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February 2008 HCV Advocate

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SVR and Disease Progression
Alan Franciscus, Editor-in-Chief

IDEAL Trial Results
Alan Franciscus, Editor-in-Chief

Adjustment of Treatment Duration Based on Early Response
Liz Highleyman

Healthwise: Blood 101
Lucinda Porter, RN

Cure for Cirrhosis?
Alan Franciscus, Editor-in-Chief

Disability & Benefits: Monitoring Your Health Insurance Coverage
Jacques Chambers, CLU

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SVR and Disease Progression
Alan Franciscus, Editor-in-Chief

In the January 2008 issue of the HCV Advocate there was a report on 2 large clinical trials that found that the long term use of low-dose pegylated interferon did little to change the clinical outcome of HCV disease progression.  Another clinical study published in 2007, “Sustained Virologic Response and Clinical Outcome in Patients with Chronic Hepatitis C and Advanced Fibrosis,” provides hope that successful treatment may indeed prevent disease progression. 

The study was a retrospective study conducted in 5 hepatology centers in Europe and Canada.  The total number of participants was 479 of whom 131 patients (27%) received interferon monotherapy, 130 patients (27%) received interferon plus ribavirin, 10 patients (2.1%) received pegylated interferon monotherapy, and 208 patients (43%) received pegylated interferon plus ribavirin.  In all, 142 patients (30%) achieved an SVR and 337 (70%) did not achieve an SVR.  All patients had biopsy-proven advanced fibrosis or cirrhosis (Ishak 4 to 6). 

The purpose of the study was to compare the incidence of outcome events in the SVR group vs. the non-SVR group. An outcome event was defined as liver failure, hepatocellular carcinoma (HCC-liver cancer), and/or liver transplantation.   

The authors found that only 4 patients who achieved an SVR had 1 outcome event compared to 83 people in the non-SVR group – with a statistically significant difference between the two groups after 5 years.  Death due to hepatitis C occurred in only 1 person in the SVR group compared to 16 people in the non-SVR group.  Furthermore, 18 patients in the non-SVR group underwent liver transplantation compared to no patients in the SVR group.  Forty-two people developed liver failure in the non-SVR group compared to no patient in the SVR group.  HCC or liver cancer developed in 3 patients in the SVR group compared to 32 people in the non-SVR group.   

The authors commented that “Our finding that therapy provides long-term clinical benefit for patients with a sustained virologic response may help to change attitudes toward screening persons who are at risk for hepatitis C infection.” 

Another important piece of information from this study is that people who are able to achieve an SVR still need to be monitored for potential future complications even though the risk of complications is low.    

Ann Intern Med 2007 Nov 20;147: 677

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IDEAL Trial Results
Alan Franciscus, Editor-in-Chief

The IDEAL (Individualized Dosing Efficacy vs. Flat Dosing to Assess optimal pegylated interferon therapy) clinical trial results were released by Schering in January 2008.  The trial was a Food & Drug Administration (FDA) mandated clinical trial to find out what dose of Peg-Intron (1.5 mcg/kg/week vs. 1.0 mcg/kg/week) is the most effective for the treatment of hepatitis C when combined with ribavirin.  In the study design Schering added an arm to compare the effectiveness of Peg-Intron (plus ribavirin) with Pegasys (plus ribavirin).  This part of the trial has been promoted as a head-to-head study of the two pegylated interferons, but as I will discuss later in this article it is not a true head-to-head study because the study design was flawed.  

There were 3,070 treatment naïve HCV genotype 1 patients enrolled in the study throughout the United States who were randomized into three different treatment arms:

  • Group A:  Peg-Intron: 1.5 mcg/kg/week and Rebetol (ribavirin):  800-1,400 mg/day
  • Group B:  Peg-Intron : 1.0 mcg/kg/week and Rebetol (ribavirin):  800-1,400 mg/day
  • Group C:  Pegasys:  180 mcg/week and Copegus (ribavirin):  1,000/1,200 mg/day

All the trial participants were treated for 48 weeks with a 24 week follow-up period, which is the standard duration of treatment for people with genotype 1.  It was reported that there were no significant differences in the patient characteristics. 

The sustained virological response (SVR) rates given in the press release were as follows:

  • Group A:  40%
  • Group B:  38%
  • Group C:  41%

It was also stated that the overall adverse events, or side effects, reported were similar between the three arms. 

The results released were listed as top line results, which means that no further information was available, just the overall SVR rates.  In addition the p-values, or confidence intervals, which would  give us a better idea of whether or not the results are truly statistically significant, were not listed.  However, it was noted that more of the data will be submitted for peer-reviewed publication and for presentations at upcoming medical meetings.  It is expected that Schering will release more information at the upcoming European Association for the Study of Liver Diseases (EASL) that will be held in April 2008. 

Bottom line:
The top line results suggest that the effectiveness of Peg-Intron at the lower dose of 1.0 mcg/kg is at least equivalent to the higher dose of 1.5 mcg/kg. 

The results comparing Peg-Intron vs. Pegasys have been promoted as a head-to-head study.  However, as I pointed out above, the part of the clinical trial comparing Peg-Intron vs. Pegasys was poorly designed because in truth the dose of ribavirin given to trial participants taking Peg-Intron was different than the ribavirin dose given to the people who were taking Pegasys.  For instance, in the Peg-Intron arms the dose of  Rebetol (ribavirin) was 800 – 1,400 mg/day (weight based), but the dose of Copegus (ribavirin) in the Pegasys arm was 1,000-1,200 mg/day (weight based).  In addition, the dose reduction schedule for Peg-Intron was different than the dose reduction schedule for Pegasys.  This is an important issue because in the last few years we have learned that taking the optimal dose of ribavirin is one of the most important factors in achieving an SVR.  In addition the different ribavirin dose reduction schedule also affects the use of growth factors for the management of ribavirin-related anemia.  Finally, it was pointed out in the Roche press release that the study arm with Pegasys was not blinded so there could be a potential for patient or provider bias. 

The FDA is the government body that approves all clinical trial designs for clinical trials that take place in the United States.  Clearly someone at the FDA was asleep at the wheel when they approved the third arm of this study.  In the future it is hoped that the FDA will take a more proactive role in determining and approving appropriate studies that will give providers and patients more clinically significant information.

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Adjustment of Treatment Duration Based on Early Response
Liz Highleyman

Pegylated interferon (Pegasys or PegIntron) plus weight-based ribavirin for 24 weeks (HCV genotypes 2 and 3) or 48 weeks (genotype 1) is the standard of care for treating chronic hepatitis C. But a growing body of research suggests that less standardization may be better.

Standard treatment, determined via large clinical trials, represents the best overall regimen for the population as a whole, but may not be optimal for a specific individual. Given the difficult side effects and expense of interferon-based therapy, patients and their clinicians would prefer treatment that lasts just long enough to cure hepatitis C – no more and no less.

Several recent studies have shown that some “fast responder” patients can achieve sustained virological response (SVR) with a shorter than usual duration of therapy, while “slow responders” may need longer treatment. The speed with which viral load declines during early treatment is a major predictor of how long treatment should last.

Treatment Duration Based on Initial Response
In a study described in the January 2008 issue of Hepatology, Alessandra Mangia and colleagues explored whether a shorter duration of therapy might be sufficient for genotype 1 patients who experience rapid virological response (RVR), or undetectable viral load at Week 4. Nearly 700 participants were treated with standard doses of Pegasys or PegIntron plus 1000-1200 mg/day weight-based ribavirin. One group was randomly assigned to receive treatment for the standard 48-week duration, while the others were treated for 24, 48, or 72 weeks, depending on whether their viral load first became undetectable at Week 4, Week 8, or Week 72, respectively.

Similar proportions first achieved undetectable viral load at Week 4 (27%) and at Week 8 (28%), with a further 11% having cleared HCV at Week 12. Overall, 45% in the standard duration arm and 49% in the variable duration arm achieved SVR. Among patients who first achieved undetectable HCV RNA at Week 4, 87% in the standard duration arm and 77% in the variable duration (24-week) arm achieved SVR. However, the subset of patients in this group who had a high baseline viral load did better with 48-week than 24-week treatment (SVR 87% vs 73%). Among individuals who achieved undetectable HCV RNA at Week 8, SVR rates were similar in the standard and variable duration (48-week) arms (70% vs 72%). But among  the slowest responders at Week 12, the SVR rates were 38% in the standard duration arm and 64% in the variable duration (72-week) arm, demonstrating a benefit from longer treatment.

Though less well studied, even earlier HCV clearance may predict ultimate treatment outcomes. In the ongoing GET-C study, looking at extended therapy for genotype 3 patients with a high baseline viral load, ultra-rapid virological response at Week 2 predicted SVR with 93% accuracy.

Response to hepatitis C treatment is described based on the amount of HCV RNA, or viral load, at different points in time:

  • Ultra-rapid virological response (URVR): undetectable HCV RNA at Week 2 of treatment.
  • Rapid virological response (RVR): undetectable HCV RNA at Week 4 of treatment.
  • Early virological response (EVR): traditionally, at least a 2-log drop in HCV RNA at Week 12 of treatment (though some researchers use undetectable viral load).
  • End-of-treatment response (EOT or ETR): undetectable HCV RNA at the completion of treatment (typically Week 24 for genotypes 2 or 3; Week 48 for genotype 1).
  • Sustained virological response (SVR): continued undetectable viral load 24 weeks after the completion of therapy (typically Week 48 for genotypes 2 or 3; Week 72 for genotype 1).

Longer Treatment for Genotype 1
As reported in the December 2007 issue of Hepatology, Brian Pearlman and colleagues specifically assessed whether longer treatment would produce a greater likelihood of SVR in previously untreated genotype 1 patients classified as “slow responders,” defined as having at least a 2-log reduction but still detectable HCV RNA at Week 12, but undetectable viral load at Week 24.

About 100 study participants were randomly assigned to receive PegIntron plus 800-1400 mg/day weight-based ribavirin for either the standard 48 weeks or an extended 72 weeks. End-of-treatment response rates were similar in the 48-week and 72-week arms, at 45% vs 48%, respectively. However, HCV relapse occurred less often with longer treatment, thus yielding a higher SVR rate (18% vs 38%). Despite longer therapy, the frequency of dose reductions and treatment discontinuation due to side effects were similar in both groups.

Longer treatment may also lead to sustained response in prior relapsers. As reported at the Digestive Disease Week 2007 conference, Jeffrey McMahon and colleagues assessed 72-week treatment with Pegasys plus ribavirin in four patients (three with genotype 1 and one with genotype 2) who relapsed after a previous 48-week course of combination therapy. During re-treatment, all experienced HCV clearance by Week 12 and achieved SVR.

Other HCV Genotypes
Tailored treatment durations may also benefit patients with other HCV genotypes. Studies have suggested that treatment shorter than the standard 24 weeks can produce sustained response in many genotype 2 and 3 patients, but the longer regimen appears to be superior overall.

In the July 12, 2007 New England Journal of Medicine, for example, Mitchell Shiffman and colleagues reported results from the ACCELERATE trial, in which 1,469 genotype 2 or 3 patients were randomly assigned to receive Pegasys plus 800 mg ribavirin for either 16 or 24 weeks. The overall SVR rates were 62% in the 16-week group and 70% in the 24-week group, and the relapse rate was significantly higher in the shorter treatment arm (31% vs 18%). However, among participants who achieved RVR at Week 4, the SVR rates were 79% and 85%, respectively. And among those with a low baseline viral load, SVR rates were similar in both treatment arms (82% vs 81%). The researchers concluded that “16 weeks may be adequate for a carefully selected subset of patients.”

Similarly, in the January 2008 issue of Hepatology, Olav Dalgard and colleagues reported that among 428 genotype 2 or 3 patients treated with PegIntron plus 800-1400 mg ribavirin who cleared HCV by Week 4, 81% achieved SVR with a 14-week course of treatment, compared with 91% of those treated for 24 weeks, which did not meet the non-inferiority criteria. “However,” they wrote, “the SVR rate after 14 weeks of treatment is high, and although longer treatment may give slightly better SVR, we believe economical savings and fewer side effects make it rational to treat patients with genotype 2 or 3 and RVR for only 14 weeks.”

Finally, as reported in the December 2007 issue of Hepatology, Sanaa Kamal and colleagues treated 358 Egyptian genotype 4 patients with PegIntron plus weight-based ribavirin for variable durations based on early response. Individuals with RVR at Week 4 were treated for 24 weeks, and 86% achieved SVR. This compared with 76% for patients with undetectable viral load at Week 12 treated for 36 weeks, and 56% for those with continued detectable HCV RNA at Week 12 treated for 48 weeks. In a control group, all participants were treated for 48 weeks regardless of early response, and 58% achieved SVR.

HIV/HCV Coinfection
Researchers have also explored variable treatment durations in HIV/HCV coinfected individuals. HIV positive patients may clear HCV more slowly, leading some experts to suggest that they might benefit from longer treatment.

As reported in several recent conference abstracts and journal articles, the Spanish PRESCO trial included 389 coinfected participants, about half with genotype 1, treated with Pegasys plus 1000-1200 mg/day ribavirin. Those who achieved early virological response at Week 12 were randomly assigned to continue treatment for either 48 or 72 weeks (genotype 1 or 4) or for either 24 or 48 weeks (genotype 2 or 3). Overall, 36% of genotype 1 patients, 72% with genotype 2 or 3, and 33% with genotype 4 achieved SVR. Undetectable HCV RNA at Week 4 was the best predictor of sustained response. Extended treatment duration did not appear to reduce the risk of relapse.

Treat Long Enough – But Not Too Long
HCV viral load at Week 4 is “emerging as an important milestone” in the management of chronic hepatitis C, according to Fred Poordad and colleagues. Based on a recent review of past research, they concluded that shortening treatment to 12-16 weeks is effective for genotype 2 or 3 patients who attain RVR; for genotype 1 patients, RVR may be used as an indicator for both shortened and extended treatment. RVR “represents a key opportunity to individualize therapy according to treatment-related viral kinetics,” they wrote in the January 1, 2008 issue of Clinical Infectious Diseases.

But clinicians should not be too quick to alter the duration of hepatitis C treatment. Even among patients who achieve RVR at Week 4, some may experience relapse with a shortened course of therapy. Conversely, in the October 2007 Journal of Hepatology, Patrick Marcellin, Jenny Heathcote, and Antonio Craxi advised against “indiscriminate extension of treatment,” since this can lead to prolonged side effects and higher cost for some patients who still will not achieve a cure. It remains a challenge, they wrote, to distinguishing at an early stage between “slow responders” and “null responders.”

In the future, the best hope for shortening hepatitis C treatment may come from targeted antiviral agents. For example, interim data from the PROVE 1 trial, looking at the HCV protease inhibitor telaprevir plus Pegasys with or without 1000-1200 mg/day ribavirin, showed that 61% of genotype 1 patients receiving the triple combination achieved SVR after 24 weeks of therapy—higher than the sustained response rate with pegylated interferon/ribavirin for 48 weeks in most studies.


  • Dalgard, O. et al. Pegylated interferon alfa and ribavirin for 14 versus 24 weeks in patients with hepatitis C virus genotype 2 or 3 and rapid virological response. Hepatology 47(1): 35-42. January 008.
  • Kamal, S.M. et al. Pegylated interferon alpha-2b plus ribavirin in patients with genotype 4 chronic hepatitis C: The role of rapid and early virologic response. Hepatology 46(6):1732-40. December 2007.
  • Jacobson, I.M. et al. Interim analysis results from a Phase 2 study of telaprevir with peginterferon alfa-2A and ribavirin in treatment-naive subjects with hepatitis C. 58th AASLD. Boston. November 2-6, 2007. Abstract 177.
  • Mangia, A. et al. Individualized treatment duration for hepatitis C genotype 1 patients: A randomized controlled trial. Hepatology 47(1): 43-50. January 2008.
  • Marcellin, P. et al. Which patients with genotype 1 chronic hepatitis C can benefit from prolonged treatment with the ‘accordion’ regimen? Journal of Hepatology 47(4): 580-587. October 2007.
  • Martin-Carbonero, L. et al. Undetectable hepatitis C virus RNA at week 4 as predictor of sustained virological response in HIV patients with chronic hepatitis C. AIDS 22(1): 15-21, January 2, 2008.
  • McMahon, J. et al. Efficacy of a 72-week course of treatment for previous relapsers to PEG/ribavirin therapy. Digestive Disease Week 2007. Washington, DC. May 19-24, 2007. Abstract S1232.
  • Pearlman, B.L. et al. Treatment extension to 72 weeks of peginterferon and ribavirin in hepatitis C genotype 1-infected slow responders. Hepatology 46(6): 1688-1694. December 2007.
  • Pianko, S. et al. Ultra rapid virologic response predicts sustained virologic response in HCV infected patients with genotype 3 and high viral load: the Get-C Study. 58th AASLD. Boston. November 2-6, 2007. Abstract 349.
  • Poordad, F. et al. Rapid virologic response: a new milestone in the management of chronic hepatitis C. Clinical Infectious Diseases 46(1): 78-84. January 1, 2008.
  • Shiffman, M.L. et al Peginterferon Alfa-2a and Ribavirin for 16 or 24 Weeks in HCV Genotype 2 or 3. New England Journal of Medicine 357(2): 124-134. July 12, 2007.

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Healthwise: Blood 101
Lucinda Porter, RN

Hepatitis C (HCV) is the most common blood-borne virus in the world.  This month’s column will focus on the vehicle that transports HCV – blood.  This vital fluid is a metaphor for life, found in literature, mythology, and religion.  The ultimate symbol of friendship is to become blood brothers or sisters.  Although a special ritual, educate your kids about the potential risks associated with this.  Friendship bracelets are safer.

The average-sized adult has about 5 quarts of blood.  It has many functions.  The blood’s major job is to transport various elements to the cells, such as oxygen, food and hormones.  It also transports waste products from the cells to the kidneys.  Blood aids in the regulation of fluids, temperature and pH.  It also plays a strong role in the immune system.

Blood circulates through the body by way of an elaborate “plumbing” system.  The heart pumps blood through large arteries, much like aqueducts.  The arteries branch off to medium-sized “pipes” called arterioles.  The pipes that carry water to our faucets are small and so are the vessels that carry blood to the cells.  These are capillaries.  Blood returns to the heart by way of veins, passing through the smallest ones first and increasing in size as it winds its way back to the beginning. 

Arteries carry oxygen-rich blood away from the heart.  Every breath we draw carries air into our lungs.  As the blood passes by, it collects oxygen from the lungs and delivers it to the rest of the body. 

Blood is classified into 4 types: A, B, AB, and O.  O is the most common, followed by A, B, and finally AB.  Blood is furthered categorized by its Rhesus factor (Rh factor).  Approximately 85% of us are Rh positive and the rest are Rh negative.  O positive is the most common blood type.  AB negative is the least common.

About 55% of blood is composed of plasma.  This liquid is mostly water with some proteins and various other ingredients.  The remaining 45% of blood are referred to as formed elements and include red blood cells, white blood cells (WBCs) and platelets.  These cells are made in the bone marrow.  A complete blood count (CBC) is the lab test that measures the blood’s components.  This is a relatively fast and inexpensive blood test. 

The most plentiful are the red blood cells (RBCs), also known as erythrocytes.  The main function of RBCs is to carry oxygen to every cell in the body.  These doughnut-shaped cells are flexible as they must endure constant bending and twisting while making their way through the tiniest capillaries.  Our body produces approximately 2.5 million new RBCs every second.  The normal ranges for RBCs vary between labs, ages and gender.  In women it is around 4 to 5 million/µL; men around 4.5 to 5.5 million/µL. 

Red blood cells contain an iron-rich substance called hemoglobin.  As red blood cells circulate past the lungs, the hemoglobin binds with inhaled oxygen.  It then carries the oxygen to the cells.  The hemoglobin deposits oxygen in the cell, exchanging it for carbon dioxide.  Carbon dioxide is carried back to the lungs, where it is exhaled. 

Normal hemoglobin ranges for men is 14 to 18 g/dL; for women 12 to 16 g/dL.  Patients undergoing HCV treatment may have low RBCs and hemoglobin.  This is primarily because ribavirin causes red blood cell death (hemolytic anemia) although interferon adds to the problem.  Hemolytic anemia is a serious condition and should not be ignored.  Symptoms include fatigue, weakness, and paleness, shortness of breath, dizziness, heart palpitations, headache and sleeping difficulties.  There are over 100 types of anemia and the treatments vary depending on the cause.  Do not take iron supplements unless under medical supervision. 

The largest cells in the blood are the white blood cells (WBCs) or leukocytes.  Their main function is to fight infection.  WBCs originate in the bone marrow.  Technically, there are three kinds of WBCs: granulocytes, monocytes, and lymphocytes.  Since there are three subtypes of granulocytes: neutrophils, eosinophils and basophils, it’s easier to think of WBCs as five types: neutrophils, monocytes, lymphocytes, eosinophils and basophils.  Each of these has their own function. 

WBC’s usually drop during HCV treatment since interferon suppresses bone marrow function.  A low white count from HCV treatment is not alarming, unless there are other factors, such as HIV.  Normal WBC ranges are around 4,000 to 11,000/µL.  Unlike anemia, a low white count does not cause any obvious discomfort.

The smallest blood components are platelets or thrombocytes.  Platelets have the ability to stick to each other and to the blood vessel walls.  Their function is to halt bleeding and repair damaged blood vessels.  For adults, the normal range for platelets is 140,000 to 400,000.

HCV patients with cirrhosis usually have a low number of platelets.  This is because the liver participates in the blood clotting process.  The platelets may drop very low before clotting is dangerously delayed.  Alpha interferons will suppress bone marrow production, so platelet count will decrease during HCV treatment – even for those without cirrhosis.  However, it is widely accepted that an HCV treatment-related platelet count as low as 50,000 is not a substantial health risk.  A platelet count of less than 20,000 is potentially serious.

Keeping copies of your labs is a good idea.  However, if you don’t know what you are looking at, lab reports can cause unnecessary anxiety or give false comfort.  All labs need to be interpreted by a qualified medical professional.  An abnormal lab does not necessarily indicate an abnormality.  Conclusions should not be made based on a single lab result.  Get the facts before you panic.  Why worry today when you can put it off until tomorrow?

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Cure for Cirrhosis?
Alan Franciscus, Editor-in-Chief

In late December 2007 there was a news item on the discovery of the protein that induces liver scarring.  That would have made our list of top news stories of 2007 if the story had been released earlier in the month. In fact the news story would have made the number one story of 2007 because the discovery will hopefully lead to new drugs to treat fibrosis/cirrhosis caused by alcohol, hepatitis B, hepatitis C or any other agent that causes liver fibrosis.  In addition, scientists believe that the protein identified to inhibit the production of the protein that causes tissue scarring will have a therapeutic value in treating other types of scarring in the body.

The protein in question was discovered by researchers led by Dr. Martina Buck at the University of California, San Diego.  The researchers identified a protein called Ribosomal S-6-Kinase-Mediated Signal (RSK) that is activated when liver tissue is damaged.  However, in the process of repairing the damage, the protein also generates excessive collagen that leads to the production of scar tissue instead of the regeneration of healthy liver tissue.  The scientists then developed a potential drug target that would inhibit and block the activation of RSK. 

The next step was to test the RSK inhibitor on mice with severe liver fibrosis – a condition that is similar to liver fibrosis found in humans.  It was found that the RSK inhibitor prevented the activation of excessive collagen, killed the cells that lead to scarring of the liver, but did not kill normal healthy cells.  In addition, the authors believe that by blocking the activation of RSK that the scar tissue would regenerate into healthy liver tissue.  The research also has implications for other types of tissue scarring such as pulmonary fibrosis in the lungs, skin burn injuries, and scleroderma – a chronic condition that causes hardening of the skin.

Buck, M, Chojkier M (2007) A Ribosomal S-6 Kinase-Mediated Signal to C/EBP-b Is Critical for the Development of Liver Fibrosis.  PloS One 2(12): 31372

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Disability & Benefits: Monitoring Your Health Insurance Coverage
Jacques Chambers, CLU

Dealing with health insurance and how it covers your medical bills can be a complicated and stressful issue, but it is not something that can be ignored. You may have an Indemnity or Preferred Provider Organization (PPO) Plan that pays medical bills after they are incurred. Or you may be covered under one of the many varieties of Health Maintenance Organization (HMO) Plans that “pre-authorize” certain treatments and disallow others. However, under either type of health plan, problems can arise in how the claims are handled, and, unless caught early, they can grow into major financial and legal dilemmas as well as affect your medical care and your health.

It’s tempting to ignore the whole medical payment process and assume that the insurance company and the doctors are handling everything satisfactorily, and many times they are.

However, a rude awakening often occurs when you receive a large bill from a medical provider for charges because insurance coverage was reduced, denied, disallowed, or just not processed.

Whether it is a claims payment or pretreatment authorization, most billing and precertification communication between a doctor and the insurance company is done in codes, and one misplaced digit can make a substantial difference in what is allowed or how much is paid. It is important to catch those small errors early, and you, as the claimant, are the best person to do it.

You do not have to become an insurance expert to be able to oversee just how your insurance company is processing the medical bills you are incurring. At the least, you can get minor errors corrected quickly; at worst, you will build a solid file of documentation that will save the attorney or benefits counselor you hire a lot of billable time. It will take some time and effort on your part to understand how the process works and how you can affect it, but it will be well worth it.

The first step is, of course, “Know Your Coverage.” Easy advice to give, but this is often the biggest problem in overseeing your coverage. Insurance contracts are scary; they’re hard to read; they don’t make a lot of sense if you’re not a lawyer. But you don’t need to memorize your plan or know every single provision to understand how the plan works and how it pays your medical bills.

Get a copy of your coverage. It may be an insurance policy, a booklet of coverage, a Summary Plan Description, or a chapter in an employee benefits manual. However, a paragraph or two in an announcement or even a couple of pages in the enrollment material is not sufficient for your needs. A complete description of your health plan will cover twenty to thirty pages or more.

If your health plan comes through your employer, they are required under a federal law called ERISA to provide you a Summary Plan Description of all of your benefit plans. If you have misplaced your copies, you should request one from your Human Resources or Benefits Department.

If you’re concerned about disclosure, just tell your employer that you are doing some financial planning with an insurance agent or estate planner, and that they have asked to you get the information for their analysis.

Don’t try to sit down and read your plan all the way through. That would put anyone to sleep. But, look through it. Note the different parts. There is usually an overview or Summary of Benefits at the front that will give the details of your specific plan, that is, what the dollar amounts are. Then there will be sections that describe different provisions of the plan.

Don’t try to understand and remember everything in every section. Just get familiar with where things are so you can refer to specific parts as you deal with the insurance company.

Things you should try to find are:

  • The Schedule of Benefits – This is often at the front of the plan. It’s the part that tells what the insurance company pays and what you pay. It lists the deductibles, the insurance percentages they pay, the co-pays you are expected to pay at each doctor’s visit, etc.
  • Covered Benefits – Often separate from the schedule of benefits, this will be a listing of what is covered. In some plans this will be a fairly long list; others will give a short list of a broad range of benefits covered. This section will also give greater detail about what and how things are covered.
  • Definitions – There is usually a separate section that defines terms used in the plan. If your plan has one, watch for words throughout the plan that are capitalized, italicized or in bold, as that usually means it is a term that has a special meaning and is defined in the definitions section. Other plans will define terms throughout the document as the terms are used.
  • Exclusions and Limitations – This lists the things that the plan will not cover, such as experimental treatment, or cosmetic surgery. It also lists the things that it will cover but puts special limits on, such as mental health, or convalescent home care, or treatment for conditions that existed when your coverage started – pre-existing conditions. You may want to paperclip this section, as you may need to refer to it more frequently, especially if you plan to appeal a denial.
  • Eligibility – This is important only if you are a relatively new employee as it tells just when your coverage actually begins. Also if you are a new employee, look for limits on coverage for Pre-Existing Conditions.  A similar section, usually in a different part of the book is the Termination of Coverage that describes when coverage ends. This section will usually include a description of how to extend coverage under COBRA and possibly other means. 
  • Claims Procedures – This will be a couple of pages that describes the claim filing procedure. The important section here is the part that tells you how to appeal denials. You may want to read that through, as there are usually some important time limits and other information there. 

Mark up the book. This is the rulebook that the insurance company must play by so don’t hesitate to use paperclips, “dog ears,” highlighting, underlining and margin notes to make it easier for you to use. Gummed tabs that label important sections are especially helpful.

Once you realize that the plan has different parts and you only need to focus on the part that fits your particular situation, learning what the plan does and doesn’t do becomes much more manageable. As an abstract description of provision, it may not seem so helpful, but you will find it valuable as you work with the insurance company and your medical provider when there are claims questions since it must contain the basis of their denials or cutbacks. To put in terms of sports: it is the rulebook and you’re at a disadvantage trying to “play” without knowing the rules.

How you watch the medical claims depends on the type of plan under which you are covered. If you have coverage through an Indemnity Plan including Medicare or a Preferred Provider Organization (PPO) Plan, the insurance company will process the claims and pay their portion after you have received the treatment.

With these plans you will receive an Explanation of Benefits (EOB) every time they process a medical bill. Medicare calls it a Medicare Summary Notice. Review each EOB or MSN carefully. Was everything “allowed” in full even if only a percentage was paid? If not, a code by the charge should lead to a reason for the denial or reduction.

If it is not clear, call and ask for an explanation. There will usually be a toll-free number on the EOB. Note down to whom you talk and what they say. Don’t be bashful about asking for more clarification. Follow the appeal procedures to challenge their decision, if you disagree. Ask for your doctor’s help in supporting your appeal.

It is important that you match the EOB or MSN with the bills the doctor gives you. Sometimes matching up the two can be daunting as every billing company seems to use a different format which makes them hard to read. But if the EOB or MSN is not reflected in the doctor’s bill, you need to contact the doctor. Many times computer generated billings contain higher charges that don’t reflect the limits on those charges by PPO contracts or Medicare assignment.

For Health Maintenance Organization (HMO) Plans, most of the claims work is done between your doctor and the HMO and consists of authorizing treatment before it is given, not in paying the bill after the treatment is received. Learn about your medical condition. Know what alternatives to treatment are available. However, even those plans usually have out-of-pocket limits so you should track all of your co-payments and other out-of-pocket costs.

You need to spend some time with your doctor (or your doctor’s insurance clerk) to understand when and what has to be pre-authorized by the HMO. How successful are they in obtaining approvals? How often are they denied? Can you be notified of denials and participate in appeals?

Health insurance is not maintenance free. It can’t be just “turned on and forgotten.” Just as you must take an active role in your health care and treatment as a patient, you must also stay alert and active as an insured individual with respect to how your medical care is authorized and paid for.

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