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June 2010 HCV Advocate

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In This Issue:

DC Rally = AWESOME
Alan Franciscus, Editor-in-Chief

Direct-Acting Antiviral Drug Update from EASL
Liz Highleyman

HealthWise: Making Friends with Fatigue
Lucinda Porter, RN


Disability & Benefits: Health Care Reform Changes for 2010
Jacques Chambers, CLU




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DC Rally = AWESOME
—Alan Franciscus, Editor-in-Chief

Some 250 viral hepatitis advocates gathered in Washington D.C. to celebrate World Hepatitis Day (May 19, 2010) and to demand that Congress show some leadership and provide funding for hepatitis B and hepatitis C by supporting and endorsing HR 3974 (Viral Hepatitis and Liver Cancer Control and Prevention Act). 

Lorren Sandt, Chair, National Viral Hepatitis Roundtable commented “We will no longer be silent—it’s time to make Congress fund viral hepatitis.”  Many signs proclaimed the same message and stressed that no one should die from viral hepatitis B or C.  Other signs stated that “Silence is Deadly” and “Pass HR 3974 NOW!” 

The rally protesters were from all walks of life and reflected the diversity and the ‘real’ population of people living with hepatitis B and C.  In addition to hepatitis B and C advocates and various hepatitis organizations, there were supporters from needle exchange, harm reduction organizations, HIV organizations, recovery organizations, veterans, medical providers and supporters from congress.

Many congressmen spoke at the rally including one of the original sponsors of HR 3974—Mike Honda (CA) as well as other congressional supporters, such as Dr. Bill Cassidy (LA), and Charles Dent (PA).

After a group photo there was a ceremony —“Silent Vigil:  Tribute to those lost to hepatitis B and hepatitis C.”  People carried placards with pictures of those who have died of viral hepatitis. 

The person who stole the hearts of everyone at the rally was Elijah who is currently undergoing HCV treatment.  Elijah is 4 going on 5 years old and talked about his treatment journey and getting shots of interferon.  Elijah received a thunderous ovation when he told the crowd “I deserve a cure.” 

Winding up the day Martha Saly, Director, National Viral Hepatitis Roundtable commented that “We stand united to demand action from Congress.”  Martha went on to comment on a recurring theme from rally participants: “We will no longer be silent. We will no longer be ignored.  The time to act is now!”

Next year the rally will be even bigger so mark your calendars and plan to attend—hopefully we will be celebrating the passage of HR 3974.

A big shout out to the rally organizers, Martha Saly (NVHR), Chris Taylor (NASTAD), Lorren Sandt (NVHR) and Ryan Clary (Project Inform) for coordinating the rally and making it a big success.


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Direct-Acting Antiviral Drug Update from EASL
—Liz Highleyman

At the 45th Annual Meeting of the European Association for the Study of the Liver (EASL) in April, researchers presented data on many experimental direct-acting antiviral drug candidates for hepatitis C. Unlike interferon-based therapy, which stimulates the immune system to fight HCV, direct-acting agents interfere with specific steps of the viral lifecycle (for more information see “How Do Targeted Anti-HCV Drugs Work?” in the December 2009 HCV Advocate).

This report covers experimental HCV protease inhibitors, which are furthest along in the development pipeline; HCV polymerase inhibitors and all-oral combinations will be covered next issue.

Comment: We are changing the way we report on coverage for the EASL conference.  Liz Highleyman will be writing up the information released and I will be providing the editorial comments about the drugs discussed in this article.  –Alan Franciscus

Telaprevir
T. Berg and colleagues presented data from Study 107, an open-label rollover study of Vertex’s NS3/4A HCV protease inhibitor telaprevir that included HCV genotype 1 patients who did not achieve sustained virological response (SVR) in the standard therapy control arms of the Phase 2 PROVE trials. Participants received 750 mg telaprevir three-times-daily for 12 weeks in combination with pegylated interferon alfa-2a (Pegasys) plus ribavirin, then continued standard therapy for 24 weeks (81 patients) or 48 weeks (34 patients), depending on response at week 4.

Overall, 59% achieved SVR (undetectable HCV RNA 24 weeks after completion of treatment). Response varied, however, according to type of previous treatment failure. Almost all prior relapsers achieved SVR when retreated for either 24 weeks (96%) or 48 weeks (100%). Partial responders and people with prior viral breakthrough had SVR rates of 60% and 86%, respectively, when retreated for 24 weeks, though none of the four patients treated for 48 weeks achieved sustained response. The SVR rate for prior null responders was just 17% with 24 weeks retreatment, but rose to 56% at 48 weeks. Among people with rapid virological response (RVR), or undetectable HCV RNA at week 4, SVR rates were higher in all groups. About half of the participants developed skin rash and 9% stopped treatment early due to adverse events.

Comments: Telaprevir continues to show impressive results especially in HCV genotype 1 treatment experienced patients—the most difficult to treat  This group is the most in need of new therapy so hopefully the larger studies will continue to show high response rates.  The study also demonstrates that a 48-week treatment period confirms the need for longer duration of treatment compared to the 24-week treatment duration for treatment naive patients.

The high rates of skin rash are an on-going problem in telaprevir studies, but since only 9% of patients stopped treatment due to all adverse events it would seem that the skin rash is manageable and for most doesn’t lead to discontinuation of therapy. –AF

Types of Non-Response

  • Prior null responders:  Patients who had a viral load reduction < 1 log10 at week 4 or < 2 log10 at week 12). 
  • Prior partial responders:  Patients who had a viral load reduction > 2 log10 at week 12, but who had detectable HCV RNA at week 24
  • Prior relapsers:  Patients who had an undetectable viral load during treatment, but had detectable viral load after treatment ended. 
  • Prior viral breakthrough:  Patients who had undetectable viral load during treatment, but detectable viral load before the end of treatment

In another trial (Study C208), X. Forns and colleagues found that telaprevir plus pegylated interferon alfa-2a or alfa-2b (Pegasys or PegIntron) and ribavirin produced high SVR rates among previously untreated genotype 1 patients when taken either twice or three times daily (1125 mg every 12 hours or 750 mg every eight hours). Participants took telaprevir for 12 weeks and continued pegylated interferon/ribavirin through 24 or 48 weeks depending on early response. About two-thirds (68%) had undetectable HCV RNA from week 4 through 20 and stopped therapy at 24 weeks, while 18% required treatment for 48 weeks. SVR rates were high regardless of telaprevir frequency or type of pegylated interferon (85% every eight hours with Pegasys; 81% every eight hours with PegIntron; 83% every 12 hours with Pegasys; and 82% every 12 hours with PegIntron). Again, the most common adverse events were skin rash and pruritus (itching), and 8% discontinued due to adverse events.

Comments:  This is the same study reported on in the December 2009 HCV Advocate.  It is important for a couple of reasons—the SVR rates for telaprevir taken with Pegasys plus ribavirin and telaprevir taken with PegIntron were similar.  But the big news is that response rates with the twice-a-day dose (every 12 hours) were comparable to the three-times-a-day dose.  Hopefully, more studies will be conducted because reducing the dosing schedule would be a big advantage in helping with adherence to treatment.  –AF

Finally, G. Foster and colleagues tested telaprevir in people with HCV genotypes 2 or 3, which respond better to interferon than genotype 1. Study C209 included 49 previously untreated patients randomly assigned to receive telaprevir alone (750 mg every eight hours), telaprevir with Pegasys plus 800 mg ribavirin, or Pegasys/ribavirin with placebo for two weeks; everyone then received standard therapy through week 24.

Among genotype 2 patients HCV RNA declined steeply in all treatment arms (-3.7, -5.5, and -4.8 log10 , respectively, at day 15), but the telaprevir monotherapy arm was less likely to achieve SVR (56%, 100%, and 89%, respectively).

Among genotype 3 patients, telaprevir monotherapy demonstrated minimal activity compared with the other arms (-0.5, -4.9, and -4.7 log10 , respectively); SVR rates were also lower (50%, 67%, and 44%, respectively) relative to genotype 2 patients. The investigators concluded that “telaprevir alone has substantial antiviral activity against HCV genotype 2 while its activity against genotype 3 is limited.”

Comments:  Although this is a study with a small patient population I believe this is one of the largest (to date) designed to see how well the telaprevir combo performs in people with HCV genotypes 2 and 3.  Genotype 2: While the SVR results were higher in the telaprevir combo group compared to the group that received only Pegasys plus ribavirin, the results were not that much better.  This could be due to the small patient population so larger studies are needed to find out if the increase in response outweighs the potential risks of subjecting patients to a direct antiviral.  Genotype 3: The results from the genotype 3 arms clearly show no benefit from the use of the triple combination of telaprevir, Pegasys and ribavirin.  –AF

Boceprevir
P. Kwo and colleagues evaluated 206 treatment-naive genotype 1 chronic hepatitis C patients in the Phase 2 SPRINT-1 trial who received PegIntron plus ribavirin for a four-week lead-in period before adding Merck/Schering-Plough’s NS3 HCV protease inhibitor boceprevir (800 mg three times daily) and continuing on triple therapy for an additional 24 or 48 weeks. A majority (64%) had undetectable HCV RNA after four weeks on triple therapy. SVR rates were high, 82% with 28 total weeks of treatment and 94% with 48 total weeks. However, among late responders (18%) who first achieved undetectable viral load after week eight, sustained response was more likely with 48 rather than 28 total weeks (79% vs 21%, respectively). While baseline characteristics could not predict in advance who would respond to shorter treatment, virological responses during early therapy appear likely to do so, allowing for response-guided therapy, the researchers concluded.

Comments:  The important finding of this study was that response-guided therapy is important with the boceprevir combo in people who are late responders.  Another interesting finding is the 82% SVR with the group that was treated for 28 weeks vs. the 94% in the group that received the combination for 48 weeks.  It will be interesting to see the results in the patient populations treated with the boceprevir combo in the phase III study because a larger patient population will give us a much clearer picture of the advantages of 28 vs. 48 weeks of treatment with the boceprevir combo.  –AF

In a related analysis, J. Vierling and colleagues reported findings from a long-term follow-up study of boceprevir. They analyzed blood samples from 604 genotype 1 chronic hepatitis C patients in three previous trials (SPRINT-1 and the PO3659 and PO4887 studies of prior nonresponders); participants were treated with boceprevir at various doses plus PegIntron, with or without ribavirin. During up to three years of follow-up, none of the 290 patients who achieved SVR experienced later relapse. Among all 604 participants, 5% experienced serious adverse events during extended follow-up. Eighteen boceprevir resistance mutations were identified.

Comments:  The finding of long term response is good news but not unexpected; however, what is interesting is the follow-up on the serious side effects with 5% of the patients experiencing these long term.  There have been reports of serious side effects occurring in people but not documented in studies.  Hopefully, this issue will be followed for many years in this and other studies to answer the important question of possible long term effects of HCV therapy.  –AF

Danoprevir
A Phase 1b trial confirmed laboratory findings that the HCV NS3/4A protease inhibitor danoprevir (formerly known as RG7227 and ITMN-191), being developed jointly by Roche and InterMune, is effective at lower doses when boosted with ritonavir (Norvir). Developed as an HIV protease inhibitor, ritonavir interferes with an enzyme (CYP3A) that processes many other drugs, causing those drugs to reach a higher concentration.

E. Gane and colleagues conducted a multiple-ascending-dose trial in which 30 treatment-naive genotype 1 patients were randomly assigned to receive ritonavir-boosted danoprevir or placebo in combination with Pegasys plus ribavirin for 15 days. Danoprevir/ritonavir was tested at doses of 100/100 mg twice-daily, 200/100 mg once-daily, and 200/100 mg twice-daily. Patients taking boosted danoprevir were more likely to achieve undetectable HCV viral load (67%, 50%, and 100%, respectively, in the three dosage arms) compared with 20% in the placebo arm and 14% in a previous trial of 900 mg unboosted danoprevir. Most patients experienced side effects, but these did not show a consistent dose-response effect. Boosted danoprevir is now being tested in prior nonresponders. 

Comments:  These findings are very good news because it shows increased levels of danoprevir when boosted with ritonavir, but without the severe side effects seen in previous studies.  –AF

BI 201335
M. Sulkowski presented results from the Phase 2 SILEN-C2 trial, evaluating Boehringer Ingelheim’s NS3/4A protease inhibitor BI 201335 in combination with standard therapy. This study included 280 genotype 1 prior nonresponders (not including relapsers) randomly allocated to receive 240 mg BI 201335 once-daily, the same BI 201335 dose after a three-day lead-in with Pegasys plus ribavirin, or 240 mg BI 201335 twice-daily after a lead-in; after 24 weeks all participants continued on pegylated interferon/ribavirin alone through week 48.

RVR rates were similar in all dose groups (62%, 64%, and 69%, respectively), as were early virological response rates at week 12 (59%, 59%, and 54%, respectively). Viral breakthrough was slightly more common in the two once-daily groups (22%) compared with the twice-daily arm (14%). Skin rash (33%-59%) and jaundice (9%-34%) occurred more often with twice-daily BI 201335; 4% of patients in the once-daily groups and 24% in the twice-daily arm discontinued early due to adverse events. “In treatment-experienced patients, BI 201335 240 mg once-daily appears to offer the best safety/efficacy balance based on this interim analysis,” the researchers concluded.

Comments:  This study found similar EVR rates among the once-a-day and twice-a-day groups.  If these results are confirmed in larger studies this could be a significant improvement in HCV therapy.  Currently, the two protease inhibitors (telaprevir and boceprevir) require dosing three times a day).  -AF

Narlaprevir
J. de Bruijne and colleagues presented a poster on narlaprevir, the HCV NS3 serine protease inhibitor formerly known as SCH 900518, which is also being tested with ritonavir boosting. This proof-of-concept study included 40 genotype 1 patients (half treatment-naive, half treatment-experienced) who received narlaprevir, with or without ritonavir, or placebo in combination with PegIntron for two weeks, followed by standard of care therapy for 24 or 48 weeks. Treatment naive patients receiving narlaprevir had a high SVR rate of 81%, but treatment-experienced patients did no better than those taking placebo (both 38%).

Comments:  This small study seems to indicate that narlaprevir may help to increase the SVR rates in treatment-naïve HCV genotype patients.  The results in prior relapsers (50%) were beneficial but the low SVR rates in the prior non-responders (17%) indicate no benefit to the addition of narlaprevirAF

ACH-1625
V. Detishin and colleagues presented data from a Phase 1 study of Achillion Pharmaceuticals’ HCV NS3 protease inhibitor ACH-1625. The first two segments of this proof-of-concept study showed that ACH-1625 monotherapy was well-tolerated in healthy HCV negative volunteers at doses up to 2000 mg. The third segment enrolled 18 genotype 1 chronic hepatitis C patients, either treatment-naive or previous relapsers or partial responders, who received ACH-1625 at doses of 500 mg or 600 mg twice-daily or placebo for five days. Maximal viral load declines were -4.3 and -3.9 log10 , respectively, in the 500 mg and 600 mg arms; two people in the 600 mg arm achieved undetectable HCV RNA. Viral load remained suppressed for at least seven days, and an average sustained HCV RNA decline of 2.5 log10 was still apparent at day 12. There were no serious adverse events and no treatment discontinuations for this reason. Additional dose cohorts have been added to evaluate lower doses and once-daily dosing.

Comments:  Since EASL, Achillion announced positive results from the additional cohorts finding that the once-a-day dose provided a mean maximal HCV RNA (viral load) reduction of 3.86 log10 . –AF

MK-5172
S. Carroll and colleagues reported on MK-5172, a second-generation HCV NS3/4A protease inhibitor. Though further back in the development pipeline, MK-5172 is notable for its activity against HCV strains with known NS3/4A and NS5A/B resistance mutations in laboratory and chimpanzee studies. The first clinical trials in humans are underway.

Comments:  Treatment of potentially resistant strains of HCV could be the focus of the next generation of research as drug induced treatment resistance emerges  –AF


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Healthwise: Making Friends with Fatigue
—Lucinda K. Porter, RN

Many of those who live with chronic hepatitis C virus infection (HCV) are all too familiar with one of its major side effects—fatigue. In fact, fatigue is the most common HCV complaint. I refer to it as the other F word, although I have been known to use the two F words together. What is this thing we call fatigue and what can we do about it?

In this article, I am going to tell you some of what you already know. Fatigue sucks.  It can feel like you are pushing your body through sludge while wearing waders and a fifty pound pack. It’s relentless and it casts a shadow on everything. Well-meaning people would tell me that if I exercised, I’d have more energy. It may be true, but how was I going to exercise if I was too tired? That’s like telling a double amputee that you could walk if you got up out of the chair.

There are thousands of causes of fatigue. Some common ones are: diseases, jet lag, inadequate sleep, anemia, alcohol, supplements, drugs (prescription and non-prescription), inactivity, pregnancy, boredom, excess iron,  stress, too much exertion, dehydration, depression, poor nutrition, pain, thyroid abnormalities, low testosterone or other hormone issues, diabetes and, of course, HCV.

Since there are so many causes of fatigue, the dilemma is figuring out if we are experiencing HCV-related fatigue, or if there is another cause. After years of debilitating fatigue, I asked myself that very question. It took a year of detective work, but I was able to figure out that my fatigue was not solely HCV-related. Now I am like the Energizer Bunny. Perhaps Energizer Turtle is a better comparison. I am slow, but I make it to the finish line with energy to spare.

If you figure out the contributors to fatigue, you may be able to fix or reduce it. Examine the common causes of fatigue mentioned in paragraph 3, and ask yourself if they could be contributing to your symptoms. Your medical provider is an essential part of the process, and will want to rule out the notorious energy-busters, such as anemia, thyroid abnormalities, sleep problems, diabetes, depression, dehydration and allergies.  A thorough and honest look at alcohol, substance use, and excessive caffeine is essential. Your medical provider will also want to look at all medications, supplements and herbs that you take. 

Determining the cause of fatigue is more a process of elimination than anything else. There are some clear connections between liver disease and chronic fatigue. Anemia may accompany liver disease. Some of the medications used to treat hepatitis cause fatigue. The liver may have an iron storage problem, which can cause tiredness. Fatty liver or autoimmune diseases that lead to hepatitis may cause fatigue. Some patients with liver disease experience a disruption of sleep patterns known as sleep reversal, which causes daytime fatigue.

Fatigue and Liver Disease
Let’s begin by discussing the type of fatigue that is associated with HCV. According to Mark G. Swain, MD of the University of Calgary, fatigue may be classified in two ways.1 

  1. Peripheral fatigue is associated with muscle, whether overused, underused, or weak.  Usually this type of fatigue is not caused by liver disease except in advanced cases, such as decompensated cirrhosis.

  2. Central fatigue is rooted in the brain and central nervous system. This type of exhaustion may be caused by chemicals in the brain. It is quite complicated, but the theory is that various factors affect this chemical system, leaving us to feel energized or tired. For more information, read “Fatigue”by Alan Franciscus in the May 2007 HCV Advocate (listed under Resources at the end of this article).

Since the liver is in the upper right-hand side of the abdomen, you may be wondering how the brain and the liver are connected. In short, our bodies are complex organisms. Just like an earthquake may lead to a tsunami, a liver problem may affect another part of the body. Our bodies are chemical plants, manufacturing and releasing hormones, neurotransmitters, and immune substances. Some of these may be related to HCV or a liver disease. Or, these reactions may be related to the neuropsychiatric features of living with a chronic disease.

Facing Fatigue
Part of your fatigue assessment will be lifestyle questions. Do you exercise, and if so, what do you do, how often and for how long?  What does your diet look like? Do you smoke? Is there a lot of stress in your life? Do you have any fun?

If you tell me that the only vegetables you eat are French fries and the only greens in your diet are lime jelly beans, there may be a problem. If the only exercise you get is pointing the remote, then there may be a big problem—a problem with a solution.

I don’t judge people about their lifestyle. I used to smoke, drink, sit, and eat chips as if these activities were a national sport.  Not only will I not judge you, I urge you to not chastise yourself. Being critical doesn’t solve problems—it just makes us feel bad about ourselves. Feeling crappy about ourselves may lead us deeper into the activities that make us tired.

Be honest, but not harsh. Ask this: What could be changed, even if you have no idea of how to make this change? Don’t censor or judge your answers. For instance, you may think some exercise would be helpful, but you have a broken leg. You can’t find a solution without identifying the problem.

Fixing Fatigue
The Resources section at the end of this article provides links to more information about fatigue. There is standard info and tips about diet, exercise, stress reduction, sleep hygiene, supplements, attitude, and so on.

Since fatigue is a tough problem to overcome, it can be difficult to figure out where to start.  I am going to share some strategies that helped to get me started. This is personal rather than scientific.

  1. First, I stopped fighting fatigue. In fact, I learned to embrace it. I started to watch how I related to fatigue. I was treating it like a huge monster, fighting it every step of the way. This fight was using up valuable mental energy that I was already short on.

  2. I changed my attitude.  I read about a study of people with chronic fatigue. After interviewing them, it was noted that people often said to themselves and others, “I am tired.” The study subjects were divided into two groups. One group was instructed not to do anything differently. The other group was instructed to substitute the phrase, “I am getting my energy back” every time they felt tired. The outcome was that the people who told themselves they were getting their energy back reported significantly reduced fatigue. I practiced this regularly.

  3. I stopped blaming hepatitis C as the sole cause of how I felt and became open to the possibility that other factors may have been contributing to how I felt. This was pivotal because it opened the door to slowly making significant lifestyle changes, which lead to more energy.

What are these changes? I sleep better because I wear ear plugs to block out my husband’s snoring. I exercise and mediate every day and eat a Mediterranean diet. I don’t smoke any longer, or drink alcohol. Remember, I wasn’t always like this. It was a slow process. If nothing else, drink a lot of water. Not only will you stay hydrated, you’ll get some exercise running to the bathroom. However, watch the water intake before bedtime so you don’t disrupt your sleep with bathroom visits.

After you have addressed all the possible factors that may cause fatigue, in the end it may still come down to hepatitis C. There is still much to be learned about this virus. Join a support group if you haven’t already. There is no substitute for being in a group with others who know what it is like to have HCV. At the very least, its one place you can go where no one will be offended if you fall asleep while others are talking. 

Resources

1Swain, Mark G., Fatigue in Liver Disease: Pathophysiology and Clinical Management, Canadian Journal of Gastroenterology, Mar 20(3):181-188 2006


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Disability & Benefits:  Health Care Reform Changes for 2010
—Jacques Chambers, CLU

Earlier this year Congress passed and the President signed into law a massive Health Care Reform, named the Patient Protection and Affordable Care Act. (PPACA) Its implementation will create major changes in how healthcare is delivered and how health insurance is purchased.
Because of the massive changes to the current health care delivery system, the effective dates of the various provisions vary. Some parts start this year, in 2010, and other parts are not coming into force until later years, 2011, 2012, 2014, 2018, and even 2020. Rather than trying to understand the entire law, perhaps, it will be easier to comprehend if we focus on the changes taking effect this year and next. The following issues will have some parts taking effect in 2010:

Children with Pre-Existing Conditions Effective September 23, 2010, insurance companies will no longer deny coverage to children because of a pre-existing condition. (This will not apply to adults until 2014.) Children applying for coverage under a health plan that requires medical underwriting, whether singly or with a family, cannot be denied coverage due to past medical history.

Transitional High Risk Insurance Pool Effective July 1, 2010, persons who are not able to purchase health insurance due to a pre-existing condition will have the opportunity to purchase “affordable” coverage through high risk insurance pools operated by the states and funded by the federal government. Rates charged will be based on the average charge for health insurance by private insurers for similar coverage in the individual health market in that geographical area.

To be eligible for the coverage this year, a person:

  • Must have a pre-existing condition that makes them otherwise uninsurable; and,
  • Must have been uninsured for at least six months prior to applying.

A person meeting these two criteria will be able to obtain coverage regardless of their health.

As of May 3, 2010, 30 states have indicated they will operate their own high risk pools. Persons living in states which do not operate such a pool will be able to purchase coverage through a federal fallback high-risk pool, currently being set up. These pools will operate until insurance companies are required to accept anyone regardless of their pre-existing condition or age in 2014.

Dependent Coverage Effective September 23, 2010 (although insurers have indicated they will implement it immediately), children may remain under their parent’s health policy until their 26th birthday. This extended coverage will be available to all adult children, including those who are no longer living with their parents and/or are not dependent on their parent’s tax return. It applies to both single and married adult children, although the children’s spouses and children are not eligible.
It should be noted that there is still no mandate that employers offer dependent coverage. If an employer chooses not to provide coverage for dependents at all, that will still be permitted.

Lifetime Maximums ProhibitedEffective at the start of plan years beginning after September 23, 2010, health plans will no longer be able to place lifetime or annual limits on new or existing health plans, both group and individual. For many employers who use December 31as the end of their plan year, this would take effect on January 1, 2011.

Rescissions ProhibitedEffective September 23, 2010, insurers will be prohibited from dropping persons from coverage when they become ill. Insurance companies have announced they will implement this provision immediately as well. It is not clear what impact this will have on persons who have obtained their insurance through fraud.

Preventive Care ExpandedNew insurance policies sold must provide first dollar coverage without co-payments for preventive care (existing plans do not have to meet this requirement until 2018). This would include all recommended screenings, preventive care and vaccines. Medicare beneficiaries will get free annual physical exams, and Medicaid will cover stop smoking programs for pregnant women.

The law requires carriers to provide coverage for all services recommended by an independent panel of experts, the U.S. Preventive Services Task Force. They must all be covered without any co-pays to be paid by the insureds.

Other features, implemented later, include:

  • A trust fund to pay for bicycle paths, playgrounds, sidewalks, and hiking trails;
  • Chain restaurants with 20 or more locations will have to provide the calorie count of each menu item including food in buffets and salad bars; and,
  • Employers will be able to offer greater incentives to employees who participate in programs to stop smoking, lose weight, and improve their health.

Medicare Part D Donut Hole Phased OutThe PPACA gradually eliminates the infamous donut hole in Medicare prescription drug coverage. That is the portion of Medical Part D Prescription Drug coverage where, after the initial coverage level, no benefits are paid until over $4,000 has been spent out of pocket. In 2010, Medicare will send checks for $250 to each Medicare beneficiary who has reached the donut hole this year. Checks will be sent out beginning June 15 with additional checks sent every six weeks through 2010.

Beginning in 2011, drug companies will have to provide medications under Part D at a 50% reduction in price in brand name drugs. That gradually increases for both brand name and generics until 2020 when coverage becomes 75%, i.e., the same amount that the first portion of Part D pays now.

Lowering Health Insurance PremiumsIn an effort to avoid excessive profits from driving health insurance rates ever higher, June 1, 2010, is the date that the National Association of [State] Insurance Commissioners (NAIC) has agreed upon to submit uniform definitions and methods of calculating medical loss ratios, i.e., the percentage of premiums collected that is spent on direct medical services to insureds. After that date, the medical loss ratio cannot exceed 85% for large groups and 80% for small groups and individuals. The goal is to limit the amount of administrative fees an insurance company pays out of the premiums collected.

Other features starting in 2010, that will eventually, but not immediately, help reduce health care costs include:

  • The Food & Drug Administration is authorized to approve generic versions of biologics for certain diseases and allow for generic medications to be marketed after 12 years;
  • Provisions to reduce fraud in the Medicare system;
  • Improved coordination of care for persons covered under both Medicare and Medicaid; and,
  • Tax credits are immediately available to small employers as an incentive for them to offer health insurance to their employees. The IRS is currently sending notices of this to small businesses and tax-exempt organizations.

Many of the regulations for these programs are still being written and will be released over the next few months.


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