severe hepatitis. Over time, the disease may progress to cirrhosis, which is irreversible scarring and damage to the liver, and ultimately, liver failure.

About a third of those with hepatitis C will eventually develop cirrhosis. But the rate of liver damage varies. In some, serious liver disease can develop in five years. In others, it may take decades. Researchers do not understand why people react so differently to the virus. HCV causes 8,000 to 10,000 deaths each year in the United States and is the leading cause of liver transplants.

Until researchers isolated and cloned the virus in 1989, HCV was referred to as “non-A, non-B” hepatitis and no test was available to detect it. Without a way to screen for HCV, donated blood supplies carried the virus to a large number of unsuspecting recipients. Since 1992, highly accurate blood screenings have nearly eliminated the chance of contracting the virus through donated blood. Currently, the highest rates of new infection are among intravenous drug users. Up to 80 percent of new addicts become infected within the first year of injecting drugs. Intravenous drug use is thought to be responsible for half of all new infections and perhaps greater than half of all chronic HCV cases, according to the National Institutes of Health. If you experimented even once with injecting drugs, you should get tested for hepatitis C.

Range of Symptoms for Hepatitis C

Symptoms of HCV and its progression toward liver disease can vary widely from person to person. Many experience no outward signs of liver disease and their liver enzymes can be completely normal. But they may have mild, nonspecific symptoms such as fatigue, nausea, poor appetite or muscle and joint pain. The majority of cases remain undetected because the people disregard their symptoms or mistake them for the flu. Even those with acute hepatitis C may not have any symptoms in the first six months. A minority may experience fatigue, nausea and jaundice, which is a yellowing of the skin and eyes.

One common symptom is elevated levels of a liver enzyme known as alanine aminotransferase, or ALT. Chronic HCV sufferers may experience periods of elevated ALT levels, followed by periods of normal enzyme activity. For some, levels will fluctuate wildly, while one-third will experience consistently normal ALT levels. It is not clearly understood how ALT levels correlate to the physical symptoms of HCV. ALT levels can be important, however, in diagnosing HCV. By picking up on elevated ALT in a routine physical?s panel of blood tests, a physician may spot the need for an HCV test and therefore diagnose the disease in an earlier stage, when treatment prognoses tend to be better.

Unfortunately for many, symptoms only appear when a person is diagnosed with advanced liver disease. As HCV progresses towards cirrhosis, the fatigue and flu-like symptoms tend to get worse. Muscle weakness, weight loss, itching, jaundice, dark urine, fluid retention and abdominal swelling are common.

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