Editorials

Flexible Sigmoidoscopy: The Unkept Promise of Cancer Prevention

WM. MACMILLAN RODNEY, M.D.
Memphis, Tennessee

The authors of the article on flexible sigmoidoscopy in this issue of American Family Physician¹ have crafted an excellent review of what many had hoped would become a diagnostic tool frequently used by generalist physicians. Gastrointestinal symptoms and colorectal cancer screening are well known in family practice, and the benefits of endoscopic examination are proved. However, too few family physicians are screening their patients.

See Article in this issue.

When introduced in the early 1980's, flexible sigmoidoscopy was going to be the catalyst leading to widespread compliance with screening recommendations for the prevention of colorectal cancer.^2-4 One published study⁵ revealed a large initial change in physician behavior. However, more recently, another round of data described widespread underuse of flexible sigmoidoscopy among family physicians.^6-9 I estimate that only one half of the 65,000 family physicians in this country maintain their diagnostic and therapeutic procedural skills in flexible sigmoidoscopy.

One reason for this low rate is that a substantial percentage of residents do not receive adequate training in this procedure. Claims of compliance with high rates of technical procedures at residency programs continue to suffer from selection bias, reporting bias and a lack of competency-based testing.^10,11

Among physicians who maintain their skills, doing so is a labor of love.^12,13 Increasingly, financial disincentives have discouraged physicians from regularly performing sigmoidoscopies in their offices. Several of my graduates have announced that they will be seeking jobs where procedures are automatically referred to subspecialists. Reimbursement for office-based flexible sigmoidoscopy is frequently in the range of $100 to $200. The family physician also has to purchase his or her own equipment, maintain staff, and understand disinfection/cleaning procedures. These additional costs and responsibilities cause some family physicians to give up flexible sigmoidoscopy and refer.

What about colonoscopy? Reimbursement for this procedure is much higher. The average Medicare reimbursement in Tennessee for colonoscopy is $300, compared with only $85 for flexible sigmoidoscopy. In addition, the hospital receives another $350 to $500 as a facility fee in supporting colonoscopy. If the patient has private insurance, the total reimbursement is over $700 for the physician and over $700 for the hospital.

Unfortunately, family physicians are even less likely to perform colonoscopy than flexible sigmoidoscopy. The higher reimbursement rates have provided an incentive for gastroenterologists to maintain an aggressive campaign for control of colonoscopy and endoscopy procedures. Besides, patients who undergo colonoscopy require sedation/analgesia.^14,15 Some physicians are uncomfortable with parenteral administration of these drugs, and, in fact, some states restrictively regulate intravenous dosing by primary care physicians.

It is a shame that flexible sigmoidoscopy and colonoscopy are not performed more frequently by family physicians. The importance of office-based screening by flexible sigmoidoscopy and fecal occult blood testing is well established. Colonoscopy is an even better screening tool: it offers greater sensitivity and therapeutic options and appears to be preferred by patients in many cases. Yet, patients are not getting the screening they need: one study¹⁶ showed that less than 9 percent of patients over the age of 50 years had flexible sigmoidoscopy in the past few years, and that less than 20 percent have received fecal occult blood testing, a much less invasive test.

In my opinion, the best hope for improved screening is to reinforce the physician-patient relationship.¹⁷ Restrictive regulations create rationing through inconvenience. Lack of training further demoralizes physicians. Both impede effectiveness of any cancer prevention program. The bond between physician and patient is the key to patient cooperation with any cancer screening procedures that are unpleasant or inconvenient. Meanwhile, we must increase family physician interest in doing flexible sigmoidoscopy. Legislators need to realize that regulations have gutted incentives for primary care physicians. Also, we must make every effort to support family physicians who wish to perform colorectal cancer screening procedures. And, just as important, our training programs must provide opportunities to improve proficiency in flexible sigmoidoscopy and colonoscopy.

Dr. Rodney is managing partner of Advanced Family Medicine Specialists in Memphis, Tenn., and editor of the Procedural Skills and Office Technology Bulletin.

Address correspondence to Wm. MacMillan Rodney, M.D., 6575 Black Thorne Cove, Memphis, TN 38119.

REFERENCES

1. Johnson BA. Flexible sigmoidoscopy: screening colorectal cancer. Am Fam Physician 1999;59:313-28.
2. Rodney WM, Felmar E. Why flexible sigmoidoscopy instead of rigid sigmoidoscopy? J Fam Pract 1984; 19:471-6.
3. Rodney WM, Ounanian LL, Werblun MN. Second-generation videosigmoidoscopy. Am Fam Physician 1985;31:127-32.
4. Rodney WM, Felmar E, Auslander M. AAFP-ASGE Conjoint course on flexible sigmoidoscopy. Fam Pract Res J 1986;5:209-15.
5. Rodney WM, Beamer RJ, Johnson RA, Quan M. Physician compliance with colorectal cancer screening (1978-1983): the impact of flexible sigmoidoscopy. J Fam Pract 1985;20:265-9.
6. Deitrich AJ, Tobin JN, Sox CH, Cassels AN, Negron F, Young RG, et al. Cancer early-detection services in community health centers for the underserved: a randomized controlled trial. Arch Fam Med 1998:7:320-7.
7. Williams RB, Boles M, Johnson RE. A patient-initiated system for preventive health care. Arch Fam Med 1998;7:338-45.
8. Ruffin MT. Can we change physicians' practices in the delivery of cancer-preventive services? Arch Fam Med 1998;7:317-9.
9. Keim DB. The level of preventive health care in an internal medicine residency clinic: still only an ounce of prevention? Southern Med J 1998;91:550-4.
10. Rodney WM. Will virtual reality simulators put an end to the credentialing arms race in GI endoscopy or an end to the need for family physician faculty with endoscopic skills. J Am Board Family Pract 1999 (in press).
11. Susman J, Rodney WM. Numbers, procedural skills and science: Do the three mix? Am Fam Physician 1994;49:1591-2.
12. Pfenninger JL. Colposcopy, LEEP, and other procedures. Fam Medicine 1996;28:505-7.
13. Rodney WM. Foreword. In: Pfenninger JL, Fowler GC, eds. Procedures for primary care physician. Mosby, St. Louis, 1994:xiii-xiv.
14. Rex DK, Erickson RL, Rodney WM. Who should do colonoscopy? Fam Pract Res J 1994;14: 109-13.
15. Rex DK. Colonoscopy by family practitioners. Gastrointest Endosc 1994;40:383-4.
16. Early DS, Fletcher R, Rodney WM. What to do now to screen for colorectal cancer. Patient Care 1998;32:206-20.
17. Rodney WM. Keeping family practice whole. Fam Pract Management 1995;2:11-2.

Hepatitis C: Who Should We Be Treating?

JEFFREY T. KIRCHNER, D.O.
Lancaster General Hospital
Lancaster, Pennsylvania

The hepatitis C virus (HCV) was first identified by molecular cloning in 1988. It was subsequently determined that this agent caused the majority of cases of transfusion-related hepatitis (formerly known as non-A, non-B hepatitis). Identification of the virus spawned the development of several diagnostic tests leading to the currently available enzyme-linked immunosorbent assay (ELISA), a confirmatory radioimmunoblot assay and, most recently, qualitative and quantitative assays that can identify specific HCV RNA. Mass screening of blood donors as well as at-risk individuals has identified approximately 4 million persons in the United States who are infected with HCV.¹

See Article in this issue.

Population-based studies have found that about 40 percent of patients with chronic liver disease are infected with HCV, resulting in 8,000 to 10,000 deaths per year.¹ Moreover, HCV-related liver disease is the leading reason for liver transplantation in this country. Data such as these led the National Institutes of Health (NIH) to publish a consensus statement on HCV in 1997 and, most recently, the Centers for Disease Control and Prevention (CDC) to issue updated guidelines for the prevention and control of HCV.^1,2 Part 2 of an overview of the guidelines is presented by Moyer and colleagues in this issue. Part 2 covers prevention counseling and treatment.³ Part 1, which covers serologic testing and diagnosis, is in the January 1, 1999, issue of AFP.⁴

The fact that 4 million Americans are infected with HCV indicates a major public health problem. However, beyond this absolute number, the clinical significance of the epidemiologic data is less certain. Although it is believed that chronic infection will develop in about 85 percent of persons infected with HCV, many of these individuals will have a latent period lasting 20 to 30 years before any serious sequelae of liver disease develop.⁵ Among persons who have persistent infection, chronic active hepatitis may develop in 25 to 50 percent, cirrhosis may develop in 8 to 40 percent, and hepatocellular carcinoma may develop in 1 to 4 percent.²

The difficulty for clinicians is identifying patients whose HCV infection will progress to more severe liver disease. Unfortunately, no clinical features, risk factors or laboratory parameters (including alanine aminotransferase [ALT] levels and HCV RNA levels) are known to help identify the subset of patients at risk for progressive disease. This paucity of current clinical information, especially as it relates to the natural history of HCV, makes it difficult for physicians and patients to decide what to do when a test result for HCV is found to be positive.

For patients between the ages of 18 and 60 years, current guidelines advocate further medical evaluation, including a liver biopsy.² If the histopathologic findings reveal portal or bridging fibrosis with inflammatory changes, a 12-month course of injected interferon given three times weekly is an option. However, interferon therapy has shown only about a 20 percent overall response rate.⁶ In most trials, a "response" is usually defined only by normalization of ALT levels, sometimes a negative HIV RNA quantitative assay at one year after therapy and, rarely, by histopathology. Interferon therapy is additionally fraught with significant side effects, including fatigue, depression, thyroid dysfunction, anemia and thrombocytopenia.^2,5 A one-year course of interferon costs about $5,000.

Unfortunately, many patients infected with HCV also have problems with substance abuse, co-infection with human immunodeficiency virus (HIV), and a history of depression--making them either poor candidates or noncandidates for the currently available therapies. In my own practice, approximately 40 percent of HIV-infected patients are HCV-positive and, for the reasons mentioned, the majority are not good candidates for interferon therapy.

Interestingly, HCV infection is similar to HIV infection and may be a cofactor for its transmission.⁵ This certainly appears to be the case among HIV-infected women, who vertically transmit HCV to their newborns at a rate three times higher than noninfected mothers.⁷ While tremendous progress has been made in the past three years in the development of more than a dozen highly effective antiviral medications to treat HIV infection, we still have only interferon and the recently approved nucleoside analog ribavirin to treat patients infected with HCV. The similarity to HIV may go even further, because it may not be possible to eradicate these RNA viruses from their human hosts.⁸ Thus, the available therapies of interferon and ribavirin may be even less effective than the currently reported 20 to 50 percent short-term success rates.^2,5

Despite published guidelines and the growing use of interferon outside of clinical trials, the critical question in 1999 is which patients should be referred for liver biopsy and possible treatment? Despite the large number of published studies that have looked at the treatment of HCV infection with interferon as well as other experimental therapies, no long-term prospective data are available that show interferon actually prevents the development of end-stage liver disease.⁹ Better data should be available in five to 10 years, but for now we really do not know if treating the majority of patients with HCV will have any effect on morbidity or mortality from cirrhosis or hepatocellular cancer.^6,9

I believe if one identifies a patient with HCV infection who could be a treatment candidate based on the NIH or CDC guidelines, it is the obligation of the testing physician, or perhaps a consulting physician, to appropriately explain the course of therapy. One must discuss the significant commitment on the part of the patient to the medication. The patient should be informed that interferon therapy may be life-altering, depending on side effects, and that even under ideal circumstances the drug(s) may not work in at least 50 percent and perhaps even 80 percent of patients. If the patient is willing to proceed and has no contraindications to interferon, performing a liver biopsy to define the degree of hepatic disease is appropriate. If a patient elects not to be treated, periodic follow-up with monitoring of hepatic function every six to 12 months is acceptable.

Until we have better long-term data on both treated and untreated patients, the hepatitis C epidemic will continue to be an uncertainty for family physicians, as well as other physicians dealing with this disease. Hopefully, ongoing research will result in the development of oral antiviral therapies such as HCV-specific protease inhibitors that will be easy to administer and be better tolerated by patients. Returning to the model of HIV treatment, combination antiviral therapy may be needed for better management of HCV infections.

The current CDC recommendations regarding counseling and screening for HCV infection are quite sound and are based on the best available data. The family physician can play a key role by identifying patients infected with HCV and advising them to avoid hepatotoxic substances, especially alcohol, which definitely will worsen their prognosis.¹⁰ Vaccination against hepatitis A and, if appropriate, hepatitis B, should be offered. Close monitoring of hepatic transaminase levels may be prudent for patients receiving hepatically metabolized medications, such as 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, or hypoglycemic agents, such as metformin or troglitazone.

Risk reduction in regard to transmission of HCV is another key role for the family physician. Beyond these interventions, many patients currently found to be HCV-antibody positive may be best served by watchful waiting. The recommendations may change when we have more effective therapies and more data are available on the natural history of HCV infections.

Dr. Kirchner is associate director of the Family Practice Residency Program at Lancaster General Hospital. He also serves as director of the HIV clinic at the hospital. He is an associate editor of American Family Physician.

Address correspondence to Jeffrey Kirchner, D.O., 585 North School Lane, Lancaster, PA 17603.

REFERENCES

1. Centers for Disease Control and Prevention. Recommendations for prevention and control of hepatitis C virus (HCV) infection and HCV-related chronic disease. MMWR 1998;47(RR-19):1-39.
2. Management of hepatitis C. NIH Consens Statement 1997; March 24-26;15(3):1-41.
3. Moyer LA, Mast EE, Alter MJ. Hepatitis C: Part II. Prevention counseling and medical evaluation. Am Fam Physician 1999;59:349-57.
4. Moyer LA, Mast EE, Alter MJ. Hepatitis C: Part I. Routine serologic testing and diagnosis. Am Fam Physician 1999;59:79-92.
5. Gross JB Jr. Clinician's guide to hepatitis C. Mayo Clin Proc 1998;73:355-61.
6. Levine RA. Treating histologically mild chronic hepatitis C: monotherapy, combination therapy, or tincture of time? Ann Intern Med 1998;129:323-6.
7. Hunt CM, Carson KL, Sharara AI. Hepatitis C in pregnancy. Obstet Gynecol 1997;89(5 Pt 2):883-90.
8. Weiland O. Can HCV infection be cleared? Lancet 1998;352:669-70.
9. Koretz RL. Interferon in wonderland. Gastroenterology 1998;115:1027-9.
10. Wiley TE, McCarthy M, Breidi L, et al. Impact of alcohol on histologic and clinical progression of hepatitis C infection. Hepatology 1998;28:805-9.

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